You are on page 1of 318

ARMY, MARINE CORPS, NAVY, AIR FORCE

POTENTIAL MILITARY CHEMICAL/BIOLOGICAL AGENTS AND COMPOUNDS
FM 3-11.9 MCRP 3-37.1B NTRP 3-11.32 AFTTP(I) 3-2.55

JANUARY 2005

DISTRIBUTION RESTRICTION: Approved for public release; distribution is unlimited.

MULTISERVICE TACTICS, TECHNIQUES, AND PROCEDURES

FOREWORD
This publication has been prepared under our direction for use by our respective commands and other commands as appropriate.

STANLEY H. LILLIE Brigadier General, USA Commandant US Army Chemical School

EDWARD HANLON, JR. Lieutenant General, USMC Deputy Commandant for Combat Development

JOHN M. KELLY Rear Admiral, USN Commander Navy Warfare Development Command

BENTLEY B. RAYBURN Major General, USAF Commander Headquarters Air Force Doctrine Center

This publication is available at Army Knowledge Online <www.us.army.mil>.

PREFACE

1. Scope
This document provides commanders and staffs with general information and technical data concerning chemical/biological (CB) agents and other compounds of military interest such as toxic industrial chemicals (TIC). It explains the use; classification; and physical, chemical, and physiological properties of these agents and compounds. Users of this manual are nuclear, biological, and chemical (NBC)/chemical, biological, and radiological (CBR) staff officers, NBC noncommissioned officers (NCOs), staff weather officers (SWOs), NBC medical defense officers, medical readiness officers, medical intelligence officers, field medical treatment officers, and others involved in planning battlefield operations in an NBC environment.

2. Purpose
This publication provides a technical reference for CB agents and related compounds. The technical information furnished provides data that can be used to support operational assessments based on intelligence preparation of the battlespace (IPB).

3. Application
The audience for this publication is NBC/CBR staff personnel and commanders tasked with planning, preparing for, and conducting military operations.

4. Implementation Plan
Participating service command offices of primary responsibility (OPRs) will review this publication, validate the information, and reference and incorporate it in service and command manuals, regulations, and curricula as follows:

Army. The United States Army (USA) will incorporate this publication in USA training and doctrinal publications as directed by the Commander, United States Army Training and Doctrine Command (TRADOC). Distribution is in accordance with Department of the Army (DA) Form 12-99-R (Initial Distribution Requirements for Publications). Marine Corps. The United States Marine Corps (USMC) will incorporate the procedures in this publication in USMC training and doctrinal publications as directed by the Commanding General (CG), United States Marine Corps Combat

i

Development Command (MCCDC). Distribution is in accordance with Marine Corps Publication Distribution System (MCPDS).

Navy. The United States Navy (USN) will incorporate these procedures in
USN training and doctrinal publications as directed by the Commander, Navy Warfare Development Command (NWDC). Distribution is according to the military standard requisitioning and issue procedures (MILSTRIP).

Air Force. The United States Air Force (USAF) will validate and
incorporate appropriate procedures according to applicable governing directives.

5. User Information
a. The United States Army Chemical School (USACMLS) developed this publication with the joint participation of the approving service commands. b. We encourage recommended changes for improving this publication. Please reference the specific page and paragraph, and provide a rationale for each recommendation. Send comments and recommendations directly to—

ii

Army
Commandant US Army Chemical School ATTN: ATSN-CM-DD 401 MANSCEN Loop, Suite 1029 Fort Leonard Wood, MO 65473-8926 COMM (573) 596-0131, extension 3-7364

Marine Corps
Commanding General US Marine Corps Combat Development Command ATTN: C42 (Director) 3300 Russell Road Quantico, VA 22134-5001 DSN 278-6234; COMM (703) 784-6234

Navy
Commander Navy Warfare Development Command ATTN: N5 686 Cushing Road Newport, RI 02841-1207 DSN 948-4201; COMM (401) 841-4201

Air Force
HQ Air Force Doctrine Center ATTN: DJ 155 North Twining Street Maxwell AFB, AL 36112-6112 DSN 493-7224; COMM (334) 953-7224

iii

*FM 3-11.9 MCRP 3-37.1B NTRP 3-11.32 AFTTP(I) 3-2.55

FM 3-11.9

US Army Training and Doctrine Command Fort Monroe, Virginia Marine Corps Combat Development Command Quantico, Virginia Naval Warfare Development Command Newport, Rhode Island Headquarters Air Force Doctrine Center Maxwell Air Force Base, Alabama 10 January 2005

MCRP 3-37.1B

NTRP 3-11.32

AFTTP(I) 3-2.55

POTENTIAL MILITARY CHEMICAL/BIOLOGICAL AGENTS AND COMPOUNDS

TABLE OF CONTENTS
Page EXECUTIVE SUMMARY ........................................................................................................... xiii CHAPTER I INTRODUCTION Background................................................................................................I-1 Threat ........................................................................................................I-2 Militarily Significant Aspects of Toxic Chemical Agents........................I-4 Militarily Significant Aspects of Biological Agents .................................I-7 Militarily Significant Aspects of Toxic Industrial Chemicals...............I-11 CHAPTER II CHEMICAL WARFARE AGENTS AND THEIR PROPERTIES Background...............................................................................................II-1 Definitions of Selected Physical and Chemical Properties ....................II-1 Definitions of Toxicity-Related Terms ....................................................II-4 DISTRIBUTION RESTRICTION: Approved for public release; distribution is unlimited. *This publication supersedes FM 3-9, 12 December 1990.

iv

........................................................................... IV-4 Rickettsiae of Potential Concern ..................................... Obscurants...... IV-1 Bacterial Agents of Potential Concern...........................................................................III-1 Respiratory Irritants.............................. D-1 CHEMICAL WARFARE AGENT PRECURSOR CHEMICALS: USES AND EQUIVALENTS ............................III-1 Riot Control Agents (Tear-Producing Compounds).............................. IV-14 Toxins of Potential Concern........................................................................................................II-64 Chemical Warfare Agent Precursors .................................................................................................................. IV-11 Viral Agents of Potential Concern............................................................... B-1 PERIODIC TABLE OF THE ELEMENTS.............................II-76 CHAPTER III MILITARY CHEMICAL COMPOUNDS AND THEIR PROPERTIES Background................. AND 3 CHEMICALS ...................................III-7 Obsolete Riot Control Agents .................................................................................................................................... G-1 TOXICITY PROFILE ESTIMATES ..................................................... E-1 CHEMICAL WARFARE AGENTS AND OTHER MILITARY CHEMICAL COMPOUNDS .......................Choking Agents .................. V-4 APPENDIX A APPENDIX B APPENDIX C APPENDIX D APPENDIX E APPENDIX F APPENDIX G APPENDIX H TABLE OF EQUIVALENTS ....................................................................................................II-13 Blood Agents..........................................................................................II-31 Blister Agents (Vesicants) ................. H-1 v ........................................................................................II-68 Other Chemical Warfare Agents .................................................................................................... 2................................................................................................ V-1 Other Information Sources ............II-9 Nerve Agents .III-16 CHAPTER IV BIOLOGICAL AGENTS AND THEIR PROPERTIES Background................................................ and Incendiaries.......................................................................................................................................II-37 Incapacitating Agents .................................. V-2 Reach-Back Capability.................. A-1 TEMPERATURE CONVERSIONS............................. C-1 CHEMICAL WEAPONS CONVENTION SCHEDULE 1.......................F-1 PROPERTIES OF CHEMICAL WARFARE AGENTS AND MILITARY CHEMICAL COMPOUNDS ..................III-14 Smokes.............................................................. IV-22 CHAPTER V TOXIC INDUSTRIAL CHEMICALS AND THEIR PROPERTIES Background.........................................................................................................................................................................................

.. G-24 Vapor Pressure of Respiratory Irritants .......................L-1 Inhalation or Aerosol Route of Entry .................. H-1 Blood Agents............................................................... K-1 Bacterial Diseases.......................................... H-32 APPENDIX I APPENDIX J PROPERTIES OF SELECTED BIOLOGICAL AGENTS....................................................II-7 Ct Profile for Dosage versus Exposure Duration........................................................................................................................................... G-23 Vapor Pressure of Riot Control Agents (Capsaicin) ............................. G-19 Vapor Pressure of Nerve Agents................................................................................................................................................................... K-5 APPENDIX L DISSEMINATION OF BIOLOGICAL AGENTS..................................................................................................................................................................................................................................................................................................................L-1 Background........... K-1 Fungal Diseases ....................................................II-8 Vapor Pressure of Choking Agents...................... H-3 vi ....... K-1 Background.......................................... G-20 Vapor Pressure of Blood Agents ......................................................Background............................................................................................. G-21 Vapor Pressure of Blister Agents ......................................................................J-1 Animal Diseases................... Glossary-1 INDEX...................................................................L-4 Covert Dissemination .................. H-1 Choking Agents .............. Index-1 FIGURES II-1 II-2 G-1 G-2 G-3 G-4 G-5 G-6 G-7 H-1 The TLE Effect on the Ct Profile .....................................................................................J-1 Background.................................................................................................................................................................................................................................................................................................................................................. G-25 GA Vapor: Dosage versus Exposure Duration ...........L-3 Oral Route of Entry...................J-1 APPENDIX K SELECTED PLANT PATHOGENS...............................L-1 Percutaneous Route of Entry.............................................................I-1 SELECTED ANIMAL PATHOGENS................................................................................................... H-17 Respiratory Irritants....... H-16 Blister Agents..........L-4 REFERENCES ........................... References-1 GLOSSARY .................................................. G-22 Vapor Pressure of Incapacitating Agents (BZ) ...................................................................................... K-2 Viral Diseases.............................................. H-1 Nerve Agents ........................................................................................................

..............................................................................................................................................II-11 DP.................II-13 GA.......................................................................H-2 H-3 H-4 H-5 H-6 H-7 H-8 H-9 H-10 H-11 H-12 TABLES II-1 II-2 II-3 II-4 II-5 II-6 II-7 II-8 II-9 II-10 II-11 II-12 II-13 II-14 II-15 II-16 II-17 II-18 GA Vapor: Concentration versus Exposure Duration................................................II-20 GD .................II-29 Vx .........................II-30 Vx Toxicity Estimates ........................................................................................................................... H-19 List of Selected CW Agents and Precursors.............................................................II-10 CG Toxicity Estimates ............. H-7 GD Vapor: Dosage versus Exposure Duration....................................................... H-15 VX Vapor: Concentration versus Exposure Duration................................................................................................................................................................... H-13 VX Vapor: Dosage versus Exposure Duration ............................................................... H-6 GB Vapor: Concentration versus Exposure Duration..................................II-24 GF Toxicity Estimates........................................ H-9 GD Vapor: Concentration versus Exposure Duration....................................................................................................................................................................II-23 GF.......................................II-17 GB..........................................I-1 CG.........................II-31 AC...............................II-12 DP Toxicity Estimates................................................................................................. H-10 GF Vapor: Dosage versus Exposure Duration .II-18 GB Toxicity Estimates ..................................................................................................................................................... H-19 HD Vapor: Concentration Versus Exposure Duration............................................................................................................................................................................... H-4 GB Vapor: Dosage versus Exposure Duration ..........II-14 GA Toxicity Estimates ..................................................................................................... H-12 GF Vapor: Concentration versus Exposure Duration.....................................................II-32 vii ...................................................II-21 GD Toxicity Estimates ..............II-26 VX...................................................................................... H-16 HD Vapor: Dosage versus Exposure Duration............................II-27 VX Toxicity Estimates.....................

.....................................................................................................II-65 BZ Toxicity Estimates .....................................II-43 HN-2 Toxicity Estimates..................................II-60 MD Toxicity Estimates.................................................................II-56 PD..............................II-33 CK...................II-54 HL Toxicity Estimates ...........................................................................................................................................................................................II-38 HD Toxicity Estimates ..................II-41 HN-1 Toxicity Estimates........................................II-48 HT Toxicity Estimates ...II-36 SA Toxicity Estimates ....II-35 SA ....................................................................................................................................................................................II-43 HN-2....II-59 ED Toxicity Estimates .II-50 L Toxicity Estimates ......................................II-19 II-20 II-21 II-22 II-23 II-24 II-25 II-26 II-27 II-28 II-29 II-30 II-31 II-32 II-33 II-34 II-35 II-36 II-37 II-38 II-39 II-40 II-41 II-42 II-43 II-44 II-45 II-46 II-47 II-48 II-49 II-50 II-51 AC Toxicity Estimates.............................................................................................................................II-48 HT.....II-71 viii .....................II-69 DF Toxicity Estimates............................................II-68 DF...............II-62 CX...............II-58 ED.............................................................................................................................................II-66 Correlation of Symptoms and Incapacitating Agent Family ...................II-63 CX Toxicity Estimates...........................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................II-53 HL.................................................................II-40 HN-1.........................................................................................................................................................................................................................................II-57 PD Toxicity Estimates.......................II-70 QL........................II-60 MD.........................II-37 HD ....II-46 HN-3 Toxicity Estimates..............II-34 CK Toxicity Estimates ............................................................................................................II-50 L..............II-64 BZ ..........................................................................................II-45 HN-3....

.II-73 NE ............. V-2 Table of Equivalents.................................................................................................................................III-13 Cl2 ......................................................III-13 Cl2 Toxicity Estimates....................................................................... IV-3 Accidents Involving Hazardous Substances ............................................................................. A-1 ix .....................................III-17 WP ...........III-19 Synthetic Graphite ...................................................................................................................................................................................................................................................III-12 DC Toxicity Estimates ..............................II-74 NE Toxicity Estimates .................................................................................................. IV-2 Animal and Plant Pathogens with Potential BW Applications ............................................................................................................III-21 List of Potential BW Agents ..........................................................................................................................................................III-15 ZnCl2.......................................................................................................II-76 Other CW Agents ...........II-72 OPA .....................................................III-5 OC Toxicity Estimates .....................II-52 II-53 II-54 II-55 II-56 II-57 II-58 II-59 III-1 III-2 III-3 III-4 III-5 III-6 III-7 III-8 III-9 III-10 III-11 III-12 III-13 III-14 III-15 III-16 III-17 III-18 III-19 III-20 III-21 IV-1 IV-2 V-1 A-1 QL Toxicity Estimates....................................III-18 TiO2 .................................................................................................................................................................................................................................................................................................II-76 List of Selected Military Chemical Compounds....................................III-2 CS Toxicity Estimates .......................................II-72 OPA Toxicity Estimates ....................................................III-20 SGF-2 ..........III-3 CR..........................................................III-1 CS ......III-4 CR Toxicity Estimates................................................................................................................................................................................................................III-7 DM...III-11 DC.................................III-5 OC......................................III-7 DM Toxicity Estimates..III-14 CN ..............II-75 NM Toxicity Estimates ...............................................................................................................................................................................................................................................III-9 DA.........................III-10 DA Toxicity Estimates .........................................II-75 NM (Containing Elemental Sulfur) .....

. H-4 GB Profile Estimates (Lethal Dose.............. H-3 GB Profile Estimates (Lethal Dose.. and Blood Agents ............................. D-2 CWC Schedule 3 Chemicals..... D-3 CW Agent Precursor Chemicals: Uses and Equivalents ................ G-12 Toxicity Estimates for CW Agents ...............................................A-2 B-1 C-1 C-2 D-1 D-2 D-3 E-1 F-1 G-1 G-2 G-3 G-4 G-5 G-6 H-1 H-2 H-3 H-4 H-5 H-6 H-7 H-8 H-9 H-10 H-11 H-12 H-13 H-14 H-15 Table of Commonly Used Prefixes... E-1 Symbols for CW Agents and Military Chemical Compounds .................... Percutaneous) .......................... H-2 GA Profile Estimates (Threshold Effects.... A-1 Temperature Conversions............... G-18 Persistency of Selected CW Agents . H-6 GB Profile Estimates (Mild Effects.......................... H-6 GD Profile Estimates (Lethal Dose..... C-2 CWC Schedule 1 Chemicals.............................................................................. Inhalation/Ocular). H-5 GB Profile Estimates (Threshold Effects................ G-7 Physical Properties of RCAs and Respiratory Irritants . H-2 GA Profile Estimates (Severe Effects....................................................... H-1 GA Profile Estimates (Lethal Dose...............................F-1 Physical Properties of Choking............................................................. G-18 CG Profile Estimates (Lethal Dose.......... Nerve............ H-1 GA Profile Estimates (Lethal Dose.......................... Inhalation/Ocular)......... H-5 GB Profile Estimates (Severe Effects......... Inhalation/Ocular) ......... Percutaneous) .......... D-1 CWC Schedule 2 Chemicals....................... Inhalation/Ocular) ........................................... H-3 GA Profile Estimates (Mild Effects. G-2 Physical Properties of Blister and Incapacitating Agents ...................... H-1 DP Profile Estimates (Lethal Dose....... Inhalation/Ocular) ........................................................... G-17 Toxicity Estimates (Exposure Duration) for Military Chemical Compounds................................................. Inhalation/Ocular)...... H-5 GB Profile Estimates (Severe Effects..................... H-7 x ........ B-1 Periodic Table of the Elements . Inhalation/Ocular) ...... Percutaneous) .... C-1 Chemical Elements and Symbols ...... Percutaneous)............ H-2 GA Profile Estimates (Severe Effects... Inhalation/Ocular) ....................................................... Percutaneous) .............. Percutaneous)... Inhalation/Ocular) .........................................................................

. H-9 GD Profile Estimates (Mild Effects.... H-18 HD Profile Estimates (Mild Effects.. Percutaneous) . Inhalation/Ocular).. H-12 VX Profile Estimates (Lethal Dose. Percutaneous) .... H-17 HD Profile Estimates (Severe Effects.. Inhalation/Ocular) ....... Inhalation/Ocular)... Percutaneous) .. Percutaneous)........ H-16 HD Profile Estimates (Lethal Dose...... Percutaneous)............. Inhalation/Ocular)... Percutaneous). H-18 HD Profile Estimates (Mild Effects....... H-14 VX Profile Estimates (Threshold Effects...... Percutaneous) ....... H-17 HD Profile Estimates (Severe Effects... H-16 SA Profile Estimates (Lethal Dose. Percutaneous) ... H-11 GF Profile Estimates (Severe Effects......... H-20 HN-1 Profile Estimates (Severe Effects. Ocular) .... Percutaneous) . H-17 HD Profile Estimates (Lethal Dose.. Percutaneous). H-8 GD Profile Estimates (Threshold Effects...H-16 H-17 H-18 H-19 H-20 H-21 H-22 H-23 H-24 H-25 H-26 H-27 H-28 H-29 H-30 H-31 H-32 H-33 H-34 H-35 H-36 H-37 H-38 H-39 H-40 H-41 H-42 H-43 H-44 H-45 H-46 H-47 H-48 H-49 GD Profile Estimates (Lethal Dose.. H-8 GD Profile Estimates (Severe Effects.. Ocular).... H-13 VX Profile Estimates (Lethal Dose. Percutaneous) ..... Percutaneous) ............ H-8 GD Profile Estimates (Severe Effects......... H-22 xi ... H-9 GF Profile Estimates (Lethal Dose... H-21 HN-1 Profile Estimates (Mild Effects....................... Inhalation/Ocular).. H-14 VX Profile Estimates (Severe Effects.... Percutaneous) ............... Ocular) ............. Inhalation/Ocular).... H-22 HN-2 Profile Estimates (Severe Effects. H-18 HN-1 Profile Estimates (Lethal Dose. H-20 HN-1 Profile Estimates (Lethal Dose............ Inhalation/Ocular) . Inhalation/Ocular).. H-15 AC Profile Estimates (Lethal Dose... H-14 VX Profile Estimates (Severe Effects.... Inhalation/Ocular) ............. H-11 GF Profile Estimates (Mild Effects.... H-15 VX Profile Estimates (Mild Effects...... Inhalation/Ocular) ...... H-10 GF Profile Estimates (Lethal Dose........ H-10 GF Profile Estimates (Severe Effects... H-22 HN-2 Profile Estimates (Lethal Dose.............. Inhalation/Ocular) ................... Percutaneous) ....... H-21 HN-1 Profile Estimates (Mild Effects....... Percutaneous) ........ Percutaneous).. H-11 GF Profile Estimates (Threshold Effects........ Ocular) . Inhalation/Ocular)...... H-21 HN-2 Profile Estimates (Lethal Dose..... Inhalation/Ocular) .. H-20 HN-1 Profile Estimates (Severe Effects...... Percutaneous).

....... Ocular)....... Inhalation/Ocular) ..... H-26 HT Profile Estimates (Severe Effects..... Inhalation/Ocular).......... H-30 HL Profile Estimates (Lethal Dose.. Ocular).............. H-27 L Profile Estimates (Lethal Dose..... H-25 HN-3 Profile Estimates (Mild Effects..... Percutaneous).......... H-24 HN-3 Profile Estimates (Lethal Dose................... Percutaneous)... H-29 L Profile Estimates (Mild Effects........ Percutaneous)...................... H-27 HT Profile Estimates (Mild Effects.......... H-24 HN-3 Profile Estimates (Severe Effects........ H-28 L Profile Estimates (Severe Effects.... H-30 HL Profile Estimates (Severe Effects... H-31 PD Profile Estimates (Lethal Dose......... H-26 HT Profile Estimates (Severe Effects....... Ocular)....... H-28 L Profile Estimates (Lethal Dose.......................... Percutaneous) ......... H-24 HN-3 Profile Estimates (Severe Effects. Inhalation/Ocular) . H-31 HL Profile Estimates (Mild Effects... H-23 HN-2 Profile Estimates (Mild Effects...........I-2 xii ....... H-28 L Profile Estimates (Severe Effects.. H-29 HL Profile Estimates (Lethal Dose..... H-25 HT Profile Estimates (Lethal Dose................... Ocular) .. H-23 HN-2 Profile Estimates (Mild Effects... H-32 Properties of Selected Biological Agents ....... Ocular) ........ Percutaneous) ................H-50 H-51 H-52 H-53 H-54 H-55 H-56 H-57 H-58 H-59 H-60 H-61 H-62 H-63 H-64 H-65 H-66 H-67 H-68 H-69 H-70 H-71 H-72 H-73 H-74 H-75 H-76 H-77 H-78 H-79 I-1 HN-2 Profile Estimates (Severe Effects...... Ocular) .. H-26 HT Profile Estimates (Lethal Dose............. Percutaneous) ... Percutaneous) . Ocular) . H-32 CX Profile Estimates (Lethal Dose...... Ocular) . Percutaneous) .. H-32 DM Profile Estimates (Lethal Dose.......... Percutaneous) ....... H-27 HT Profile Estimates (Mild Effects. H-30 HL Profile Estimates (Severe Effects.................................. H-31 HL Profile Estimates (Mild Effects........... Inhalation/Ocular) ............ Percutaneous) ........ Percutaneous)....... Inhalation/Ocular)....... Percutaneous).................... Ocular)... Percutaneous) .... Ocular)........ H-29 L Profile Estimates (Mild Effects.... H-25 HN-3 Profile Estimates (Mild Effects. H-23 HN-3 Profile Estimates (Lethal Dose..... Inhalation/Ocular)... Inhalation/Ocular)..................

Chapter III Military Chemical Compounds and Their Properties Chapter III discusses military chemical compounds such as the riot control agents (RCAs). blood. xiii . and incapacitating agents. It discusses chemical agent physical characteristics and toxicity data of choking. Chapter V Toxic Industrial Chemicals and Their Properties Chapter V addresses TIC and a summary of available TIC information sources.EXECUTIVE SUMMARY Potential Military Chemical/Biological Agents and Compounds Chapter I Introduction Chapter I briefly addresses the threat and the significant military aspects of chemical and biological agents and TIC. Chapter IV Biological Agents and Their Properties Chapter IV addresses general characteristics of biological agents (including toxins) and provides a summary of selected antipersonnel agents that may be employed in weapons systems. nerve. blister. Chapter II Chemical Warfare Agents and Their Properties Chapter II provides information on chemical agents that might be encountered in the field. It provides physical and chemical characteristics and toxicity data for military chemical compounds.

FL 32403-5319 xiv .PROGRAM PARTICIPANTS The following commands and agencies participated in the development of this publication: Joint Joint Requirements Office. Suite 1029. 2200 Amphibious Drive. Suite 1309. RI 02841 United States Navy Surface Warfare Development Group. 155 North Twining Street. Fort Leonard Wood. Fort Leonard Wood. Sims Hall. Tyndall AFB. MO 65473 Army United States Army Chemical School. Suite 1. Norfolk. Newport. 3300 Russell Road. ATTN: DJ. Maxwell AFB. 139 Barnes Drive. AL 36112-6112 HQ Air Force Civil Engineer Support Agency. Aberdeen Proving Ground. VA 22134-5021 Navy United States Navy Warfare Development Command. MD 21040 Marine Corps United States Marine Corps Combat Development Command. Suite 318A. Quantico. 401 MANSCEN Loop. 401 MANSCEN Loop. 686 Cushing Road. VA 23521 Air Force HQ Air Force Doctrine Center. MO 65473 United States Army Edgewood Chemical and Biological Center.

To meet this challenge. or stockpiling of these weapons. identification. US Policy.” also known as the Geneva Protocol of 1925. Most parties interpret the protocol as a prohibition only of the first use of these agents in war.2 a. In many of the regions where the US is likely to deploy forces.3 Adversaries may employ CB agents and other toxic materials to achieve specific effects. and can have significant physiological effects. can be persistent or nonpersistent. production.3 This paragraph contains brief descriptions of treaty. (3) The means available to adversaries for delivery of CB weapons range from specially designed. (2) Biological agents can produce lethal or incapacitating effects over an extensive area and can reproduce. legal. In addition to the physical effects.1 Additionally. The protocol entered into force for the US on 10 April 1975. asymmetrical means. the US ratified the protocol subject to this reservation. It did not ban the development. both in the immediate target area and in other vulnerable areas that may be potential targets. Use of CB Weapons. potential adversaries may use CB weapons. US forces must be properly trained and equipped to operate effectively and decisively in the face of NBC attacks. (1) Chemical agents have effects that can be immediate or delayed. there exist psychological effects. While relatively large quantities of an agent are required to ensure an area remains contaminated over time. and of Bacteriological Methods of Warfare. The delayed onset of symptoms and detection. small-scale selective use that exploits surprise can cause significant disruption and may have lethal effects. Potential adversaries may seek to counter US conventional military superiority using less expensive and more attainable. subject to the reservation that the US would not be bound by the provisions with respect to an enemy state or its allies who fail to respect the prohibitions of the protocol. the US Senate gave advice and consent to ratification of this protocol. and policy strictures on chemical and biological warfare (CBW). US forces could be confronted in an environment where TIC present a hazard to US forces. and verification difficulties for biological agents can also confer important advantages to adversaries who decide to use biological agents. (1) The Protocol for the Prohibition of the Use in War of Asphyxiating. sophisticated weapon systems developed by nations to relatively inefficient improvised devices employed by terrorists and other disaffected individuals and groups. On 22 January 1975. Poisonous or Other Gases. prohibits chemical and bacteriological methods of warfare. Background The threat or use of CB weapons is a possible condition of future warfare and could occur in the early stages of war to disrupt United States (US) operations and logistics. In 1974.Chapter I INTRODUCTION 1. The relevance of the Geneva Protocol is largely superseded by the more I-1 . b.

transfer. CB industrial capabilities. (2) The Presidential Statement on Chemical and Biological Weapons. Stockpiling.4 In the next several years. production. Intelligence efforts include collection and analysis of nations’ dual-use. The US ratified the BWC on 29 March 1975. parties undertake not to develop. It provides for the destruction of all chemical weapons stocks within 10 years after entry into force. It contains a vigorous challenge regime to ensure compliance.4 Proliferation of CBW technology also raises several important issues. d. 25 November 1969. or use of chemical weapons. Proliferation: Threat and Response. 11850. stockpile. pathogens with biological warfare (BW) applications. Under the terms of the BWC. b. or acquire biological agents or toxins “of types and in quantities that have no justification for prophylactic. and development of the indications and warning of adversarial use of dual-use capabilities. Threat a. Challenges. and Use of Chemical Weapons and on their Destruction (also known as the Chemical Weapons Convention [CWC] and by the Convention on the Prohibition of Bacteriological and Toxic Weapons (also known as the Biological Weapons Convention [BWC]) summarized below. renounced first use of herbicides in war (except for specified defensive uses) and first use of RCAs in war except for defensive military modes to save lives. the threat from the proliferation of CBW may increase. including Australian group-controlled items to numerous countries of proliferation concern. (4) The CWC. Many of these are detailed in the January 2001 report published by the Office of the Secretary of Defense (OSD). stockpiling. the sophistication of CBW capabilities is increasing. Renunciation of Certain Uses in War of Chemical Herbicides and Riot Control Agents. renounced the US use of lethal biological agents and weapons and confined biological research to defensive measures such as immunization and safety. States with existing programs may master the production processes for complete weapons development and will be less dependent on outside suppliers. (3) Executive Order No. Various nations could export a wide array of chemical products. which entered into force on 29 April 1997. 2. The US ratified the CWC on 25 April 1997. Similarly. protective and other peaceful purposes. acquisition. Changes. I-2 . The BWC does not establish a specific verification regime.4 Countries with chemical weapons programs are adding agents and more sophisticated delivery systems.restrictive Convention on the Prohibition of the Development. precision navigation technology.” as well as weapons and means of delivery. and dual-use equipment that can be used in both CBW programs. Proliferation of weapons technology. Production. The US faces a number of regional proliferation challenges. bans the development. The controlled items include specific chemical agent precursors.5 c. and CBW technology in developing nations presents the US with a complicated national security challenge. Increases in Proliferation. This could result from the development of CB agents that are more difficult to detect and from the adoption of more capable delivery systems. Proliferation. 8 April 1975. produce. At least 25 countries now possess—or are in the process of acquiring and developing—capabilities to inflict mass casualties and destruction: NBC weapons or the means to deliver them.

virulence. infectious organisms can be modified to bring about disease in different ways. I-3 . Microorganisms resistant to antibiotics. An example of a recent new pathogen (though not necessarily ideal BW agents) includes streptococcus pneumonia S23F. but there is enormous potential—based on advances in modern molecular biology. standard vaccines. Historically. The BW agents may emerge in two likely categories: man-made manipulations of classic BW agents and newly discovered or emerging infectious diseases. when new genetic engineering techniques were introduced. nevertheless. Novel BW Agents. and drug delivery technology—for making more sophisticated weapons. and related scientific fields provide ever-increasing potential to control more of these factors. With today’s techniques. identification. however.1 Advances in biotechnology and genetic engineering may facilitate the development of potentially new and more deadly BW agents. (d) Immunologically altered microorganisms able to defeat standard identification. Genetically engineered microorganisms also raise the technological hurdle that must be overcome to provide for effective detection. and early warning of BW attacks. Such weapons might be capable of inflicting only limited numbers of casualties. (4) Numerous characteristics need to be controlled for a highly effective BW agent. e. (1) The potential types of novel biological agents that could be produced through genetic engineering methodologies are listed below. and diagnostic methods. possibly leading to an enhanced ability to use BW agents as battlefield weapons. (e) Combinations of the above four types with improved delivery systems. detection. (b) therapeutics. Each of these techniques seeks to capitalize on the extreme lethality. almost any nation or group could fabricate crude agent dispersal devices. or infectivity of BW agents and exploit this potential by developing methods to deliver more efficiently and to control these agents on the battlefield. Advances in biotechnology. possibly even rendering the modified agent ineffective as a weapon. a naturally occurring strain of pneumonia resistant to at least six of the more commonly used antibiotics. (c) Microorganisms with enhanced aerosol and environmental stability. (2) On the other hand. Efficient weaponization of these agents. they could have significant operational repercussions due to the psychological impact created by fears of CBW agent exposure. genetic engineering. fermentation. the accentuation of one characteristic often resulted in the attenuation of one or more other characteristics. venom. The ability to modify microbial agents at a molecular level has existed since the 1960s.(1) Any nation with the political will and a minimal industrial base could produce CBW agents suitable for use in warfare. does require design and production skills usually found in countries that possess a munitions development infrastructure or access to such skills from cooperative sources. but the enterprise tended to be slow and unpredictable. and Benign microorganisms genetically altered to produce a toxin. (a) or bioregulator. The current level of sophistication for many biological agents is low.4 (3) Genetic engineering gives BW developers the tools to pursue agents that could defeat the protective and treatment protocols of the prospective adversary.

7 Choking agents cause damage to the lungs. blister.7 Arsine (SA) is different. can cause death. It causes hemolysis of the red blood cells. 3. which transmits many nerve impulses. It is now possible to transform relatively benign organisms to cause harmful effects. Militarily Significant Aspects of Toxic Chemical Agents a. At sufficient doses. nerve. and respiratory and cardiovascular collapse resulting from AC and CK poisoning. or permanent harm to humans or animals. (1) CW Agents. Their physiological actions are as follows: (a) Choking Agents. the proximal cause of death is myocardial failure. This inhibition permits acetylcholine (ACh). I-4 . and incapacitating agents. Classification. blood. Hydrogen cyanide (AC) and cyanogen chloride (CK) are cellular poisons. In the case of SA poisoning. and pulmonary edema (“dry-land drowning”). (c) Blood Agents. (e) Many bioengineering companies (both US and foreign) now sell all-inone kits to enable researchers to perform recombinant deoxyribonucleic acid (DNA) experiments. perhaps to the point where classic BW agents will offer less utility as a means of causing casualties. chemical agents are further divided into chemical warfare (CW) agents and military chemical compounds. The terms “persistent” and “nonpersistent” describe the time chemical agents remain in an area and do not classify the agents technically.(2) The future likelihood of infectious agents being created for BW purposes will be influenced by technological trends such as— (a) Genetically engineered vectors in the form of modified infectious organisms may become increasingly available as medical tools and techniques become more widely available. irritation to the eyes and the respiratory tract. These agents include choking. through its chemical action on life processes. The availability of free online gene sequence databases and analytic software over the Internet further amplifies and disseminates this capability.7 The blood transports these agents to all body tissues.8 The central nervous system (CNS) is especially vulnerable to lack of oxygen regardless of the etiology. (b) Nerve Agents.7 The body’s muscles and glands become overstimulated due to excessive amounts of ACh. and they disrupt the oxidative processes used by the cells.6 For the purpose of this manual. to collect at its various sites of action. Nerve agents inhibit cholinesterase (ChE) enzymes. (b) Strides will be made in the understanding of infectious disease mechanisms and in microbial genetics that are responsible for disease processes. this can lead to an inability of the body to sustain breathing. temporary incapacitation. The CW agents are toxic chemicals and their precursors prohibited under the CWC. A toxic chemical agent is any chemical which. (c) An increased understanding of the human immune system function and disease mechanisms will shed light on the circumstances that cause individual susceptibility to infectious disease. (d) Vaccines and antidotes will be improved over the long term.

They can then be evaporated or desorbed (off-gas) from surfaces. At high concentrations they irritate the respiratory tract and the skin. or both. freezing point (FP). but the eyes and respiratory tract are more sensitive than the skin. Their primary action is irritation of the respiratory tract. Since missions vary. An incapacitating agent is an agent that produces temporary physiological or mental effects.7 (e) Incapacitating Agents. They sometimes cause nausea and vomiting. volatility. Medical treatment is not essential but can facilitate a more rapid recovery. Inhaled mustard damages mucous membranes and the respiratory tract. for the purpose of this manual.(d) Blister Agents (Vesicants). RCAs. These include. The term excludes CW agents. these agents cause lacrimation (tearing). and melting point (MP). and the physical and chemical properties of the agent. nausea. wind speed. leaving no residual injury.7 (2) Military Chemical Compounds.11 Chemical agents are usually disseminated in the field in the form of vapors (gases). vapor pressure (VP). Military chemical compounds are less toxic and include materials such as respiratory irritant agents. initially the cloud expands. causing a vapor hazard. relative humidity. The RCAs are chemicals that rapidly produce in humans sensory irritation or disabling physical effects which disappear within a short time following termination of exposure. causing intense pain and tearing. uncontrollable coughing.10 In addition. Duration of Effectiveness. and incendiary materials.11 Many weather factors and terrain conditions influence the duration of effectiveness of chemical agents. temperature gradient. These agents were previously called vomiting agents. (b) Respiratory Irritant Agents. in very low concentrations. Some of the important physical properties are vapor density. soil. act primarily on the eyes.7 b. and a general feeling of bodily discomfort. or liquids. Usually symptoms disappear in 20 minutes to 2 hours. which will render individuals incapable of concerted effort in the performance of their assigned duties. but are not limited to. Their physiological actions are as follows: (a) RCAs (Lacrimators). grows cooler and heavier. Several factors determine the time a chemical agent remains effective. (2) Weather and Terrain Conditions. sneezing. and tends to retain its form. and precipitation.6 They are local irritants that. irritation of the eyes. Vapor I-5 . and terrain contours. the method of dissemination. Liquid agents can be absorbed (soaked into) and adsorbed (adhered to) by surfaces. incapacitation means the inability to perform any military task effectively. weather and terrain conditions. Aerosols are finely divided liquid and/or solid substances suspended in the atmosphere and behave in much the same manner as vaporized agents. Blister agents are noted for producing reddening and blistering of the skin. Most important weather factors include temperature. (3) Physical Properties. aerosols. smoke and obscurants. Important terrain conditions include vegetation. incapacitation is understood to mean inability to perform one’s military mission. (1) Method of Dissemination. Eye exposure results in reddening of the eyes and temporary blindness or permanent effects.9 Used in a military context. When a chemical agent is disseminated as a vapor from a bursting munition.

14 (2) Schedule 2 chemicals (See Table D-2. Emphasis is placed on acute toxic effects. and Appendix C for the periodic table of elements.14 Chemicals covered under the CWC are divided into three categories as follows: (1) Schedule 1 chemicals (See Table D-1. There are. Vapor pressure is used to determine the volatility of an agent. Note that not all factors are applicable to all exposure scenarios. Additional toxicological data are required to determine if the toxicity estimates can be applied to women. 12. minute volume (MV). See Chapter II for definitions of selected physical properties. Acute toxic effects are those occurring within moments to a few days of the toxic exposure. dosage. These references define the medical surveillance program for personnel who support chemical demilitarization operations. f.000 or more chemicals subject to the CWC regulation—listing each chemical by name is not practical. See Appendix F for the symbols of CW agents and other military chemical compounds. The toxicity estimates provided are not applicable to the general population. they also have legitimate uses in other industrial areas. Dual-Use Precursors. groups of chemicals. See Appendix A for information on table of equivalents and commonly used prefixes. Dosages are given for a 70-kilogram (kg) male with an MV of 15 liters per minute (L/min). Potency and Physiological Actions. 25. (4) Chemical Properties. d.14 (3) Schedule 3 chemicals (See Table D-3. temperature. c. CW Agents and Other Military Chemical Compounds.14 e. They pose a high risk to the object and purpose of the CWC by virtue of their high potential for use in activities prohibited under the CWC.10. page D-3) have legitimate uses in industrial areas and pose a risk to the object and purpose of the CWC. and rate of action (ROA). Appendix B for information on temperature conversions. The examples given in Appendix D are not all-inclusive. Appendix D contains the list of toxic chemicals. The boiling and freezing points of chemical agents influence their operational use and the means of disseminating them. page D-1) have little or no use in industrial and agricultural industries. page D-2) may be useful in the production of chemical weapons. CWC Chemicals. thus determining whether the agent will settle to low areas or float away and dissipate in the atmosphere. exposure duration. however. by conservative estimates. MV is not applicable to a percutaneous liquid exposure. The volatility has an effect upon the vapor concentration. It also affects the duration of an agent hazard after dissemination. route of exposure (ROE). 13 NOTE: Occupational health guidelines for the evaluation and control of occupational exposure to nerve and blister agents is promulgated separately by the US Army Surgeon General in DA Pamphlets 40-8 and 40-173. Factors that contribute to the adverse human health effects of chemical agents include toxicity.density determines whether the agent is lighter or heavier than air. Precursors for CW agents also have civil uses in industrial and agricultural industries (see Appendix E). The chemical properties of an agent include its stability and reactivity with water and other substances. See Appendix G for a I-6 . For example. endpoint. physiological stressors. and precursors subject to the CWC. See Chapter II for definitions of selected chemical properties. They pose a significant risk to the object and purpose of the CWC. rate of detoxification (ROD).

Mixtures may lower the freezing point. There are no known therapies effective against prions. Biological agents can be disseminated and used against personnel. The addition of thickeners or thinners to agents will increase or decrease persistency: for example.6 Biological agents can be classified as pathogens. Pathogens are either naturally occurring or altered by random mutation or recombinant DNA techniques. mixing agents together will create special problems through their physiological effects. (1) Pathogens. the infected brain cells die and release prions into the tissue.15 (4) Prions. When prions enter brain cells. sea creatures. or prions. or viruses. III. 4. Militarily Significant Aspects of Biological Agents a. or material. Associated with the I-7 . immediate and delayed effects. increasing agent effectiveness over a wider temperature range. These problems can produce difficulty in identification. soman (GD) mixed with thickeners will increase persistency. Some mixtures would make it difficult to maintain the seal of the protective mask. g. plants. RCAs mixed with thinners will decrease persistency. animals.6 Toxins are produced by a variety of organisms.18 b.17 Transmission of the prions from cows to man is suspected to cause human illness.16 Proteins have a unique. Pathogens are disease-producing microorganisms. as distinguished from inorganic poisons. Mixing chemical agents with each other or with other materials can alter the characteristics and effectiveness of the agents. and Appendix H for detailed information on toxicity of CW agents and military chemical compounds. insects. A biological agent is a microorganism that causes disease in personnel. In addition to changing the physical properties. they apparently convert normal proteins into prions. snakes. or contact and vapor hazards occurring simultaneously. infect. Agent Mixtures. toxins. either by a synergistic effect or by an improved absorption through the skin. or animals or causes the deterioration of material. Mixing some agents can also increase the toxic effects. Food and industrial products can be rendered unsafe or unfit for use by contamination or by the effects resulting from contamination with biological agents. Uses. Toxins are poisons formed as a specific secreting product in the metabolism of a vegetable or animal organism. NOTE: See information in Chapters II. Prions are proteins that can cause neurodegenerative diseases in humans and animals. Prions entered the public’s consciousness during the mad cow epidemic that hit England in 1996. (2) Toxins. plants. Classification.consolidation of the information given in the chemical agent tables and toxicity tables in Chapters II and III. spiders.15 (3) Bioregulators. Normal cell proteins have the same amino acid building blocks but they fold differently than prions. These prions enter. rickettsiae. Although they can be found in the human body in small quantities. and destroy other brain cells. Ultimately. The US military forces are deployed throughout the world. Such poisons can also be manufactured by synthetic processes. and plants. Bioregulators include biochemical compounds that regulate cell processes and physiologically active compounds such as catalysts and enzymes. genetically defined amino acid sequence that determines their specific shapes and functions. including microbes. bioregulators.6 such as bacteria. introduction of large quantities can cause severe adverse effects or death.

vegetables. rubber products. and biological medicinal products such as adrenalin. insulin. wind speed.g. Some bacteria can use petroleum products as an energy source and cause residues that might clog fuel or oil lines. and temperature gradient are important weather factors in determining duration of effectiveness. I-8 . and dairy products. Biological antipersonnel agents are those that are effective directly against humans.3 (1) Biological agent characteristics such as encapsulation (natural. Some bacteria produce highly acidic compounds that cause pitting in metals. other food items. and antisera). Potential biological antipersonnel agents include toxins.. cortisone. Biological antianimal agents are those that could be employed against animals to incapacitate or destroy them through disease. or manmade protective coverings).) (1) Antipersonnel. The resistant spore might remain dormant for years without requiring nutrients or water and might survive under extreme ranges of temperature. trophies). The duration of effectiveness of a biological agent refers to the persistency of the agent in the environment. The United States Department of Agriculture (USDA). These agents may be used intentionally by an enemy to attack food or economically valuable crops.20 See Appendix K. relative humidity.20 c. equipment. Biological antiplant agents are organisms that cause disease or damage to plants. The bacterium (vegetative cell) makes a copy of its DNA. fats. The purposeful spreading of infectious agents that attack cattle or other domestic animals can lead to serious consequences for a country’s food supply or export of animal products (hides. It depends on the characteristics of the agent and environmental factors. mail. leather goods. pituitary extracts. Spore formation is not a method of reproduction inasmuch as each vegetative cell forms only a single spore and each spore germinates to form a single vegetative cell. Animal and Plant Health Inspection Service (APHIS) oversees the entry of cargo. (3) Antiplant. and their means of conveyance into the US. When conditions become favorable. dipicolinic acid (heat-resistant factor). fungi may damage fabrics. Antimaterial agents are organisms that degrade or break down some item of material. and toxins. thereby reducing a nation’s ability to resist aggression.movement of troops are risks of introduction of exotic agricultural pests and animal disease agents through soil contamination and transportation of regulated items such as fruits.19 (See Appendix I for selected properties of some biological agents. such as bacterial spores.20 See Appendix J. viruses. For example. (4) Antimaterial. wool. and animal products (e. bacteria. and protein layers. addition of dyes to the spray fluid.3 Bacteria that are resistant to environmental extremes frequently produce spores to allow survival during adverse conditions. or possibly genetic engineering (of pathogens) may protect some agents from sunlight and other destructive natural forces. The DNA becomes surrounded by a series of membranes that accumulate calcium. these agents could create potential problems with stockpiled material. Duration of Effectiveness. personal property. The threat would select these agents on the basis of the agents’ ability to cause death or disability.21 (2) Ultraviolet (UV) radiation. rickettsiae. (2) Antianimal. personnel. or foodstuffs. meat. vaccines. the spore develops into an actively growing vegetative cell.

23 Personnel can encounter biological agents by natural routes. staphylococcal enterotoxin B when ingested in food causes acute gastrointestinal (GI) illness. Human toxicity estimates are based on animal data.24 For example. This is particularly true of abraded (broken) surfaces and some toxins such as mycotoxins. liquid droplets (toxins only). Dried agents require an increased level of technological sophistication to produce. units of micrograms (µg) or even nanograms (ng) may be used instead of milligrams (mg) in expressing toxicity. which is a stationary device for aerosolization of the agent.25 The infectivity of an agent reflects the relative ease with which microorganisms establish themselves in a host species. and the ROE for the animals is not always what would be expected on the battlefield. The body is more resistant to invasion by microorganisms through the skin.3 The respiratory system is much more susceptible to penetration. See Appendix L for additional information on dissemination of biological agents.15 (a) Infective Dose. A modified point source would be a group of spray devices. it produces respiratory disease. botulinum. Most commonly.23 In a biological attack the respiratory route would be the primary route of entry. such as a stationary sprayer. delivery methods use aerosolized agents.23 Toxins absorbed through the respiratory tract can produce signs and symptoms different from those acquired through natural occurrence. Some pathogens produce toxins that can result in disease (for example. (2) Dosage. The important portals of entry are the respiratory tract. however. cholera. or dry powders. Hence. A line source would be released perpendicular to the direction of the wind. diphtheria. The BW agents are inherently more toxic than CW nerve agents on a weight-for-weight basis and can potentially provide broader coverage per pound of payload than CW agents. and eyes). The extreme toxicity of many toxins causes the lethal dose to be much smaller than that of chemical agents. the exposed mucosal surfaces (moist surfaces of nose. and the digestive tract. Dry powders composed of very small particles tend to have better dissemination characteristics and have advantages in storage. when delivered via aerosol to the respiratory tract. and contamination of food and water. such as specially designed bomblets dispersed in a pattern on the ground or a missile or artillery shell designed to release such bomblets. I-9 . penetration across the skin can occur.d. Physiological Aspects. however. (b) Lethal Dose. (2) The BW agents might be released against our forces or against civilian populations by means of sprays. anthrax. and typhus). e. Pathogens with high infectivity cause disease with relatively few organisms. although freeze-drying and spray-drying technologies have been available in the industry for a number of years. (1) Biological agents may be delivered in either wet or dry form. Employment considerations for BW agents include the following: (1) ROE. mouth. explosive devices. such as in water and food or by vectors. Methods of Dissemination.22 Biological agents may be disseminated as aerosols. upwind of the intended target area. (b) A second type of aerosol source is a point source. (a) A BW agent can be released as a line source.

a cloud of such particles would not generally be detected by those attacked. However. however. stability (while maintaining virulence) after production in storage. or even placed in a stationary position. An alternative method would be to disseminate the agent in an enclosed space (e. appropriate particle size in aerosol. ease of dissemination. and many toxins are produced in nature in such low quantities that harvesting them is impractical (shellfish toxins are a good example).22 The key factors that make a biological agent suitable for an attack include availability or ease of production in sufficient quantity. I-10 . An agent such as Venezuelan equine encephalitis (VEE) virus could cause incapacitation among large numbers of unit personnel. or inhalation of these natural poisons. and the environment. The rate of reaction to toxins varies widely. are widely available because their source in nature is ubiquitous and the process necessary to harvest the toxin is technically straightforward. Particles larger than this would either settle out into the ground or more likely be filtered out in the upper respiratory tract of those who inhale them. Rapid-acting toxins generally incapacitate within minutes. These could be mounted on an airplane. (2) Incapacitation and Lethality. (1) Availability or Ease of Production. On the other hand. The size range of particles that meets both of these conditions is 1 to 5 microns in diameter. If lethality is desired. car. An effective weaponized BW agent is of a particle size that would allow it to be carried for long distances by prevailing winds and inhaled deeply into the lungs of the unsuspecting victims.. even if such a cloud were to be carried through their position. some replicating agents are very difficult to grow in quantity. Requirements for a Weaponized BW Agent. or other moving vehicle. BW agents are likely to be selected for their ability to either incapacitate or kill the human targets of the attack. that particles outside this size range are still dangerous and able to cause deadly illnesses. It is worth noting. An effective weaponized BW agent is easily disseminated in the open air by using off-the-shelf devices such as industrial sprayers or other types of aerosol-producing devices. Some toxins. (3) ROA. A BW agent does not necessarily have to be lethal to be useful as a military weapon. a building) where it could more efficiently infect or intoxicate humans living or working in the area. even though their transmission efficiency is less. (4) Ease of Dissemination. boat. Many replicating agents (bacteria and viruses) can be produced in large quantities with modern fermentation and viral production technologies. ingestion.g. the ability to cause either lethal or incapacitating effects in humans at doses that are achievable and deliverable. Delayed-acting agents may take several hours to days to incapacitate. thus. f. agents such as anthrax have high case fatality rates once infection is established in unimmunized hosts. and susceptibility of intended victims with nonsusceptibility of friendly forces. weapons. Particles in this size range are invisible to the human eye. the incubation periods of microorganisms used in BW may be far shorter than those expected by examining the natural disease. (3) Appropriate Particle Size in Aerosol. like ricin. The time for maximum effects for pathogens is normally more than 24 hours (unless the pathogen produces a toxin).Some human toxicity data are based on accidental contact.

they disrupt bodily functions. b. For many cases. The TIC are found in abundance in all countries.(5) Stability after Production. Militarily Significant Aspects of Toxic Industrial Chemicals a. It must. can cause incapacitation or I-11 . (2) Corrosiveness. Many TIC are highly corrosive. processed.. Unlike CW agents. The sheer volume and widespread availability of TIC present a serious danger in the event of a release. and conditions at the release site. (6) Susceptibility and Nonsusceptibility. 5. Factors include the physical properties of the TIC as well as weather. A large portion of these chemicals may exhibit characteristics or be sufficiently hazardous to be a threat in a military situation. not immunized against). TIC include many lethal compounds. Physiological Aspects. toxicity of the chemical. including air. and are used in chemical manufacturing processes. Like CW agents. TIC can be highly explosive and present a serious threat when handled. Many TIC react violently with water or other materials.2 c. Each year. more than 70. agriculture (pesticides). animals. Once an adversary produces a BW agent in quantity. The effects are dependent on the routes of entry. but to which the adversary possesses high levels of immunity. A number of factors determine the amount of time a TIC would present a danger after release. liquids. Exposure to TIC affects the body in a variety of ways. Classification. transportation. Special equipment containers and procedures are necessary to ensure safe handling. The TIC of military concern may exist as solids. therefore. and the concentration to which exposed. therefore making protection difficult. These factors affect TIC in the same manner as that for chemical agents. many TIC produce additional highly toxic byproducts.3 e. (5) Reactivity. Generally. mixed. water treatment (chlorination). usually via vaccination. it must be fairly stable—either in bulk storage or once put into a weapon or delivery system. or consumed by the global chemical industry. (7) Quantities available. or humans. Characteristics of TIC. (4) Explosiveness. storage. d. and thus present dangers upon contact with other materials.e. and many other areas.000 different chemicals amounting to billions of tons of material are produced. Duration of Effectiveness. Many TIC. or exploded. or gases. The TIC are chemicals that are toxic to plants. When burned. (6) Byproducts. An effective BW agent is one to which the target force is known to be susceptible (i. Many TIC are highly flammable and present a major fire Toxicity. retain its viability and virulence or toxicity during production. release of a TIC may involve a change of the state of the chemical. Uses. (1) death. terrain. (3) hazard. and delivery. Flammability. due to their toxicity.

The primary concern for exposure is that of the inhalation of a TIC as a gas. However. In determining IDLH values. the 30-minute period was not meant to imply that workers should stay in the work environment any longer than necessary. Civilian personnel remaining may be pressured to operate equipment beyond their training/technical expertise in a area of combat. airfields and rail yards often contain significant amounts of transiting TIC. Large stockpiles of obsolete pesticides have been accumulated in virtually all developing countries over periods sometimes exceeding four decades. f. Pesticides. The TIC can enter the body through inhalation.” as used by US forces include insecticides. ports. (b) Refer to the United States Army Center for Health Promotion and Preventive Medicine (USACHPPM) Technical Guide 230. The highly reliable breathing apparatus providing maximum worker protection was permitted. a planner must assess the likelihood of a release or exposure as well as the actual TIC material. In fact. disorientation or lack of coordination) that could prevent escape. Standards have been developed for industry for different exposure scenarios. TIC Hazard Assessment.(1) ROE.2 (2) Exposure Concentration and Levels of Concern.g. or a combination of these methods. ingestion. In general. the SCP IDLH values were based on the effects that might occur as a consequence of a 30minute exposure. dermal absorption. for obtaining the military exposure guidelines for assessing exposure concentrations for TIC. This not only presents opportunities for improvised use against US forces. The purpose for establishing an IDLH value in the SCP was to ensure that a worker could escape without injury or irreversible health effects from an IDLH exposure in the event of the failure of respiratory protection equipment. TIC tend to be at least one order of magnitude less potent than nerve agents and tend not be rapidly lethal in small quantities. (2) Pipelines can offer a very attractive target for terrorists because actions can be planned well in advance of execution and pipelines do not rely on shipping or transportation scheduled. As part of the IPB process. every effort should be made to exit immediately. Chemical Exposure Guidelines for Deployed Military Personnel.28 The term “pesticides. the ability of a worker to escape without loss of life or irreversible health effects was considered along with severe eye or respiratory irritation and other deleterious effects (e. but also presents increased possibility of accidents and targets for those who want to destroy the TIC (such as ammunition precursor chemicals).3(t). (a) Immediately Dangerous to Life and Health (IDLH):24 The definition of IDLH that was derived during the Standards Completion Program (SCP) was based on the Mine Safety and Health Administration (MSHA) definition stipulated in 30 CFR 11. (3) Storage yards. As a safety margin. fungicides. This concentration and time relationship is unique to every chemical. g. Some example considerations are3— (1) Accidents in civilian operations significantly increase when technically trained personnel flee an area. such as a combat zone (CZ). rodenticides. and I-12 .. The type and seriousness of effects from exposure to TIC. like any chemical is dependent upon the concentration and length of time one is exposed. The dosages of TIC are expressed in parts per million (ppm).

29 The US Environmental Protection Agency (EPA) has recognized the dangers of many pesticides and publishes lists of those pesticides that are either banned or severely restricted in their use. public health) can provide information on specific pesticides that could be used in specific areas of operation (AOs).. Others may irritate the skin or eyes. The health effects of pesticides depend on the type of pesticide. I-13 . such as the organophosphates and carbamates.g.herbicides. Others may affect the hormone or endocrine system in the body. Applicable service personnel (e. Air Force civil engineering. Some. affect the nervous system. Army preventive medicine (PVNTMED). Some pesticides may be carcinogens.

US Government Printing Office. “BMBL Section VII: Agent Summary Statements. Office of Health and Safety (OHS). 2002. Final Rule. Office of the Surgeon General. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. Final Report of International Task Force-25: Hazard From Toxic Industrial Chemicals. I.. Chemical and Biological Defense Program Annual Report to Congress. Steumpfle et al.htm. Department of Commerce. of the Secretary of Defense. January 2001. 19 August 2003. Fishbein and S. General (BG) Russ Zajtchuck. “Research in the News: Prions: Puzzling Infectious Proteins.gov/OD/OHS/BIOSFTY/bmb14/bmbl4s7d.gov/nihHTML/ose/snapshots/multimedia/ritn/prions/prions1. Register. ISBN: 0-16-0427274. Assistant to the Secretary of Defense. Field Behavior of NBC Agents (Including Smoke and Incendiaries). Report of the Workshop on Chemical Agent Toxicity for Acute Effects: Institute for Defense Analyses. 1997.. 8-285/Navy Medical (NAVMED) P-5041/Air Force Joint Manual (AFJMAN) 44149/Fleet Marine Force Manual (FMFM) 11-11. April 2002. 1998. Department of Defense Dictionary of Military and Associated Terms. Bureau of Export Administration. Chapter 11..” http://scienceeducation. 7FM 6Joint 5Office of the US President.” 17 June 1999. 15Office 14Federal 13Anna 12Jeffrey 11FM 10Sharon 9Brigadier 8L. Joint Doctrine of Operations in NBC Environment. March 18. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. 17Ruth 16Centers I-14 . H. PhD. Vol. June 2001. for Disease Control and Prevention (CDC). September 2003. 1999. Section VII-D: Prions. 1999.html. 3 November 1986.” December 30. The Biological and Chemical Warfare Threat.).” Reutter et al. Subject: Interim Certification of Chemical and Biological Data. 3Joint 4DOD 2A.nih. Chemical Weapons Convention Regulations. November 1997. December 27. US Government Printing Office. 22 December 1995. Publication 1-02. May 11-12. Review and Recommendations for Human Toxicity Estimates for FM 3-11. Czerczak. Johnson-Winegar. Proliferation: Threat and Response. http://www.9. Memorandum. IDA Document D-2176. Grotte and Lynn I Yang. 8 August 2003.cdc. 2001. 1Office Publication 3-11. (eds. 1996. Levy Guyer.K.NOTES of the Secretary of Defense. Proliferation: Threat and Response. WHO. “Incapacitating Agents. Concise International Chemical Assessment Document 47: Human Health Aspects. 3-6/FMFM 7-11-H/Air Force Manual (AFM) 105-7. as amended through 05 June 2003. ECBC-TR0349. “15 CFR Part 710 et al. et al. 11 July 2000.

1997. National Technical Information Service (NTIS) Publication No. “Defense Against Toxin Weapons. Nuclear. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. Technical Aspects of Biological Defense. “The Biological Warfare Threat. Baseline Study on the Problem of Obsolete Pesticide Stocks.epa. et al. Office of the Surgeon General.” 18 June 2001. Treatment of Biological Warfare Agent Casualties. Davis.). Russ Zajtchuk.). 20BG 18AFMAN APHIS.10-2602. Office of the Surgeon General.9. 12 January 1971. et al. Chemical. EPA.gov/pesticides/health/human. (eds. Chapter 30. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. Food and Agriculture Organization of the United Nations (FAO) Pesticide Disposal Series N. “Pesticides: Health and Safety: Human Health Issues. 28US 27Mark 26CDC. 19 August 2003. 1997.1C. PB-94195047.” 8-284/NAVMED P-5042/AFMAN (I) 44-156/Marine Corp Reference Publication (MCRP) 4-11.” 21TM 22BG 3-216/AFM 355-6. 19USDA. (eds. “Use of Biological Weapons. 1 February 1996. et al.” 19 May 2003. and Conventional (NBCC) Defense Operations and Standards (Operations). Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. NOISH. Chapter 21. Documentation for Immediately Dangerous to Life or Health Concentrations. (eds. 1 December 2002. Russ Zajtchuk. http://www.). 17 July 2000. Office of the Surgeon General. May 1994.htm. I-15 . Biological. 2001. Russ Zajtchuk. Chapter 20. “Protocol for Military Clearance. 1997. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDD-6(B).” 25FM 24BG 23FM 8-9/NAVMED P-5059/AFJMAN 44-151.

0079) Cl (atomic weight = 35. Boiling Point. and physiological action. duration of effectiveness.91 MW = 174. Table II-1.453) x 2 = 24.02 x5= 5.92 x 2 = 70. and the physical. a.9216) x 1 = 74. It also determines the type of munitions used for its dissemination. they include choking. and incapacitating agents. c. or gases.89 b. and physiological properties of selected CW agents and precursors listed in Table II-1. blister.1 This chapter contains definitions for selected physical and chemical properties. Chemical agents may exist as solids.3 d. is computed as follows: C (atomic weight = 12. The normal boiling point is the temperature at which the vapor pressure of a liquid equals one atmosphere (atm).2 e. the MW of ethyldichloroarsine (ED). At high altitudes where the atmospheric pressure is less than one atm. liquids. MW is the value represented by the sum of the atomic weights of all the atoms in a molecule. Odor. water boils below 100 degrees Celsius (C) or 212 degrees Fahrenheit (F). The FP is the temperature at which the solid and liquid phases of a given substance are in equilibrium and is generally equivalent to the MP.2 NOTE: Some liquids can be cooled well below their freezing temperatures and still remain in a liquid state. FP/MP.2 See Table C-1 (page C-1) for the Periodic Table of Elements and Table C-2 (page C-2) for the list of elements and their symbols. nerve. This extended form of the liquid physical state is called “supercooling.011) H (atomic weight = 1. Physical State.Chapter II CHEMICAL WARFARE AGENTS AND THEIR PROPERTIES 1. chemical. Molecular Weight (MW).2 To a certain extent the state in which an agent normally exists determines its use. The boiling point is the temperature at which the vapor pressure of a liquid equals the pressure of the gas above it. blood. Definitions of Selected Physical and Chemical Properties The definitions for the physical and chemical properties are given in the same order listed in the chemical agent tables. definitions for selected toxicity terms. Background The CW agents can be classified according to their physiological effects or their military use.” Supercooled liquids are unstable and can crystallize II-1 .04 As (atomic weight = 74. For example. Odor is the emanation from any substance that stimulates the olfactory cells in the organ of smell. List of Selected CW Agents and Precursors 2. C2H5AsCl2.

pores. The VP increases as temperature increases. The VP varies with temperature.spontaneously.4 f. Due to the potential for supercooling. However. Constant agitation and/or the use of seed crystals can sometimes prevent or reduce the amount of supercooling that occurs. It is calculated numerically by an equation derived from the perfect gas law: II-2 . h.6 For the purpose of this manual. the gas will generally settle on the ground. To calculate the vapor density. Vapor density is the ratio of the weight of a given volume of a gaseous substance and that of the same volume of another gas measured under the same conditions of pressure and temperature. The VP is the pressure exerted by a vapor when a state of equilibrium exists between the vapor and its liquid (or solid) state. If the vapor density is greater than 1. many chemical agents experience some degree of supercooling. It is the pressure in a closed space above a substance when no other gas is present. the gas will generally rise in the air. Volatility is the tendency of a solid or liquid material to pass into the vapor state at a given temperature. Bulk density includes the volume of the voids. If the vapor density is less than 1. VP. Whenever possible. or empty spaces between particles.5 g. the other gas is air. MP valves should be used because they are more thermodynamically reproducible than the FP. especially the G agents. Vapor Density. The density of a liquid or solid is usually given as grams per milliliter (g/ml) or grams per cubic centimeter (g/cm3). Because volume varies with temperature. a specified temperature should be given. Density (Liquid/Solid). so the temperature should be stated. divide the MW of the compound of interest by 29 (the average MW of air). The density of a chemical agent is the mass per unit volume of the substance.2 NOTE: Solid density can be further specified as bulk (or apparent) density or crystalline (or true) density. whereas crystalline density includes only the volume occupied by the material itself.7 The volatility depends on vapor pressure and varies with temperature. Volatility is expressed as milligrams of vapor per cubic meter (mg/m3).2 i. freezing point values should be used with caution. Volatility. Both properties describe the mass per unit volume.

9 The more complex the molecules in a liquid and the stronger the intermolecular forces between them.15) j. Flash Point. Also. The latent heat of vaporization is the quantity of energy absorbed or given off as a substance undergoes a change in state with no change in temperature.V = 16020 x MW x VP T Where V = Volatility (mg/m3) MW = molecular weight VP = vapor pressure (in torr at a specified temperature) T = Kelvin temperature (degrees C + 273. the more difficult it is for the molecules to move past each other and the greater the viscosity of the liquid. Latent Heat of Vaporization.7 n.987 cal K-1 mol-1) = Temperature in degrees C B. the molecules on the surface of a liquid are attracted only into the liquid and to either side.7 It is calculated using the following equation:8 ∆Hv = ln 10 RBT2 (C + t)2 Where ∆Hv = Enthalpy of vaporization (latent heat of vaporization) T R t = Kelvin temperature = (degrees C + 273.2 Units for viscosity are given in centipoises (cP). The flash point is the temperature at which a liquid or volatile solid gives off sufficient vapor to form an ignitable mixture near the surface of the liquid. The decomposition temperature is the temperature at which a chemical breaks down into two or more substances. l. as temperatures increase.C = Vapor pressure constants (from Antoine or Clausius Clapeyron fit) k. Decomposition Temperature. The molecules within a liquid are attracted equally in all directions by the cohesive forces within the liquid. A fluid with a large viscosity resists motion.2 Units for surface tension are dynes per centimeter (dynes/cm). Surface tension is the force that causes the surface of a liquid to contract. II-3 . m.15) = Ideal gas law constant (1. Viscosity is resistance that a gaseous or liquid system offers to flow when it is subjected to a shear stress.4 Because reaction rates vary. the viscosity of the liquid decreases. decomposition temperature is a function of both temperature and time (some reactions are slower than others). Viscosity. Surface Tension. reducing its surface area to a minimum. This unbalanced molecular attraction tends to pull the surface molecules back into the liquid such that the minimum number of molecules possible are on the surface. However.

Dosage is the amount of substance administered (or received) per 11 In this manual. For some agents. Any part of the respiratory tract. Hydrolysis is the reaction of a compound with water whereby decomposition of the substance occurs. Plastics. The choking agents exert their effects only if inhaled. dosage is usually expressed as milligrams per kilogram body weight. Stability in Storage.o. Stability in storage determines the practical usefulness of a compound. such as prostration.g. Nerve agents exert their toxic effects through the skin. and mucous membranes can absorb droplets of liquids and solid particles.2 New substances (hydrolysis products) form when a compound reacts with water. Action on Metals.. The solubility of a solute is the quantity that will dissolve in a given amount of solvent to produce a saturated solution. The onset and severity of signs may vary. severe. effects are more severe in normally sweaty areas. eyes. The skin can also absorb vapors. Solubility. eyes. from the nose to the lungs. Fabrics. may absorb inhaled gases and aerosols. skin. Hydrolysis. eyes. some chemicals can react with and degrade materials they contact. and Paint. depending upon the ROE and dosage. q. This is the time required for half of the original concentration of the limiting reactant to be consumed. the body can absorb them through the gastrointestinal tract.1 The ROEs have been limited to those that are likely to be encountered in the field: vapor inhalation with eye exposure. and skin exposure to liquid. The specific heat is the quantity of heat required to raise the temperature of 1 gram of a substance 1 degree C2 (given in lieu of latent heat of vaporization for military chemical compounds only). s. II-4 . Effective dosages of liquid on the skin are based upon data for bare skin. t. The toxicity estimates for mustard agent percutaneous vapor exposure are based on clothed skin exposures. it will have little military operational value. Chemical agents enter the body through the respiratory tract. to include eyes and lungs. The addition of stabilizers will typically slow down decomposition and polymerization in storage. Half-Life of a Reaction (t1/2). Dosage.4 r. Specific Heat. Dosages are given for a 70-kg man.9 b. This item describes the action between a given compound and different materials. skin exposure to vapor.9 (1) Median Lethal Dosage (LD50) of Liquid Agent. Depending on their activity. 3. Inhalation is the usual route of exposure for blood agents. Chemical agents can contaminate food or drink. (mg/kg) of body weight for liquid agents and as milligrams-minute per meter cubed for (mgmin/m3) for vapor exposure. and therefore. and lungs.2 p. The toxicity estimates given for percutaneous vapor exposure for the nerve agents are based on bare skin exposures. Definitions of Toxicity-Related Terms a. The LD50 is the amount of liquid agent expected to kill 50 percent of a group of exposed. If a compound decomposes in storage. and by ingestion. The surface of the skin. Blister agents damage skin and other tissues that they contact. Wounds or abrasions are probably more susceptible to absorption than the intact skin. unprotected individuals. The ED50 is the amount of liquid agent expected to cause some defined effect (e. (2) Median Effective Dosage (ED50) of Liquid Agent. Chemical agent-resistant coating (CARC) can minimize this effect. ROE.

the apparent dosage decreases because more agent is inhaled into the lungs. as the MV increases. unprotected personnel for a defined MV and exposure duration. Such calculations require knowledge of the probit (Bliss) slope and use the probit equation.g. unprotected personnel for a defined MV and exposure duration. a person may show signs and symptoms that are less or more severe than expected. Proper fit of the mask. (4) Median Effective Dosage (ECt50) of a Vapor or Aerosol. Modifying Factors. Selected toxicity estimates are assigned provisional values. The MV is the volume of air exchanged in one minute. MV. especially if exposure was long. After exposure to a chemical agent vapor. NOTES: 1.collapse. In general. A toxicity estimate is considered provisional based on only having limited data. mild. Physical exertion of the person at the time of exposure.. (3) Median Lethal Dosage (LCt50) of a Vapor or Aerosol. heat. For example. LCt25. Speed with which he or she donned the mask. Rate of detoxification. for an MV of 15 liters. Effective dosages can be calculated for more or less than the median dosage (e. The LCt50 of a chemical agent in vapor form is the dosage that is lethal to 50 percent of exposed. Physiological stressors include anxiety. unprotected individuals. convulsions. Physiological Stressors. it would be approximately 50 mg-min/m3 for an MV of 10 liters and approximately 15 mg-min/m3 for an MV of 30 liters. but the data are within the range of available animal data or when the agent is presumed to be comparable in toxicity to a related agent. MV of the person at the time of exposure. the agent is potentially more effective. The relationship of MV to dosage is approximately linear over ranges of MV from 10 to 50 liters. ED84). if the LCt50 is given as 35 mg-min/m3. Whether the agent increased the MV. and humidity and are likely to reduce toxicity estimates. The severity of the effects may depend upon some of the following potential variables: (1) (2) (3) (4) (5) (6) (7) (8) (9) How long the person held his or her breath during short exposure. In other words.10 c. II-5 . such as erythema) in 50 percent of a group of exposed. d. Previous exposure to chemical agents and type of agent. Whether the body absorbed the agent through the skin. It is important to note that increasing respiratory rate does not necessarily increase MV and may actually decrease it.10 3. The ECt50 is the effective dosage of a chemical agent vapor that is sufficient to cause some defined effect in 50 percent of exposed. MV profile tables are provided in Appendix H.10 2.3 Where available.

As seen in some Ct profile tables. ChE inhibition and/or localized sweating. The official interim standards for inhalation/ocular exposures are for a 2-minute duration. blepharospasm. as data are available.10 (2) For percutaneous exposure to blister agents.e. a given dosage (Ct) produces a given effect—independent of concentration or exposure duration. a default exponent value of one is used (TLE is assumed to be 1). the equation Cnt=k is used. The human body can detoxify some toxic materials. Endpoint (Physiological Effects). (b) When the TLE value is less than 1. threshold effects.10 h.10 g. In order to describe the effective dosages better mathematically. Selected agents have toxicity estimates for hot and moderate temperatures. Toxicity estimates are provided for different endpoints to include lethality. collapse. not necessarily significant. Hot temperatures are defined as greater than 85 degrees F. severe effects include vesication and mild effects include erythema. and mild effects. Dosage is a function of Ct. Threshold effects for percutaneous vapor exposure include slight. More data have become available since the interim standards were defined. Concentration-Time (Ct) Profile. ROA. severe effects. as the temperature increases. These effects can occur in the absence of measurable ChE inhibition in the blood. rhinorrhea. (c) When the TLE value equals 1 (Haber’s Law). Exposure Duration. however. (1) For nerve agents. Some deaths will occur. even between those of similar tactical or physiological classification. Mild effects following inhalation/ocular exposure include miosis. Temperature. The dosages for hot temperatures are about half of those for moderate temperatures.10 f. the effective dosage decreases. edema. conjunctivitis. j. ROD. When the Ct profile is unknown. The ROA of a chemical agent is the rate at which the body reacts to or is affected by that agent. the equation k=Ct does not describe all cases of injury from chemical agent exposure. and tight chest. The exponent “n” is called the toxic load exponent (TLE). severe effects include prostration. effective dosages decrease as the exposure duration increases (the agent is more potent following long exposures to low concentrations than short exposures to high concentrations). and they are also given for longer exposures. mild effects consist of erythema and minimal conjunctivitis. pain. a given effective dosage does not always produce a specific effect for all duration exposures. those for percutaneous vapor exposure (masked personnel) are for a 30-minute duration. effective dosages increase as the exposure duration increases (and the exposure concentration decreases). Severe effects following ocular exposure include pain. The ROD is an important factor in determining the hazards of repeated exposure to CW agents. and itching—depending upon the agent. II-6 . and temporary blindness. The rate varies widely. Many CW agents are essentially cumulative in their effects. See Figure II-1 and II-2 (page II-8) (a) When the TLE value is greater than 1. and/or convulsions. Moderate temperatures are defined as 65 to 85 degrees F. In general. i.

• There is a single LCt/ECt for a specific type of exposure and endpoint.5 exposures to low concentrations than short exposures to high concentrations. Figure II-1. exposure to low levels for an extended period of time can cause effects.The effect the TLE has on the effective dosage is illustrated in the following Ct profile tables.3 • There is no single LCt/ECt for a specific 120 15 0. Case 2: TLE<1 NOTES: Ct Profile (15L MV) • LCt50/ECt50 decreases as exposure Concentration Exposure LCt50 3 3 duration increases. • Concentration decreases. there are three possible cases for the value of the TLE(n).5 0. The TLE Effect on the Ct Profile II-7 .7 type of exposure and endpoint.2 can cause effects.5 low levels for an extended period of time 60 70 1. Case 1: TLE>1 NOTES: Ct Profile (15L MV) • LCt50/ECt50 increases as exposure Concentration Exposure LCt50 3 3 duration increases. (mg/m ) Duration (min) (mg-min/m ) • Concentration decreases. exposure to 2 35 17.5 0. In the n equation k-C t. 60 20 0. • There is no single LCt/ECt for a specific 120 80 0.125 type of exposure and endpoint.3 NOTES: • LCt50/ECt50 remains constant as exposure duration increases. Case 3: TLE =1 (Haber’s Law) Ct Profile (15L MV) Exposure Duration (min) 2 60 120 LCt50 (mg-min/m3) 35 35 35 Concentration (mg/m3) 17. (mg/m ) Duration (min) (mg-min/m ) • The agent is more potent following long 2 35 17.

Ct Profile for Dosage versus Exposure Duration II-8 . Severe effects can include some deaths. LCt50/ECt50 remains constant as exposure duration increases. Case 3: TLE = 1. The line gives the effective dosages where 16 percent of 70-kg males would experience severe effects. this is for an inhalation/ocular vapor exposure to a CW agent. Figure II-2. The region shows the effective dosages that would cause mild effects in 16-84% of 70-kg males exposed. This is roughly equivalent to the lethal dosage for 1 percent. Case 2: TLE < 1. the effective dosage (LCt/ECt) increases. There is no single LCt or ECt for an exposure.0 Time (minutes) Upper Band: The endpoint is lethality. Line: The endpoint is severe effects (specific symptoms depend on the type of CW agent exposure). Case 1: TLE > 1. LCt50/ECt50 increases as exposure duration increases. The region shows the effective dosages that would be lethal to 16-84% of 70kg males exposed. Case 1 Ct (mg-min/m ) 3 Case 2 Example: TLE > 1 Case 3 1) (Case Time (minutes) Example TLE > 1 (Case 1) CW Agent Vapor: Dosage versus Exposure Duration 10 Ct (mg-min/m ) 3 This is an example of the Ct profile graphs for dosage versus exposure duration given in Appendix H. LCt50/ECt50 decreases as exposure duration increases. Notice as exposure duration (time) increases. Exposure Duration The graph on the left is a representation of a Ct profile for dosage versus exposure duration. Lower Band: The endpoint is mild effects (specific symptoms depend on the type of CW agent exposure). The graph shows the three cases.Dosage vs. In the quotation k=C t there are three possible cases for the value of the TLE (n). Given: Upper Band: LCt16 and LCt84 region Line: ECt16 (severe) [roughly LCt01] Lower Band: ECt16 and ECt84 region for mild effects 1 10 100 1 0. they are time-dependent. The graph is constructed by plotting the exposure duration (t) on the horizontal axis and the dosage n (k) on the vertical axis.

Dose response curves can be used to assess from a graphical depiction the results of an exposure to a CW agent. a graphical x-axis plot) and response (i. and death results from lack of oxygen.. lungs become filled with liquid.” Of the choking agents. CG is a colorless gas with an odor similar to musty hay or rotting fruit. The dose response curve is impacted by the concentration of the CW agent and duration of the exposure (i. larynx. these agents “choke” an unprotected person. Degree of Confidence (DOC).13 Vapors can linger for some time in trenches and low-lying areas under calm or light winds.10 II-9 . and there are sufficient data for mathematical modeling.10 Lung damaging concentrations may not be detected by smell.14 Any activity or stress after exposure is likely to exacerbate the effects and turn a sublethal exposure into a lethal exposure.12 The severity of poisoning cannot be estimated from the immediate symptoms.e. 4. With very potent agents. thus. It is a subjective evaluation based on the quality and quantity of the underlying data and the method(s) by which the estimate was derived. phosgene (CG) is the only one considered likely to be used in the future. primarily causing pulmonary edema.12 The protective mask gives protection against choking agents. trachea. Initial symptoms may include tears.k. and nose. (3) High. a small change in the dose can also make a big change in the level and severity of the effects produced. tightness of chest. choking. Fatalities of this type are called “dry-land drownings. They cause irritation to the bronchi. Probit Slope. (b) A low probit slope value means that a relatively large change in the dose will make for a relatively minor change in the number of individuals responding to the given dose. vomiting. nausea.10 The DOC is an indication of the level of confidence in each toxicity estimate and is provided to indicate uncertainty. and the full effect can be delayed up to 72 hours after exposure. and headache.1 a. and there is good statistical confidence in the value. There are primary data for both humans and animals. coughing. (a) A high probit slope value means that a small change in the dose will make a large change in the number of individuals responding to the chemical agent. Choking Agents Choking agents are CW agents that attack lung tissue. (2) Moderate. There are ample primary data for both humans and animals. and/or the data are extremely limited. a graphical y-axis plot).. CG (see Table II-2 [page II-10]). dry throat.e. The following definitions are provided: (1) Low. There are no primary data. The probit slope is derived from dose response curve data and corresponds to the variability in the response of the population to the chemical agent. pharynx. membranes swell. l.1 In extreme cases.

Phosgen (German). D–gas (German). 1. Zusatz (German).402 @ 7.Table II-2. Carbonyl dichloride.4 -128oC (MP) 5 Liquefied phosgene 1.92 @ 25oC. 1.4 (calculated) 1.8oC.11 Hydrochloric acid and carbon dioxide 9 Stable in steel containers @ ambient temperatures for at least one year if CG is dry.8oC. MM1 17 Protective mask 15 Not required in the field except in very cold climates 18 Delayed action casualty agent 19 II-10 .40 x 103 @ 25oC. 5. Fosgeen (Dutch). 3. 14 Causes pulmonary edema 15 Immediate to 3 hours.360 @ 25oC. 7. @ 13oC. stability decreases at elevated temperatures 12 None when CG is dry. 5.29 x 106 @ 7.46 x 106 @ 25oC.25 sec. Fosgene (Italian). Carbonic chloride. CG Alternate Designations: Collongite (French).96 @ 0oC (calculated from vapor pressure) 3. does not react quickly with water vapor.4 5.60 x 102 @ 0oC 3.420 @ 0oC 6 3. acidic and corrosive when moist 13 Other Data Initial effects resemble those of tear gas. Carbonylchlorid (German). and lubricating oil 9.4 7. NCI-C60219 Chemical Name: Carbonyl chloride Synonyms: Carbon oxychloride.8oC. 5.92 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials Eye toxicity Inhalation toxicity Rate of action Means of detection in field Protection required Decontamination Use Colorless gas that is readily liquefied 1 Musty hay or rotting fruit 2 7. Fosgen (Polish).10 C Cl t1/2 = 0. Carbon dichloride oxide.8oC. 8 miscible with common organic solvents. Koolstofoxychloride (Dutch) CAS Registry Number: 75-44-5 RTECS Number: SY5600000 Physical and Chemical Properties Structural Formula: Cl O Molecular Formula: COCl2 Molecular Weight: 98.4 Data not available Data not available Data not available Nonflammable 1 Complete @ 800oC 7 Limited in water.60 x 102 @ 7.95 @ 7. Carbone (oxychlorure de) (French).8oC 3.53 x 106 @ 0oC (calculated from vapor pressure) 3. Carbonio (ossiclorurodi) (Italian). Green Cross (German). Chloroformy chloride. depending on concentration 16 M18A2 CADK. 4. but it immediately reacts with liquid water to yield carbon dioxide and hydrochloric acid 8. petroleum.

13 Patten. The Chemical Warfare Threat and the Military Healthcare Provider. 1410-1426. Chemical Warfare Service. 13. A.H. 1 February 1996. NJ. p. 1928. Eng. c. “The Preparation and Physical Properties of Carbonyl Chloride.. Chemical Warfare Service. 1997. Office of the Surgeon General. N. EACD 11. DP is described as a respiratory irritant and a lachrymator. et al. II-11 . Chemical Defence Experimental Establishment. CG (Continued) NOTES ¹Matheson Gas Data Book. 120. Heats of Fusion and Vaporization. “Die Dissociation des Kohlenoxychlorids. An Investigation on the Solubility and Rate of Hydrolysis of Phosgene in Water. P. Chem. December 1944. Summary Technical Report of Division 9. Chem.. 1948.. 1154 –1159. UNCLASSIFIED Report (ADB959731). Soc. Chem. p. 7 Bodenstein.. 10 Baskerville. ETF 100-41/Vol-3. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. EACD 124. The Matheson Company. G. Chem. 1946. 1921.. c Based on secondary human data and TM 3-215 (1952). Steel Gas Shell Extending Over a Period of One Year. 4 Germann. Soc.. February 2000. Vol.E. Vol. Kirner. CG Toxicity Estimates (see Table II-3). UNCLASSIFIED Report (ADB955133). “The Density and Thermal Expansion of Liquid Phosgene. Entropy. Edgewood Arsenal. 14 BG Russ Zajtchuk. 1946. F. C.. Chemical Warfare Agents.W. 9 Atkinson. and Related Chemical Problems Part I-II.9 See Table II-5 (page II13) for DP toxicity estimates. and Conventional (NBCC) Defense Operations and Standards (Operations). Chapter 4.. 7 (U). 61.. 48.” Z.” J. Properties of War Gases Volume III: Vomiting & Choking Gases & Lacrimators (U). 48(5). p. “The Critical Constants and Vapor Tension of Phosgene.M. Vapor Pressure. 1966. MD.. W. Washington. and Taylor. Inc.W. CONFIDENTIAL Report (AD108458). 6 Davies. C. R.13 DP is not a polymer of CG. S. Although the probit slope for CG is unknown. Biological.W. 5 Giauque. MD.Table II-2. UNCLASSIFIED Report (AD234270). Surveillance Tests on 75 MM. Soc. Chemical Corps Board. East Berlin. F. CG Toxicity Estimates10 Endpoint Lethality Odor Detection a Toxicity (mg-min/m3) LCt50: 1500 a EC50 : 6 mg/m3 c MV (L) 15 N/A Exposure Duration 2-60 min Few Seconds ROE Inhalation/Ocular Inhalation NOTES Probit Slope Unknown N/A TLE 1b N/A ROD Probably Insignificant Probably Insignificant DOC Moderate Low Based on ECBC modeling of 10 mammalian species. Vol. DC.R. 70. It is more easily detected than CG because of its lacrimatory effects. DP is a colorless liquid with an odor similar to that of musty hay. Diphosgene (DP) (see Table II-4 [page II-12]). 2 Franke. 8 Hall. UNCLASSIFIED Technical Manual (AD849866). 18 FM 8-9/NAVMED P-5059/AFJMAN 44-151.. “Carbonyl Chloride. but does produce similar physiological effects...” 15 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. et al. Ind. Q. 17 AFMAN 10-2602 Nuclear. Porton.F. ECBC Notebook # NB 98-0079. Amer. ACSI-J-3890. it is known to be so steep that “incapacitating” or “severe effects” dosages could include some lethality. 19 W. and Jones.. W. 1908. pp.. Chemical Properties of Phosgene.M. and Cohen. Vol... 3 Abercrombie. Office of Scientific Research and Development. Porton Report 2663. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries.” J.. Comments on Solid Sulfur Dioxide Structures. East Rutherford. Vol. June 1920. H. UNCLASSIFIED Report. 12 Henley. b See Appendix H for supporting toxicity profile estimates. and Bouder.” J. March 1923. 16 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. April 1968. P. MD. Chem. Manual of Military Chemistry Volume I-Chemistry of Chemical Warfare Agents. Vol. Chemie der Kampfstoffe. p. R.O.” J.. 29 May 2003.. 4th ed. 117.. Phys.” J. and Durant. 411. Chemical. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP6(B). 22 December 1995. Heat Capacity. Edgewood Arsenal.. (eds. 437. 333. N. 19 December 1944. p. NDRC Volume 1. England.. M. pp.).M. Physik. Chem.. Army Chemical Center. 14.10 Table II-3. 1920. 11 b. p. “Solvents for Phosgene. Amer.

2 Other Data Lachrymator 7 Causes pulmonary edema 8 Immediate to 3 hours depending on concentration 9 MM1 Protective mask 8 Not required in the field except in very cold climates.83 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/mL) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials Colorless oily liquid 1 Musty hay 2 127oC 3. converts to CG.4 Data not available Data not available Data not available None 5 300oC to 350oC (yields two molecules of CG) 1 Solubility in water is 44. 6 readily soluble in common organic solvents 2 Slow @ ambient temperature and fairly rapid @ 100oC 1 Hydrogen chloride (HCl) and carbon dioxide 1 Unstable.4 12.Table II-4. trichloromethyl ester.687 @ 0oC 2 6. Trichloromethyl carbonochloridate. Trichloromethyl chlorocarbonate. DP Alternate Designations: Difosgene.4 and cement.656 @ 20oC. chloro-. cork. 1 Metals act as catalyzers in conversion to CG.2 @ 20oC. Superpalite (British). Surpalite(French). 2.77 x 104 @ 20oC. 1.6 g DP/L solution @ 20oC. 10 Delayed or immediate action casualty agent. 12. Carboncohloridic acid trichloromethyl ester CAS Registry Number: 503-38-8 RTECS Number: LQ7350000 Physical and Chemical Properties Structural Formula: O Cl Molecular Formula: C2Cl4O2 Molecular Weight: 197. Chloroformic acid trichloromethyl ester.41 @ 20oC. 9.4 -57oC (MP) 2 C Cl O C Cl Cl Munitions grade: 1. Green Cross (German) Chemical Name: Trichloromethyl chloroformate Synonyms: Trichloromethyl chlorocarbonic acid ester. Perstoff (German).4 4. 1. Formic acid.14 x 10-1 @ 0oC 3.06 x 104 @ 0oC (calculated from vapor pressure) 3.8 @ 0oC (calculated from vapor pressure) 3. depending on dosage rate Eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination Use II-12 . 1.2 Also attacks rubber.8 (calculated) 4.

.” Kolloid Beihefte.R. 3 Abercrombie. “Superpalite. Vol. 7 Sharon Reutter. 6 Carter. 9 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. Fundamental Study of Toxicity Solubilities of Certain Toxics in Water and in Olive Oil. low volatility.. and cramps.10 Nerve agents are cumulative poisons..1 They are divided into the G agents and V agents. 4 Herbst.. and resultant high persistency. DP Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LCt50: 1500a (Provisional) EC50: 4 mg/m3 d MV (L) 15 Exposure Duration 10-60 min ROE Inhalation/ Ocular Inhalation Probit Slope Unknown TLE 1 b.. Physiological Effect.Table II-4. Military Chemistry and Chemical Agents. ACh is not hydrolyzed. As a result. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B). H. 498. MD. ²Potts.15 Individuals poisoned by nerve agents may experience symptoms in the following order: • • • Miosis. December 1963. OEMCMR-114. 23. c See Appendix H for supporting toxicity profile estimates.M. UNCLASSIFIED Report.12 Even though the V agents are considered primarily a contact hazard12.. and even a minute amount of airborne material is extremely hazardous. R. 34 (U).. Nausea. ECBC Notebook # NB 98-0079. 1945. Chemical Warfare Service. They may cause effects within seconds and death within minutes. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. Probably Insignificant N/A DOC Low Odor Detection a N/A Few Seconds N/A N/A Low NOTES Based on recommendations for CG. 1 Table II-5. H.15 The nerve agents are all liquids. P. They can be absorbed through any body surface and can penetrate ordinary clothing rapidly.1 a. May 1928. H. b The TLE value is assumed to be 1 because the Ct profile is unknown. ECBC-TR-349. Normally. p. V. 22 December 1995. and Knight.1 Level 4 mission-oriented protective posture (MOPP4) is required for protection. EACD 445.The Physical and Chemical Properties of Phosgene and Diphosgene. Chem. the nerve agents bind to AChE. 23. 5. Upon exposure. 330. p. Edgewood. 1 February 1996. making it unable to bind with ACh.. et al. runny nose. not nerve gas per se. d Based on secondary human data. vomiting.C. which terminates the activity of ACh at the receptor sites.” J. Nerve Agents Nerve agents are more toxic than other CW agents. DP (Continued) NOTES Hood. Vol. September 2003. A. UNCLASSIFIED Report (ADB955216). 10 FM 8-9/NAVMED P-5059/AFJMAN 44-151.c OD Unknown. 5 TM 3-215/AFM 355-7.H. Both the G and V agents have the same physiological action on humans. UNCLASSIFIED Technical Manual. 1919. The accumulation of ACh causes hyperactivity of the body organs stimulated by cholineraic neruons.9. Dim vision and headache. The V agents have high boiling points. 1927. and chest tightness. February 2000. Review and Recommendations for Human Toxicity Estimates for FM 3-11. Repeated exposure to low concentrations may produce symptoms. “Uber die Fluchtigkeit und Vernebelung einer Reihe organischer Stoffe. Edgewood Arsenal. the enzyme acetylcholinesterase (AChE) binds and hydrolyzes the neurotransmitter ACh. Phys..P. and Murdock. p.H. II-13 . 8 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. they are at least twice as potent as GB.

ethyl ester. Table II-6. and pyridostigmine bromide (PB). Atropine is still needed to counteract the excess ACh and 2-PAM Cl is still needed to reactivate AChE active sites that were protected by PB. Dmethylaminecyanoethoxyphosphine oxide.15 Prompt treatment is essential because after the agent binds to AChE.15 GA is primarily an inhalation hazard. FM-511. Difficulty breathing. 2-PAM chloride. Tabun (GA) (see Table II-6). and staggering. Miosis. GA was the first of the nerve agents developed by the Germans. When airborne vapor comes in contact with the eyes. Ethyl dimethylphosphoramidocyanidate. miosis is one of the last effects to occur before death. This phosphorylated AChE is called an “aged” enzyme and is completely resistant to both spontaneous and oxime-medicated (2PAM Cl) reactivation. miosis occurs as a result of a direct local effect of the nerve agent on the eyes and can occur prior to any inhibition of ChE in the blood. Dimethylphosphoramidocyanidic acid. Gelan I (German). The carbamoylated AChE is fully protected from attack by nerve agents.16 For GD. Dimethylamidoethoxyphosphoryl cyanide. a second reaction occurs in which the agent loses one alkyl or alkoxy group. excessive sweating. and any or all other symptoms can occur. T-2104 (British). Le-100 (German). it is unlike nerve agents in that the interaction between PB and AChE is freely and spontaneously reversible and it does not undergo the aging process. In cases of nerve agent exposure not involving vapor contact with the eyes. Although PB is also an AChE inhibitor. Dimethylaminocyanphosphorsaeureaethylester (German). b. Convulsions and coma. Cyanodimethylaminoethoxyphosphine.17 PB is available to US forces in active theaters of operation (TOs). See Table II-7 (page II-17) for GA toxicity estimates.1 d. (2) 2-PAM Cl acts by reactivating ChE inhibited by a nerve agent. TL-1578 (UCTL). convulsant antidote for nerve agents (CANA). Dimethylaminoethoxyphosphoryl cyanide. (1) Atropine binds to receptor sites blocking the excess acetylcholine caused by nerve agent poisoning. GA Alternate Designations: EA 1205. PB and AChE bind and form what is called a carbamoylated AChE. Ethyl dimethylaminocyanophosphonate Phosphoramidocyanidic acid. ethyl ester. Treatment of nerve agent poisoning includes use of atropine. Ethylester-dimethylamid kyseliny kyanfosfonove (Czech) CAS Registry Number: 77-81-6 RTECS Number: TB4550000 II-14 .• • • Drooling. This type of exposure is frequently accompanied by tightness of the chest and/or rhinorrhea.10 c. Trilon 83 (German). and confusion. drowsiness.17 (3) The CANA prevents and treats convulsions caused by exposure to nerve agents in moderate to severe cases. Dimethylaminocyanophosphoric acid ethyl ester. the “aging” half-time is within 2 minutes. dimethyl. N-dimethylphosphoroamidocyanidate Synonyms: Ethyl dimethylamidocyanophosphate. MCE. Taboon A Chemical Name: Ethyl N.1 (4) PB is a pretreatment for exposure to GD. The “aging” period varies from minutes to hours depending on the type of agent. jerking. twitching. Treatment. T-83 (German).

M18A3 CADK16.0o C.10 slow in water but fairly rapid with strong acids and alkalis with self-buffering @ pH 4 to 5. 17 NOTE: GA may react to form CK in bleach slurry. and absorbents (earth. liquid nerve agents penetrate ordinary clothing rapidly 13 Flush eyes with water immediately.5 @ 25oC.5 hrs @ 20oC and pH 7. M90 AMAD. 1. sawdust. IPDS.5 @ 25.0756 @ 25oC. liquid penetrates skin. Water. and other products 10 When stabilized with 5% chlorobenzene. 3 readily soluble in common organic solvents 2 t1/2 = 8. Use the M291 SDK to remove any liquid nerve agent on skin or clothing.2g GA/100g solution @ 20oC and 9.6 (calculated) 5. steam. M272 Water Testing Kit. 16.13 STB is effective on equipment. 13 Inhalation Toxicity Rate of action Means of detection Protection required Decontamination Use Primarily inhalation hazard 14 Rapid 15 M8 paper.000034 inch/month @ 65oC.13 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage O P CN N CH3 CH3 Action on Metals or Other Materials Skin and eye toxicity Colorless to brown liquid 1 Faintly fruity. M256A1 CADK.75 x 10-3 @ 0oC (extrapolated) 3-7 4. M9 paper. 4. The degree of stability decreases @ elevated temperatures with decomposition occurring within 6 months @ 50oC and 3 months @ 65oC. Skin: highly toxic. MM1.20 x 10-3 @ 25.0oC. 5. dimethylaminocyanophosphonic acid. AN/KAS-1 CWDD16 MOPP4.97 x 102 @ 25oC. much greater through eyes than through skin. CAM/ICAM. GA can be stored in steel containers for several years @ ambient temperatures. M21 ACAA.320@ 0oC3 6. 4. M22 ACADA.18 Quick-acting casualty agent II-15 . 35. 12 Other Data Eyes: very high.0oC.Table II-6.0 @ 0oC3 78oC (closed cup) 8 Decomposes completely @ 150oC after about 3 to 3 1/4 hrs 9 Solubility in water is approximately 7.8g GA/100g @ 0oC.7 @ 0oC (calculated from vapor pressure) 3-7 2.60 x 10-3 @ 0oC3 32. ashes. M8A1 ACAA. Use the M295 IEDK for individual equipment.0999 @ 0oC 3 5. decontamination of smallest drop of liquid agent is essential. 1 autocatalytic below pH 4 11 AC. M18A2 CADK.70 x 10-2 @ 25oC. GA (Continued) Physical and Chemical Properties Structural Formula: O CH3CH2 Molecular Formula: C5H11N2O2P Molecular Weight: 162. and rags) are effective for physical removal.277@25.52 x 101 @ 0oC (calculated from vapor pressure) 3-7 15. 12 Corrosion rate of steel on crude GA with 5 to 20% chlorobenzene is 0. none when pure 2 248oC (extrapolated) 3-7 -50oC (FP) 5 1. 4. CAPDS.

H. England. 7 Belkin. Washington. Army Chemical Center..W. 4 Abercrombie. Porton.L. NBC Decontamination. 2 Welchman. D. Benjamin. England. 45 (PTP 45). Review of Reactions of Chemical Agents in Water. Battelle. Porton. and Brown. 1946. R. March 1948.. GA (Continued) NOTES ¹Witten. UNCLASSIFIED Report. J. Thermal Studies on MCE. 13 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. UNCLASSIFIED Report (ADB 964103). Physical Constants of MCE. 36 (U). 9 Miller.J. Physical Properties of Standard Agents. USA Chemical Research and Development Laboratories.. A.A. MD. P. 10 Marsh. Candidate Agents..R.. Volume I. and Related Compounds at Several Temperatures (U).N. D. UNCLASSIFIED Report (ADB964104). Office of Scientific Research and Development. June 1975. September 1945. 14 Sharon Reutter. ARCSL-SP-83015. Chemical Defense Experimental Establishment.L. Chemical Defence Experimental Establishment. 16 DOD Chemical And Biological Defense Program Annual Report to Congress.. Part III. USA Chemical Research and Development Laboratories. USA Chemical Research and Development Laboratories. 8 Walpole. December 1946. UNCLASSIFIED Report (ADC033491).. Technical Division Memorandum Report 1121. Military Intelligence Division. Chemical Defence Experimental Establishment. Army Chemical Center. August 1945. UNCLASSIFIED Report. C.A. April 2003. et al. et al. Determination of the Flash Points of GA and GB. 85 (PTP-85). June 1983. Summary Technical Report of Division 9. MD. DC. Storage Stability of German GA in Uncoated and Lacquered 75mm Shell at 50°C and 65°C. 28 July 2000. UNCLASSIFIED Report (AD234270). USA Chemical Research and Development Laboratories. January 1947. R. Porton Report No. July 1945. Army Chemical Center. F. December 1948. ECBC Notebook # NB 98-0079. The Hydrolysis of MCE. ¹¹Clark. Porton. and Related Chemical Problems Part I-II. ECTR-75032. USA Armament Research and Development Command. 17 FM 3-5/MCWP 3-37. MD. January 1989. Kinetics of the Hydrolysis of Ethyl Dimethylamino Cyanophosphonate (and certain other related compounds) in Water. OH. 18 W. NDRC Volume 1. Edgewood Arsenal. Final Report to USA Biomedical Research and Development Laboratory. September 2003. 6 Balson. UNCLASSIFIED Report (ADA010666).... UNCLASSIFIED Report.3. Proton Technical Paper No.L. Chemical Warfare Agents. MD. Agents. B. Aberdeen Proving Ground. Porton. 5 Harris. B. 2747 (PR 2747). p. Determination of the Vapor Pressure of T. 22 December 1995. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. ¹²Harris.M. Review and Recommendations for Human Toxicity Estimates for FM 3-11. February 2000. Aberdeen Proving Ground..3804/3..B. April 1945. Technical Division Memorandum Report 1299. Kirner.W. Technical Division Memorandum Report 1094. Chemical Defence Experimental Establishment. England. 3 Samuel. UNCLASSIFIED Report (ADB964902). England. Vapor Pressure Measurements of Some Chemical Agents Using Differential Thermal Analysis. et al.E. Corrosion Rate of Steel by GA at 65oC. Army Chemical Center. Porton Technical Paper No. II-16 . Columbus. and Macy. UNCLASSIFIED Report. E. J. Technical Division Memorandum Report 1132. MD. Preliminary Report on the Potential Value of Nerve Gases as C. 15 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report.9. UNCLASSIFIED Report (ADB964102). MD.Table II-6.. ECBC-TR-349. UNCLASSIFIED Report (ADA213287).2104.

c See Appendix H for supporting toxicity profile estimates. Note that for an inhalation/ocular expouse the TLE is greater that 1.d ECt50: 1000 g. Sarin (GB) (see Table II-8 [page II-18]).10 See Table II-9 (page II-20) for toxicity estimates.h (Provisional) ECt50: 0.f 1 c.Table II-7.h (Provisional) ECt50: 2000 a. f The TLE value is assumed 1 because the Ct profile is unknown. This means that the effective dosage increases with longer exposure durations and the concentration of the agent decreases. f. 70-kg man 2 min 30-360 min 30-360 min 30-360 min 30-360 min 2 min ROE Percutaneous Liquid b Inhalation/Ocular Percutaneous Vapor e Percutaneous Vapor e Percutaneous Liquid b Inhalation/Ocular Percutaneous Vapor e Percutaneous Vapor e Percutaneous Vapor e Percutaneous Vapor e Inhalation/Ocular Probit Slope 5 12 5 5 5 10 5 5 5 5 10 TLE N/A 1. II-17 . e. Unlike many other agents. includes deaths Threshold effects (slight ChE inhibition) Mild effects (miosis. d Moderate temperatures (65-85°F).13 It is a volatile liquid at room temperature. e Assumes personnel are masked with eye protection and bare skin.5 c ROD Unknown Some Unknown Unknown Unknown Some Unknown Unknown Unknown Unknown Some DOC Low Moderate Low Low Low Moderate Low Low Moderate Moderate Low Severe effects. for which clothing affords some protection against a liquid agent.4 h MV (L) N/A 15 N/A N/A N/A 15 N/A N/A N/A N/A N/A Exposure Duration N/A.d ECt50: 6000 g.f 1 c.000 a.000a.5 c 1 c. It is hypothesized that clothing retards evaporation. g Hot temperatures (greater than 85°F). clothing may enhance the potency of GB liquid on the skin. The Germans developed GB after they developed GA.d LCt50: 7500 g.f 1.h (Provisional) ED50: 900 mga ECt50: 50 a ECt50:12. GA Toxicity Estimates. GA Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LD50: 1500 mg a LCt50: 70 a LCt50: 15.f N/A 1.f 1 c. thereby increasing the effective dose. h Based on recommendations for GB. b Bare skin. rhinorrhea) a NOTES Based on Grotte and Yang (2001). Pure GB is odorless and colorless.15 hence the designation GB. 70-kg man 2 min 30-360 min 30-360 min N/A.f 1 c.5 c 1 c.

t1/2 = 5. T-144 (German).51 x 10-3 @ 0oC7 25. methylfluorophosphonic acid (MFPA) and isopropyl alcohol are initially formed which further hydrolyze to produce MPA and HF.583 @ 0oC (extrapolated)7 7. TL-1618 (UCTL).0oC.0964 @ 25oC. K-monel.7 @ 0oC (calculated from vapor pressure) 3 1. T-2106 (British). At elevated temperatures up to 71oC. 5.0887 @ 25oC. Phosphine oxide. isopropyl ester. IMPF.0oC.2 Varies with pH and temperature. and lead as well as slight to severe amounts of corrosion on aluminum. depending on the type.6 min @ pH 11.48 x 10o @ 25oC. methyl-. 28. fluoroisopropoxymethyl-.1255 @ 0oC (extrapolated) 6 4.6 @ 25oC. storage life decreases slightly.87 x 104 @ 25oC.10 x 10-1 @ 0oC 3 1. @ pH 1.397 @ 25. 1. hydrogen fluoride (HF) and isopropyl methylphosphonic acid (IMPA) are formed which further hydrolyze to produce methylphosphonic acid (MPA) and isopropanol. 4. Methylfluorphosphorsaeureisopropylester (German) CAS Registry Number: 107-44-8 RTECS Number: TA8400000 Physical and Chemical Properties Structural Formula: O CH3 Molecular Formula: C4H10FO2P Molecular Weight: 140. t1/2 = 27 min. t1/2 = 80 hr @ pH 7.9 @ 25. Propoxyl-2-methylphosphoryl fluoride.8 (calculated) 2.37 x 103 @ 0oC (calculated from vapor pressure) 3 11.09 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products CH3 O CH CH3 P F Colorless liquid 1 None when pure 2 150oC (extrapolated) 3 -56oC (FP) 3-5 Pure: 1. Trilon 46 (German). 2. 12 At 71oC. Isopropoxymethylphosphoryl fluoride. 13 Stability in Storage Action on Metals or Other Materials II-18 . T 46 German). 11. 10 Under acidic conditions. at 20oC. copper.Table II-8. Under alkaline conditions. 11 GB stabilized with tributylamine can be stored in steel containers for at least 5 to 10 years @ ambient temperature.0oC.19 x 10-3 @ 25. Methylphosphonofluoridic acid 1methylethyl ester. Isopropyl methylfluorophosphate. Methylphosphonofluoridic acid isopropyl ester. inconel.8 @ 0oC (extrapolated)7 Nonflammable 8 Complete decomposition occurs within 2 1/2 hr @ 150oC 9 Completely miscible with water and common organic solvents 1. 3. Trilon 144 (German). 1. methylfluoro-. Isopropyl methanefluorophosphonate. Sarin II Chemical Name: Isopropyl methylphosphonofluoridate Synonyms: Fluorisoproopoxymethylphosphine oxide. Isopropylester kyseliny methylfluorfosfonove (Czech). isopropyl ester.1182 @ 0oC (extrapolated) 6 Munitions grade: 1. Phosphoric acid. and t1/2 = 0.4 min @ pH 10. MFI. slightly corrosive on steel. brass. GB Alternate Designations: EA 1208. O-Isopropyl methylphosphonofluoridate. t1/2 = 3 1/2 hr @ pH 2. Isopropyl-methylphosphoryl fluoride. Phosphonofluridic acid.

B. May 1955. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. UNCLASSIFIED Report.. 15 Sharon Reutter.. 14 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. B. November 1957. MD. S. UNCLASSIFIED Report.. ashes.B. OH.S. Special Report: Corrosion Resistance of Metals Toward Isopropyl Methylphosphonofluoridate (GB).M. Final Report to USA Biomedical Research and Development Laboratory. April 2003. Chemie der Kampfstoffe. UNCLASSIED Report (ADB187225). 278 (PTP-278). MD. March 1948.. 8 Walpole. USA Chemical and Radiological Laboratories. ERDEC-TR-166. M22 ACADA. 2 Welchman. 4 Zeffert.. Water.M. February 1948. GB (Continued) Other Data Eyes: very high. Volume I. England. September 2003. UNCLASSIFIED Report (ADA213287). UNCLASSIFIED Report (AD498968). MM1 Protection required MOPP4. Elwin C. A.. 6 Wardrop. Porton Report No. NBC Decontamination. D. MD.. et al. Porton Technical Paper No. and Zeffert. 10 Epstein. USA Chemical and Biological Defense Command.W. 9 Perry. Chemical Warfare Laboratories. Chemical Defence Experimental Establishment. USA Armament Research and Development Command. The Properties of 2-Propyl Methylfluorophosphonate (GB) I. Skin and eye toxicity II-19 . B. CAM/ICAM. 16 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. 31 August 1951. Manual of Military Chemistry Volume I. M8A1 ACAA.M. decontamination of smallest drop of liquid agent is essential. Chemical Warfare Laboratories.. CRLR 510.A. Battelle.N.14 STB is effective on equipment. II. Aberdeen Proving Ground. 18 FM 3-5/MCWP 3-37. The Chemistry of the Alkylfluorophosphonites and Related Compounds. UNCLASSIFIED Report. M18A2 CADK.. 7 Samuel. R. Chemical Defense Experimental Establishment. P. and Bryant. Vapor Pressure Data Review and Analysis.. 22 December 1995. Agents. MD. . M21 ACAA. ACSI-J-3890.W.H.. UNCLASSIFIED Report (ADE481528). UNCLASSIFIED Report (ADE471275). MD. 11 Clark. sawdust. et al. UNCLASSIFIED Report (ADE481350). et al. Slow Fractional Crystallization of GB. ARCSL-SP-83015. 17 DOD Chemical And Biological Defense Program Annual Report to Congress. Determination of the Flash Points of GA and GB. February 2000. UNCLASSIFIED Report (AD474404). MD. Skin: highly toxic. Physical Properties of Standard Agents and Related Compounds at Several Temperatures (U). January 1947. England. 18 Use Quick-acting casualty agent NOTES 1 Franke. November 1949. CAPDS.. 5 Tannenbaum. Review of Reactions of Chemical Agents in Water. Porton. April 1951. 3 Penski. Army Chemical Center. and rags) are effective for physical removal. 13 Hutchcraft. H. April 1968. AN/KAS-1 CWDD. ECBC-TR-349. MDR 132. Aberdeen Proving Ground.L. UNCLASSIFIED Report (AD849866).. Preliminary Report on the Potential Value of Nerve Gases as C. TCIR-513. 258. Army Chemical Center. Use the M291 SDK to remove any liquid nerve agent on skin or clothing. Jr. MD. Army Chemical Center. 45 (PTP 45). USA Chemical and Radiological Laboratories. Porton. Effect of pH and Temperature on Hydrolysis Rates. Porton Technical Paper No. USA Chemical and Radiological Laboratories.R. clothing may enhance the potency of GB liquid on the skin 15 Decontamination Flush eyes with water immediately. M272 Water Testing Kit. June 1994. J.. Army Chemical Center..Table II-8. liquid penetrates skin 14 Inhalation toxicity Most toxic route of exposure 15 Rate of action Rapid 16 Means of detection M8 paper. UNCLASSIFIED Report (ADC033491). Chemical Defence Experimental Establishment.. J. Physico-Chemical Properties of Phosphorus Esters Part II: Some Constants of Isopropyl methylfluorophosphinate (GB). Porton. 12 Comparison of GA and GB as Chemical Warfare Agents (U). Army Chemical Center. much greater through eyes than through skin.. MD. USA Chemical Warfare Laboratories. M256A1 CADK.9. England. liquid nerve agent penetrates ordinary clothing rapidly. M90 AMAD.Chemistry of Chemical Warfare Agents. Studies on Hydrolysis of GB I. Porton Technical Paper No. Use the M295 IEDK for individual equipment. M18A3 CADK16. June 1983. Review and Recommendations for Human Toxicity Estimates for FM 3-11.J. and absorbents (earth. 2747 (PR 2747). A. 28 July 2000.J.. UNCLASSIFIED Report (ADE481544). Army Chemical Center. Columbus. March 1952. IPDS.3. et al. Observations on Hydrolysis of GB in Sodium Bicarbonate Buffered Waters. et al. J. CRLR 2. CWL-SP-1. East Berlin. Crystallization of GB. January 1989. M9 paper. steam.

4 j NOTES Based on Grotte and Yang (2001). c d LD50 could be less with clothing.g 1.g N/A 1. j ROD Unknown Some Unknown Unknown Unknown Some Unknown Unknown Unknown Unknown Some DOC Low c Moderate Low Low Low Moderate Low Low Moderate Low Moderate ECt50: 600 h. includes some deaths ED50: 1000 mg a ECt50: 25 a ECt50: 8000 a. h.g.15 See Table II-11 (page II-23) for toxicity estimates.5 d. 70-kg man 2 min 30-360 min 30-360 min 30-360 min 30-360 min 2 min ROE Percutaneous Liquid b Inhalation/ Ocular Percutaneous Vapor f Percutaneous Vapor f Percutaneous Liquid b Inhalation/ Ocular Percutaneous Vapor f Percutaneous Vapor f Percutaneous Vapor f Percutaneous Vapor f Inhalation/ Ocular Probit Slope 5 12 5 5 5 12 5 5 5 5 10 TLE N/A 1.5 d 1 d. b Bare skin.g 1 d. II-20 . GB Toxicity Estimates (Table II-9).g 1 d.5 d 1 d. e f Moderate temperatures (65-85°F) Assumes personnel are masked with eye protection and bare skin.g 1 d. Table II-9. Note that for an inhalation/ocular expouse the TLE is greater than 1.e LCt50: 6000 h. 70-kg man 2 min 30-360 min 30-360 min N/A. h i Hot temperatures (greater than 85°F) Based on Grotte and Yang (2001) and Letter (25 Mar 03). i (provisional) ECt50: 0. rhinorrhea) a MV (L) N/A 15 N/A N/A N/A 15 N/A N/A N/A N/A N/A Exposure Duration N/A.000 a. This means that the effective dosage increases with longer exposure durations and the concentration of the agent decreases.13 2 PAM Cl is not as effective for GD poisoning as it is for other nerve agents1 because the “aging” process halftime is within 2 minutes. GB Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LD50: 1700 mg a LCt50: 35 a LCt50: 12.e ECt50: 4000 h. (2002). See Appendix H for supporting toxicity profile estimates. GD is a colorless liquid when pure.i (provisional) Severe effects. GD (see Table II-10).g 1 d.e Threshold effects (Slight ChE inhibition) Mild effects (miosis. j Based on human data and recent rat data of Mioduszewski et al.i (provisional) ECt50: 1200 a. g The TLE value is assumed 1 because the concentration-time profile is unknown.

Phosphine oxide. 13.789 @ 0oC (extrapolated)5 5. t1/2 = 3 hr. 13 Corrosion rate on steel is 0. 3.6 generally solidifies to a noncrystalline.1 stabilized GD decomposes in 200 hrs @ 130oC.33 x 10-3 @ 0oC5 24. Fluoromethylpinacolyloxyphosphine oxide.2-Trimethylpropyl methyphosphonofluoridate.3-Dimethyl-2-butyl methylphosphonofluridate.3-dimethyl-. T-2107 (British. Pinacolyl methylphosphonofluoride. Zoman (USSR).0oC.003 molar solution of GD @ 25oC. Pinacolyl methane fluorophosphonate. 2-Butanol.2-trimethylpropoxy)-.3-Dimethyl-n-but-2-yl methylphosphonofluoridate.2. unstabilized GD decomposes in 4 hrs @ 130oC 9 Solubility of GD in water is 2.2.2.93 x 103 @ 25oC. 3. fluoromethyl (1. GD Alternate Designations: EA 1210 (US). 12 Stabilized GD can be stored for at least 6 months @ elevated temperatures (71oC) in glass. Pinacolyloxy methylphosphoryl fluoride. Methyl pinacolyloxyfluorophosphine oxide. and aluminum containers. Pynacolyl methylfluorophosphonate CAS Registry Number: 96-64-0 RTECS Number: TA8750000 Physical and Chemical Properties Structural Formula: O CH3 Molecular Formula: C7H16FO2P Molecular Weight: 182.2 @ 25oC. Methylphosphonofluoridic acid 1. 1.0oC. t1/2 = 45 hrs @ pH 6. 9 very soluble in organic solvents 1 Varies with pH. 1.17 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m ) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis 3 CH3 O CH C CH3 CH3 CH3 P F Colorless liquid when pure 1 Fruity. glasslike material 7 1. Methyl pinacolyloxy phosphorylfluoride.96 x 10-2 @ 0oC 4 3.0456 @ 0oC (extrapolated) 7 6. Pinacoloxymethylphosphoryl fluoride. Methylphosphonofluoridic acid.2-trimethylpropyl ester. 5.0222 @ 25oC.01 x 10-1 @ 25oC.65. 6.1 g GD/100g @ 20oC.8 Above 150oC. @ pH 2.5oC5 121oC (open cup) 5. complete hydrolysis occurs in less than 5 min in a 5% NaOH solution 11 Essentially PMPA and HF 11 Relatively stable in glass for 5-1/2 months @ ambient temperature with or without a stabilizer. steel. Methylfluorphosphorsaeurepinakolylester (German). methylphosphonofluoridate. Methyl pinacolyl phosphonofluoridate. Trilon (German). Methylfluoropinacolylphosphonite.2.2-trimethylpropyl ester.167 @ 25.2. methyl-. Phosphonofluoridic acid. Pinacolyl methylfluorophosphonate. 5.90 x 10-3 @ 25.10 3. 5. t1/2 = 60 hrs @ pH 10.3-dimethyl-2-butyl ester. UK). impurities give it the odor of camphor 2.31 x 102 @ 0oC (calculated from vapor pressure) 4 13. 4.3 (calculated) 4. Pinacoloxymethylphosphoryl fluoride.3 198oC (extrapolated) decomposes 4 -42oC (MP).4 g GD/100g solution @ 0oC.8 @ 0oC (calculated from vapor pressure) 4 3. 9.2-Trimethylpropylester kyseliny methylfluorfosfonove (Czech). PMFP Chemical Name: Pinacolyl methyl phosphonofluoridate Synonyms: 3.00001 inch/month @ 65oC 14 Hydrolysis Products Stability in Storage Action on Metals or Other Materials II-21 . 1. Methyl pinacolyl phosphonofluoridate. using a 0. 3.5 @ 25.Table II-10. 1.

December 1965. FM 3-5/MCWP 3-37. East Berlin. USA Chemical Research and Development Laboratories Notebook # NB 7265.... D. ACSI-J-3890. and absorbents (earth. Edgewood Arsenal. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. TDMR 1346.Chemistry of Chemical Warfare Agents. 8 Fielder. GD (Continued) Other Data Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Eyes: very high toxicity. EC-TR-76058. M9 paper.B. Chemical Corps Technical Command. ARCSL-SP-83015. p.. The Search for Toxic Chemical Agents (U).. 28 July 2000. Military Chemistry and Chemical Agents. EA 1212. ashes. MD. II-22 . 4 Savage. Aberdeen Proving Ground. M22 ACADA. 22 December 1995. IPDS. EA 3547. J. CRDLR 3342. R..W. December 1963. M21 ACAA. CAPDS. EA 1211. P. EA 5365. GF and EA 1356 (U). August 1976. 6 Stern. MD. 9 Chemical Agent Data Sheets Volume I. Army Chemical Center. CONFIDENTIAL Report (AD369299). MD. Edgewood Arsenal. VX. UNCLASSIFIED Report (AD507852). et al.. Agents. 16 M18A3 CADK. L. Porton. December 1974. J. Preliminary Report on the Potential Value of Nerve Gases as C. January 1947. B. 5 Samuel. Chemical Corps Technical Compound. 12 Newman. 3 TM 3-215/AFM 355-7. et al. EC-TR-77016. UNCLASSIFIED Report (ADB013164). S.. USA Armament Research and Development Command. UNCLASSIFIED Report (ADC033491). UNCLASSIFIED Report (ADB964759). much greater through eyes than through skin. March 1947. CONFIDENTIAL Report (ADC009719).M. 14 Hormats. MD. M8A1 ACAA. and EA 5533. Use the M295 IEDK for individual equipment.9. R. November 1969.A. J. 2 Welchman. Army Chemical Center. UNCLASSIFIED Report (ADB966291). Benjamin. Volume I. and Fielder. April 1977. D. Manual of Chemistry Volume I. . steam. September 2003.. p. Quick-acting casualty agent Use 1 NOTES Franke. The Hydrolysis Rate of GD. sawdust. M272 Water Testing Kit. UNCLASSIFIED Report (ADB028222).. et al. 11 Buckles. CAM/ICAM. July 1947. Army Chemical Center. Edgewood Arsenal Research Laboratories. 15 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. USA Chemical Research and Development Laboratories. M256A1 CADK. and Coulter. M18A2 CADK. April 2003. EA 1213. UNCLASSIFIED Report (ADE470188). Physical Properties of Standard Agents. TCIR 373. MD. 15 decontamination of smallest drop of liquid agent is essential. and 19 rags) are effective for physical removal. MD.M. STB is effective on equipment. 10 Witten. UNCLASSIFIED Report (ADB964904). 18 19 DOD Chemical And Biological Defense Program Annual Report to Congress. June 1983. Aberdeen Proving Ground. 13 Grula. J. et al. AN/KAS-1 CWDD.Table II-10. MD. UNCLASSIFIED Technical Manual (ADA292141). 16 Sharon Reutter. Chemical Defence Experimental Establishment. 45 (C). Corrosion Rate of Steel at 65°C. M90 AMAD. 2747 (PR 2747). Physical Constants of G-Series Compounds: Compounds EA 1210. et al. England. Aberdeen Proving Ground. February 2000. Water. EATR 4210.S. Chemie der Kampfstoffe.. Aberdeen Proving Ground. 7 Zeffert.... MD. SBCCOM Report Review and Recommendations for Human Toxicity Estimates for FM 3-11. S. NBC Decontamination.C. Storage Stability of GD. Edgewood Arsenal Special Report EO-SR-74001.H.. MM1 MOPP4. Porton Report No. Use the M291 SDK to remove any liquid nerve 15 agent on skin or clothing. EA2223. liquid penetrates skin. 17 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. A Thickener for GD (U).A. Most toxic route of exposure Rapid 17 16 M8 paper. Storage Stability in Steel at 65°C of Pure GD. MD. USA Chemical Research and Development Laboratories.3.B. ECBC-TR349. Candidate Agents. R. Edgewood Arsenal. UNCLASSIFIED Technical Manual (AD849866). EA 1214. Skin: highly toxic. April 1968. Technical Division Memorandum Report 1292.. 72 (C). March 1948. liquid nerve agents penetrate ordinary clothing rapidly 15 Protection required Decontamination Flush eyes with water immediately.. and Related Compounds at Several Temperatures (U). The Vapor Pressure of Chemical Agents GD. EA 3580. USA Chemical Warfare Laboratories Notebook # NB 6695.

13 See Table II-13 (page II-26) for toxicity estimates.i.f ECt50: 150 g.f ECt50: 0. b Bare skin. rhinorrhea) a N/A N/A Percutaneous Vapor e Percutaneous Vapor e Inhalation/ Ocular c. i Based on recommendations for GB and relative potency of GD and GB.d N/A N/A N/A 15 LCt50: 1500 g.25 c 1 1 1 1 c. GF is a colorless and odorless liquid when pure. This means that the effective dosage increases with longer exposure durations and the concentration of the agent decreases. 70-kg man 2 min 30-360 min 30-360 min ROE Percutaneous b Liquid Inhalation/ Ocular Percutaneous e Vapor Percutaneous e Vapor Percutaneous b Liquid Probit Slope 6 12 6 TLE N/A 1.2 i 2 min 1. GD Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LD50: 350 mg LCt50: 35 a a MV (L) N/A 15 Exposure Duration N/A.f N/A. Assumes personnel are masked with eye protection and bare skin.h (provisional) Threshold effects ECt50: 300 a. Table II-11. Cyclosarin (GF) (see Table II-12 [page II-24]). j.h (provisional) Severe effects. g h Hot temperatures (greater than 85°F).d N/A N/A N/A ECt50: 1000 g. II-23 . 70-kg man 2 min 30-360 min 30-360 min 30-360 min 30-360 min N/A Inhalation/ Ocular Percutaneous e Vapor Percutaneous e Vapor 1. includes some deaths ED50: 200 mg ECt50: 25 a a 6 6 12 6 c.f c ROD Unknown Some Unknown Unknown Unknown DOC Low Low Low Low Low Low Low Low Low Low Low LCt50: 3000 a. The TLE value is assumed 1 because the concentration time profile is unknown. c See Appendix H for supporting toxicity profile estimates. d e f Moderate temperatures (65-85°F). Based on recommendations for GB.d 6 6 6 10 c.h (provisional) Mild effects (miosis.25 1 1 c. GD Toxicity Estimates (Table II-11).4 c Some NOTES Based on Grotte and Yang (2001). Note that for an inhalation/ocular expouse the TLE is greater than 1.f c.f Some Unknown Unknown Unknown Unknown ECt50: 2000 a.

98 x 102 @ 25oC. steam. 14 M18A2 CADK. Methyl cyclohexylfluorophosphonate CAS Registry Number: 329-99-7 RTECS Number: TA 8225000 Physical and Chemical Properties Structural Formula: O CH3 Molecular Formula: C7H14FO2P Molecular Weight: 180.000053 inch/month @ 65oC 10 Other Data Eyes: very high toxicity. 14.15 x 10-3 @ 25. M272 Water Testing Kit. . Most toxic route of exposure 12 Rapid 13 M8 paper.78 x 10-3 @ 0oC (extrapolated) 3 8.11 STB is effective on equipment.8 @ 0oC (calculated from vapor pressure) 3 94oC 6 5. Cyclohexyl methylfluorophosphate. Flush eyes with water immediately. ashes.03 x 102 @ 0oC (calculated from vapor pressure) 3 14. M9 paper.27 x 10-2 @ 25oC.003 M solution of GF in distilled water 8 Hydrogen fluoride and cyclohexyl methylphosphonic acid 5 Stabilized GF can be stored @ 71oC for at least 6 months in glass containers and at least 1 year in steel and aluminum containers. 4 -12oC (MP). 1. T-2139 (British).3 @ 25. much greater through eyes than through skin. decontamination of smallest drop of liquid agent is essential. MM1 MOPP4. Phosphonofluoridic acid. methyl-.1276 @ 25oC.5oC6 Completely decomposes within 2 hrs @ 150oC 7 Solubility in water is 3.1 g GF/100 g @ 0oC 6 t1/2 = 42 hrs @ 25oC using a 0. 1. Use the M291 SDK to remove any liquid nerve agent on skin or clothing. cyclohexyl ester.3 @ 25oC. M256A1 CADK. 14. GF Alternate Designations: EA 1212 (US). and absorbents (earth. and rags) are effective for physical removal. AN/KAS-1 CWDD M18A3 CADK. a metastable crystalline form of GF is produced which slowly converts into a stable form that melts @ –12oC 5 1. below –30oC.7 g GF/100g @ 20oC. 5. Use the M295 IEDK for individual equipment. sawdust.16 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Flash Point Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials Skin and eye toxicity P F O Colorless liquid 1 None if pure 2 228oC (extrapolated) 3 –30 to –50oC (FP).Table II-12.762 @ 0oC (extrapolated)6 6. 15 Quick-acting casualty agent Inhalation toxicity Rate of action Means of detection Protection required Decontamination Use II-24 . Water.0oC. M90 AMAD. 5. IPDS.1525 @ 0oC (extrapolated) 4 6. 9 Corrosion rate on steel is 0. CAPDS. Skin: highly toxic. liquid penetrates skin 11.0oC. 9. M22 ACADA. liquid nerve agents penetrate ordinary clothing rapidly 11.5 x 10-3 @ 0oC6 32.41 @ 25.2 (calculated) 9. M21 ACAA. CMPF Chemical Name: Cyclohexyl methylphosphonofluoridate Synonyms: Cyclohexyloxyfluoromethylphosphine oxide. M8A1 ACAA. CAM/ICAM.

and Related Compounds at Several Temperatures (U).A. D.. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. Army Chemical Center.E.. 9 Grula. December 1947. EA1213. 13 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. EA1214. 3 Tevault. EA1211.. J. USA Chemical Research and Development Laboratories. MD. 12 Sharon Reutter. UNCLASSIFIED Report (ADB966236). Joint CB Technical Data Source Book.Table II-12. 258. B. W.. Army Chemical Center. MD. USA Chemical Research and Development Laboratories. et al.. Edgewood Arsenal..3. GF Toxicity Estimates (Table II-13. July 1947. The Hydrolysis Rate of G Agents. G Nerve Agents. September 2003. January 1969. June 1983. Porton. TCIR 393. II. P. SECRET Report (ADC032927). Part Three: Agents GD and GF (U). K. USA Armament Command. 6 Samuel. Physical Constants of G-Series Compounds: EA1210. December 1974. Volume III. 22 December 1995. 10 Kaiser. USA Chemical Research and Development Laboratories. Army Chemical Center. Chemical Defense Experimental Establishment. GF and EA 1356 (U). UNCLASSIFIED Report (ADB969120). Fort Douglas. USA Dugway Proving Ground. Edgewood Arsenal Special Report EO-SR-74002. MD. TR-304S. GF (Continued) NOTES Eakle. EA1212. February 2000. Technical Study 69-C4.. MD. and Coulter. et al. Aberdeen Proving Ground.B. This means that the effective dosage increases with longer exposure durations and the concentration of the agent decreases. S. April 2003. CRDLR 3342. Summary of Information on Agent GF. CONFIDENTIAL Report (AD369299). Aberdeen Proving Ground. July 1947.J. The Chemistry of the Alkylfluorophosphonites and Related Compounds. Aberdeen Proving Ground. 5 Chinn..B. 15 FM 3-5/MCWP 3-37. DPG-TR-82-004. Utah. ¹¹FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11.9. 7 Perry. UNCLASSIFIED Report (ADE481528).. December 1965. USA Desert Test Center.C. CRLR 164.. Storage Stability of GD.. submitted for publication 2 May 2003. USA Armament Research and Development Command. ECBC-TR-349. Physical Properties of Standard Agents. B. Review and Recommendations for Human Toxicity Estimates for FM 3-11. B. 14 DOD Chemical And Biological Defense Program Annual Report to Congress. UNCLASSIFIED Report. MD. Edgewood Arsenal. CONFIDENTIAL Report (AD000020). page II-26). MD.F.. August 1983. Vapor Pressure of GF. 1 k. Technical Division Memorandum Report 1292).. Porton Technical Paper No. UNCLASSIFIED Report (AD509689). ARCSL-SP-83015. Chemical Agent GF (U). 4 Zeffert. March 1954. 2 Chemical Agent Data Sheets Vol. Kenneth. et al.. Utah. II-25 . R. Candidate Agents. USA Chemical Research and Development Laboratories. et al. MD. Note that for an inhalation/ocular exposure the TLE is greater than 1. England. UNCLASSIFIED Report (ADC033491). NBC Decontamination. USA ECBC. UNCLASSIFIED Report (ADB964904). 31 August 1951. et al.M. 8 Buckles. Volume I.S.. 28 July 2000. L.

i Based on recommendations for GD.f 1 c. A significant component of the hazard or airborne VX is percutaneous absorption of the vapor.f N/A 1.25 c 1 c.25 c 1 c. c See Appendix H for supporting toxicity profile estimates.13 Although VX is significantly less volatile than the other agents.2 i Threshold effects Mild effects (miosis.f 1 c. O-ethyl methyl phosphonothiolate (VX) (see Table II-14).f 1 c.d LCt50: 1500 g.d ECt50 1000 g. II-26 .4 c ROD Unknown Some Unknown Unknown Unknown Some Unknown Unknown Unknown Unknown Some DOC Low Moderate Low Low Low Moderate Low Low Low Low Low LCt50: 35 a LCt50: 3000 a. d Moderate temperatures (65-85°F). h Based on recommendations for GB. b Bare skin. l. VX is a colorless and odorless liquid when pure.h (provisional) ECt50: 0. 70-kg man 2 min 30-360 min 30-360 min 30-360 min 30-360 min 2 min ROE Percutaneous Liquid b Inhalation/ Ocular Percutaneous Vapor e Percutaneous Vapor e Percutaneous Liquid b Inhalation/ Ocular Percutaneous Vapor e Percutaneous Vapor e Percutaneous Vapor e Percutaneous Vapor e Inhalation/ Ocular Probit Slope 5 12 5 5 5 12 5 5 6 6 10 TLE N/A 1. g Hot temperatures (greater than 85°F).10 See Table II-15 (page II-29) for toxicity estimates. rhinorrhea) a NOTES Based on Grotte and Yang (2001). it does vaporize to some extent and is extremely potent.f 1. 70-kg man 2 min 30-360 min 30-360 min N/A. includes some deaths ECt50 25 a ECt50: 2000 a.d ECt50: 150 g.Table II-13.h (provisional) ED50: 200 mg a Severe effects. GF Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LD50: 350 mg a MV (L) N/A 15 N/A N/A N/A 15 N/A N/A N/A N/A N/A Exposure Duration N/A. f The TLE value is assumed to be 1 because the Ct profile is unknown. e Assumes personnel are masked with eye protection and bare skin.h (provisional) ECt50: 300 a.f 1 c.

methyl-.5oC. and t1/2 = 60 hrs [pure H2O] 9 VX hydrolyzes via three different pathways (P-S.8 min [1.(bis(methylethyl)amino)ethyl) O-ethyl ester.62 x 10-1 @ 0oC (calculated from vapor pressure) 2 19. Methylphosphonothioic acid S-(2. t1/2 = 36 sec @ 295oC 5 Water solubility of VX is 5% @ 21. Ethyl-S-dimethylaminoethyl methylphosphonothiolate. t1/2 = 1.532 @ 0oC (extrapolated)3 5.0oC. 4 soluble in common organic solvents 5 Hydrolysis rate of VX varies with temperature and concentration. 4. 8 t1/2 = 1. t1/2 = 31 min.6 10.3 hrs [0. t1/2 = 34. 6. t1/2 = 4 min @ 250oC. At 22oC.Table II-14. and aluminum.5 hrs @ 150oC.001M NaOH]. S-(2-(diisopropylamino)ethyl) O-ethyl ester. steel.3 @ 25.0083 @ 25oC.25M NaOH]. [0.0M NaOH)] eventually producing less toxic products. 11 Relatively stable @ ambient temperature.26 x 101 @ 25oC. TX60 Chemical Name: O-Ethyl-S-(2-diisopropylaminoethyl) methyl phosphonothiolate Synonyms: S-(2-Diisopropylaminoethyl) O-ethyl methyl phosphonothiolate. Phosphonothioic acid. the P-O bond cleavage path produces ethyl methylphosphonate (EMPA) and the toxic S-[2diisopropylaminoethyl] methylphosphonothiolate ion (EA 2192). and C-S).0oC. P-O.10M NaOH].0oC.[EA 2192. At room temperature EA 2192 reacts very slowly with OH.8 hrs [0.78 x 10-4 @ 25oC. 1. t1/2 = 20. (calculated from vapor pressure) 2.0209 @ 0oC (extrapolated) 4 9.041 @ 25. t1/2 = 7. Ethyl-S-diisopropylaminoethyl methylthiophosphonate. unstabilized VX of 95% purity decomposes at a rate of 5% a month @ 71oC. 4 miscible with water below 9.1 @ 0oC.7 @ 0oC3 127oC (continuously closed cup method) 7 t1/2 = 502 days @ 71oC. 20.2 @ 25oC.22 x 10-5 @ 0oC (extrapolated) 2 1. O-Ethyl-S-2-diisopropylaminoethylester kyseliny methylthiofosfonove (Czech) CAS Registry Number: 50782-69-9 RTECS Number: TB1090000 Physical and Chemical Properties Structural Formula: O CH3CH2 Molecular Formula: C11H26NO2PS Molecular Weight: 267. t1/2 = 10 hrs @ 170oC.6 hrs @ 200oC. 37.4oC. t1/2 = 41 days @ 100oC. 37. 9. Ethyl S-2diisopropylaminoethyl methylphosphonothiolate.2 (calculated) 8.8 min [0.01M NaOH]. t1/2 = 3. which vary significantly with temperature and pH.63 x 10-3 @ 0oC3 31. slight corrosion with copper 12 Hydrolysis Products Stability in Storage Action on Metals or Other Materials II-27 . At pH below 12. VX Alternate Designations: EA 1701.4 days (1.10 Using an equimolar ratio of VX and water at elevated temperatures appears to reduce the persistency of EA 2192.13 x 10-3 @ 25. 1 Negligible on brass.37 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m ) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis 3 O P S CH2CH2 N CH(CH3)2 CH(CH3)2 CH3 Colorless liquid when pure 1 Odorless when pure 1 292oC (extrapolated) 2 Below –51oC and –39 to –60oC (FP) 3-5 1. 4. 13 Highly purified VX is stable in both glass and steel.25M NaOH]. t1/2 = 10.

6965. UNCLASSIFIED Report (ADB963125). CV and EA 2192. UNCLASSFIED Report (ADA334105). If it does obey the toxic load principle (Cnt = k) where the TLE (n) is less than one. CWLR 2346.K. and Related Compounds at Several Temperatures (U). UNCLASSFIED Report (ADA313080). MD. UNCLASSIFIED Paper (ADE487572). Vapor Pressure of VX. October 1997. HTH. The Search for Toxic Chemical Agents (U). ERDEC-SP-048. steam. MD. M18A3 CADK. USA Armament Research and Development Command. USA Edgewood Research. USA Chemical Warfare Laboratories.17 M18A2 CADK. Vol.. Candidate Agents. 599-605.3.. June 1983. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. Use the M291 SDK to remove any liquid nerve agent on skin or clothing. liquid nerve agents penetrate ordinary clothing rapidly 14 Flush eyes with water immediately. Aberdeen Proving Ground. MD. P. June 1959. 2 Buchanan. et al. 15 Sharon Reutter. ERDEC-SP-036. April 2003. M256A1 CADK.9. M9 paper. Aberdeen Proving Ground. M. CWL Technical Memorandum 31-73. ARCSL-SP-83015. Thermal Decomposition of VX.. MD. December 1974. MD. in fact. et al. Agent VX. et al. December 1959. 4 Coulter. or household bleach are effective on equipment. VX (Continued) Other Data Skin and eye toxicity Inhalation toxicity ROA Means of detection Extremely toxic by skin and eye absorption 14 Extremely potent 15 Rapid 16 M8 paper. M90 AMAD. M22 ACADA. 7 Butrow. 5 Chemical Agent Data Sheets Volume I. May 1996. et al... UNCLASSIFIED Report (AD507852). UNCLASSIFIED Report (ADA371297). 17 DOD Chemical And Biological Defense Program Annual Report to Congress. 28 July 2000.14 STB. Review and Recommendations for Human Toxicity Estimates for FM 3-11.. Development and Engineering Center. UNCLASSIFIED Report (ADC033491). ECBC-TR-349. 58. Development and Engineering Center. 11 Yang. pp. ashes. EATR 4210. soaps. VX is unlike the G agents in that the Ct profile for vapor inhalation appears to obey Haber’s Law. 18 FM 3-5/MCWP 3-37. CRDEC-TR-88056. MD. Army Chemical Center. Edgewood Arsenal Special Report EO-SR-74001. Development and Engineering Center. Use the M295 IEDK for individual equipment. AN/KAS-1 CWDD. UNCLASSIFIED Report (ADB124301). USA Armament Command. Aberdeen Proving Ground. 3 Samuel. February 2000. February 1959. 10 Yang. ECBC Notebook # NB 98-0079. 6 Abercrombie. B. J. 22 December 1995.. Water. UNCLASSIFIED Paper (ADE479900). p. USA Chemical Warfare Laboratories.R. November 1969.” In Proceedings of the 1996 ERDEC Scientific Conference on Chemical Biological Defense Research 19-22 November1996..K. D. sawdust. Army Chemical Center. 18 Quick-acting casualty agent Protection required Decontamination Use 1 NOTES Witten. May 1988.. 11 (U). 13 Salamon.B. Org. 14 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11..” J. detergents. Edgewood Arsenal Research Laboratories. et al. 375-382. Studies in Support of SUPLECAM (Surveillance Program for Lethal Chemical Agents and Munitions) II. MM1 MOPP4. Y.. J. “Hydrolysis of VX: Activation Energies and Autocatalysis... 12 Eckhaus. UNCLASSIFIED Report (ADB028222). Y. et al. However. P. ECBC-TR-068. Aberdeen Proving Ground. Physical Constants of Thirteen V Agents. USA Edgewood Research.” In Proceedings of the 1994 ERDEC Scientific Conference on Chemical Biological Defense Research 15-18 November1994. Chem. NBC Decontamination.. 1. Physical Properties of Standard Agents. 8 Rohrbaugh. et al. pp. CWL Special Publication 4-10. Volume I. November 1999. 1993. Aberdeen Proving Ground. Edgewood Arsenal. S. Army Chemical Center. CAM/ICAM. USA Chemical Research and Development Laboratories. and rags) are effective for physical removal.. MD.B. “Hydrolysis of VX with Equimolar Water at Elevated Temperatures: Activation Parameters of VX. p. September 2003. USA Soldier and Biological Chemical Command. VX Toxicity Estimates (see Table II-15). B. “Perhydrolysis of Nerve Agent VX. MD. et al. it means that the ECt50 does not increase with longer exposures at lower concentrations. m. ECBC Notebook # NB 97-0109 (C). M272 Water Testing Kit. Aberdeen Proving Ground...H. Resistance of Various Materials of Construction in Contact with Transester Process. IPDS. CAPDS. Y.Table II-14. 9 Yang. and absorbents (earth. UNCLASSIFIED Report (ADE471109). M8A1 ACAA. 16 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. MD. it may actually decrease. et al. USA Chemical Research.. UNCLASSIFIED Report (AD314520). MD..9 II-28 . some data indicates that the TLE may be less than one..

i (Provisional) ED50: 2 mg a ECt50: 10 a ECt50: 25 a.g.e LCt50: 75 h. b Bare skin. Assumes personnel are masked with eye protection and bare skin. n. includes some deaths Threshold effects (Slight ChE inhibition) Mild effects (miosis. 70-kg man 2-360 min 30-360 min 30-360 min N/A.Table II-15.j ROD Unknown Little.g 1 c. It is also noted that it is more volatile than VX.g 1 c. if any Unknown Little. it appears to be less potent than VX.g 1 c.g 1 c. Based on recommendations for GB and Cummings and Craig (1965). c d e f See Appendix H for supporting toxicity profile estimates.i ECt50: 0. Another V agent of interest is Vx. so its potential airborne hazard is greater than that for VX. if any Little.e ECt50: 12 h. called “V sub x”. it is decidedly more potent than the G agents. Based upon percutaneous liquid exposure. h i j Hot temperatures (greater than 85°F). rhinorrhea) a NOTES Based on Grotte and Yang (2001). Estimates should be revised as new data becomes available.10 See Table II-17 (page II-31) for toxicity estimates.g N/A 1c 1 c.e ECt50: 5 h. if any Little. VX Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LD50: 5 mg a LCt50: 15 a LCt50: 150 a.I (Provisional) ECt50: 10 a. II-29 . human estimate for miosis may go down. The TLE value is assumed to be 1 because the Ct profile is unknown. 70-kg man 2-360 min 30-360 min 30-360 min 30-360 min 30-360 min 2-360 min ROE Percutaneous Liquid b Inhalation/ Ocular Percutaneous Vapor f Percutaneous Vapor f Percutaneous Liquid b Inhalation/ Ocular Percutaneous Vapor f Percutaneous Vapor f Percutaneous Vapor f Percutaneous Vapor f Inhalation/ Ocular Probit Slope 6 6 6 5 6 6 6 6 6 6 4 TLE N/A 1c 1 c. if any Unknown Unknown Unknown Unknown Some DOC Low Low d Low Low Low Low d Moderate Low Moderate Low Low Severe effects. However. LCt50 /ECt50 could be less. Information on this agent is limited.1 a MV (L) N/A 15 N/A N/A N/A 15 N/A N/A N/A N/A N/A Exposure Duration N/A.g 1 c. Vx (see Table II-16) [page II-30]. g Moderate temperatures (65-85°F).

steam. M9 paper. 5.02 @ 0oC (calculated from vapor pressure) 3.5 STB.4 16. soaps.64 x 101 @ 25oC.7 x 10-4 @ 0oC (extrapolated) 3.26 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials Skin and eye toxicity Inhalation Toxicity Rate of action Means of detection Protection required Decontamination CH3 S CH2CH2 N CH3 O P CH3 Use Liquid 1 Odorless2 256oC (extrapolated) 3. sawdust.73 x 10-3 @ 25oC.0oC.4 @ 25. CAM/ICAM.Dimethylaminoethyl-O-ethylester kyseliny methylthiofosfonove (Czech).Table II-16. Water. detergents.0oC. 7.8 x 10-3 hr-1 (based on a nonlinear least square fit) 5 Ethanol and the toxic product compound S-(2-dialkylamino-ethyl) methylphosphonothioic acid that is very stable in neutral water3 Data not available Data not available Other Data Extremely toxic by skin and eye absorption 6 Extremely potent 7 Rapid 8 M8 paper. 5. S-[2-(dimethylamino)ethyl] O-ethyl ester. 10 Quick-acting casualty agent II-30 . 33.0 @ 25oC. and rags) are effective for physical removal. HTH. or household bleach is effective on equipment. methyl-.56 x 10-3 @ 25.0820 @ 0oC (extrapolated) 1 7. M8A1.4 7. Medemo Chemical Name: O-ethyl S-(2-dimethylaminoethyl) methylphosphonothiolate Synonyms: Phosphonothioic acid. 16.628 @ 25. EDMM. O-Ethyl-S(dimethylaminoethyl)-methylphosphonothioate CAS Registry No: 20820-80-8 RTECS Number: 51366-09-7 Physical and Chemical Properties Structural Formula: O CH3CH2 Molecular Formula: C7H18NO2PS Molecular Weight: 211. 1. Use the M295 IEDK for individual equipment.060 @ 25oC.0oC. IPDS. S-2.02 x 10-3 @ 0oC3 31. O-Aethyl-S-(2-dimethylaminoaethyl)methylphosphonothioat (German).1 @ 0oC (calculated from vapor pressure) 3. 4 Data not available 1. MM17 MOPP4. and absorbents (earth.4 5.335 @ 0oC (extrapolated)3 5.3 (calculated) 6. ashes. slightly soluble in water (source unidentified) The rate coefficient for 7. liquid nerve agents penetrate ordinary clothing rapidly 6 Flush eyes with water immediately. Use the M291 SDK to remove any liquid nerve agent on skin or clothing. 15. Vx Alternate Designations: EA 1699. M18A2 CADK.7 @ 0oC (extrapolated)3 Data not available Data not available Soluble in organic solvents.

therefore. December 1959. ARCSL-SP-83015. Candidate Agents. Physical Constants of Thirteen V Agents (U).J.B. UNCLASSIFIED Report (ADA225952). 3 Samuel. 7 Sharon Reutter. NBC Decontamination. It has a faint odor. and ultimately unconsciousness. palpitation and pain in the chest and region of the heart. 9 DOD Chemical And Biological Defense Program Annual Report to Congress. L. that sometimes cannot be detected even in lethal concentrations. and SA. P.10 Inhalation of high concentrations can initially cause breathing that is deeper and more rapid than is normal at rest. and death. CWLR 2346. On the Stoichiometry of Phosphonothiolate Ester Hydrolysis. December 1963. 2 TM 3-215/AFM..18 Exposure to AC causes an increase in respiration within a few seconds.B. Pure AC is a nonpersistent. Military Chemistry and Chemical Agents. MD. et al.1 See Table II-19 (page II-33) for toxicity estimates. USA Armament Research and Development Command. followed closely by a loss of consciousness. 64 (U).. MD..3. Edgewood Arsenal Notebook # NB 9298. MV (L) N/A Exposure Duration ROE Probit Slope TLE N/A ROD Unknow n DOC N/A N/A N/A N/A 6. J. a. colorless liquid that is highly volatile. 22 December 1995. Vx (Continued) NOTES Coulter. UNCLASSIFIED Report (AD314520). Aberdeen Proving Ground. September 2003. 10 FM 3-5/MCWP 3-37. Review and Recommendations for Human Toxicity Estimates for FM 3-11. ECBC-TR-349.18 SA causes hemolysis of the red blood cells. p. nonpersistent.20 Exposure at high concentrations causes effects within seconds and death within minutes in unprotected personnel. Volume I. CRDEC-TR-212. Physical Properties of Standard Agents. USA Chemical Research Development & Engineering Center. This progresses to respiratory arrest. Blood Agents Blood agents include AC. J. February 2000.Table II-16...9.12 See FM 3-11.. 1 Table II-17.4 for filter change criteria. CK. a casualty may not be able to hold his breath.12 Inhalation of small amounts causes giddiness. USA Chemical Warfare Laboratories. The cyanogen blood agents AC and CK affect the bodily functions by inactivating the cytochrome oxidase system.18 The protective mask with fresh filters gives adequate protection against field concentrations. and Related Compounds at Several Temperatures (U). 5 Szafraniec. confusion. headache and faintness. 6 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. difficulty breathing. Washington DC. AC (see Table II-18 [page II-32]). July 1990.1 After exposure to AC and CK. UNCLASSIFIED Report (ADC033491).H. et al. Vx Toxicity Estimates10 Endpoint N/A Toxicity (mg-min/m3) No toxicity estimates are recommended at this time because data are lacking.19 Cyanogen agents are highly volatile and. MD. 4 Newman.. June 1983. UNCLASSIFIED Technical Manual (ADA 292141). 28 July 2000. cessation of cardiac activity. II-31 . et al. similar to bitter almonds. filters should be changed. April 2003. Army Chemical Center. Aberdeen Proving Ground.. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. The pink color of the casualty’s skin suggests AC poisoning. et al. 8 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report.18 This poisoning prevents cell respiration and the normal transfer of oxygen from the blood to body tissues.

10 Rapid 11 M256A1 CADK. Cyanwasserstoff (German). M18A2 CADK. formic acid (HCOOH). Forestite (French).1 Data not available Data not available Data not available -18oC (closed cup). 2. Cyaanwaterstof (Dutch).6797 @ 25oC. sulfur dioxide. cast iron.03 Physical State Odor Boiling Point FP/BP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage C N Colorless liquid 1 Bitter almonds or peach kernels 2. and lead 2 Other Data None Can cause death within minutes. 6 forms explosive polymer on standing. 6.1 -13. MMI Protective mask with fresh filter.3.6 with the use of a stabilizer such as phosphoric acid.3oC (MP) 1 0. Formonitrile CAS Registry Number: 74-90-8 RTECS Number: MW6825000 Physical and Chemical Properties Structural Formula: H Molecular Formula: HCN Molecular Weight: 27. Prussic acid. 2. MOPP 4 when exposed to or handling liquid AC 13 Move to fresh air. Aero Liquid HCN Chemical Name: Hydrogen cyanide Synonyms: Hydrocyanic acid.1 1. AC Alternate Designations: Cyclone (Russian).5oC. and amorphous brown solids 9 Pure AC is unstable in storage. Acide cyanhydrique (French).6 Corrodes iron.72 @ 25. Blausaeure (German). rapid with traces of base or basic salts 8 Ammonia. Cyjanowodor (Polish).Table II-18.72 @ 25. Carbon hydride nitride (chn). M272 water testing kit. or powdered copper. 1. 7. AC may be stored in metal containers for long periods of time @ temperatures up to 65oC 2.5oC 4.0oC.0oC.0oC.5oC.60 x 102 @ 25.1 6.5oC. Blauwzuur (Dutch).65 x 102 @ 0oC 4.10 x 106 @ 25. 3 frequently ignites when explosively disseminated6 Above 65. Cyclone B. 2.7162 @ 0oC 5 0. Evercyn. Formic anammonide.08 x 106 @ 25.12 M18A3.3 25. forms explosive polymer on long standing.3 stabilized material can be stored up to 65oC 6 Miscible with water and common organic solvents including alcohol and ether 7 Slow under acidic conditions. Acido cianidrico (Italian). 4.46 x 102 @ 25. none required under field conditions 14 Quick-acting casualty agent Action on Metals or Other Materials Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination Use II-32 . 6.5oC when stabilized. 0.71 @ 0oC (calculated from vapor pressure)4. chromium steel.20 x 105 @ 0oC (calculated from vapor pressure) 4.93 (calculated) 7. Cyclon.

p. ³Lewis.” ¹¹NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. Chap. UNCLASSIFIED Report (AD234270). Maryland.Table II-18. Chemical Corps Board. lung irritation can lead to pulmonary edema.. Biological.13 It is nonpersistent and is used as a quick-acting casualty agent. Office of Scientific Research and Development. 29 May 2003.20 See Table II-21 (page II-35) for CK toxicity estimates. R. Battelle. Soc. 1194.H. p. 1992.10 However. and Biologicals. Merck & Company.. NDRC Volume 1. 16 (U). Inc. p.20 It is readily detectable by its immediate lacrimatory effect and its irritant effect on the nasal passage. Chem. Nuclear. 9 Clark. c Based on TM 3-215 (1952) and secondary human data. Drugs.” J. Kirner. 7. p. 13 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. and Conventional (NBCC) Defense Operations and Standards (Operations). UNCLASSIFIED Report (ADA213287). John Wiley & Sons.J. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. Whitehouse Station. 22 December 1995.. Soc.A. p. II-33 . W. Washington. 4 Abercrombie.. Am. 2001. 1997. Army Chemical Center.E. Sax’s Dangerous Properties of Industrial Materials. NY. Review of Reactions of Chemical Agents in Water. 10 BG Russ Zajtchuk et al.F. 2001. ACSI-J-3890. 2626. New York. “Studies on Hydrogen Cyanide. Part XVIII. AC (Continued) NOTES ¹Giauque. December 1956. 1 February 1996. R. and Ruehrwein. Table II-19.. c. 8 Properties of War Gases Vol. Heat of Vaporization and Vapor Pressure. Summary Technical Report of Division 9. This means that the effective dosage increases with longer exposure durations and the concentration of the agent decreases. ²Franke. D.Chemistry of Chemical Warfare Agents. AC Toxicity Estimates10 Endpoint Lethality Severe effects Threshold/odor (odor detection) a b Toxicity (mg-min/m3) LCt50: 2860 a (Provisional) ECt50: NR EC50: 34 mg/m3 c MV (L) 15 N/A N/A Exposure Duration 2 min ROE Probit Slope 10 Unknown Unknown TLE 1. CK is a colorless gas with an irritating odor. OH.. J.. Heat Capacity. Manual of Military Chemistry Volume I.. 857. “The Entropy of Hydrogen Cyanide.. “Cyanide Poisoning. AC Toxicity Estimates (Table II-19). Chem. February 2000. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B). ECBC Notebook # NB 98-0079.85 b Unknown N/A ROD Some Some N/A DOC Low N/A Low Inhalation/ Ocular N/A Inhalation/ Ocular Seconds Inhalation/ Ocular NOTES Based on McNamara (1976).20 At high concentrations CK produces effects similar to AC. 6 W. S. April 1968.” J. UNCLASSIFIED Report (AD849866). Vol. 14 FM 8-9/NAVMED P-5059/AFJMAN 44-151. Chemical. NJ. 61.. Final Report to USA Biomedical Research and Development Laboratory.. II: Blood and Nettle Gases (U). 13th ed. p. 1939. P. and Davies. CK (see Table II-20 [page II-34]). 1946. Vol. ETF 100-41/Vol-2. 12 AFMAN 10-2602. Chemie der Kampfstoffe. East Berlin. Note that for an inhalation/ocular expouse the TLE is greater than 1. January 1989. No toxicity effects for severe effects is recommended. 10th ed. R. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries.. Columbus. Hydrogen Bond Polymerization of the Gas in Chains of Indefinite Length. (eds). Office of the Surgeon General. in occasional instances. Some Physical Properties of Anhydrous Hydrogen Cyanide. 1950. CONFIDENTIAL Report (AD108457). b. 10. Chemical Warfare Agents. 3.N. and Related Chemical Problems Part I-II. 5 Coates. The existing estimate is not supported by the available data.R. DC. Chapter 2. Inc. See Appendix H for supporting toxicity profile estimates. 7 The Merck Index: An Encyclopedia of Chemicals.

powdered sodium pyrophosphate.Table II-20. sulfur mustard.8°C. munitions grade CK with a water content of less than 0.62 x 106 @ 0°C (calculated from vapor pressure) 3-5 6. 2 None if CK is dry. Chlorocyanogen.1 (calculated) 7. slowly polymerizes when stored unstabilized in steel and other common metals @ elevated temperatures (see stability in storage section) 2 Other Data Irritation to eyes similar to RCAs 11 Can cause death within minutes 11 Rapid 12 M256A1 CADK. 6.48 x 10² @ 0°C 3-5 2. 7 soluble in common organic solvents. 1.37 x 106 @ 10°C.80 x 10² @ 10°C.9°C (FP)5 1. CC. M18A3 CADK.47 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage C N Colorless gas 1 Lacrimatory and irritating 2 12. none required under field conditions 15 Quick-acting casualty agent Action on Metals or Other Materials Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination Use II-34 .41 @ 10°C.8°C.5% can be stored in most common metals for extended periods of time @ temperatures up to 100°C.60 x 10² @ 12.8°C. Chlorocyan. 10. 1.2 When stabilized using 5% anhydrous. cyanuric chloride.62 x 106 @ 12. 6.40 @ 12. but only about 9 weeks @ 60°C. M272 water testing kit. Chlorure de cyanogene (French) CAS Registry Number: 506-77-4 RTECS Number: GT2275000 Physical and Chemical Properties Structural Formula: Cl Molecular Formula: CNCl Molecular Weight: 61. Stable in steel containers for at least 1 year @ ambient temperature. after which time the gas begins to polymerize with formation of the corrosive solid. MMI 13 Protective mask with fresh filters 14 Move to fresh air. 6. 2.4 g/L @ 20°C. and AC 1 The hydrolysis rate of CK with tap water is t1/2 = 180 hrs @ ambient temperature and pH 7 8 Hydrogen chloride and cyanic acid (CNOH) 9 CK is stable in glass containers for long periods of time even @ elevated temperatures.222 @ 0°C 4 2. M18A2 CADK.44 @ 0°C calculated from vapor pressure) 3-5 Data not available Data not available Data not available Nonflammable 2 Approximately 149°C 6 Solubility of liquefied CK in water is 71. Chlorine cyanide. Impurities have a tendency to promote explosive polymerization.202 @ 10°C. Chlorocyanide. Klortsian Chemical Name: Cyanogen chloride Synonyms: Chlorcyan. 4. CK Alternate Designations: Mauguinite (French).8°C (calculated) 3-5 -6.

. CK Toxicity Estimates10 Endpoint Lethality Severe effects Threshold (odor detection. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. Vol. et al. Marguerite E. D.. CK Toxicity Estimates (Table II-21)..” Ca. C. Chemical. Fundamental Study of Toxicity: Solubility of Certain Toxics in Water and in Olive Oil. Surveillance Tests on 75 mm Steel Gas Shell Extending Over a Period of One Year. No toxicity estimates for lethal and severe effects are recommended. Chem.M. ARCSL-TR-79040. Table II-21. Edgewood Arsenal. Soc. 29 May 2003. Chap. vomiting. SA (see Table II-22 [page II-36]). EACD 11. Research. UNCLASSIFIED Report (AD234270). NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B). UNCLASSIFIED Report (ADB042888). The existing estimates are not supported by the available data. 1001. 11 BG Russ Zajtchuk et al. nausea. and Related Chemical Problems Part I-II.” ¹²NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report.19 See Table II-23 (page II-37) for toxicity estimates. MD. Chemical Warfare Service. shortness of breath. e. R. 1640. 13 AFMAN 10-2602. MD.13 Symptoms from inhalation exposure include abdominal pain. p. p. 7 Carter. Chemical Warfare Service. 8 Price. 9 Edwards. Chemical Warfare Agents. Office of Scientific Research and Development. Note that for an inhalation/ocular expouse the TLE is greater than 1. P. and Conventional (NBCC) Defense Operations and Standards (Operations). Chem. and Robinson. UNCLASSIFIED Report (ADA090556). 10. 2 W.. 69. “The Preparation.. CK (Continued) NOTES Franke. ACSI-J-3890.Table II-20. 4 Cook. Manual of Military Chemistry Volume I . February 2000. Summary Technical Report of Division 9. October 1979. NDRC Volume 1.. headache.. Vol. 15 FM 8-9/NAVMED P-5059/AFJMAN 44-151. East Berlin. UNCLASSIFIED Report (ADB959731). Amer. tearing) a Toxicity (mg-min/m3) LCt50: NR ECt50: NR EC50: 12 mg/m3 a MV (L) N/A N/A N/A Exposure Duration N/A N/A Few Seconds ROE Inhalation/ Ocular Inhalation/ Ocular Inhalation/ Ocular Probit Slope Unknown Unknown N/A TLE More than 1 More than 1 N/A ROD Probably Insignificant Probably Insignificant N/A DOC N/A N/A Low NOTES Based on human data and TM 3-215 (1952). June 1920.. April 1968. Chemical Reactivity of Cyanogen Chloride in Aqueous Solution.Chemistry of Chemical Warfare Agents.E. 1935. 22 December 1995.. p. p. Soc. 381. J. garlic-like odor. Chemie der Kampfstoffe. DC. 1946. et al. This means that the effective dosage increases with longer exposure durations and the concentration of the agent decreases. 16 (U). M. “Certain Physical Properties of Cyanogen and its Halides. (eds). and Sauer.. 3 Abercrombie.O.L. and Knight. 1947. USA Chemical Laboratories. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. P. “Hydrolysis and Chlorinolysis of Cyanogen Chloride”. DAAA15-71-C-0478-QSR 3. H. 1 d. 14 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. and Winkler. S. 10 Henley. EACD 445. ECBC Notebook # NB 98-0079.H. causing anemia and kidney damage.R. 25B. Quarterly Status Report (March through May 1972)..C. May 1928. 5 Douglas. Office of the Surgeon General. dizziness. 1 February 1996. confusion. III.. “Cyanide Poisoning. Washington. 1997. SA is a colorless gas with a disagreeable.P. MD. Chapter 2..A.” J.. F. R..19 Exposure from liquid can cause frostbite. Edgewood Arsenal. Incineration/Pyrolysis of Several Agents and Related Chemical Materials Contained in Identification Sets. UNCLASSIFIED Report (ADB955216). Edgewood Arsenal. Nuclear. February 1973. Purification. J. 6 Brooks. UNCLASSIFIED Report (AD849866). Kirner. Physical Properties and Hydrolysis of Cyanogen Chloride. J. Report No.C. 1947. Biological. and weakness. Severe exposure damages blood.. C. II-35 .

5°C and pH ~ 7.028 g/100 g @ 20°C.734 @ -100°C 2 2. garlic-like 1 -62. SA Alternate Designations: Arthur Chemical Name: Arsenic trihydride Synonyms: Hydrogen arsenide.69 x 10¹ @ -100°C 2 2. Aresenwasserstoff (German) CAS Registry Number: 7784-42-1 RTECS Number: CG6475000 Physical and Chemical Properties Structural Formula: H Molecular Formula: AsH3 Molecular Weight: 77. depositing shiny black arsenic 1 Corrosive to most metals 6 Other Data Exposure to liquid causes frostbite 7 Acute toxicity is high 7 1-24 hours (dependent on concentration and exposure duration)7 MM1 Protective mask with fresh filter.4 Rapid in the presence of light.7 (calculated) 4. Arsenous hydride. in the absence of light and air @ 15. metals catalyze decomposition.17 (calculated from Clausius Clapeyron equation which assumes constant heat of vaporization as a function of temperature) 2 Data not available Data not available Data not available Flammable. forms explosive mixtures with air 3 300°C 1 Solubility of SA in water is 0.27 x 105 @ -100°C (calculated from vapor pressure) 2 4. Arseniuretted hydrogen.2°C (extrapolated) 2 -116°C (MP) 2 1. and benzene 3.00 x 10² @ -75°C and 8. none required under field conditions8 Delayed-action casualty agent II-36 . 32% of SA is hydrolyzed within 5 hrs and about 66% within 24 hrs 5 SA hydrolyzes to produce shiny black arsenic. Arsenic hydride. MOPP4 when exposed to or handling liquid SA 7 Move to fresh air.4 soluble in alkalis. hydrocarbons. halogen alkanes.Table II-22. Arsenowodor (Polish). which is also highly toxic 1 Unstable in most metal containers.1 Slow. 1.6 on exposure to light. moist SA decomposes quickly.667 @ -75°C.95 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination Use As H H Colorless gas 1 Disagreeable.55 x 106 @ -75°C and 6.

John Wiley & Sons.10 The severity of a blister agent burn relates directly to the concentration of the agent. which cause immediate pain on contact. Mustards. Warm.” J. and blood-forming organs. p. and Pechukas. 1 February 1996. Departments of the Army and the Air Force. Merck & Company. With an increase in temperature (>85 degrees F) and humidity. 2002. skin.10 Both mustard vapor and liquid rapidly penetrate the skin. inside elbow.J. CONFIDENTIAL Report (AD108457). NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B). UNCLASSIFIED Technical Manual (ADA292141). “Concise International Chemical Assessment Document 47: Arsine: Human Health Aspects. East Berlin. underarms. mucous membranes. Chem.21 It is possible to increase their persistency even more by dissolving them in thickeners. New York. Blister Agents (Vesicants) Blister agents are used to produce casualties. evaporation increases as the temperature increases. Most blister agents are insidious in action except for lewisite (L) and phosgene oxime (CX). I. Manual of Chemistry Volume I. Inc. moist areas with thin skin (perineum.. A.” WHO. 2065. mustards are persistent under cool conditions. R. Chemical Corps Board. “Hydrogen Compounds of Arsenic. 13th ed. SA Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LCt50: 7500 a (Provisional) MV (L) 15 Exposure Duration 2 min ROE Inhalation/Ocular NOTES a Probit Slope Not Calculated TLE 1. p. b See Appendix H for supporting toxicity profile estimates. NY.. 8 FM 8-9/NAVMED P-5059/AFJMAN 44-151. 5 Properties of War Gases Volume II: Blood and Nettle Gases (U). the duration of contact with the skin. to degrade fighting efficiency. arsenicals.1 Blister agents are CW agents that act on the eyes. Army Chemical Center. ACSI-J-3890. Maryland.Table II-22. 4 Lewis.4 b ROD Some DOC Low Based on modeling of 6 species.. W.12 (1) Distilled Mustard (HD) (see Table II-24 [page II-38]). ETF 100-41/Vol-2. 2001. Drugs.Chemistry of Chemical Warfare Agents. and to restrict use of terrain and equipment. 2001.1 and the location on the body. 10th ed..21 Sweaty skin absorbs more mustard than dry skin. Vol.13 The eyes and respiratory tract are the most sensitive target organs. a. external genitalia. and HN-3). NJ. 59. S. Whitehouse Station. Soc. Table II-23. Fishbein and S.10 The latency period for ocular effects is shorter than that for pulmonary effects. and acutely. Am. 309. ocular effects are more debilitating. Sax’s Dangerous Properties of Industrial Materials. II-37 . April 1968. p. Chemie der Kampfstoffe. HD is a pale yellow to dark brown oily liquid with a garlic-like odor..12 The most toxic route of exposure is inhalation/ocular. ²Johnson. Preparation of Arsine in Liquid Ammonia Some Physical Properties of Arsine. and neck) are much more sensitive... 2. however. This group of agents includes the sulfur mustards (H and HD) and the nitrogen mustards (HN-1.10 Mild symptoms caused from vapor exposure include tearing. 6 TM 3-215/AFM 355-7. 138. the effective dosages decrease and are about half of those for temperatures from 65 to 75 degrees F. Assume MOPP4 whenever liquid or vaporized agents are known to be present. Inc.21 The blister agents are divided into three groups: mustards. and Biologicals.. December 1963. Military Chemistry and Chemical Agents. SA (Continued) NOTES ¹The Merck Index: An Encyclopedia of Chemicals. 7 L. HN-2. December 1956. Vol. Because of their physical properties. Czerczak. and urticants. lungs. Washington DC. 7.1 Decontaminate within 1 or 2 minutes after exposure to help prevent or decrease tissue damage. 3 Franke. UNCLASSIFIED Technical Manual (AD849866). 1937.

gritty feeling in the eyes. which were detected at the bottom of the containers. Sulfur mustard. 45.5 @ 25. 2. and sulfonium ion aggregates—one of which is also highly toxic11 A small amount of degradation occurs when stored in steel ton containers for over 50 years.9 @ 0°C7 105°C 5 180°C 8 HD is practically insoluble in water. 5 t1/2 = 5 min @ 25°C via a Sn1 mechanism. 7. gasoline.746 @ 0°C (extrapolated)7 6. 1’-Thiobis(2-chloroethane).06 x 10² @ 25°C (calculated from vapor pressure) 4 15. Bis (2chloroethyl)sulfide. sneezing. 1-Chloro-2-(beta-chloroethylthio)ethane. and CW agents. at atmospheric pressure HD starts to decompose below the boiling point 4 14. Y. Bis (2-chloroethyl) sulphide.21 See Table II-25 (page II-40) for toxicity estimates.65 x 10-3 @ 25. 2’-dichloroethyl sulfide. M. solubility of HD in distilled water is 0. Mustard HD. hoarseness.21 Repeated exposures can cause an increase in sensitivity.13 Very little when pure. 14 Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials II-38 .5 (calculated) 1. and vesication. Gelbkreuz (Czech). 1.beta-Dichlor-ethyl-sulphide.2 Garlic-like 1.0°C.0°C. S mustard. G. 1 colorless when pure 1.9 t1/2 = 60 min @ 25°C in salt water.372 @ 0°C.10 HD on or under water undergoes hydrolysis only if dissolved. Bis (beta-chloroethyl)sulfide. Sulfide.2’-Dichloroethyl sulphide. Table II-24. Severe symptoms include marked lid edema.3 or horseradish 3 218°C (extrapolated).β´dichloroethylsulfide di – (2-chloro-ethyl) sulfide. Mustard Sulfur.0°C. productive cough. rhinorrhea. Sulphur mustard.1’-Thiobis(2-chloroethane) CAS Registry Number: 505-60-2 RTECS Number: WQ0900000 Physical and Chemical Properties Structural Formula: Cl-CH2-CH2-S-CH2-CH2-Cl Molecular Formula: C4H8Cl2S Molecular Weight: 159.beta’-Dichloroethyl sulfide. and erythema. Di-2chloroethyl sulfide. HD is freely soluble in fats and oils. 1. S-Lost.2685 @ 25°C 6 5. HS. β . The rate of HD hydrolysis is controlled by the rate of mass transfer and is very slow. most organic solvents. HD. Mustard gas. Kampstoff “Lost”. possible corneal damage. and Fe. burning. Schewefel-lost. HD Alternate Designations: EA 1033.O.β ‘-dichlorodiethyl sulphide.07 Physical State Odor Boiling Point FP/MP Solid Density (g/mL) Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Pale yellow to dark brown oily liquid.4-dithianium chloride}.3 The corrosion rate of HD on steel is 0.2’-Dichlorodiethyl sulfide. beta.34. severe pain in the eyes. Yellow Cross liquid. beta.itchy.0001 inch/month @ 65°C using munitions grade HD. thiodiglycol. kerosene. 1. Sulphur mustard gas. dyspnea.06 x 10-¹ @ 25°C 4 9.45°C (FP) 2 1. bis (2-chloroethyl).0 @ 25°C (calculated from vapor pressure) 4 3.951 @ 25. 2. 6. Yperite (French & German) Chemical Name: Bis (2-chloroethyl) sulfide Synonyms: 2.92g HD/100g solution at 22°C. Mustard vapor.333 @ 10°C 5 1.12 This degradation appears to be caused by the formation of solid deposits “heels” comprised of a six-membered ring cyclic sulfonium ion {1-(2chloroethyl) -1. β.11 Hydrogen chloride.00 x 10-3 @ 0°C7 42. hacking cough. Sulfur mustard gas.

P.. E. NBC Decontamination.” J.. ERDEC-TR450.C.L. November 1942. 12 Abercrombie.. p. 7 Samuel. and Related Compounds at Several Temperatures (U). Technical Division Memorandum Report 1031. 15 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. September 2003. Properties of Di-(2-Chloroethyl) Sulfide I. HN-3. USA Edgewood Research. USA Edgewood Research. Vol. p. M256A1CADK. and Q (U). Chem..G. Manual of Chemistry Volume I-Chemistry of Chemical Warfare Agents. Military Intelligence Division..Table II-24.. steam. Aberdeen Proving Ground.. Review and Recommendations for Human Toxicity Estimates for FM 3-11. MD..D. CAM/ICAM. UNCLASSIFIED Report (ADB963161).9. Development and Engineering Center. M18A2 CADK MOPP4 whenever liquid or vaporized agents are present 15 Flush eyes with water immediately. “The Melting Point of Mustard Gas. Special Report CRLR 542..B. Vapor Pressure Data Review and Analysis.” Chem. pp 353-360. Mostly at 65°C. Development and Engineering Center.” J. 19 FM 3-5/MCWP 3-37.A. “The Thermal Decomposition of 2:2’-Dichlorodiethyl Sulphide. UNCLASSIFIED Technical Manual (AD849866). July 1998.. 92. 1948. Chem. and Engineering Center. 1992.. MM1. USA Armament Research and Development Command.L. Data on Chemical Warfare. MD. The Kinetics of the Hydrolysis of Vesicants Part II-2:2’-Dichlorodiethylsulphide (H). UNCLASSIFIED Paper.. ERDEC-SP-048. ARCSL-SP-83015. UNCLASSIFIED Report (AD108272). and Butrow. A. 1949. Technical Division Memorandum Report 456. Rev. Use the M291 SDK to remove any liquid nerve agent on skin or clothing. Part XV of the Thermal Decomposition of the Secondary Alkylfluorophosphonites. W. Y. HN-1 and L. UNCLASSIFIED Report. 14 Harris. USA Edgewood Research.3.. M90 AMAD. Vol. 71.. T. detergents. June 1983. 70. Vol. et al. ACSI-J-3890.H. 17 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. et al. B. The Surface Tension.. MD.A. P. Soc. Aberdeen Proving Ground. K. M22 ACADA... September 1941. 11 Yang. 10 Brookfield. ERDEC-TR-043. incapacitating effects by skin absorption require higher concentrations.. MD. sawdust. Chemical Corps Chemical and Radiological Laboratories. p. MD.F. M21 ACAA. A. UNCLASSIFIED Report.19 Delayed-action casualty agent Use 1 NOTES Franke. Great Britain. East Berlin. “Decontamination of Chemical Warfare Agents. 5 Buckles. M9 paper. R.. Use the M295 IEDK for individual equipment. Volume I. February 2000. Chemie der Kampfstoffe. MD. 16 Sharon Reutter. Soc. Sutton Oak Report 544. HD (Continued) Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination Other Data Eyes are very susceptible to low concentrations. UNCLASSIFIED Report (ADB969725). soaps. 1729. 1947. USA Chemical Research and Development Laboratories. Corrosion by Vesicants: Rate of Corrosion of Steel and Other Metals by H. et al. et al. 6 Moelwyn-Hughes. 28 July 2000. et al. 9 Bartlett. and absorbents (earth.” In Proceedings of the 1996 ERDEC Scientifiec Conference on Chemical and Biological Defense Research 19-22 November 1996. Amer.. p. Aberdeen Proving Ground. M272 water testing kit. April 1968. and rags) are effective for physical removal. and Owens. April 2003. M18A3 CADK18. Y. ashes. Army Chemical Center. Soc. 22 December 1995. ECBC-TR-349. E. SO/R/576. 3 Kibler..B. 318.. STB does not effectively decontaminate mustard if it has solidified at low temperatures.. Chemical Warfare Center..” J. Physical Properties of Standard Agents. Water. 1406. 2 Felsing. March 1942. A. “Characterization of HD Heels and the Degradation of HD in Ton Containers. and Swain. England. MD.15 HTH or household bleach is effective on equipment. 18 DOD Chemical And Biological Defense Program Annual Report to Congress.. II-39 . April 1993. Army chemical Center. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries.Chem. UNCLASSIFIED Report (ADA350462). October 1997.L. 15 Most toxic route of exposure 16 Delayed—hours to days 17 M8 paper. M. April 1945.. UNCLASSIFIED Report (ADA334105). The Molecular Surface Energy and the Parachor of Toxic Compounds and of Certain Chlorides Used in Their Manufacture. UNCLASSIFIED Report (ADC033491). S. J... Selected Physical Properties of Ton Container HD (Mustard) and VX. 1966. Edgewood Arsenal. HQ. “Kinetics of Hydrolysis and Displacement Reactions of β-β’-(Dichlorodiethyl Sulfide (Mustard Gas) and of β-Chloro-β’-hyroxidediethyl Sulfide (Mustard Chlorohydrin). 13 Yang. May 1956. Development.J. Aberdeen Proving Ground. 8 Williams.. CW Vesicants: Selected Values for the Physical Properties of H. Sutton Oak. C. et al. et al. Candidate Agents. 4 Penski. UNCLASSIFIED Report (ADA 267059).

protection against. and physical and chemical properties II-40 . j Based on temperature factor given in Grotte and Yang (2001) and analysis of lethal data for GB percutaneous vapor exposure. fishy or soapy odor.g 1 d. 70-kg man 2 min 30-360 min 30-360 min N/A. if any Little. if any Little.6-1mg/m 3 n N/A NOTES Based on Grotte and Yang (2001). Levinstein mustard is the original mustard (gas) of World War I vintage. 70-kg man 30-360 min 30-360 min 2-360 min 30 min 30 min 2-360 min Few seconds ROE Percutaneous Liquid b Inhalation/ Ocular Percutaneous Vapor f Percutaneous Vapor f Percutaneous Liquid b Percutaneous Vapor f Percutaneous Vapor f Ocular Percutaneous Vapor f Percutaneous Vapor f Ocular Inhalation Probit Slope 7 6 7 7 3 3 3 3 3 3 3 N/A TLE N/A 1. elevated temperature.e ECt50: 25 a. laryngitis. n Based on primary human data. d See Appendix H for supporting toxicity profile estimates. if any Some Probably insignificant DOC Low Low Low h Low Low Moderate Moderate h High Moderate Moderate High High Severe effects (vesication) ECt50: 75 m ECt50: 50 a. HN-1 is a colorless liquid when pure with a faint. e Moderate temperatures (65-85°F). Properties of H are essentially the same as those for HD. l Based on human data. bronchitis. coughing.k Severe effects (eyes) Mild effects (erythema.j (Provisional) ED50: 600 mg a ECt50: 500 e. and vomiting. i Hot temperatures (greater than 85°F).l 1 d.Table II-25. if any Some Unknown Unknown Little. (3) Nitrogen Mustard (HN-1) (see Table II-26). (2) Levinstein Mustard (H). The most prevalent symptoms in men inadvertently exposed to HN-1 vapor were conjunctivitis. h True human LCt50/ECt50 values could be lower.13 It is used as a delayed-action casualty agent. In this accidental exposure.g. The effective dosages of H and HD have been demonstrated to be quite comparable. if any Little. g The TLE value is assumed to be 1 because the Ct profile is unknown.g. nausea.000 a. b Bare skin.l 1d 1d 1d 1d N/A ROD Little. some pain) Mild effects (eyes) Odor detection a MV (L) N/A 15 N/A N/A N/A N/A N/A N/A N/A N/A N/A Exposure Duration N/A. itching. c Based on Grotte and Yang (2001) and Sommerville (2002). hoarseness.5 d 1 d.e LCt50: 5000 I. f Assumes personnel are masked with eye protection and clothed skin. the fact that these men. if any Little. k Based on Grotte and Yang (2001) and Letter (Dec 2001). if any Little. HD Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LD50: 1400 mg a LCt50: 1000 c LCt50: 10.k ECt50: 200 i.i ECt50: 25 a EC50: 0. m Based on re-analysis of human data. with all the knowledge available at their command as to precautions.10 This manual does not differentiate between H and HD. It contains H and about 30 percent impurities.g N/A 1 d.

M256A1 CADK. flashing has occurred on static detonation 3 For HN-1 ٠ HCl. M9 paper.9 (calculated) 2. NSC 10873.2’-Dichlorotriethylamine Synonyms: Bis (2-chloroethyl)ethylamine. a dimer. 6 Polymerizes with the formation of solid deposits. 9 Most toxic route of exposure 10 Delayed: 12 hours or longer 11 M8 paper. 12. when stored in steel containers.2°C (MP) 2 1.4. Table II-26. cyclic imonium salts.44 x 10-¹ @ 25°C.7% is destroyed @ 149°C and @ 426°C >99% is destroyed. but increases @ temperatures above 50°C. HN-1 Alternate Designations: Ethyl S. Nitrogen mustard gas –1. NH-Lost. 7 Corrosion of HN-1 on steel @ 65°C is 1 x 10-5 to 5 x 10-5 inch/month 8 Other Data Eyes are very susceptible to low concentration. fishy or soapy 3 192°C (extrapolated).2 13. MM1 12 MOPP4 whenever liquid or vapor is present 9 Stability in Storage Action on Metals or Other Materials Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required II-41 . 1. bis (β -chloroethyl)amine Ethylbis (betachloroethyl)amine CAS Registry Number: 538-07-8 RTECS Number: YE1225000 Physical and Chemical Properties Structural Formula: CH3CH2 Molecular Formula: C6H13Cl2N Molecular Weight: 170.08 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products N CH2CH2Cl CH2CH2Cl Dark oily liquid.23 x 10³ @ 25°C. CH3CH2N(CH2CH2OH)2. 3. 12. were severely affected without knowledge of their exposure.2 Faint. this amount is slight @ ambient temperature.2 2. N-ethyl.10 See Table II-27 (page II-43) for HN-1 toxicity estimates. TL 1149 Chemical Name: 2.0 @ 25°C. Miscible with common organic solvents. incapacitating effects by skin absorption require higher concentrations. CAM/ICAM. etc.3 min @ 25°C in aqueous solution 3 Complete hydrolysis yields the following: hydrochloric acid and ethyl diethanolamine. 5 Solubility in water is approximately 4 g HN-1/L solution @ ambient temperature.1 colorless when pure 1. 1 The process involves a complex series of reactions. serves to further emphasize the insidious nature of this agent.110 @ 0°C (extrapolated) 2 5. TL 329. 3.9 @ 0°C (calculated from vapor pressure) 4. 3 t1/2 = 1.31 x 10² @ 0°C (calculated from vapor pressure) 4. Ethylbis(2-chloroethyl)amine.086 @ 25°C. NOR nitrogen mustard.of HN-1.2 Data not available Data not available Data not available Data not available. with formation of the hydrochloride.32 x 10-²@ 0°C (extrapolated) 4.2 at atmospheric pressure HN-1 decomposes below the boiling point 5 -34.

Technical Division Memorandum Report 706. DC. USA Chemical Research and Development Laboratories. ECBC-TR-349. T. UNCLASSIFIED Report (ADB962153).R. USA ECBC. 7 Harris.R. and rags) are effective for physical removal. and absorbents (earth. NBC Decontamination. July 1999. Chemical Warfare Agents.3. Office of Scientific Research and Development. NDRC Volume 1. II-42 . Technical Division Memorandum Report 1031. HN-1. Kirner. ARCSL-TR-79040. 1946. ECBC Notebook # NB 98-0079. ERDEC-SP-004.. and L. ³W.13 Delayed-action casualty agent Use NOTES ¹Cheicante.. UNCLASSFIED Report (ADB960467). 4 Abercrombie. R. Chapter 19. HQ. Review and Recommendations for Human Toxicity Estimates for FM 3-11. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. September 2003. 13 FM 3-5/MCWP 3-37. 10 Sharon Reutter. Technical Division Memorandum Report 552. detergents. and Parker. UNCLASSIFIED Report (AD234270). HN-1 (Continued) Decontamination Liquid on eyes and skin requires immediate decontamination. 28 July 2000. et al. 6 W. ²Dawson. Army Chemical Center. sawdust. HN-3. July 1943. Thickened Vesicants: Storage Stability of Unthickened and Thickened Nitrogen Mustards and Their Mixtures with Levinstein Mustard.. April 2003. Incineration/Pyrolysis of Several Agents and Related Chemical Materials Contained in Identification Sets.L. MD.A. E. STB does not effectively decontaminate mustard if it has solidified at low temperatures. 9 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. G.Table II-26. M. UNCLASSFIED Paper (ADE491775). et al. April 1945. DC. Mostly at 65°C.. ashes. and Related Chemical Problems Part I-II. p. P. 9 HTH. 24 (U). USA Chemical Research and Development Laboratories. UNCLASSIFIED Report (AD234270). steam.2’ Dichlorotriethylamine. USA Chemical Research and Development Laboratories. 389. B. MD. andMacy. B. p. 8 Harris. 1946. Chemical Warfare Agents. MD.. February 1943. Water. et al.L. MD. Army Chemical Center.. 22 December 1995..L. 12 DOD Chemical and Biological Defense Program Annual Report to Congress. Army Chemical Center. Summary Technical Report of Division 9. Washington. “Investigation for the Determination of Nitrogen Mustard and Related Compounds in Air by Gas Chromatography Using Solid Sorbent Collection and Thermal Desorption. Office of Scientific Research and Development. Summary Technical Report of Division 9.9. Corrosion by Vesicants: Rate of Corrosion of Steel and Other Metals by H. p. UNCLASSIFIED Report (ADB042888). Chapter 6. UNCLASSFIED Report (ADA375171). and Related Chemical Problems Part I-II. 11 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. Kirner. soaps. household bleach is effective on equipment. pp 781-792.. NDRC Volume 1. Washington. A Memorandum Report New Compounds 2. Aberdeen Proving Ground. R. October 1979.” In Proceedings of the 1998 ERDEC Scientific Conference on Chemical and Biological Defense Research 17-20 November 1998.. Volume I. et al.. UNCLASSIFIED Report (ADB963161). 5 Brooks. 59. February 2000.

13 HN-2 is irritating to the eyes.Table II-27. ENT-25294. and it has a fishy or soapy odor. Di(2chloroethyl)methylamine. HN-2 Alternate Designations: Dichloren.d N/A 1 c. Table II-28. itching) Mild effects (eyes) a ECt50: 500 e ECt50: 200 g ECt5: 75 ECt50: 50 e ECt50: 25 g ECt50: 25 N/A N/A N/A 30 min 30 min 2 min Unknown Unknown Unknown Unknown Unknown Unknown Low Low Low NOTES All toxicity values given are provisional and based on recommendations for H/HD. f Assumes personnel are masked with eye protection.d 1 c. Bis(beta-chloroethyl)methylamine. (4) Nitrogen mustard (HN-2) (see Table II-28). N-Methyl-bis(2-chloroethyl)amine.2’dichlorodiethylamine.20 For other symptoms. 70kg man 30 min 30 min 2 min ROE Percutaneous Liquid b Inhalation/Ocular Percutaneous Vapor f Percutaneous Vapor f Percutaneous Liquid Percutaneous Vapor f Percutaneous Vapor. N. Chlorethazine. N-Methyl-bis(beta-chloroethyl)amine. see discussions of HN-1. N-bis(2-chloroethyl)methylamine. Nitrogen mustard. e Moderate temperatures (65-85°F). N-methyl-Lost (German).d 1 c.d 1 c. Methyldi(2-chloroethyl)amine CAS Registry Number: 51-75-2 RTECS Number: IA750000 II-43 . See Table II-29 (page II-45) for HN-2 toxicity estimates.d 1 c. Ethanamine.N-Di(chloroethyl)methylamine. b Bare skin.f Ocular Percutaneous Vapor f Percutaneous Vapor f Ocular Probit Slope Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown TLE N/A 1 c. Mecloretamina (Italian). MBA Chemical Name: Bis-(2-chloroethyl)methylamine Synonyms: 2. Mechlorethamine. Chloramine. 2-chloro-N-(2-chloroethyl)-N-methyl-.2’-Dichloro-N-methyldiethylamine. HN-2 is a colorless liquid when pure. N. HN-1 Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) a LD50: 1400 mg LCt50: LCt50: LCt50: ED50: 1000 10. g Hot temperatures (greater than 85°F).2’-Dichlorodiethyl-methylamine. Mutagen. T-1024. d The TLE value is assumed to be 1 because the Ct profile is unknown. Methylbis(beta-chloroethyl)amine. Methylbis(2-chloroethyl)amine.000 e 5000 g 600 mg MV (L) N/A 15 N/A N/A N/A N/A N/A N/A Exposure Duration N/A. beta’-Dichlorodiethyl-N-methylamine. Chlormethine. S.d 1 c. Mustargen. 2. TL 146. beta. 70kg man 2 min 30 min 30 min N/A. N-Methyl-bischloraethylamin (German). bis(β chloroethyl)amine. Mustine. c See Appendix H for supporting toxicity profile estimate. 2-Chloro-N-(2-chloroethyl)-Nmethylethanamine. NSC 762. N-methyl.d ROD Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown DOC Low Low Low Low Low Low Low Low Severe effects (vesication) Severe effects (eyes) Mild effects (pain.d 1 c. N-Methyl-2. erythema.d 1 c.

the reactions involved could generate enough heat to cause an explosion.1425 @ 0°C (extrapolated) 3. 2 t1/2 = 4 min @ 25°C in an aqueous solution. ashes. HN-2 (Continued) Physical and Chemical Properties Structural Formula: Molecular Formula: C5H11Cl2N Molecular Weight: 156. 1. detergents.22 x 10² @ 0°C (calculated from vapor pressure) 3. dimerizes on storage and deposits crystalline dimers 2 None on steel and brass 2 Other Data Eyes are very susceptible to low concentration.4 (calculated) 4. cyclic imonium salts. M9 paper.2.4 at atmospheric pressure. incapacitating effects by skin absorption require higher concentrations 7 Most toxic route of exposure 8 Delayed: 12 hrs or longer 9 M8 paper. MM1 10 MOPP4 whenever liquid or vapor is present 7 Liquid on eyes and skin requires immediate decontamination. Miscible with common organic solvents. 5.8 @ 0°C (calculated from vapor pressure) 3.118 @ 25°C.11 Delayed-action casualty agent Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination Use II-44 .2. M256A1 CADK. steam. 5. sawdust.49 x 10³ @ 25°C. Water.70°C (FP) 2 1. Slow except where alkali is present. etc.9 @ 25°C.2. 12.70 x 10-² @ 0°C (extrapolated) 3.2.4 3. STB does not effectively decontaminate mustard if it has solidified at low temperatures.16 x 10-¹ @ 25°C.3. instability of HN-2 is associated with its tendency to polymerize or condense.4 5. soaps. a dimer. 2 The process involves a complex series of reactions. dimerizes fairly rapidly in water. 7 HTH or household bleach is effective on equipment.Table II-28. CAM/ICAM. 5 Solubility in water is approximately 13 g HN-2/L solution @ ambient temperature. and rags) are effective for physical removal. HN-2 decomposes below its boiling point 5 . and absorbents (earth.4 Data not available Data not available Data not available Data not available Decomposes before boiling point is reached.4 12. 6 Not stable. with formation of the hydrochloride.05 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature CH3 N CH2CH2Cl CH2CH2Cl Colorless liquid when pure 1 Fishy or soapy 2 177°C (extrapolated).

Chemical Warfare Agents. Office of Scientific Research and Development. P. Chapter 6. Volume I..e Percutaneous Vapor e Ocular Probit Slope Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown TLE N/A Unknown c 1 c.f 1 c. p. April 2003. Office of Scientific Research and Development. HN-2 (Continued) NOTES ¹Witten.9. 59. November 1969. 389. 8 Sharon Reutter.f ROD Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown DOC Low Low Low Low Low Low Low Low 1 c. et al. 6 W.f 1 c. The Search for Toxic Chemical Agents (U).R. Kirner.. f Unknown Unknown Unknown Low Low Low II-45 .f 1 c. 10 DOD Chemical and Biological Defense Program Annual Report to Congress. 70-kg man 30-360 min 30-360 min ROE Percutaneous Liquid b Inhalation/ Ocular Percutaneous Vapor e Percutaneous Vapor e Percutaneous Liquid b Percutaneous Vapor.f 1 c. UNCLASSIFIED Report (ADB960331). Edgewood Arsenal Research Laboratories. ³Abercrombie. Bis (2-chloroethyl) methylamine. 27 (U). Benjamin. September 2003. 4 Dawson. Decontamination. p. UNCLASSIFIED Technical Manual (ADA292141). NDRC Volume 1. Chemical Warfare Agents. Edgewood Arsenal.3. Summary Technical Report of Division 9. Chapter 19. 2 W. Preparation. and Related Chemical Problems Part I-II. 1946. Kirner.f N/A 1 c.. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. MD. UNCLASSIFIED Report (AD507852). Washington. itching) Mild effects (eyes) ECt50: 75 N/A ECt50: 50 d ECt50: 25 g ECt50: 25 N/A N/A N/A 2 min 30-360 min 30-360 min 2 min Percutaneous Vapor e Percutaneous Vapor e Ocular Unknown Unknown Unknown N/A N/A N/A MV (L) N/A 15 N/A N/A Exposure Duration N/A. 28 July 2000. Washington. Review and Recommendations for Human Toxicity Estimates for FM 3-11. 1946. T. Chemical Warfare Center.f 1 c. NDRC Volume 1. UNCLASSIFIED Report (AD234270). 22 December 1995..Table II-28. B. Technical Division Memorandum Report 442. 7 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. DC. DC. February 2000. 5 TM 3-215/AFM 355-7. Table II-29. UNCLASSIFIED Report (AD234270). 70-kg man 2 min 30 min 30 min N/A. 11 FM 3-5/MCWP 3-37. 9 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. HN-2 Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3)a LD50: 1400 mg LCt50: 1000 LCt50: 10. MD. and Related Chemical Problems Part I-II. December 1963. ECBC Notebook # NB 98-0079 p. Military Chemistry and Chemical Agents.R.000 d LCt50: 5000 g Severe effects (vesication) ED50: 600 mg ECt50: 500 d ECt50: 200 g Severe effects (eyes) Mild effects (pain. and Stability.P. erythema. EATR 4210. Summary Technical Report of Division 9. NBC Decontamination. and Witten. September 1942. ECBC-TR-349.

c See Appendix H for supporting toxicity profile estimates. e Assumes personnel are masked with eye protection. d Moderate temperatures (65-85°F).8 @ 25°C. a (5) Nitrogen Mustard (HN-3) (see Table II-30).1 @ 0oC3 Data not available Above 150°C. TO. TS 160 Chemical Name: 2.2 x 10² @ 25°C. 1.Table II-29.9 @ 25.2 x 10-4 @ 0°C (extrapolated) 3 1.20 See HN-1 discussion for additional symptoms. Table II-30. 2’. 16. 44.97 x 10-3 @ 25. Tris (β-chloroethyl)amine CAS Registry Number: 555-77-1 RTECS Number: YE2625000 Physical and Chemical Properties Structural Formula: ClCH2CH2 Molecular Formula: C6H12Cl3N Molecular Weight: 204. See Table II-31 (page II-48) for HN-3 toxicity estimates. 5.0oC. and vomiting. Miscible with common organic solvents.2596 @ 0°C (extrapolated) 3 7. hydrolysis is not complete even after several days unless alkali is present 5 II-46 . none when pure 2 257°C (extrapolated). Tris (2-chloroethyl)amine.08 g HN-3/L @ ambient temperature. HN-2 Toxicity Estimates9 (Continued) NOTES All toxicity values given are provisional and based on recommendations for H/HD. 9.073 @ 25. Nitrogen mustard-3.20 Symptoms noted among humans inadvertently exposed to HN-3 vapor include local irritation of eyes and upper respiratory tract.0 @ 0°C (calculated from vapor pressure) 3 0. odorless liquid when pure.74°C (MP) 3 1.1 x 10¹ @ 0°C.13 It is the most stable in storage of the three nitrogen mustards.0oC.2352 @ 25°C. colorless when pure 1 Geranium-like. 2”-Trichlorotriethylamine Synonyms: Tri (2-chloroethyl)amine.1 (calculated) 1. 0. 2 Very slow.177 @ 0oC (extrapolated)3 5.0oC. 3 at atmospheric pressure HN-3 decomposes below the boiling point 4 -3. f The TLE value is assumed to be 1 because the Ct profile is unknown. 4 remains stable when explosively disseminated 2 Solubility in water is approximately 0. b Bare skin. (calculated from vapor pressure) 3 15. headache. 1. TL 145.38 x 10-3 @ 0oC3 40.1 x 10-² @ 25°C. g Hot temperatures (greater than 85°F). HN-3 Alternate Designations: EA 1053. HN-3 is a colorless.53 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis N CH2CH2Cl CH2CH2Cl Oily dark liquid.

ARCSL-SP-83015.. Washington. Aberdeen Proving Ground.R. Chemical Warfare Agents. etc. 6 In storage HN-3 darkens and forms crystalline deposits. ECBC-TR-349. MM1 11 MOPP4 whenever liquid or vapor is present8 Liquid on eyes and skin requires immediate decontamination. and Related Compounds at Several Temperatures (U). Chem. USA ECBC. Office of Scientific Research and Development. Review and Recommendations for Human Toxicity Estimates for FM 3-11. 1946. NDRC Volume 1. CAM/ICAM. Water. M256A1 CADK.9..12 Delayed-action casualty agent Stability in Storage Action on Metals or Other Materials Use NOTES ¹Cheicante. Aberdeen Proving Ground. Technical Division Memorandum Report 1031. Soc. 389.L. Am. April 2003.3. HN-1. βChloroethyldiethylamine and tris-β-Chloroethylamine. 71. NBC Decontamination. et al. UNCLASSFIED Report (ADA375171).UNCLASSIFIED Report (ADB969725). Kirner. MD. detergents.” J. DC. Army Chemical Center.D. June 1983. 12 FM 3-5/MCWP 3-37.4 Corrodes steel @ a rate of 1 x 10-5 to 5 x 10-5 inch/month @ 65°C. and Macy.R. Candidate Agents. Office of Scientific Research and Development. 8 HTH or household bleach is effective on equipment. with formation of the hydrochloride. Chemical Warfare Agents. November 1942. 1946. 8 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. 7 Harris.. M9 paper. STB does not effectively decontaminate mustard if it has solidified at low temperatures. NDRC Volume 1. July 1999. cyclic imonium salts. 4 Kibler. HQ. “Kinetics and Mechanism of the Reactions of Tertiary β-Chloroethylamines in Solution. Chapter 6. incapacitating effect by skin absorption require higher concentrations 8 Most toxic route of exposure 9 Delayed: 12 hours or longer 10 M8 paper. UNCLASSIFIED Report (AD234270). and absorbents (earth. and Related Chemical Problems Part I-II. soaps. a dimer. February 2000. UNCLASSIFIED Report (ADB963161). R. et al. 11 DOD Chemical and Biological Defense Program Annual Report to Congress. ashes. DC.L. Chemical Warfare Center. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. II-47 . HN-3. Edgewood Arsenal. and rags) are effective for physical removal. 22 December 1995.” In Proceedings of the 1998 ERDEC Scientific Conference on Chemical and Biological Defense Research 17-20 November 1998. “Investigation for the Determination of Nitrogen Mustard and Related Compounds in Air by Gas Chromatography Using Solid Sorbent Collection and Thermal Desorption. USA Armament Research and Development Command. p.. MD. steam. 10 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. and L. et al.. Volume I. 59. Data on Chemical Warfare. Chapter 19.Table II-30. B. ERDEC-SP-004. A. MD. et al. p. HN-3 (Continued) Hydrolysis Products Complete hydrolysis gives the following products: Hydrochloric acid and triethanolamine (TEA). Vol. 1415. 6 W. N(CH2CH2OH)3. 5 Bartlett. 9 Sharon Reutter. pp 781-792. Washington. 4 Relatively stable in steel containers. 1949. USA Chemical Research and Development Laboratories. and Related Chemical Problems Part I-II. September 2003. P. MD. 1 The process involves a complex series of reactions. 28 July 2000.. 2 W. UNCLASSFIED Paper. April 1945. Technical Division Memorandum Report 456. ³Samuel. UNCLASSIFIED Report (ADC033491). Mostly at 65°C. sawdust.. p.B. 2 No attack on iron if dry. Physical Properties of Standard Agents. UNCLASSIFIED Report (AD234270). Corrosion by Vesicants: Rate of Corrosion of Steel and Other Metals by H. Summary Technical Report of Division 9. Kirner. J. Summary Technical Report of Division 9. III..L. R. if dry.7 Other Data Skin and eye toxicity Inhalation Toxicity Rate of action Means of detection Protection required Decontamination Eyes are very susceptible to low concentration.

d 1 c.000 e LCt50: 5000 g Severe effects (vesication) ED50: 600 mg ECt50: 500 e ECt50: 200 g Severe effect (eyes) Mild effects (pain. 70-kg man 2-360 min 30-360 min 30-360 min N/A. 70-kg man 30-360 min 30-360 min 2-360 min 30-360 min 30-360 min 2-360 min ROE Percutaneous Liquid b Inhalation/Ocular Percutaneous Vapor f Percutaneous Vapor f Percutaneous Liquidb Percutaneous Vapor f Percutaneous Vapor f Ocular Percutaneous Vapor f Percutaneous Vapor f Ocular Probit Slope Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown TLE N/A 1 c. f Assumes personnel are masked with eye protection.d 1 c. Average: 188.Table II-31.96 (based on 60:40 wt %) Physical State Odor Boiling Point Pale yellow to brown liquid 1 Garlic-like.d 1 c. c The TLE value is assumed to be 1 because the Ct profile is unknown. Table II-32.d 1 c.d N/A 1 c. T: 263.d 1 c.07. however. HT is a pale yellow to brown liquid with a garlic-like odor.d 1 c. erythema. b Bare skin. it is less vesicant through wet or dry clothing and is somewhat less effective than H on the eyes. T: 63918-89-8 RTECS Number: HD: WQ0900000. T: KN1400000 Physical and Chemical Properties Structural Formula: 60wt% HD: Cl-CH2-CH2-S-CH2-CH2-Cl 40 wt% T: (ClCH2CH2SCH2) 2O Molecular Formula: HD: C4H8Cl2S. HT Alternate Designations: Distilled mustard and T mixture Chemical Name: HD: Bis-(2-chloroethyl) sulfide.13 It is somewhat more vesicant than H on bare skin.10 See Table II-33 (page II50) for HT toxicity estimates. less pronounced than mustard 1 No constant boiling point 2 II-48 . itching) Mild effects (eyes) a MV (L) N/A 15 N/A N/A N/A N/A N/A N/A N/A N/A N/A ECt50: 75 ECt50: 50 e ECt50: 25 g ECt50: 25 Exposure Duration N/A.d 1 c. g Hot temperatures (greater than 85°F).24. T: Bis {2(2-chloroethylthio)ethyl} ether Synonyms: N/A CAS Registry Number: HD: 505-60-2.d ROD Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown DOC Low Low Low Low Low Low Low Low Low Low Low NOTES The toxicity values given are provisional and based on recommendations for H/HD. HN-3 Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3)a LD50: 1400 mg LCt50: 1000 LCt50: 10. It is a mixture of 60 percent HD and 40 percent T. (6) Mustard-T Mixture (HT) (see Table II-32). e Moderate temperatures (65-85°F). T: C8H16Cl2OS2 Molecular Weight: HD: 159. d See Appendix H for supporting toxicity profile estimates.

TDMR 575. HN-3. UNCLASSIFIED Report. 4 Properties of War Gases Volume IV: Vesicants (U). NBC Decontamination. Volume I. MD. February 1943. CAM/ICAM. and Rouiller. R. USA Armament Command. incapacitating effects by skin absorption require higher concentrations than does eye injury 8 Most toxic route of exposure 9 No data available M8 paper. p. and L. M9 paper.. HQ. Mostly @ 65°C. 22 December 1995. 6 Yang. USA Chemical Research and Development Laboratories. UNCLASSIFIED Report (ADB960651). Corrosion by Vesicants: Rate of Corrosion of Steel and Other Metals by H. p. December 1956. 92. soaps. STB does not effectively decontaminate mustard if it has solidified at low temperatures. and sulfonium aggregates.B. 11 FM 3-5/MCWP 3-37. USA Chemical Research and Development Laboratories. CLASSIFIED Report (AD108459).. April 1945.3°C (MP) 3 1. 4 Hydrogen chloride. HQ & HT Review of British & US Literature.L. M18A3 CADK.” Chem.7 x 10-² @ 25°C (calculated based on Raoult’s Law equation) 4 7. et al. Edgewood Arsenal. 9 Sharon Reutter. and Macy. Chemical Corps Board. 7 Other Data Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination Eyes are very susceptible to low concentrations. A. UNCLASSIFIED Report (ADB963161). MD. Rev.00007 inch/ month @ 65°C. Draft. Water. 8 HTH or household bleach is effective on equipment..A. ashes. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. January 1943. N. MD. MD December 1974. thiodiglycol. SBCCOM Report Review and Recommendations for Human Toxicity Estimates for FM 3-11. HN-1... 2 Hydrolyzed by prolonged boiling with water or treatment with caustic alkalis. II. 1992. Army Chemical Center. and absorbents (earth.83 x 10² @ 25°C (calculated from vapor pressure) 4 Data not available Data not available Data not available Data not available Flash point range 109 to 115°C 5 165°C to 180°C 4 Slightly soluble in water. 50 (U). steam. Army Chemical Center.. 5 Butrow. B. M256A1 CADK. 8 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. Aberdeen Proving Ground.3. TDMR 1031. HT (Continued) FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials 1. C. II-49 ..5 (calculated based on 60:40 HT mixture) 7. Edgewood Arsenal Special Report EO-SR-74002. and rags) are effective for physical removal. 1729. USA Chemical Research and Development Laboratories. Vol. Canadian HT corrodes steel at a rate of 0. soluble in most organic solvents. Army Chemical Center.10 M18A2 CADK. ETF 100-41/Vol-4. T. 7 Harris. 28 July 2000. TDMR 534. detergents..Table II-32. ECBC Notebook # N 03-0025. ³Dawson. MD. CONFIDENTIAL Report (AD000020). Y. April 2003.P. A Memorandum Report: New Compounds Bis(B-Chloroethylthioethyl) Ether (T) and its Mixtures with Mustard (HT). based on HD 6 Pressure develops in steel 2 Very little when pure.11 Delayed-action casualty agent Use NOTES ¹Cone. 8 Liquid on eyes and skin require immediate decontamination. ²Chemical Agent Data Sheets Vol. et al. Army Chemical Center.263 @ 20°C 3 6. 10 DOD Chemical and Biological Defense Program Annual Report to Congress.M. “Decontamination of Chemical Warfare Agents. sawdust. MM1 MOPP4 whenever liquid or vapor is present.9.

Table II-33. HT Toxicity Estimates10
Endpoint Lethality Toxicity (mg-min/m3)a LD50: 1400 mg LCt50: 1000 LCt50: 10,000 e LCt50: 5000 g Severe effects (vesication) ED50: 600 mg ECt50: 500 e ECt50: 200 g Severe effect (eyes) Mild effects (pain, erythema, itching) Mild effects (eyes)
a

MV (L) N/A 15 N/A N/A N/A N/A N/A N/A N/A N/A N/A

Exposure Duration N/A; 70-kg man 2-360 min 30-360 min 30-360 min N/A; 70-kg man 30-360 min 30-360 min 2-360 min 30-360 min 30-360 min 2-360 min

ROE Percutaneous Liquid b Inhalation/Ocular Percutaneous Vapor f Percutaneous Vapor f Percutaneous Liquid b Percutaneous Vapor f Percutaneous Vapor f Ocular Percutaneous Vapor f Percutaneous Vapor f Ocular

Probit Slope Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown

TLE N/A 1 c,d 1 c,d 1 c,d N/A 1 c,d 1 c,d 1 c,d 1 c,d 1 c,d 1 c,d

ROD Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown

DO C Low Low Low Low Low Low Low Low Low Low Low

ECt50: 75 ECt50: 50 e ECt50: 25 g ECt50: 25

NOTES The toxicity values given are provisional and based on recommendations for H/HD. b Bare skin. c The TLE value is assumed to be 1 because the concentration time profile is unknown. d See Appendix H for supporting toxicity profile estimates. e Moderate temperatures (65-85°F). f Assumes personnel are masked with eye protection. g Hot temperatures (greater than 85°F).

b. Arsenicals. The arsenical vesicants are organic dichloroarsines. They are respiratory tract irritants and produce lung injury on sufficient exposure. The vapors are irritating to the eyes and the liquid may produce serious eye lesions. Skin damage leading to vesication is produced by sufficient exposure to the vapor or by contact with the liquid. Absorption of vapor or liquid through the skin may lead to systemic intoxication or death.20 (1) Lewisite (L) (see Table II-34). L is a brown liquid with a geranium-like odor.13 L is the principal arsenical of military interest.12 It is extremely irritating to the eyes and quickly produces copious tearing. Liquid on the skin is immediately painful and is absorbed more promptly than H.10 Blistering starts within several hours.21 See Table II-35 (page II-53) for toxicity estimates.
Table II-34. L
Alternate Designations: EA 1034; Lyvizit; LI; M-1; Lewisite (arsenic compound) Chemical Name: Dichloro(2-chlorovinyl)arsine Synonyms: Arsonous dichloride, (2-chloroethenyl)-; Chlorovinylarsine dichloride; 2-Chlorovinyldichloroarsine; βChlorovinyldichloroarsine; (2-Chloroethenyl) arsonous dichloride; Arsine, dichloro (2-chlorovinyl)CAS Registry Number: 541-25-3 RTECS Number: CH2975000

II-50

Table II-34. L (Continued)
Physical and Chemical Properties Structural Formula:

Cl ClCH
Molecular Formula: C2H2AsCl3 Molecular Weight: 207.32 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Brown liquid; colorless when pure 1 Geranium-like; odorless when pure 1 196°C (extrapolated); 2,3 decomposes prior to boiling 4 –44.7 to –1.8°C (FP) (depending on purity and isomers present) 5 1.8793 @ 25°C; 1.9210 @ 0°C (extrapolated) 2 7.1 (calculated) 3.46 x 101 @ 25°C (extrapolated); 2.71 x 10-2 @ 0°C (extrapolated) 2,3 3.86 x 103 @ 25°C; 3.30 x 102 @ 0°C (calculated from vapor pressure) 2,3 15.5 @ 25°C; 17.5 @ 0°C (calculated from vapor pressure) 2,3 2.053 @ 25.0oC, 3.521 @ 0oC (extrapolated)2 8.53 x 10-3 @ 25.0oC, 7.70 x 10-3 @ 0oC2 41.1 @ 25.0oC, 44.2 @ 0oC2 Nonflammable 6 At 149°C, 0.5% of L is destroyed and @ 493°C > 99.99% is destroyed 4 Lewisite on contact with water immediately hydrolyzes to form Lewisite oxide (solid), which dissolves very slowly in water. 1,7 Readily soluble in common organic solvents, oils, and CW agents. 8 Rapid 1,7 2-Chlorovinylarsonous acid (CVAA), 2-chlorovinylarsenious oxide (lewisite oxide), and hydrochloric acid 9 Fairly stable in glass and steel containers, but decomposes considerably upon detonation; alkalis decompose L @ ambient temperatures 1 None if L is dry; corrosive penetration on steel is 1 x 10-5 to 5 x 10-5 inch/month @ 65°C.10 Extremely corrosive towards aluminum and aluminum alloys. 8 Other Data Extremely irritating to the eyes and produces copious tearing,11 also causes immediate burning sensation on skin. Most toxic route of exposure 11 Rapid 12 M9 paper, M256A1 CADK, M21 ACAA, M22 ACADA, M272 Water Testing Kit,13 MM1 MOPP4 whenever liquid or vapor is present 14 Liquid on eyes and skin requires immediate decontamination. 14 STB, HTH, or household bleach is effective on equipment. Water, soaps, detergents, steam, and absorbents (earth, sawdust, ashes, and rags) are effective for physical removal. 15 Quick-acting casualty agent

HC As Cl

Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials

Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination

Use

II-51

Table II-34. L (Continued)
NOTES ¹W.R. Kirner, Summary Technical Report of Division 9, NDRC Volume 1, Chemical Warfare Agents, and Related Chemical Problems Part I-II, Chapter 7, p. 83, Office of Scientific Research and Development, Washington, DC, 1946, UNCLASSIFIED Report (AD234270). ²Samuel, J.B., et al., Physical Properties of Standard Agents, Candidate Agents, and Related Compounds at Several Temperatures (U), ARCSL-SP-83015, USA Armament Research and Development Command, Aberdeen Proving Ground, MD, June 1983, UNCLASSIFIED Report (ADC033491). ³Sumner, J.F., et al., The Vapour Pressure of Arsenious Chloride and of Lewisite I, Sutton Oak Report 561(SO/R/561), Military Intelligence Division, Great Britain, December 1941, UNCLASSIFIED Report. 4 Brooks, M. E. and Parker, G.A., Incineration/Pyrolysis of Several Agents and Related Chemical Materials Contained in Identification Sets, ARCSL-TR-79040, October 1979, UNCLASSIFIED Report (ADB042888). 5 Macy, R., Constants and Physiological Action of Chemical Warfare Agents, EATR 78, Chemical Warfare Service, Edgewood Arsenal, MD July 1932, UNCLASSIFIED Report (ADB956574). 6 Chemical Agent Data Sheets Volume I, Edgewood Arsenal Special Report EO-SR-74001, USA Armament Command, Edgewood Arsenal, Aberdeen Proving Ground, MD December 1974, UNCLASSIFIED Report (ADB028222). 7 Buswell, A.M., et al., The Chemistry of Certain Arsenical Chemical Warfare Agents as Water Contaminants, OSRD 4193, Division 9 National Defense Research Committee of the Office of Scientific Research and Development, June 1944, UNCLASSIFIED Report. 8 Franke, S., Manual of Chemistry Volume I- Chemistry of Chemical Warfare Agents, ACSI-J-3890, Chemie der Kampfstoffe, East Berlin, April 1968, UNCLASSIFIED Technical Manual, (AD849866). 9 Bossle, P.C., et al., Determination of Lewisite Contamination in Environmental Waters by High Performance Liquid Chromatography, CRDEC-TR-042, USA Chemical Research Development and Engineering Center, Aberdeen Proving Ground, MD, January 1989, UNCLASSIFIED Report (ADA206000). 10 Harris, B.L. and Macy, R., Corrosion by Vesicants: Rate of Corrosion of Steel and Other Metals by H, HQ, HN-3, HN-1, and L, Mostly at 65°C, Technical Division Memorandum Report 1031, USA Chemical Research and Development Laboratories, Army Chemical Center, MD, April 1945, UNCLASSIFIED Report (ADB963161). 11 Sharon Reutter, et al., Review and Recommendations for Human Toxicity Estimates for FM 3-11.9, ECBC-TR-349, September 2003. 12 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report, February 2000. 13 DOD Chemical and Biological Defense Program Annual Report to Congress, Volume I, April 2003. 14 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11, Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries, 22 December 1995. 15 FM 3-5/MCWP 3-37.3, NBC Decontamination, 28 July 2000.

II-52

Table II-35. L Toxicity Estimates10
Endpoint Lethality Toxicity (mg-min/m3) LD50: 1400 mg a (Provisional) LCt50: 1000 a (Provisional) LCt50: 5000 – 10,000 e,f (Provisional) LCt50: 2500 – 5000 f,I (Provisional) ED50: 600 mg a (Provisional) ECt50: 500 a,e (Provisional) ECt50: 200 a, i (Provisional) ECt50: 75 a (Provisional) ECt50: 50 a,e (Provisional) ECt50: 25 a,I (Provisional) ECt50: 25 a (Provisional) EC50: 8 j MV (L) N/A 15 N/A N/A N/A N/A N/A N/A Exposure Duration N/A; 70-kg man 2-360 min 30-360 min 30-360 min N/A; 70-kg man 30-360 min 30-360 min 2-360 min ROE Percutaneous Liquid b Inhalation/ Ocular Percutaneous Vapor g Percutaneous Vapor g Percutaneous Liquid b Percutaneous Vapor g Percutaneous Vapor g Ocular Probit Slope Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown TLE N/A 1 c,d 1 c,d 1 c,d N/A 1 c,d 1 c,d 1 c,d 1 c,d 1 c,d 1 c,d N/A ROD Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown DOC Low Low Low h Low h Low Low Low Low

Severe effects (vesication)

Severe effects (eyes) Mild effects (erythema, pain) Mild effects (eyes) Threshold/ odor detection
a

N/A N/A N/A N/A

30-360 min 30-360 min 2-360 min Few Seconds

Percutaneous Vapor g Percutaneous Vapor g Ocular Inhalation/ Ocular

Unknown Unknown Unknown N/A

Unknown Unknown Unknown Unknown

Low Low Low Low

NOTES Based on recommendations for H/HD. b Bare skin. c The TLE value is assumed 1 because the Ct profile is unknown. d See Appendix H for supporting toxicity profile estimates. e Moderate temperatures (65-85°F). f Based on H estimate and animal data. g Assumes personnel are masked with eye protection. h True human values could be lower. i Hot temperatures (greater than 85°F). j Based on TM-215 (1952) and secondary human data.

(2) Mustard-Lewisite Mixture (HL) (see Table II-36 [page II-54]). HL has a garlic-like odor from its HD content.13 Table II-36 lists the properties for the mixture with 37 percent HD and 63 percent L by weight. Statistical analysis of comparative data for HL, H, and L indicates that HL is equipotent to H and both are statistically less potent than L.10 See Table II-37 (page II-56) for toxicity estimates.

II-53

Table II-36. HL
Alternate Designations: Distilled mustard gas and lewisite mixture Chemical Name: HD: Bis-(2-chloroethyl) sulfide; L: Dichloro-(2-chlorovinly)arsine Synonyms: N/A CAS Registry Number: HD: 505-60-2; L: 541-25-3 RTECS Number: HD: WQ0900000; L: CH2975000 Physical and Chemical Properties Structural Formula:

Molecular Formula: Molecular Weight: HD: 159.07; L: 207.32; Average: 186.39 (based on 37:63 wt %) Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Flash Point Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Decomposition Temperature

37 wt% HD: Cl-CH2-CH2-S-CH2-CH2-Cl Cl 63 wt% L: CICH HC-As Cl HD: C4H8Cl2S; L: C2H2AsCl3
Liquid 1 Garlic-like (HD) 2 200°C (extrapolated) 3,4 Munitions grade: -42°C (FP); pure: -25.4°C (FP) 4 1.6383 @ 20°C (calculated) (based on 67 wt% L) 1 6.4 (calculated) 3.63 x 10-1 @ 25°C; 4.93 x 10-2 @ 0°C; (calculated based on Raoult’s law; actual values are assumed to be somewhat lower than calculated values.) 3,4 3.64 x 10³ @ 25°C, 5.39 x 10² @ 0°C (calculated based on Raoult’s law; actual values are assumed to be somewhat lower than calculated values.) 3,4 12.8 @ 25°C; 13.1 @ 0°C (calculated from vapor pressure) 3,4 Data not available for the mixture; HD flashes @ 105°C 5 Data not available Data not available Data not available Above 100°C; based on data which shows that HD decomposes @ 180°C 6 and that L starts to decompose @ 150°C; 7 this might suggest that HL also decomposes in this temperature range Both HD and L are soluble in most organic solvents but only slightly soluble in water, suggesting that HL has a similar degree of solubility towards organic solvents and water.8 HD t1/2 = 5 min @ 25°C;9 HD on or under water undergoes hydrolysis only if dissolved. The rate of HD hydrolysis is controlled by the rate of mass transfer and is very slow. 10 Lewisite on contact with water or moist surfaces immediately hydrolyzes to form lewisite oxide (solid), which dissolves very slowly in water. 11,12 Hydrogen chloride, thiodiglycol, sulfonium aggregates, (CVAA), and lewisite oxidebased on HD and L 13,14 Stable in lacquered steel containers for approximately 3 months @ 65°C, 6 months @ 50°C, and for a year or more @ ambient temperature when using a 50:50 mixture of HD and L. Less stable in uncoated steel containers @ temperatures above 50°C. Stable in glass @ 65°C. 15 Little or none if dry 8 Other Data Equal to L in vesication action;16 both H and L are irritating to the eyes. Most toxic route of exposure 16 Prompt stinging; blistering delayed approximately 12 hours 17 CAM/ICAM, M256A1 CADK, M18A2 CADK,18 MM1 MOPP4 whenever liquid or vapor is present 19

Solubility

Rate of Hydrolysis

Hydrolysis Products Stability in Storage

Action on Metals or Other Materials Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required

II-54

Table II-36. HL (Continued)
Decontamination Liquid on eyes and skin requires immediate decontamination. 19 HTH or household bleach is effective on equipment. Water, soaps, detergents, steam, and absorbents (earth, sawdust, ashes, and rags) are effective for physical removal. STB does not effectively decontaminate mustard if it has solidified at low temperatures. 20 Delayed-action casualty agent

Use

NOTES ¹Mumford, S.A. and Parry, G.A., Report on Physical Properties of Mixtures of H and Lewisite I, PR-1342, USA Chemical Research and Development Laboratories, Army Chemical Center, MD, March 1935, UNCLASSIFIED Report. ²TM 3-215/AFM 355-7, Military Chemistry and Chemical Agents, Washington DC, December 1963, UNCLASSIFIED Technical Manual (ADA292141). ³Abercrombie, P., ECBC Notebook # NB 98-0079, p. 29 (U). 4 Macy, R, Freezing Point and Volatilities of Mustard and Lewisite Mixtures, TCIR 512, USA Chemical Research and Development Laboratories, Army Chemical Center, MD, March 1935, UNCLASSIFIED Report (ADB9670444). 5 Buckles, M.F., CW Vesicants: Selected Values for the Physical Properties of H, T, and Q (U), Special Report CRLR 542, Chemical Corps Chemical and Radiological Laboratories, Army Chemical Center, MD, May 1956, UNCLASSIFIED Report (AD108272). 6 Williams, A.H., “The Thermal Decomposition of 2:2’-Dichlorodiethyl Sulphide,” J. Chem. Soc., p. 318, 1947. 7 Brooks, M. E. and Parker, G.A., Incineration/Pyrolysis of Several Agents and Related Chemical Materials Contained in Identification Sets, ARCSL-TR-79040, October 1979, UNCLASSIFIED Report (ADB042888). 8 Properties of War Gases Volume IV: Vesicants (U), ETF 100-41/Vol-4, Chemical Corps Board, Army Chemical Center, MD, December 1956, CONFIDENTIAL Report (AD108459). 9 Bartlett, P.D., and Swain, C.G., “Kinetics of Hydrolyisis and Displacement Reactions of β,β’-[Dichlorodiethyl Sulfide (Mustard Gas)] and of β-Chloro- β’-hyroxidediethyl Sulfide (Mustard Chlorohydrin),” J. Chem. Soc., Vol. 71, p. 1406, 1949. 10 Yang, Y., et al., “Decontamination of Chemical Warfare Agents,” Chem. Rev., Vol. 92, p. 1729, 1992. 11 W.R. Kirner, Summary Technical Report of Division 9, NDRC Volume 1, Chemical Warfare Agents, and Related Chemical Problems, Part I-II, Office of Scientific Research and Development, Washington, D.C., 1946, UNCLASSIFIED Report (AD234270). 12 Buswell, A.M., et al., The Chemistry of Certain Arsenical Chemical Warfare Agents as Water Contaminants, OSRD 4193, Division 9 National Defense Research Committee of the Office of Scientific Research and Development, June 1944, UNCLASSIFIED Report. 13 Yang, Y., et al., “Characterization of HD Heels and the Degradation of HD in Ton Containers,” In Proceedings of the 1996 ERDEC Scientific Conference on Chemical and Biological Defense Research 19-22 November 1996, UNCLASSFIED Paper (ADE487543), ERDEC-SP-048, pp 353-360, USA Edgewood Research, Development and Engineering Center, Aberdeen Proving Ground, MD, October 1997, UNCLASSFIED Report (ADA334105). 14 Bossle, P.C., et al., Determination of Lewisite Contamination in Environmental Waters by High Performance Liquid Chromatography, CRDEC-TR-042, USA Chemical Research Development and Engineering Center, Aberdeen Proving Ground, MD, January 1989, UNCLASSIFIED Report (ADA206000). 15 Harris, B.L. and Macy, R., Memorandum Report Storage Stability of HL, Mixtures of Mustard and Lewisite, Technical Division Memorandum Report 1302, USA Chemical Research and Development Laboratories, Army Chemical Center, MD, February 1947, UNCLASSIFIED Report (ADB96498). 16 Sharon Reutter, et al., Review and Recommendations for Human Toxicity Estimates for FM 3-11.9, ECBC-TR-349, September 2003. 17 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report, February 2000. 18 DOD Chemical and Biological Defense Program Annual Report to Congress, Volume I, April 2003. 19 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11, Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries, 22 December 1995. 20 FM 3-5/MCWP 3-37.3, NBC Decontamination, 28 July 2000.

II-55

g (Provisional) ECt50: 25 a (Provisional) EC50: 2 mg/m3 h MV (L) N/A 15 N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A Exposure Duration N/A. c The TLE value is assumed to be 1 because the Ct profile is unknown.000 a. II-56 .d N/A ROD Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown N/A DOC Low Low Low Low Low Low Low Low Low Low Low Low Severe effects (vesication) Severe effect (eyes) Mild effects (erythema. (3) Phenyldichloroarsine (PD) (see Table II-38). PD is an odorless and colorless to yellow liquid. HL Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LD50: 1400 mg a (Provisional) LCt50: 1000 a (Provisional) LCt50: 10. 70-kg man 30-360 min 30-360 min 2-360 min 30-360 min 30-360 min 2-360 min ROE Percutaneous Liquid b Inhalation/ Ocular Percutaneous Vapor f Percutaneous Vapor f Percutaneous Liquid b Percutaneous Vapor f Percutaneous Vapor f Ocular Percutaneous Vapor f Percutaneous Vapor f Ocular Probit Slope Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown Unknown N/A TLE N/A 1 c. pain) Mild effects (eyes) Odor Detection a b Few Inhalation Seconds NOTES Based on recommendations for H/HD.g (Provisional) ED50: 600 mg a (Provisional) ECt50: 500 a.10 See Table II-39 (page II-58) for toxicity estimates.e (Provisional) ECt50: 25 a.d 1 c. but the primary action is lung injury. e Moderate temperatures (65-85°F).d 1 c.e (Provisional) ECt50: 200 a.13 PD does have marked vesicant and sternutatory properties. h Based on TM 3-215 (1952).g (Provisional) ECt50: 75 a (Provisional) ECt50: 50 a.Table II-37.d 1 c. it is a fairly potent vesicant. f Assumes personnel are masked with eye protection.d 1 c.d N/A 1 c. itching. Although PD is somewhat less vesicant than H and L by the percutaneous liquid route of exposure.d 1 c. g Hot temperatures (greater than 85°F). Bare skin.d 1 c. 70-kg man 2-360 min 30-360 min 30-360 min N/A.e (Provisional) LCt50: 5000 a.d 1 c. d See Appendix H for supporting toxicity profile estimates.

DJ.A. detergents.Table II-38. 2.7 (calculated) 2. ashes. Phenylarsonous dichloride.3 x 101 @ 0°C (calculated from vapor pressure) 3 15. 12 Delayed-action casualty agent Use II-57 . Sternite. and absorbents (earth.5°C (FP) 3 1.6 kerosene. Fenildicloroarsina (Italian).4 miscible with alcohol. soaps. petroleum. Fenyldichlorarsin (Czech) CAS Registry Number: 696-28-6 RTECS Number: CH5425000 Physical and Chemical Properties Structural Formula: Cl As Cl Molecular Formula: C6H5AsCl2 Molecular Weight: 222. 1. benzene. 2. acetone. 7 Other Data Fairly potent vesicant 8 Toxic lung injurant 8 Immediate effect on eyes.5.1 x 10-3 @ 0°C (both values are extrapolated) 3 2. Dichlorophenylarsine. PD Alternate Designations: Pfiffikus.. MM1.93 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination Colorless to yellow liquid 1 None 2 233°C (extrapolated) 3 -22. Phenylarsinedichloride. Water. 11 Household bleach is effective on equipment. effects on skin are delayed approximately 1 hour 9 M18A2 CADK. Dichlor-fenylarsin (Czech). sawdust. dichlorophenyl-.1 (calculated from Clausius Clapeyron equation which assumes constant heat of vaporization as a function of temperature) 3 Data not available Data not available Data not available Data not available Stable to the normal boiling point 3 Immediately hydrolyzes in the presence of water. FDA Chemical Name: Phenyldichloroarsine Synonyms: Arsine. steam. ether.677@ 0°C 3 7. M18A3 CADK 10 MOPP4 whenever liquid or vapor is present 11 Liquid on eyes and skin requires immediate decontamination. and olive oil 6 Very rapid 4 Hydrochloric acid and phenylarsine oxide which are also highly toxic 4 Data not available No serious effects on mild steel and cast iron. and rags) are effective for physical removal. phenyl-. TL 69.645 @ 25°C.64 x 102 @ 25°C.2 x 10-2 @ 25°C. Arsonous dichloride. M.

Inc. 10 DOD Chemical and Biological Defense Program Annual Report to Congress. liquid. R. ED is a more powerful irritant than L and produces sneezing and lacrimation. Review and Recommendations for Human Toxicity Estimates for FM 3-11. OSRD 4193. f Based on secondary human data. SO/R 488. UNCLASSIFIED Report. Edgewood Arsenal Special Report EO-SR-74001. Volume 3. PD (Continued) NOTES Lewis. R. NY. December 1940.M. 11 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. p. June 1944. Volume I. p. Edgewood Arsenal. Sutton Oak. 8 Sharon Reutter. Sutton Oak. D. T. 3 Owens.13 Although ED is a fairly powerful sternutator and vesicant. CRC Handbook of Chemistry and Physics. or vapor exposures or sever percutaneous liquid exposure.3. Aberdeen Proving Ground. and D.C. et al. 2 TM 3-215/AFM 355-7. 4 Buswell. September 2003.. Table II-39.10 See Table II-41 (page II-60) for toxicity estimates.. b The TLE value is assumed to be 1 because the Ct profile is unknown.. 6 Chemical Agent Data Sheets Volume I. Division 9 National Defense Research Committee of the Office of Scientific Research and Development. December 1963.. 1 (4) PD Toxicity Estimates (Table II-39).A. 22 December 1995. Diphenylcyanoarsine Part III – The Pope-Turner Process. No toxicity estimates are recommended for lethal percutaneous. 82nd ed. DC. England.A.J... England. ED is a colorless liquid with a fruity but biting and irritating odor. c See Appendix H for supporting toxicity profile estimates. R. SO/R 492. John Wiley & Sons. 9 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report.9. 1215.2 min 1 min ROE Percutaneous Liquid Inhalation/Ocular Percutaneous Vapor d Percutaneous Liquid Percutaneous Vapor d Inhalation/Ocular Inhalation/Ocular Probit Slope Unknown Unknown Unknown Unknown Unknown Unknown Unknown TLE Unknown 1 b. 2001. e Based on currently accepted estimates for H/HD. et al. D. New York. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. 12 FM 3-5/MCWP 3-37. MD December 1974.A.. UNCLASSIFIED Report (ADB028222).. The Chemistry of Certain Arsenical Chemical Warfare Agents as Water Contaminants. Diphenylcyanoarsine: Part V – The Physical Properties of M.. 7 Owens. PD Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LD50: NR LCt50: 2600 a (Provisional) LCt50: NR Severe effects (vesication) Intolerable Threshold (odor detection) a MV (L) N/A 15 N/A N/A 15 15 N/A Exposure Duration N/A 2-360 min N/A N/A 30-50 min 1 . UNCLASSIFIED Report. Washington. (5) Ethyldichloroarsine (ED) (see Table II-40).Table II-38. Sax’s Dangerous Properties of Industrial Materials. it is primarily a toxic lung injurant. 3-15.c Unknown Unknown ROD Unknown Unknown Unknown Unknown Unknown Unknown N/A DOC N/A Low N/A N/A Low Low Low ED50: NR ECt50: 200-500 e (Provisional) ECt50: 16 f ECt50: 1 f NOTES Based on existing estimates. 28 July 2000. UNCLASSIFIED Technical Manual (ADA292141). II-58 . 2001.R.. 10th ed. UNCLASSIFIED Report. 5 Lide. December 1940. Military Chemistry and Chemical Agents. ECBC-TR-349. February 2000. The existing estimates are not supported by available data. CRC Press. NBC Decontamination. d Assumes personnel are masked with eye protection. April 2003..c Unknown Unknown 1 b. A...

29 @ 21. Green Cross 3. and rags) are effective for physical removal.5°C 2 2.5 Attacks brass @ 50°C and is destructive to rubber and plastics 3 Other Data Fairly potent vesicant and lacrimator 6 Primarily a lung injurant 6 Immediate irritation.742 @ 14°C 2 6. MM1 MOPP4 whenever liquid or vapor is present 9 Liquid on eyes and skin requires immediate decontamination. 2 decomposes 3 Below –65°C (MP) 2 1.8 M18A2 CADK. when ED is dry. biting. Yellow Cross 1 Chemical Name: Ethyldichloroarsine Synonyms: Dichloroethylarsine. Arsonous dichloride. Arsenic dichloroethane. dichloroethyl-.19 x 104 @ 20°C 2 9. alcohol. ethylCAS Registry Number: 598-14-1 RTECS Number: CH3500000 Physical and Chemical Properties Structural Formula: Cl CH3CH2 As Cl Molecular Formula: C2H5AsCl2 Molecular Weight: 174.0 (calculated) 2. detergents. benzene. TL 214. ashes. 9 Household bleach is effective on equipment. Ethylarsonous dichloride.18 3 Data not available Data not available Data not available Data not available Stable to boiling point 3 Immediately hydrolyzes in the presence of water. steam.89 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials Colorless liquid 1 Fruity. ether. which are also highly toxic 4 Stable 3 None on steel when pure. Arsine. delayed blistering 7 M18 A3 CADK. soaps. ED Alternate Designations: DICK (German). sawdust. and absorbents (earth. kerosene and cyclohexane. and irritating 1 156°C. 10 Delayed-action casualty agent Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination Use II-59 .2 noncorrosive towards iron @ temperatures up to 50°C. Water.4 Soluble in ethyl chloride. acetone.Table II-40.3 Very rapid 4 Hydrochloric acid and ethylarsine oxide.

. which produces sneezing and finally extends to the chest where it gives rise to pain. Methylarsonous dichloride CAS Registry Number: 593-89-5 RTECS Number: CH4375000 II-60 . OSRD 4193. 1968. ED (Continued) NOTES ¹Sax.L. Table II-41. MD. MD Alternate Designations: TL 294. 28 July 2000.13 It has been described as a vesicant. EATR 325. (6) ED Toxicity Estimates (Table II-41). et al. 8 DOD Chemical and Biological Defense Program Annual Report to Congress. 7 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. 4 Buswell. p. September 2003. April 2003.. Data on Chemical Warfare. T. TDMR 456. Table II-42. Ethyldichloroarsine (ED): Preliminary Investigation (1939). Volume I. and respiratory irritant. Edgewood Arsenal. Chemical Warfare Service. NBC Decontamination. The Chemistry of Certain Arsenical Chemical Warfare Agents as Water Contaminants. 741. Division 9 National Defense Research Committee of the Office of Scientific Research and Development. Medikus Chemical Name: Methyldichloroarsine Synonyms: Arsine.. Albany.9. UNCLASSIFIED Report (ADB969725). A. Edgewood Arsenal. Review and Recommendations for Human Toxicity Estimates for FM 3-11. ED Toxicity Estimates10 Endpoint Lethality Toxicity (mg-min/m3) LCt50: NR LCt50: NR MV (L) N/A N/A Exposure Duration N/A N/A 1 min ROE Inhalation/ Ocular Percutaneous Vapor Inhalation/ Ocular Inhalation/ Ocular Probit Slope Unknown Unknown Unknown TLE Unknown Unknown N/A ROD Unknown Unknown Unknown DOC N/A N/A Low Severe effects (temporary incapacitation) Odor detection ECt50: 5 –10 a N/A EC50: 1 mg/m 3 b N/A 1 min Unknown N/A Unknown Low NOTES a Based on secondary human data and TM 3-215 (1952). MD. UNCLASSIFIED Report (ADB957078). Methyl-dick. et al.M. ³TM 3-215/AFM 355-7. December 1963.3.10 See Table II-43 (page II-62) for toxicity estimates.Table II-40.P. UNCLASSIFIED Technical Manual (ADA292141). (7) Methyldichloroarsine (MD) (see Table II-42). The existing estimates are not supported by the available data. June 1944. 9 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. Arsonous dichloride.. methyl-. Chemical Warfare Center. February 2000. November 1941. Inhalation causes a severe irritation in the nose. A. 5 Kibler. UNCLASSIFIED Report. MD is a colorless and odorless liquid when pure. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries.I. Reinhold Book Corporation. November 1942. ECBC-TR-349. N. 3rd ed. Dangerous Properties of Industrial Materials. dichloromethyl-. NY. Dichloromethylarsine. Methylarsine dichloride. 22 December 1995.. Military Chemistry and Chemical Agents. toxic lung injurant. No toxicity estimates are recommended for lethal exposure. b Based on existing estimate. ²Dawson. 10 FM 3-5/MCWP 3-37.. 6 Sharon Reutter.

2 @ 0°C (calculated from vapor pressure) 2 Data not available Data not available Data not available Data not available Stable up to the boiling point 2 Immediately hydrolyzes in the presence of water. MD (Continued) Physical and Chemical Properties Structural Formula: Cl CH3 As Cl Molecular Formula: CH3AsCl2 Molecular Weight: 160. none when pure 1 132. 5 Soluble in common organic solvents @ ambient temperatures. soaps. and absorbents (earth. 1. eye and skin irritant 9 Toxic lung injurant and respiratory irritant 9 Immediate irritation.063 @ 0°C 2 6.6°C 2 -54. detergents. MM1 MOPP4 whenever liquid or vapor is present 12 Liquid on eyes and skin requires immediate decontamination. Water.68 x 104 @ 20°C.Table II-42.875 @ 0°C 4 5. sawdust. 8 Satisfactory with steel for at least 1 year @ ambient temperature.86 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials Colorless Liquid 1 Extremely irritating.5 (calculated) 7. but @ elevated temperatures (60°C) crude pitting occurs within 15 weeks.1 Very rapid.593 @ 20°C. 12 Household bleach is effective on equipment. steam. 10. 2.5 @ 20°C. ashes. 1. 7 Other Data Blistering action less than that of HD and L. delayed blistering 10 M18A3 CADK. 13 Delayed-action casualty agent Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required Decontamination Use II-61 .8°C (FP) 3 1.11 M18A2 CADK. 5 complete in less than 2 min @ 25°C in dilute solution 6 Hydrogen chloride and methylarsenic oxide 5 Stable in steel containers @ 60°C for a period of at least 15 weeks and for at least 1 year @ ambient temperatures 7 No appreciable amount of corrosion on steel when MD is pure and acid-free. and rags) are effective for physical removal.839 @ 20°C.95 x 104 @ 0°C (calculated from vapor pressure) 2 10.

Important Constants of Fourteen Common Chemical Warfare Agents. April 2003. Edgewood Arsenal. It can penetrate garments and rubber much more quickly than other agents.H. EACD 170. May 1922. S.G. UNCLASSIFIED Report (ADB958296). 9 Sharon Reutter. 13 FM 3-5/MCWP 3-37. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. and lungs. Review and Recommendations for Human Toxicity Estimates for FM 3-11. P. 7 Henley. Edgewood Arsenal. Methyldichloroarsine and Methyldifluoroarsine Field Tests. M. 4 Klosky.P. in particular. UNCLASSIFIED Report (ADB95011). P.9.21 Droplets on the skin are potentially lethal. Edgewood. December 1924. Edgewood. 12 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11.M. Edgewood Arsenal.21 CX is the primary urticant of military interest (see Table II-44). Chemical Warfare Service. et al. Edgewood Arsenal. February 2000. The Physico Chemical Properties of Methyldichloroarsine and Arsenic Trichloride. 5 Buswell.21 It affects the skin.. MD. EACD 63. March 1931.. June 1944. NBC Decontamination. MD. Edgewood Arsenal. B. Chemical Warfare Service. are similar to those caused by a strong acid. MD..D. No other chemical agent produces such an immediately painful onset that is followed by rapid tissue necrosis. MD. 10 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. UNCLASSIFIED Report (ADB955153). 22 December 1995.. Chemical Warfare Service. Edgewood. 28 July 2000. UNCLASSIFIED Report. they do not produce fluid-filled blisters.. June 1920. The skin lesions. The existing estimates are not supported by the available data. Chemical Warfare Service. The rapid skin damage renders the skin more susceptible to a second type of agent. eyes. F.10 See Table II-45 (page II-64) and Appendix H for toxicity estimates. Chemical Warfare Service. Chemical Warfare Service. 11 DOD Chemical and Biological Defense Program Annual Report to Congress.. 6 Beebe. II-62 . EACD 176. 8 Siegel. Urticants are not true vesicants because. September 2003. EACD 113. A. unlike mustard and L. Freezing Points of Mixtures of Methyldichloroarsine and Mustard Gas and of Lewisite and Mustard Gas..3. CX has also been classified as a lung poison. Table II-43.F. Surveillance Tests on 75 mm Steel Gas Shell Extending Over a Period of One Year.. Edgewood. May 1922. The Chemistry of Certain Arsenical Chemical Warfare Agents as Water Contaminants. et al.M. Determination of the Vapor Pressure of Methyldichloroarsine. UNCLASSIFIED Report (ADB959731). EACD 11. ECBC-TR-349. December 1921. (temporary incapacitation) Odor Detection Toxicity (mg-min/m3) LCt50: NR ECt50: 25 a (Provisional) EC50: less than 1 mg/m3 a MV (L) N/A N/A Exposure Duration N/A 1 min ROE Inhalation/ Ocular Inhalation/ Ocular Inhalation/ Ocular NOTES Probit Slope Unknown Unknown TLE Unknown N/A ROD Unknown Unknown DOC N/A Low N/A 1 min Unknown N/A Unknown Low a Based on secondary human data and TM 3-215 (1952). C.Table II-42.. and Stricker. Edgewood Arsenal. OSRD 4193. MD (Continued) NOTES Macintire. UNCLASSIFIED Report (ADB955243). MD. they produce solid lesions resembling urticaria. Volume I. 3 Mead. UNCLASSIFIED Report (ADB959625). MD Toxicity Estimates10 Endpoint Lethality Severe effects. 2 Watson. W. The Corrosive Effect of War Gases on Metals and Materials. No toxicity estimates are recommended for lethal exposure. rather. EACD 328. Division 9 National Defense Research Committee of the Office of Scientific Research and Development. Chemical Warfare Service. c. MD. August 1921. Edgewood Arsenal. UNCLASSIFIED Report (ADB955049). MD.. Urticants. et al. 1 (8) MD Toxicity Estimates (Table II-43). EACD 410.

Phosgen-oxime Chemical Name: Dichloroformoxime Synonyms: 1. CX causes pain. cause rapid decomposition of CX.2 @ 50oC (calculated from vapor pressure) 3 Data not available Data not available Data not available Data not available Below 129oC 4 Very soluble in both water and common organic solvents 5 Slow in water @ ambient temperature and pH 7. even trace amounts of iron chloride may cause explosive decomposition.Table II-44. trace amounts of iron chloride may cause explosive decomposition. MM1 7 MOPP4 8 NOH Hydrolysis Products Stability in Storage Action on Metals or Other Materials Skin and eye toxicity Inhalation toxicity Rate of action Means of detection Protection required II-63 . 1 resembles new-mown hay at low concentrations 2 129oC 3 (with decomposition unless highly pure) 39oC (MP) 3 Data not available 3. and hydroxylamine 2 Pure. crystalline. 5 Other Data Causes pain. Dichloroformaldoxime. If stored @ -20oC it can be kept indefinitely. Carbonyl chloride oxime CAS Registry No: 1794-86-1 RTECS Number: Data not available Physical and Chemical Properties Structural Formula: Cl C Cl Molecular Formula: CHCl2NO Molecular Weight: 113. CX Alternate Designations: Fosgen Oksim. especially iron. Dichlorformaldehyd-oxime. 2 Metals. and inflammation of the cornea of the eye. especially upon heating.9 (calculated) 2. M18A2 CADK. conjunctivitis. Dichloroximinomethane.2-Dichloroformoxime.93 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Viscosity (cP) Viscosity of Vapor (cP) Surface Tension (dynes/cm) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Colorless. 2 Also attacks rubber. M18A3 CADK.37 x 105 @ 50oC (calculated from vapor pressure) 3 11. 1 CX is extremely unstable in the presence of impurities such as metals. 6 Can cause pulmonary edema 6 Almost instantaneous 6 M256A1 CADK. unstabilized CX decomposes on storage @ ambient temperature. hydrolyzes 5% within six days @ ambient temperature. whereas basic solutions react very violently with CX 2 Carbon dioxide. Dichlormethylen-hydroxylamine. Kohlensaure-dichlorid-oxime. hydrogen chloride. irritation.43 x 101 @ 50oC 3 1. and severe tissue damage on skin. dilute acids slow down the hydrolysis rate even further. deliquescent-solid when pure 1 Unpleasant and irritating.

T. sawdust. motivation. If the M291 kit is not available. b The TLE value is assumed to be 1 because the concentration-time profile is unknown. 9 FM 3-5/MCWP 3-37. planning. ERDEC-TR-042. CONFIDENTIAL Report (AD367890). Aberdeen Proving Ground. EATR 4210.c Unknown Unknown ROD Unknown Unknown Unknown DOC Low Low Low NOTES Based on animal data and existing estimate.3. CRDL Special Publication 7.22 These are drugs that produce delirium. hallucinosis. Volume I. Chemical Corps Board. USA Chemical and Biological Defense Agency. UNCLASSIFIED Report (AD507852). memory. Vapor Pressure Data Analysis of Dichloroformoxime. 4 Properties of War Gases Volume II: Blood and Nettle Gases (U). and psychedelics. Many II-64 . 6 BG Russ Zajtchuk et al. “Trichloronitrosomethane. 22 December 1995. incapacitation is understood to mean inability to perform one’s military mission. October 1965. B. USA Chemical Research and Development Laboratories. they do not seriously endanger life except in cases exceeding many times the effective dose. orientation.. detergents.. stimulants. flush the area with large amounts of water to remove any agent that has not reacted with the skin. April 2003.Table II-44. K. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. soaps. 9 Use Rapid-acting casualty agent NOTES 1 Witten. 22 a. ETF 100-41/Vol-2. Army Chemical Center. They interfere with the higher functions of the brain such as attention. depressants. W. 3 Penski. and judgment. 7. Agent CX (Phosgene Oxime) Summary Report (U). NBC Decontamination. Thus. and absorbents (earth.G. Office of the Surgeon General. 8 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. d Based on secondary human data. MD. and they produce no permanent injury. The Search for Toxic Chemical Agents (U). and Sennewald. November 1969. decontamination will not be entirely effective after pain occurs.22 Incapacitating agents differ from other CW agents in that the lethal dose is theoretically many times greater than the incapacitating dose. “Vesicants. (eds). perception. MD. Water. March 1993. for the purpose of this manual.1 Virtually all drugs whose most prominent effects are psychological or behavioral can be classified into four fairly discrete categories: deliriants. 8 Household bleach is effective on equipment. and disorganized speech and behavior. Incapacitating Agents Used in a military context. Chap. Dichloroformoxime (Phosgene Oxime) and Their Derivatives. MD.C. 1929. Edgewood Arsenal Research Laboratories.. 1997. and rags) are effective for physical removal. MD. Deliriants. E. 2 Petersen. which is an incapacitating syndrome involving confusion. December 1956. CX Toxicity Estimates10 Endpoint Lethality Incapacitation/ intolerable Threshold (odor detection) a Toxicity (mg-min/m3) LCt50: 3200 a (Provisional) ECt50: 3 d (Provisional) ECt50: 1 d (Provisional) MV (L) 15 15 15 Exposure Duration 10 min 1 min 10 min ROE Inhalation/ Ocular Inhalation/ Ocular Inhalation/ Ocular Probit Slope Unknown Unknown Unknown TLE 1 b. Since missions vary. conceptual thinking. 5 Prandtl. ashes. p. nevertheless. steam.” Chemische Berichte. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. 28 July 2000. Edgewood Arsenal. 8. c See Appendix H for supporting toxicity profile estimates. Decontamination Table II-45.” 7 DOD Chemical and Biological Defense Program Annual Report to Congress. 62. Vol. CONFIDENTIAL Report (AD108457).. decontaminate as rapidly as possible with M291 SDK. UNCLASSIFIED Report (ADA265873). 1766. CX (Continued) Because of the rapid reaction of CX with the skin. incapacitation means the inability to perform any military task effectively and implies that the condition was achieved via the deliberate use of a nonlethal weapon.

6 (calculated) 1.2 (calculated from Clausius Clapeyron equation which assumes constant heat of vaporization as a function of temperature) 4 Pure: 246°C.6 t1/2 = 3 to 4 wks @ 25°C in moist air and pH 7. producing carbon dioxide. Skin absorption is possible with proper solvents. benzophenone. BZ intoxication requires from two to three days to reach full recovery. 1 Solubility in water is approximately 1.2) octan-3-ol. The rate of decomposition is both temperature. CS 4030. During prolonged heating at temperatures approximately 170°C. slightly soluble in water. 3-(2.7 hrs @ 25°C and pH 9.6 t1/2 = 1. 1-Azabicyclo (2. BZ begins to decompose.2.5. however.6 t½ = 12 min @ 34° and pH 12. the chemicals in the subgroup anticholinergics are regarded as most likely to be used as military incapacitating agents.5 t½ = 1.0 x 10-9 @ 0°C (calculated from vapor pressure)4 21.2)oct-3-yl ester. QNB Chemical Name: 3-Quinuclidinyl benzilate Synonym: Benzilic acid. alphahydroxy-alpha-phenyl-. Of these drugs.18 g/L5. 1 t1/2 = 6.2-Diphenyl-2-hydroxyethanoyloxy)quinuclidine.33 2 11. 3-Chinuclidylbenzilate.5 t½ = 9.and purity-dependent. 3-Quinuclidinol benzilate. soluble in dilute acids and common organic solvents such as alcohol and chloroform.43 x 10-10 @ 25°C (extrapolated). See Table II-47 (page II-66) for toxicity estimates.5 3-Quinuclidinol and benzylic acid 6 Stable in aluminum and stainless steel @ 71°C for at least 2 years 5 Slight pitting of aluminum and stainless steel occurs after 2 years @ 71°C7 Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials II-65 . BZ Alternate Designation: EA 2277. Oksilidin.51. Benzeneacetic acid. and other products. benzhydrol.5 hr @ 100°C and pH 0.2.8.5°C 3 (MP) 412°C (extrapolated) 4 Bulk: 0. insoluble in aqueous alkali. BZ is capable of producing delirium at a very low dosage with a high safety margin.2 Crystal: 1. 4. See Table II-48 (page II-68) for symptoms.4 hr @ 50°C and pH 8. 3-Quinuclidyl benzilate CAS Registry Number: 6581-06-2 RTECS Number: DD4638000 Physical and Chemical Properties Structural Formula: OH O C C O N Molecular Formula: C21H23NO3 Molecular Weight: 337.42 Physical State Odor FP/MP Boiling Point Solid Density (g/cm3) Vapor Density Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Flash Point Decomposition Temperature White crystalline solid 1 None 2 167.2 Munitions grade: 220°C 2 Stable up to the melting point.60 x 10-6 @ 25°C. 3Quinuclidinyl benzilate (BZ) is considered the most likely candidate for military use (see Table II-46).74 x 10-13 @ 0°C (extrapolated)4 2.drugs can produce delirium.9. Table II-46. 3-quinuclidinyl ester.8 min @ 25°C and pH 13.1-azabicyclo (2. benzilate.

Clarksville.E. 1970. and Master. USA Munitions Command. 1967). UNCLASSIFIED Report (ADB030349). CRDL-SP-4-28. 4 Cogliano. Aberdeen Proving Ground. March 1961. MD. UNCLASSIFIED Report (ADB028222). May 1964. DA18-108-CML-6602. et al. S. D. 1 to 4 hours depending on exposure 10 MM1 MOPP4 11 Decontaminate skin with soap and water or use M291 kit if soap and water are not available 12 Use Delayed-action incapacitating agent NOTES ¹Witten. Clarksville. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. B... Stimulants.9. The Physical Properties of the Glycolates (U). The Search for Toxic Chemical Agents (U). Edgewood Arsenal. Edgewood Arsenal. Grace and Company. 8 BG Russ Zajtchuk et al. 1963. caffeine. Edgewood Arsenal Special Report EO-SR-74001. “Incapacitating Agents. UNCLASSIFIED Report (AD507852). Basic Esters of Glycolic Acids (U): Part III Analysis and Chemical Properties of Microgram and Larger Quantities of EA 2277 and Related Compounds. Stimulants are drugs that produce a temporary increase of the functional activity or efficiency of an organism or any of its parts. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. MD. UNCLASSIFIED Report (AD350755). et al. USA Chemical Research and Development Laboratories. EATR 4210. I. February 2000. 1977.. ECBC-TR-349. Corrosion. Final Report – Task I. MD. DA18-108-CML-6602 (A). CONFIDENTIAL Report (AD508308).. Corrosion. MD. Table II-47.. Chap. UNCLASSIFIED Report (AD325351). Army Chemical Center.A.L.H.Compatibility. M. Fort Detrick.R. USA Medical Bioengineering Research and Development Laboratory. ²Chemical Agent Data Sheets Volume I.. W. 11 FM 8-9/NAVMED P-5059/AFJMAN 44-151.M. (eds). Compatibility and Other Physicochemical Studies (U). ³Lochboehler. and epileptogenic substances such as strychnine II-66 . Washington Research Center. 6 Sass. Review and Recommendations for Human Toxicity Estimates for FM 3-11. Problem Definition Studies on Potential Environmental Pollutants VIII: Chemistry and Toxicology of BZ (3-Quinuclidinyl Benzilate). 10 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. CRDLR 3088. 5 Rosenblatt. MD. Grace and Company. nicotine. EA 2277 (U): A Summary Report as of 15 March 1961. cocaine. 1 February 1996. Army Chemical Center. CONFIDENTAL Report. Chemical Research Laboratory. 22 December 1995. The existing estimates are not supported by the available data. Final Report-Task II. 12 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. No toxicity estimates are recommended for lethal or threshold effects. BZ Toxicity Estimates10 Endpoint Lethality Severe effects (temporary incapacitation) Threshold effects (odor detection) Toxicity (mg-min/m3) LCt50: NR ECt50: 100 a (Provisional) ECt50: NR MV (L) N/A 15 Exposure Duration N/A Less than 5 min N/A ROE Inhalation/ Ocular Inhalation/ Ocular Probit Slope Unknown Unknown TLE Unknown N/A ROD Unknown Unknown DOC N/A Low Inhalation/ Ocular NOTES a Based on human data and “official” estimate (HEC. 11. C. et al. N/A Unknown N/A Unknown N/A c.Table II-46. and Braude.. J. BZ (Continued) Other Data Can cause blurred vision and dilation of pupils 8 Primary route of exposure 9 Delayed action. MD. BZ Toxicity Estimates (Table II-47). Washington Research Center.. USAMBRDL-TR 7710. USA Chemical Research and Development Laboratories. G. Office of the Surgeon General. Edgewood Arsenal Research Laboratories. and other Physiocochemical Studies (U). 1997. November 1969. August 1961. Skin and eye toxicity Inhalation toxicity Rate of action Means of detection in field Protection required Decontamination b. 7 Brooks. MD.3 They include amphetamines. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B). September 2003.” 9 Sharon Reutter.. W. MD December 1974. UNCLASSIFIED Report (AD359603).R. EASP-100-61.

Short-term and long-term effects of the fentanyls are indistinguishable from those of heroin.22 As a potential class of agents. The lethal dose for morphine and other opioids is only 10 to 20 fold greater than the incapacitating dose. phencyclidine (PCP). Symptoms and possible agent families are shown in Table II-48 (page II-68).23 Fentanyls are opiates with actions similar to those of morphine.1 (2) Phenothiazine-like compounds have a very high safety index and would not likely involve any special medical care.22 (1) Cannabinols.and Metrazole. Psychedelics. Cannabinols are another a group of potential incapacitating agents that seem to act basically as CNS depressants. Psychedelic drugs have been found unsuitable for military use. Russia used a derivative of fentanyl in a Moscow theatre where Chechen rebels held 800 hostages. in particular. Affected individuals usually cannot carry out a series of instructions or concentrate on a complex task.1 e. None of the conventional stimulants appears to have sufficient potency to be usable as an airborne incapacitating agent.3 They include drugs such as barbiturates.24 Fentanyls depress respiration and heart rate and cause lethargy.3 They include D-lysergic acid diethylamide (LSD). since moderate stimulation might easily lead to a soldier’s more energetic and aggressive performance. they have a rapid onset of action. See documents such as FM 8-285 for diagnosis and treatment for incapacitating agents. the capacity to relieve pain. and tranquilizers. morphine and other opioids. however. Psychedelics are drugs capable of producing abnormal psychological effects and sometimes psychological states resembling mental illness. MDMA (popularly known as ecstasy). and immobilization. although they reduce hyperactivity. Symptoms. but might be capable of isolated. On 27 October 2002. Depressants. The onset of action for phenothiazines is about 5 minutes and often lasts about 1 hour. Decontamination would involve washing with soap and water. Depressants are drugs that reduce a bodily functional activity or an instinctive desire. II-67 . sedation. Primary effects of these agents. (3) Fentanyls.22 f. are sedation and destruction of motivation rather than disruption of the ability to think. and low doses could even prove counterproductive. but they are hundreds of times more potent. and indoles. impulsive actions such as firing a weapon accurately enough to be dangerous. Major tranquilizers often produce relatively little sedation.22 d.

lethargy. erratic behavior. II-68 . easy laughter. decrease in disturbance with reassurance. other intoxications (e. sedation. elevated temperature. The Human Estimates Committee of what is now Edgewood Chemical and Biological Center (ECBC) stated that many alkyl organophosphorous compounds produce neurotoxicity in various animal species. lead) Anticholinergics (BZ) Indoles (schizophrenic psychosis may mimic in some respects) Cannabinols Anxiety reaction Fentanyls 9. bromides. failure to obey orders. before the appearance of lung damage. anxiety reaction. papillary dilation. slow pulse. tachycardia at rest. history of nervousness or immaturity Respiratory depression.. with death resulting from a central action. flushed face. vomiting Dryness of mouth. Deaths that occur within a few hours of exposure. Correlation of Symptoms and Incapacitating Agent Family 1. relaxed. Deaths occurring after 24 hours postexposure are thought to result from lung damage. destructibility.Table II-48. unconcerned daydreaming attitude.22 Signs and Symptoms Restless. hallucinatory behavorior. indoles. and blood pressure. perceptual distortions. or giddiness. clinging or pleading. stumbling or staggering. slurred or nonsensical speech. difficulty in expressing self. a. Methyl Phosphonic Acid (DF) (see Table II-49). barbiturates. are perhaps due to central respiratory failure. stomach cramps and vomiting Euphoric. labile increase in pupil size. immobilization Possible Agent Family Anticholinergics (BZ). low blood pressure and dizziness on sudden standing Tremor. See Table II-50 (page II-70) for toxicity estimates. stupor. confusion. blurred vision. cannabinoids. dizziness. they are binary agent components and are relatively nontoxic—at least when compared with the CW agents. central respiratory failure. or a combination of the two. Chemical Warfare Agent Precursors10 These materials are not CW agents. heart rate. irrational fear. The toxic syndrome includes weakness and paralysis.g. crying. DF is an organophosphorous compound that is an intermediate component of binary GB. coma Inappropriate smiling or laughing. alcohol.

1 Never store DF with alcohols. 9. 1. natural rubber. and t1/2 = 47 days @ pH 3.0 x 104 @ 0°C (calculated from vapor pressure) 2 9.4 (calculated) 3. metals. alkaline materials.Table II-49. 8. MF and HF. Difluoromethyl phosphonate.5 @ 0°C (calculated from vapor pressure) 2 Nonflammable 4 Data not available Immediately decomposes with the addition of water 5 Virtually instantaneous to produce methylphosphonofluoridic acid (MF) and hydrogen fluoride (HF) which are also toxic.9 x 105 @ 25°C. 5 Hydrolyzes to give toxic products. Difluoromethylphosphine oxide.00 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Liquid 1 Pungent. Methylphosphonyldifluoride. 1. methylCAS Registry Number: 676-99-3 RTECS Number: TA1840700 Physical and Chemical Properties Structural Formula: O CH3 Molecular Formula: CH3F2PO Molecular Weight: 100. MF t1/2 = 162 days @ pH 7. methyl-.4060 @ 0°C (extrapolated) 2 3. which is mainly due to the acidic corrosive nature of the hydrolysis products. such as crude GB. acid like1 99. Further hydrolysis is a slow reaction that produces methylphosphonic acid (MPA).7°C 2 –36. and some organics. Methyl difluorophosphite. 8 most metals.9°C (FP) 3 1. 5.10-12 HF may react with some metals. Phosphonodifluoridic acid. EA 1251 Chemical Name: Methylphosphonic difluoride Synonyms: Phosphonic difluoride. 10. 6 Avoid contact with water mist or sprays. 9 and organic materials like glycols.2 @ 25°C. a potential fire and explosive hazard. 7 Incompatible with water. when stored in high-density polyethylene containers enclosed in steel.13 P F F Hydrolysis Products Stability in Storage Action on Metals or Other Materials II-69 . DF Alternate Designations: Difluoro. t1/2 = 90 days @ pH 4. to give off hydrogen gas. Further hydrolysis of MF results in MPA and a second mole of HF. glass. DF will react with alcohols to form a lethal chemical. concrete.5 @ 0°C (extrapolated) 2 1.3595 @ 25°C.6 x 10¹ @ 25°C. 5 Remains stable for at least 20 years.

J. P. USA Armament Research and Development Command. 9 Schweitzer. Aberdeen Proving Ground.” J. & Chem. 6 Jackson. CRDEC-TR-88032. Acute Toxicity of Methylphosphonic Difluoride (DF) Methylphosphonic Dichloride (DC) and their Hydrolysis Products by Inhalation and other Routes in Mice. DC. DF (Continued) NOTES ¹Buchi.. K.. 4.. ARCSL-TR-77061. Nonmetallics. M. 8 Ellzy. USA Armament Research and Development Command. and Semiatin. Mixed Binary Agents New Approach Toward Meeting Expanded Chemical Munitions Effectiveness Requirements. June 1986. June 1983.. Chemical Systems Laboratory. Long-Term Storability of the M20 DF Canister Used in the M687 Binary Projectile. USA Chemical Research Development and Engineering Center. p. May 1991. MD. C. MD. The only human data for QL are from occupational exposures for which the dosage is unknown. 82.” J. USA Chemical Research Development and Engineering Center.A. ‘Thermodynamic Properties of Some Methylphosphonyl Dihalides From 15 to 335°K.T. NBS Phy. Aberdeen Proving Ground. UNCLASSIFIED Report (ADB117574). 572. and Rubbers. CRDC-TR-84104. UNCLASSIFIED Report (ADB096058). MD. August 1986. INC. pp. Environmental Overview of Common Industrial Chemicals with Potential Application in the Binary Munitions Program. B. Vol. b. Chem. Rats and Guinea Pigs. Vol.. ¹³Tarantino. MD.M.. November 1987. APG. Plastics. January 1985. et al. See Table II-52 (page II-72) for toxicity estimates. Tony Man. UNCLASSIFIED Report (ADB155651). Marcel Dekker. Aberdeen Proving Ground. By-Products. UNCLASSIFIED Report (ADB105158). CONFIDENTIAL Report (ADC033576). USA Chemical Research Development and Engineering Center... 1986.A. USA Chemical Research Development and Engineering Center. and Products in the Production of QL. USA Chemical Research Development and Engineering Center. Table II-50. Chester. CRDEC-TR-87041. USA Chemical Research Development and Engineering Center. M. Soc. UNCLASSIFIED Report (ADB092563). ³Furukawa.. USA Chemical Research Development and Engineering Center. CRDEC-TR-229. 3843. P.. 1964. Aberdeen Proving Ground.J. Aberdeen Proving Ground.. 2nd ed. Rsch. NJ. p. The Relationship Between Oxygen Index and the Flashing Propensity of Explosively Disseminated Liquids. Am. MD. ¹²Kay Lau.R. MD. L. Research and Development for Candidate Materials for Use as a DF Containment Vessel... and DF. II-70 .. Environmental Overview of Intermediates.M. et al.M. G. CRDC-CR85058. K. et al. et al. CONFIDENTIAL Report (ADC039896). Aberdeen Proving Ground. Aberdeen Proving Ground. Electrochemical Corrosion Study of Miscellaneous Metals/Alloys with Methylphosphonic Difluoride.. MD.M. Interaction and Esterification of Methylphosphonic Dihalides.Table II-49. “Properties. 68A. MD. 367.T. October 1977.. 7 Hyttinen. May 1991. Corrosion Resistance Tables: Metals. USA Chemical Research Development and Engineering Center. 5 Dahl. CRDEC-TR-076. Difluor (DF) – Flooring Compatibility Studies. No toxic signs have been observed in workers who have handled large quantities of QL or who have become highly contaminated with it. CRDEC-CR-86049. UNCLASSIFIED Report (ADB154752)..R. ²Zeffert. DF Toxicity Estimates10 Endpoint Permanent Corneal Damage Temporary Corneal Damage a Toxicity a (mg/eye) ED50: 10 ED50: 0. Aberdeen Proving Ground. 10 Buchi. et al. UNCLASSIFIED Report (ADA045976). No. MD. CRDEC-TR-86074. ¹¹Thomas. UNCLASSIFIED Report (ADA186083). 4 Allan. A..573.2 MV (L) N/A N/A Exposure Duration N/A N/A ROE Liquid in eye Liquid in eye NOTES Probit Slope Unknown Unknown TLE Unknown Unknown ROD Unknown Unknown DOC Moderate Moderate Based on “official” existing human toxicity estimate. W. July 1987.. Glass or Polymer Etching Due to the Reaction of Methylphosphonic Difluoride (DF) with Water (U). Aberdeen Proving Ground... 1960. September 1985. MD.. O-(2 Diisopropylaminoethyl)-O’Ethyl Methyl Phosphonite (QL) (see Table II-51). ARCSL-TR-83080. A. Ed.

8 @ 0°C (calculated from vapor pressure) 2 19. if kept dry and pure. many chlorinated hydrocarbons.1 x 10-4 @ 0°C (extrapolated) 2 2. 7 Satisfactory against aluminum. 5 Reacts with sulfur and sulfur compounds to produce highly toxic VX or VX-like compounds.1 (calculated) 1.4 @ 25°C. has a flash point of 28°C 4 and an autoignition temperature of 40°C. 6 With excess of water by weight.9080 @ 25°C.3 x 102 @ 25°C. 2-propanol. fishy 1 244. and stainless steel containers for at least 6 months @ 71°C.9307 @ 0°C 2 8. steel.Table II-51. 5 Always store QL away from heat or ignition sources and sulfur compounds because of the potential to form highly toxic V-agents. methyl-. acetone. Soluble in methanol. Phosphonous acid. 1 Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials II-71 .8 x 10-2 @ 25°C.31 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Flash Point P O CH2CH2N[CH(CH3)2]2 Liquid 1 Strong. moisture. 4 Stable in aluminum. 0. With traces of water or other proton donors. QL Alternate Designations: EA 1724.O’-bis-(2-diisopropylaminoethyl) methylphosphonite (LT).3 @ 0°C (calculated from vapor pressure) 2 89°C (closed cup). QL has an autoignition temperature of 129°C. 22. 9. EDMP Chemical Name: O-(2-Diisopropylaminoethyl) O’-ethyl methylphosphonite Synonyms: O-Ethyl-O’-(2-diisopropylaminoethyl) methylphosphonite. 2 A hydrolysis product. selenium compounds. 1 and is flammable. 7. and stainless steel. selenium. 7 It is incompatible with HTH. 2-[bis(1methylethyl)amino]ethyl ethyl ester CAS Registry Number: 57856-11-8 RTECS Number: Data not available Physical and Chemical Properties Structural Formula: CH3 CH3CH2O Molecular Formula: C11H26NO2P Molecular Weight: 235.O’-diethyl methylphosphonite (TR) and O. QL can be completely hydrolyzed within 5 hrs.8°C (extrapolated) 2 Data not available 0. but not glass unless a stabilizer is used. QL will produce O. QL primarily forms O-ethyl methylphosphonic acid (YL) and 2-diisopropylaminoethanol (KB). 1 TR has a boiling point of 120°C. but also forms O-(2diisopropylaminoethyl) methylphosphonic acid (QA) and ethanol (ZS) as secondary products. 1 Data not available Slightly soluble in water. and carbon tetrachloride. O.O’-diethylmethylphosphonite (TR). steel. and benzene. 5 Rapid. oxidants. 4 a vapor pressure of 10 mm Hg @ 20°C. 3 In addition.

7 Nowlin. QL (Continued) NOTES ¹Buchi. Detection and Identification of QL Impurities by Electron and Chemical Ionization Gas Chromatography/ Mass Spectrometry. MD.. %) II-72 . June 1964. and Products in the Production of QL. Aberdeen Proving Ground. UNCLASSSIFIED Report (AD352753). By-Products. 4 Kinkead. Chemical Research and Development Center Notebook #NB 83-0155. A. T.10. CRDEC-TR-076. MD. K. Physical Properties of Standard Agents. May 1991. ³Butrow. Edgewood Arsenal. Evaluation of the Acute Toxicity of Four Compounds Associated with the Manufacture of O-Ethyl-O’. Corrosion. OPA is most likely to be encountered in liquid form. Final Report – Task VII RES-64-86. Aberdeen Proving Ground. E. et al. Isopropyl amine: NT8400000 Physical and Chemical Properties Structural Formula: CH3 OH CH CH3 72 wt% 2-Propanol CH3 + CH NH2 CH3 28 wt% Isopropylamine Molecular Formula: C3H8O and C3H9N Molecular Weight: 2-Propanol: 60. Candidate Agents.E. Table II-52.. W. UNCLASSIFIED Report (ADB113969). 6 Rohrbaugh. Clarksville. Aberdeen Proving Ground. ARCSL-SP-83015. USA Chemical Research. Development. UNCLASSIFIED Report (ADB155651). and Related Compounds at Several Temperatures. J. Grace & Co. infection. Isopropyl amine: 59. July 1989. & Engineering Center. OPA has an inflammatory and corrosive action when in contact with mucous membranes. R. UNCLASSIFIED Report (ADC033491). USA Chemical Research Development and Engineering Center.11. D. MD.(2Diisopropyaminoethyl) Methylphosphonite. OPA Alternate Designations: N/A Chemical Name: 2-Propanol (isopropyl alcohol) and Isopropyl amine mixture Synonyms: N/A CAS Registry Number: 2-Propanol: 67-63-0. UNCLASSIFIED Report (ADB136428). November 1972. CRDEC-CR-87077. Final Report – Task VII. and obstruction. A New Binary VX Reaction-Two-Liquid System (U). These effects are the results of the concentration of the material. Aberdeen Proving Ground. and DF. M. Environmental Overview of Intermediates. p. EATR 4700. Table II-53. tissues. perforation. hemorrhage. Washington Research Center. USA Munitions Command. 5 Brooks.. or skin. shock. Isopropyl amine: 75-31-0 RTECS Number: 2-Propanol: NT8050000.E. QL Toxicity Estimates10 Endpoint N/A Toxicity (mg-min/m3) No toxicity estimates are recommended at this time due to lack of data MV (L) N/A Exposure Duration N/A ROE N/A Probit Slope N/A TLE N/A ROD Unknown DOC N/A c. rather than the total quantity applied. Isopropylamine and Isopropyl Alcohol (OPA) (see Table II-53). ²Samuel. See Table II-54 for toxicity estimates. with secondary complications such as toxemia... Average: 59. MD. et al. DC. MD.81 (based on 72:28 wt.. USA Armament Research and Development Command. Compatibility and Other Physicochemical Studies (U).Table II-51. 45 (U).R. USA Chemical Research.. June 1987.. Development & Engineering Center.K. Contract DA18-108-CML-6602 (A). Death could occur from severe local tissue injury. et al.B. UNCLASSIFIED Report (AD524088).M. June 1983. Maryland.

alcohol. 45 (U). March 1983.. 1 Reacts readily with oxidizing materials and organophosphorus halides. APG. II-73 .C. Mixed Binary Agents New Approach Toward Meeting Expanded Chemical Munitions Effectiveness Requirements. OPA Toxicity Estimates10 Endpoint N/A Toxicity (mg-min/m3) No toxicity estimates are recommended at this time due to lack of data MV (L) N/A Exposure Duration N/A ROE N/A Probit Slope N/A TLE N/A ROD Unknown DOC N/A d. L. pp. C...7759 @ 0°C (extrapolated) 4 2. USA Armament Research and Development Command. and soluble in acetone. R. 6. CRC. ²The Merck Index: An Encyclopedia of Chemicals. open flame... 13th ed.. ARCSL-TR-82019.Table II-53. OH. MD.152 x 105 @ 0°C (calculated from vapor pressure) 3 7. See Table II-56 (page II-75) for toxicity estimates. Merck & Company.S. et al.6 Data not available Data not available Relatively stable for at least 5 years at temperatures between ambient and 71°C. 4 Fielder. p. if stored in carbon steel containers lined with an ethylenebutylene copolymer. such as DF. J. P. Cleveland. CRC Handbook of Chemistry and Physics. R.M. 5 Allan. NJ. and chloroform—suggesting that OPA has a similar degree of solubility. NE is a component of binary VX. and ether. C-453 and C-440. and DF because they react to form highly toxic compounds such as crude GB. D. CONFIDENTIAL Report (ADC033576). June 1983. 1 NOTES Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials ¹Hyttinen. 2001.J. Aberdeen Proving Ground. Chemical Systems Laboratory. Binary GB: A Compilation of Relevant Data. 6 Weast. Sulfur with a Small Amount of Silica Gel (NE) (see Table II-55 [page II-74]).R.8°C (based on Raoult’s law calculation) 3 Less than –88°C (FP) 1 0. ³Abercrombie. OPA (Continued) Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m ) Latent Heat of Vaporization (kcal/mol) Flash Point Decomposition Temperature Solubility 3 Colorless liquid 1 Alcohol and ammonia (based on the two components) 2 60. Inc. Contact with DF can produce extremely toxic compounds such as crude GB. ARCSL-TR-83080. p.. p.7520 @ 25°C 1. USA Armament Research and Development Command. Drugs.1 (calculated) 1. Chemical Systems Laboratories Notebook #NB-CSL-82-0213. benzene.. UNCLASSIFIED Report (ADA045976).4 0. 13 (U). USA Armament Research and Development Command. The Relationship Between Oxygen Index and the Flashing Propensity of Explosively Disseminated Liquids.288 x 105 @ 25°C. eyes.128 x 10¹ @ 0°C (based on Raoult’s law calculation) 3 6. APG. ARCSL-TR-77061. 50th ed. October 1977. 5225.. and Simak. 2. 1969. and Biologicals. nose and throat. 7 Store OPA away from heat. MD.51 (calculated from Clausius Clapeyron equation which assumes constant heat of vaporization as a function of temperature)3 Less than 0°C 5 Data not available Both 2-propanol and isopropyl amine are miscible in water. Table II-54.955 x 10² @ 25°C.. 2. ECBC Notebook #NB 98-0079. It has very low toxicity and may irritate skin. 7 Sze. MD. Whitehouse Station.. CONFIDENTIAL Report (ADC030931).

Table II-55. Edgewood Arsenal. Brimstone.21°C 1 2. Inc. but many sulfur compounds tend to be vile-smelling 444. A New Binary VX Reaction-Two-Liquid System (U).. et al. NY. Precipitated sulfur.. USA Munitions Command. benzene 1. DC. yellow crystals 1 Odorless when pure 2. Sulfur atom.. Sulfidal. Merck & Company. 2001. slightly soluble in alcohol. 5 Nowlin.R. EATR 4700. Colsul. Spersul thiovit. Washington. Colloidal sulfur. Sulphur. R. Flowers of sulfur. Rhombic sulfur. Crystex.0 x 10³ @ 184°C (calculated from vapor pressure) 3 2. UNCLASSIFIED Report (AD524088). MD.6°C 1 The rhombic form of sulfur transforms into the monoclinic form @ 95.48 Physical State Odor Boiling Point FP/MP Solid Density (g/cc) Vapor Density (relative to air) Vapor Pressure (torr) Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Flash Point Decomposition Temperature Solubility S S S S Rhombic..07 @ 20°C 2 8. Sulfur ointment. John Wiley & Sons.2 toluene. ether.. Kumulus. Sulkol. D.. Spersul. CRC Handbook of Chemistry and Physics. Whitehouse Station. Sulfur vapor. 10th ed.. soluble in carbon disulfide. NE Alternate Designation: Brimstone Chemical Name: Sulfur (with small amount of silica aerogel) Synonyms: Alpha sulfur. Drugs. liquid NH3.E. Kolofog.21 4 207°C (closed cup) 3 Data not available Insoluble in water.8 (calculated) 1 @ 183. Sulforon. CRDEC-TR-87041. the MP of monoclinic sulfur is 115. Cosan. Super cosan. Aberdeen Proving Ground. Thiovit CAS Registry Number: Sulfur: 7704-34-9 and 10544-50-0 RTECS Number: Data not available Physical and Chemical Properties Structural Formula: S S S S Molecular Formula: S8 Molecular Weight: 256.. Sofril. NJ. New York. Tesuloii. Vol. Environmental Overview of Common Industrial Chemicals with Potential Application in the Binary Munitions Program. Thiolux. II-74 . Flour sulfur. Atomic sulfur. and chloroform1 Rate of Hydrolysis Data not available Stability in Storage Always store NE away from heat or ignition sources and QL because of the potential to form highly toxic VX 5 Action on Metals or Other Materials Reacts with QL to produce extremely toxic VX 5 NOTES ¹The Merck Index: An Encyclopedia of Chemicals. ³Lewis. 82nd ed. ²Lide. July 1987. Sulsol. 3328. acetone. 3. Hexasul. CRC Press. and Biologicals. Bensulfoid.3°C. Elemental sulfur.8°C 3 9. 4 Buchi.M. T. 13th ed. Ground vocle sulphur. Collokit. K.J. Kocide. Sublimed sulfur. MD. Inc... 2001. 1599. Beta sulfur. Microflotox. p. UNCLASSIFIED Report (ADA186083). p. 2001. methylene iodide. Sperlox-s. Kolospray. Sax’s Dangerous Properties of Industrial Materials. USA Chemical Research Development and Engineering Center. Sulfur flower. November 1972. Orthorhombic sulfur.

8 Data not available Data not available Satisfactory in storage for at least 1 year at temperatures between –40 to 71°C. the latent heat of vaporization for NM will probably be above 9. 3 Reacts with QL to produce extremely toxic VX. Methyl disulfide. NE Toxicity Estimates10 Endpoint N/A Toxicity (mg-min/m3) No toxicity estimates are recommended at this time due to lack of data MV (L) N/A Exposure Duration N/A ROE N/A Probit Slope N/A TLE N/A ROD Unknown DOC N/A e. Very high vapor concentrations are required to produce toxic effects.864 x 10¹ @ 25°C. but insoluble in water 7.21 kcal/mol based on DMDS 105 to 108°C 6 Data not available Dimethyl disulfide is soluble in alcohols. 4 generally vapor pressure decreases with increasing molecular weight. DMDS: 1. NM will probably have a lower vapor pressure than DMDS since its molecular weight will generally be higher. it is most likely to be encountered in an occupational setting. NM (Containing Elemental Sulfur) Alternate Designation: NM5 Chemical Name: Dimethyl polysulfide mixture [powdered sulfur + dimethyl disulfide (DMDS)] Synonyms: Dimethyl disulfide: 2. 5 thus. 6 Volatility (mg/m3) Latent Heat of Vaporization (kcal/mol) Flash Point Decomposition Temperature Solubility Rate of Hydrolysis Hydrolysis Products Stability in Storage Action on Metals or Other Materials II-75 . See Table II-58 (page II-76) for toxicity estimates. 1 Always store NM away from heat or ignition sources and QL because of the potential to form highly toxic VX. NM is a binary intermediate. Table II-57.6 (calculated) DMDS: 2.3895 @ 25°C 1 6. Disulfide. 6 Stains the surface of steel and various metal-plated steels when stored in glass vessels for 4 months @ 71°C.45 x 105 @ 25°C (calculated from vapor pressure) 4 DMDS: 9. as such.3-Dithiabutane. dimethyl CAS Registry Number: Dimethyl disulfide: 624-92-0 RTECS Number: Data not available Physical and Chemical Properties Structural Formula: 1 CH3 Molecular Formula: C2H6S5 Molecular Weight: 190. 1 DMDS: -84.Table II-56. 4 generally latent heat of vaporization increases with molecular weight of similar compounds.72°C (FP) 4 1. (Methyldithio) methane.37 Physical State Odor Boiling Point FP/MP Liquid Density (g/mL) Vapor Density (relative to air) Vapor Pressure (torr) Liquid 1 S S S S S CH3 Very noxious 2 117°C 3 < -40°C (FP). The Department of Transportation (DOT) shipping classification is not a class B poison. No estimates of human toxicity of NM have been derived.21 @ 25°C. Dimethylpolysulfide (NM) (see Table II-57). 5 thus.

UNCLASSIFIED Report (ADE470951). 72. “2. 2424. H.. 1950. MD. M. MD. USA Armament Command. MD. Washington. NM Toxicity Estimates10 Endpoint N/A Toxicity (mg-min/m3) No toxicity estimates are recommended at this time due to lack of data MV (L) N/A Exposure Duration N/A ROE N/A Probit Slope N/A TLE N/A ROD Unknown DOC N/A 10. Chem. p. DC. UNCLASSIFIED Report (AD524088).E.A.. NM (Containing Elemental Sulfur) (Continued) NOTES ¹Brown. R. Chemical Corps Board. Edgewood Arsenal. Other Chemical Warfare Agents In the past. December 1956.W. Vol..M. MD.. Most compounds were found unlikely to be used for various reasons (e. Modified NM: An Improved Liquid Binary VX Reactant (U). A New Binary VX Reaction-Two-Liquid System (U). et al. CLASSIFIED Report (AD108459).J.3-Dithiabutane: Low Temperature Heat Capacity. Table II-58. Jr. 82nd ed. EATR 4700. Compatibility Studies with Candidate Binary VX2 Components. D. Aberdeen Proving Ground. Heat of Fusion. CRDEC-TR-87041. 8 Lide.. Aberdeen Proving Ground. Edgewood Arsenal. February 1976. 2001. November 1976. MD.B. CRC Handbook of Chemistry and Physics. other compounds were studied and evaluated to determine their potential as CW agents. Army Chemical Center. USA Armament Command. Soc. VE. Edgewood Arsenal. D. USA Armament Command. 7 Buchi. Heat of Vaporization.” J. November 1972.. Environmental Overview of Common Industrial Chemicals with Potential Application in the Binary Munitions Program. November 1976. UNCLASSIFIED Report (ADA186083). UNCLASSIFIED Report (ADC008561). unstable in storage). ³Grula. Vapor Pressure. CONFIDENTIAL Report (ADC008383). Amer. Aberdeen Proving Ground. 6 Nowlin. USA Munitions Command... 4 Scott.. 5 Properties of War Gases Volume IV: Vesicants (U). MD.R. Some CW agents studied but not commonly known are listed in Table II-59. Edgewood Arsenal. CRC Press. et al. T. et al... Table II-59.. Aberdeen Proving Ground. K. Other CW Agents Classification Choking Agents Nerve Agents Blister Agents CW Agent Chloropicrin (PS) Ethyl Sarin (GE).. EC-TR-76075. July 1987. Entropy and Thermodynamic Functions. ETF 100-41/Vol-4.Table II-57. ²Riordan. Amiton (VG). USA Chemical Research Development and Engineering Center. EM-TR-76055. Pilot-Scale Operations of Process for Manufacture of VX Binary Intermediate NM (U).. VS Sesqui mustard (Q) II-76 . EC-TM-76009.g.

Roberts and Don Etherington. McGraw Hill Companies. General Chemistry with Qualitative Analysis. “Vapor Density. MD. 3Stedman’s 4Holzclaw. et al. John Wiley & Sons. Russ Zajtchuk et al. and Engineering Center. Draft. Vapor Pressure Data Analysis Methodology.. Chemical Research. Inc. 9.. Chap. UNCLASSIFIED Report (AD-A255090). 5. D. (eds). Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. “Pretreatment for Nerve Agent Exposure. Jr.” CRC Press. 1997. D.stanford. College Chemistry with Qualitative Analysis. Heath and Company. Chap. MA. and Applications. Holtzclaw. Chap.NOTES 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. H. 7 January 2002. Lexington. Aberdeen Proving Ground. Williams &Wilkins. 6. MA. Jr. 7Richard 6Matt 5American J. (eds). SBCCOM Report Review and Recommendations for Human Toxicity Estimates for FM 3-11. 2003. Office of the Surgeon General.. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. http://palimpsest. Hawley’s Condensed Chemical Dictionary. Office of the Surgeon General. Jr. CR DEC-TR-386. 1997. F.. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare.C. and Chemical Agents and Defense Equipment.” 17BG 16Satu 15BG II-77 . (eds).. Lexington. Abercrombie. New York. 13 14BG Russ Zajtchuk. E. Office of the Surgeon General. T. Statistics. Draft. TG 204. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B). and Robinson. “Toxic Inhalational Injury. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. Somani and James A. 1992. Inc. Standard Test Method for Apparent and True Specific Gravity and Porosity of Lump Coke. 12FM 11USACHPPM 10Sharon 8-9/NAVMED P-5059/AFJMAN 44-151. 22 December 1995.. Chemical Warfare Agents: Toxicity at Low Levels.F.. 9th ed. 2Henry 1FM Medical Dictionary. (eds).. Heath and Company. 1997. 2001.” M. Sr.9.C. Romano. 6th ed. Glossary of Terms for Nuclear..html (8 April 2003). Biological.” Russ Zajtchuk et al. 8Penski.R.. 1988. et al. 8th ed. 1991. W. Reutter.C.. Physical Property Data Review of Selected Chemical Agents and Related Compounds. Development. 13th ed.edu/don/dt/dt3670. New York.” Bookbinding and the Conservation of Books: A Dictionary of Descriptive Terminology. Society for Testing and Materials (ASTM) Method D 167.. 1997. MD. “Nerve Agents. 25th Edition. Baltimore. December 2001. 1990. Lewis. 1 February 1996. et al. 9McGraw Hill Dictionary of Scientific and Technical Terms. NY. Patrice L.

“Cyanide Poisoning. “Opioids: Fentanyls. 18BG Kirner. (eds).” WHO. Policy Development and Analysis Branch. Czerczak. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. Section (Laboratory).R.com/2002/WORLD/europe/10/30/moscow.com.” Russ Zajtchuk et al. 1997. 22BG 21BG “Russia names Moscow siege gas./World. 8 August 2003. “Incapacitating Agents. Summary Technical Report of Division 9. 7.” October 1998. Terminology and Information on Drugs: Part I. Office of the Surgeon General. Washington. http://www. 11. Chap. 1997. and Related Chemical Problems Part I-II.html. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. UNCLASSIFIED Report (AD234270). Division for Operations and Analysis. DC. 20W. 1997. 27 August 2003. “Concise International Chemical Assessment Document 47: Arsine: Human Health Aspects. Chemical Warfare Agents.org/unodc/report_1998-10-01_1_page016. 10.” Fishbein and S. Office of the Surgeon General. (eds). http://www.” 23CNN.” 30 October 2002.cnn. (eds). 1946. Office of the Surgeon General. “Vesicants.unodc. NDRC Volume 1. Russ Zajtchuk et al.gas/. 19L. United Nations Office on Drugs and Crime. Chap. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. 24Scientific II-78 . 2002.Russ Zajtchuk et al. Office of Scientific Research and Development. Chap.

Fog Oil [Smoke Generator Fuels (SGF-2)]. sneezing.Chapter III MILITARY CHEMICAL COMPOUNDS AND THEIR PROPERTIES 1. When inhaled.2 NOTE: Bleach reacts with RCAs to form a strong irritant.3 Symptoms include an initial burning feeling or irritation to the eyes that progresses to pain accompanied by blepharospasm and lacrimation. obscurants. and gloves. Thermite and Thermate Incendiaries. with excess salivation. Tantalum (Ta). other agents in the same family (CS1. Rhinorrhea is accompanied by pain inside the nose.1 The standard tear-producing agents currently in the US inventory for RCAs are o-chlorobenzylidene (CS). these agents cause tingling or burning. On unprotected skin. they produce a rapid onset of effects (seconds to several minutes) and they have a relatively brief duration of effects (15 to 30 minutes) once the victim has escaped the contaminated atmosphere and has removed the contamination from clothing. Symptoms. Diphenylcyanoarsine (DC). these compounds cause a burning sensation or a feeling of tightness in the chest. CSX. List of Selected Military Chemical Compounds Classification RCAs Respiratory irritants Smoke and obscurants Military Chemical Compounds O-Chlorobenzylidene Malononitrile (CS). See Table III-1 for a list of the selected military chemical compounds discussed. CS1. and ankles provide protection against field concentrations of RCAs.f)-1:4-oxazepine (CR). smoke.f)-1:4-oxazepine (CR). and situations where long-term incapacitation is unacceptable. When used against poorly equipped forces.3 Because tear compounds produce only transient casualties. Brass. these compounds have proven extremely effective. they are widely used for training. and increased secretions. When released indoors. Background This chapter addresses military chemical compounds including RCAs. JP-8. Riot Control Agents (Tear-Producing Compounds) The RCAs are chemicals that rapidly produce sensory irritation or disabling physical effects that disappear within a short time following termination of exposure. Titanium Tetrachloride (FM Smoke). Protection. Diphenylchloroarsine (DA). wrists. Phosphorous. DF-2.3 Do not decontaminate RCAs with any form of bleach.2 a. and incendiaries. CSX). riot control.2 III-1 . Table III-1. Chlorine (Cl2) Hexachloroethane (HC). they cause serious illness or death. b. Dibenz(b. especially if the air is warm and moist. and dibenz (b. The mucous membranes of the mouth have a sensation of discomfort or burning. masks.2 Generally. hoods. respiratory irritants. Synthetic Graphite. Capsaicin (OC) Adamsite (DM). Oil and metal Incendiary Mixtures Incendiaries 2.4 When handling and loading bulk CS. Signaling Smoke Magnesium Incendiaries. CS2. CS2. DF-1. with coughing. personnel should wear protective clothing. The protective mask and ordinary field clothing secured at the neck.

00034 @ 20°C 2 0. Crystal: 1.2 CS has been found to persist in snow for as long as 30 days but its persistency in soil varies.2 CS produces an intense burning and irritation of the eyes. CS is also a primary skin irritant. and CSX. In 1959. the USA adopted CS for combat training and riot control purposes. 1.24-0. edema.6 1 Physical state Odor Boiling point FP/MP Solid density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m³) Latent heat of vaporization (kcal/mol) Flash point Decomposition temperature Solubility Rate of hydrolysis Hydrolysis products Stability in storage Action on metals or other materials White crystalline solid 1 Pepper-like 1 310°C to 315°C (590-599°F)1 95°C to 96° C (203-205°F) (MP) 1 Bulk: 0.26. CS1. dissemination. OCBM 1 CAS registry number: 2698-41-1 1 RTECS number: OO3675000 1 Physical and Chemical Properties Structural formula: 2 CN CH C CN Molecular formula: C10H5ClN2 Molecular weight: 188. O-Chlorobenzylidene Malononitrile (CS) (see Table III-2). Different forms of CS have different persistence characteristics because of their formulation.6 See Table III-3 for CS toxicity estimates. There are a number of different formulations and methods of dispersion for the RCAs. CS2. may burn but does not ignite readily.04 2 6. CS Chemical name: O-Chlorobenzylidene Malononitrile 1 Synonym: 2-Chlorbenzalmalonitrile.4 incompatible with strong oxiders.2 moderate in alcohol. Containers may explode when heated. with a sensation of choking and being unable to breathe.c. and good in acetone. and vesication. followed by draining of the nasal sinuses. chloroform. Table III-2. methylene dichloride. depending on the condition of the soil. The chest feels constricted. and benzene 3 Data not available Data not available Combustible material.1 Contact with metals may evolve flammable hydrogen gas 4 Cl III-2 . It also produces a burning sensation in the nose and mucous membranes of the respiratory tract.5 d. The estimates recommended by the former Human Estimates Committee at what is now ECBC were often based upon the most potent formulation.5 CS exists as a family of four forms: CS. Toxicity. CS. ethylacetate. and the different systems/formulations impact the potency of the materials.71 @ 25°C 2 Data not available Data not available Data not available Insoluble in water.5 (calculated) 0. and can produce erythema. with mild to severe conjunctivitis. and rate of hydrolysis.

CS1.9.000 a (Provisional) ECt50 : 7 b MV (L) 15 Exposure Duration 5-90 min ROE Inhalation/ Ocular Inhalation/ Ocular NOTES Probit Slope Unknown TLE More than 1 ROD Some DOC Low Intolerable a b 15 1 min Unknown Unknown Unknown Moderate Based on existing human estimates. One gram of powdered CS is dissolved in 99 grams of trioctyl phosphite (TOF). Do not use oil-based lotions.2 e. “Riot Control Agents. Riot Control Agents and Herbicide Operations. February 2000. skin. 7 FM 3-11. CSX stings and irritates the eyes.” ³FM 8-9/NAVMED P-3059/AFJMAN 49-151.2 CR is more potent and less toxic than III-3 . 4 2000 Emergency Response Guidebook. throat.. or CS2. Do not use any form of bleach. Dibenz (b. Do not rub eyes. 6 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. (1) CS1 has been especially formulated to prolong persistency and increase effectiveness.2.2 (3) CSX is a form of CS developed for dissemination as a liquid rather than a powder. and ankles. Flush eyes and skin with water. Office of the Surgeon General. microencapsulated form of CS1. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. Table III-3. Guide 153. September 2003.00061. ²BG Russ Zajtchuk et al. masks. This form of CS prolongs the effectiveness for both immediate and surface contamination effects. 19 August 1996 (Renumbered from FM 3-11). CS1 reaerosolizes and can cause respiratory and eye effects. wrists. primary skin irritant 5 Causes sensation of choking 5 Instantaneous 6 A protective mask and dry field clothing secured at neck. Review and Recommendations for Human Toxicity Estimates for FM 3-11.11/MCRP 3-3. (eds). 2 (2) CS2 is a siliconized. Chap. and gloves.f)–1:4-oxazepine (CR) (see Table III-4 [page III-4]). 12. Use soap and water on equipment contaminated with CS. 5 Sharon Reutter. increases fluidity. 1997. As with CS. “o-Chlorobenzylidene malononitrile. Unlike CS. 1969). NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP6(B). 7 Move to fresh air. and lungs of exposed personnel. This formulation reduces agglomeration.” CAS 2698-41-1. Flame. and achieves the desired respiratory effects when dispersed as a solid aerosol. ECBC-TR-349.7 Training and RCA 7 NOTES ¹NIOSH Pocket Guide to Chemical Hazards. CS1 is a free-flowing agent powder consisting of 95 percent crystalline CS blended with 5 percent silica aerogel.Table III-2. CS (Continued) Skin and eye toxicity Inhalation toxicity Rate of action Protection required Decontamination Use Other Data Burning and irritation to eyes. 1 February 1996. CS Toxicity Estimates5 Endpoint Lethality Toxicity (mg min/m3) LCt50: 52. et al. Based on “official” estimates (HEC. Personnel handling and loading bulk CS should wear protective clothing. Substances-Toxic and/or Corrosive (Combustible).3 This treatment improves the physical characteristics of CS by reducing agglomeration and hydrolysis. When disturbed. In 1974.7. nose. the USA approved the use of CR in riot control situations.

wrists.1 percent CR solution.2 (See Table III-5) for CR toxicity estimates Table III-4. vesication. shoveling. remove by using towels. Flush eyes with copious amounts of cold water. masks. or any other method such as scraping. CR can persist on certain surfaces (especially porous) for up to 60 days. CR 2 CAS registry number: 257-07-8 RTECS Number: HQ395000 Physical and Chemical Properties Structural formula: 1 O N CH Pale yellow crystalline solid 3 Pepper-like 3 Data not available 73°C (163°F) (MP) 3 Data not available 6. and it is quite persistent in the environment. The severity of symptoms increases with the CR solution concentration and in any environment of high temperature and humidity. absorbent paper. 5 Move to fresh air. Soap and water can be used on skin. rags.7 (calculated) Data not available Data not available Data not available Data not available Data not available Sparingly soluble 1 Not hydrolyzed in aqueous solutions 3 Data not available Stable in organic solutions 3 Data not available Other Data Irritant.22 Physical state Odor Boiling point FP/MP Solid density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m3) Latent heat of vaporization (kcal/mol) Flash point Decomposition temperature Solubility Rate of hydrolysis Hydrolysis products Stability in storage Action on metals or other materials Skin and eye toxicity Inhalation toxicity Rate of action Protection required Decontamination Use III-4 . or sweeping. and gloves. CR does not degrade in water. Do not rub your eyes. hoods. To decontaminate equipment or surfaces. CR Chemical name: Dibenz(b. or contact sensitization 1 Causes almost no effects in the lower airways and lungs1 Instantaneous 4 Personnel exposed to CR should wear protective clothing (secured at neck. Do not use any form of bleach.f)-1:4-oxazepine 1 Synonym: Dibenzoxazepine. and ankles). CR does not induce inflammatory cell infiltration.3 CR is not used in its pure form but is dissolved in a solution of 80 parts of propylene glycol and 20 parts of water to form a 0.CS. however.5 RCA 5 Molecular formula: C13H9NO Molecular weight: 195. Under suitable conditions.

CR (Continued) NOTES ¹BG Russ Zajtchuk. is derived from cayenne peppers. 8-Methyl non-6-enoyl vanillylamide. 6-Nonenamide. causing reflex changes in blood pressure and respiration. Contact with the eyes is extremely painful. (E)-.15a ECt50 : 0.Table III-4. It causes pain. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. OC stimulates sensory nerve endings. Chemical Name: Trans-8-methyl-N-vanillyl-6-nonenamide Synonym: Vanillyl decenamide.0020. Pepper Spray. Riot Control Agents and Herbicide Operations. Capsaicin (OC) (see Table III-6). (eds). 12. 3 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. Capsaicin. February 2000.5 See Table III-7 (page III-7) for toxicity estimates. just discernable respiratory tract/ocular symptoms a Toxicity (mg min/m3) LCt50: N/A ECt50 : 0. 4 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. OC is a powerful irritant and lacrimator. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries.11/MCRP 3-3. (E)-N-[(4-Hydroxy-3-methoxyphenyl)methyl]-8-methyl-6-nonenamide. 1 February 1996. Although it may not have been the proximal cause of death.7. 5 FM 3-11. It also produces bronchoconstriction and edema of the airway mucosa. edema. “Riot Control Agents. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP6(B).004b MV (L) N/A 15 N/A Exposure Duration N/A 1 min 1 min ROE Inhalation/Ocular Inhalation/Ocular Inhalation/Ocular Probit Slope N/A Unknown Unknown TLE N/A N/A N/A ROD N/A Apparently Rapid Apparently Rapid DOC N/A Moderate Moderate NOTES Based on “official” estimates (HEC. f. also called oleoresin capsicum. and erythema of the tissues with which it makes contact. 6-Nonenamide.42 III-5 . intolerable Threshold effects. it has been associated with deaths in humans. b Based on human data. 22 December 1995. Flame. 19 August 1996 (Renumbered from FM 3-11).2. Table III-5. Trans8-methyl-N-vanillyl-6-nonenamide. 8 Methyl nonen-6-oxyl-vanillyl amide. 8-methyl-N-vanillyl-. 1997. Office of the Surgeon General. (E) CAS Registry Number: 404-86-4 RTECS Number: RA8530000 Physical and Chemical Properties Structural Formula: * CH3O O HO CH2NHC(CH2)4CH CH3 CHCHCH3 Molecular Formula: C18H27NO3 Molecular Weight: 305. CR Toxicity Estimates5 Endpoint Lethality Severe effects. OC Alternate Designations: DC. Table III-6.” 2 FM 8-9/NAVMED P-5059/AFJMAN 44-151. N-((4-Hydroxyl-3-methoxyphenyl)methyl)-8-methyl-. N-(4-Hydroxy-3methoxybenzyl)-8-methylnon-trans-6-enamide. et al. 1967). Chap.

III-6 . Evaluation and Synthesis of Chemical Compounds Vol. UNCLASSIFIED Report (ADB955131).7.5 x 10-7 @ 65oC (extrapolated) 3 2.R. ketones. September 2003.. Edgewood Arsenal. L. EACD 445. 2.. February 1965. (ADB955216). Fundamental Study of Toxicity: Solubility of Certain Toxics in Water and in Olive Oil. ether.5 (calculated) 1. irritating 1 340. et al.Physical state Odor Boiling point FP/MP Liquid density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m3) Latent heat of vaporization (kcal/mol) Flash point Decomposition temperature Solubility Rate of hydrolysis Hydrolysis products Stability in storage Action on metals or other materials Skin and eye toxicity Inhalation toxicity Rate of action Protection required Decontamination Use Colorless monoclinic plates 1. MD. Riot Control Agents and Herbicide Operations. Isolation of Capsaicin from Capsicum. P. Flush face with cool water. 6 Carter. if burning persists. Edgewood Arsenal. December 1921.. EACD 79. and aqueous alkali 1. 9 FM 3-11. wrist. MD.K. Chem.. UNCLASSIFIED Report (ADB959611)..H. 6 soluble in alcohol.). 19 August 1996 (Renumbered from FM 3-11). also has applications for SF and stability and support operations.4oC (extrapolated) 3 65oC (FP) 2. MD. E. The Pungent Principle of Capsicum. it has the potential of being an effective riot control agent... R. water. 3 Watson. Vol.2.9. II. June 1922. Chemical Warfare Service. Decontaminate required areas with soap and water. methylene chloride. 5 Above 150oC 3 Solubility in water is 0. Flame.. et al. 5 Daroff. EACD 188. Determination of the Vapor Pressure of D. carbon disulfide. “The Constitution of Capsaicin.2 x 10-3 @ 65oC (calculated from vapor pressure) 3 33. and ankles 9 Table III-6. M.090 g/L @ 37oC.4 (calculated from Clausius Clapeyron equation which assumes constant heat of vaporization of a function of temperature) 3 Capsaicin in the form of pepper spray may be flammable or nonflammable depending on the type of delivery (carrier) system used. Am.L. Final Comprehensive Report November 1961 – February 1965. hydrocarbons. UNCLASSIFIED Report (ADB955292). chloroform. UNCLASSIFIED Report (ADB225032).. A.C. April 1924. USA Dugway Proving Ground. DA-18-108-CML-6673 (A). 9 Most often used by the MP for incapacitating violent or threatening subjects. Oleoresin Capsicum: An Effective Less-Than Lethal Riot Control Agent. Chemical Warfare Service. III. USA Chemical Research Laboratories. Investigation of the Synthesis of Capsaicin and Related Compounds. use ice pack. USA Chemical Research Laboratories. May 1928. H. concentrated HCl. When pepper spray is combined with various carrier systems (i. Soc. 9 NOTES *Capsaicin is the principal capsaicinoid compound present in oleoresin capsicum (OC). 7 Data not available Alkaline hydrolysis yields vanillylamine and isomeric decenoic acid 7 Data not available Data not available Other Data Powerful irritant and lacrimator 8 Causes bronchoconstriction and edema 8 Almost immediate 9 A protective mask and ordinary field clothing secured at the neck..S. Do not rub area. 2 Pungent..” J.11/MCRP 3-3.. UT.M. Chemical Biological Defense. 4 Nelson. P. 8 Sharon Reutter..E. etc..D. EACD 307. January 1997. 2 Steadman. DPG/JCP-097-002. Edgewood Arsenal.e. and Sharp. Edgewood Arsenal. UNCLASSIFIED Report (ADB253543). MD. H. Review and Recommendations for Human Toxicity Estimates for FM 3-11.4 Data not available 10. USA Chemical Research Laboratories. and Dawson. and Knight. S. MD.C. Edgewood Arsenal. OC is commonly known as pepper spray. aromatic solvents. isopropyl alcohol. 7 Rosenberg. 1923. ECBC-TR-349. 45. OC (Continued) Move to fresh air. 1 Sherrill..

diphenylcyanoarsine (DC) and chlorine (Cl2). diphenylchloroarsine (DA). In the absence of symptoms.5 See Table III-9 (page III-9) for DM toxicity estimates. They were originally designed as “mask breakers” during WWI. OC Toxicity Estimates5 Endpoint Lethality Toxicity (mg min/m3) LCt50: N/A MV (L) N/A Exposure Duration N/A ROE Inhalation/Ocular Probit Slope N/A TLE N/A ROD N/A DOC N/A 3. The second characteristic of these compounds is that there may be more prolonged systemic effects—such as headache. vomiting. and diarrhea—which last for several hours after exposure. a significant amount of the compound will have been absorbed. The degree of severity and the duration of effects vary directly with the concentration used. DA. however. and they produce their effects by inhalation or by direct action on the eyes. Rl5 Chemical Name: 10-Chloro-5.10-dihydro-phenarsazine CAS Registry Number: 578-94-9 RTECS Number: SG0680000 Physical and Chemical Properties Structural Formula: Cl As Molecular Formula: C12H9AsClN Molecular Weight: 277.3 They are dispersed as aerosols. Phenazsarine chloride. nausea. The effects may then cause an individual to unmask. Their intended purpose was to penetrate the canister. 10-Chloro-5.10-dihydroarsacridine. Phenarsazine chloride. by the time they mask. DM. Diphenylaminechlorarsine. there is burning and tightening across the chest with a persistent rasping cough.6dihydrophenarsazine.Table III-7. their primary action is irritation of the respiratory tract. abdominal cramps. DM Alternate Designations: Azine. they can cause serious illness or death. but irritating 2 III-7 . 10-chloro-5. 6-Chlorophenarsazine. 5-Aza-10arsenaanthracene chloride. No protective clothing is required. Fenarsazinchlorid (Czech). DM has caused a few human deaths. The first characteristic is that the effects do not appear immediately on exposure or seconds afterwards. forcing troops to remove their masks and be exposed to more toxic materials. 10-chloro-9. and acute general depression. personnel will not mask immediately. burning in the nose and throat. but several minutes later.10-dihydrophenarsazine Synonyms: Diphenylamine chloroarsine. Table III-8. 10-Chlorophenarsazine. When released indoors.10-dihydro-.4 The protective mask gives adequate protection against field concentrations.4 a.58 Physical state Odor NH Light yellow to green crystals 1 No pronounced odor. 1-Chloro-1. Phenarsazine. After exposure.5 Two characteristics make these compounds different than RCAs. Diphenylamine arsenious chloride. Respiratory Irritants The principal respiratory irritants are diphenylaminochloroarsine (DM) (Adamsite). chills. Symptoms are decidedly more marked after an exposure than during it. DM (see Table III-8). mental depression. and DC were previously called vomiting agents.

7 Slightly soluble in benzene xylene. causes extensive corrosion on aluminum and stainless steel @ 71oC. 8. 4 Diphenylaminearsenious oxide and hydrochloric acid 4 At room temperature.044 g/L @ 37oC. 14 Previously used as an RCA and “mask breaker” 11 Table III-8. mouth. the eyes. 10 After 3 months.6 (calculated) Negligible @ ambient temperature 5. 10 Stable in aluminum and stainless steel for at least 2 years @ 71oC when pure. @ 200oC. alcohols. 0. it slowly hydrolyzes and a protective oxide coating forms that hinders further hydrolysis.15% per min @ 250oC 5 Solubility in water is 0. 3 0.Boiling point FP/MP Solid density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m3) Latent heat of vaporization (kcal/mol) Flash point Decomposition temperatures Solubility Rate of hydrolysis Hydrolysis products Stability in storage Action on metals or other material Skin and eye toxicity Inhalation toxicity Rate of action Protection required Decontamination Use 410oC (extrapolated) decomposes 3 195oC (MP) with slight decomposition 3 1. Finely divided DM hydrolyzes rapidly. 6 14.8% at temperatures between 70-80oC.5% HCl @ room temperature and 0. carbon tetrachloride. DM is stable for at least 1 year when pure and 6 months with plant grade material. 4 Acidic solutions prevent hydrolysis. 9 acetone. 1. and 0. but the containers are severely pitted.648 @ 20oC.672 @ 0oC 4 9. and skin may be washed with water. 6 Negligible @ ambient temperature 5. bronze and brass. 10 Also corrodes iron. tetrachorethane9 When solid DM is covered with water. DM (Continued) III-8 .2 @ 410oC (calculated from vapor pressure) 5 Nonflammable 2 Slight decomposition @ 195oC. 8 Other Data Causes eye irritation and burning 11 Primary action on upper respiratory tract 11 Rapid 12 Protective mask 13 If symptoms persist.02% per min. Do not swallow water.

New York. e Based on secondary data. Whitehouse Station. 1997. July 1987. Chemical Warfare Service. Brief Evaluation of the Possibilities of Using Arsenicals as Incapacitating Agents.M. 3. Grace and Company. R. EACD 445. Vol. Table III-9. Chemical Warfare Service Edgewood Arsenal. NJ. Chemical Warfare Service Edgewood Arsenal. 5 Parker. Merck & Company. 22 December 1995. MD.Table III-8. Corrosion. Washington Research Center. Final Report – Task I. “Riot Control Agents. May 1928. 7 Carter.. EATR 46.. UNCLASSIFIED Report (ADB955216). Clarksville. Chap. R. Chemical Warfare Service Edgewood Arsenal. ETF 100-41/Vol-3. Fundamental Study of Toxicity Miscellaneous Data. May 1964. and nasal discharge. b The TLE value is assumed to be 1 because the Ct profile is unknown. 13th ed. John Wiley & Sons. 8 The Merck Index: An Encyclopedia of Chemicals. (Diphenylaminechloroarsine). c See Appendix H for detailed toxicity profile estimates.. 1928 UNCLASSIFIED Report (ADB955210). 12. Constants and Physiological Action of Chemical Warfare Agents.. 10 Brooks. 2001. Office of the Surgeon General. MD. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B). (eds). DA causes severe irritation of the mucous membranes. d Based on human data. Vapor Pressure of D. A. 6 Properties of War Gases Volume III: Vomiting & Choking Gases & Lacrimators (U). throat irritation a 15 1 min Inhalation/Ocular Unknown Unknown Unknown Low NOTES Based on existing “official” estimates. UNCLASSIFIED Report (AD108458).R..K... Sax’s Dangerous Properties of Industrial Materials.. et al..5 See Table III-11 (page III-11) for toxicity estimates. Inc. 1 February 1996.000a (Provisional) ECt50 : 22 – 150d (Provisional) ECt50 : less than 1e MV (L) 15 15 Exposure Duration 2-240 min 1 min ROE Inhalation/Ocular Inhalation/Ocular Probit Slope Unknown Unknown TLE 1b.c Unknown ROD Unknown Unknown DOC Low Low Threshold effects. Chemical Corps Board. Edgewood Arsenal. p. D. MD. 10th ed.. UNCLASSIFIED Report (ADB114319).. NY. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare.” 12 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. MD. 9 Kibler. 2001. 5225. salivation.J. 2875. and Stricker. MD.. coughing. b. December 1944. DA has also been classified as a sternulator. R. MD. Aberdeen Proving Ground.. July 1921. Inc. Compatibility and Other Physicochemical Studies (U). H. T. DM Toxicity Estimates5 Endpoint Lethality Intolerable Toxicity (mg min/m3) LCt50: 11. Fundamental Study of Toxicity: Solubility of Certain Toxics in Water and in Olive Oil.F. W. 4 Macy. USA Chemical Research Development and Engineering Center. Edgewood Arsenal. DA (see Table III-10 [page III-10]). MD.M. and Biologicals.C. DA18-108-CML-6602 (A). DM (Continued) NOTES ¹Lewis. P. p.. and Knight. M. Physico Chemical Constants of Diphenylaminochlorarsine. 14 FM 8-9/NAVMED P-3059/AFJMAN 49-151. EATR 78. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. It may lead to serious disturbances of the nervous system from absorption. UNCLASSIFIED Report (AD350755). 13 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. July 1932. EACD459. Drugs. III-9 . 11 BG Russ Zajtchuk. S. ³Klosky. MD.L. CRDEC-TR-87061.H.H. UNCLASSIFIED Report (ADB956574). UNCLASSIFIED Report (ADB955024). June 1921. Chemical Warfare Service. UNCLASSIFIED Report (ADB955053). et al. ²Lau. February 2000.E. Army Chemical Center. EATR 58.

Table III-10. DA
Alternate Designations: Clark I (German); Blue Cross (German); Sternite (French); Sneezing gas; DIK Chemical Name: Diphenylchloroarsine Synonyms: Arsine, chloro, diphenyl; Chlorodiphenylarsine; Diphenylarsenious chloride; Chlorodiphenylarsine; Arsinous chloride, diphenyl-; Diphenyl arsenic chloride; Chlor-difenylarsin (Czech); Chlorodiphenylarsine; Difenylchlorarsin (Czech); Diphenylarsinous chloride; Diphenylchloorarsine (Dutch) CAS Registry Number: 712-48-1 RTECS Number: CG9900000 Physical and Chemical Properties Structural Formula:

Cl As

Molecular Formula: C12H10AsCl Molecular Weight: 264.59 Physical state Odor Boiling point FP/MP Liquid density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m3) Latent heat vaporization (kcal/mol) Flash point Decomposition temperature Solubility Rate of hydrolysis Hydrolysis products Stability in storage Action on metals or other materials Skin and eye toxicity Inhalation toxicity Rate of action Protection required Decontamination Use Colorless crystalline solid when pure 1 None 1 383°C (extrapolated) decomposes 2 37.3°C 3; 39 to 44°C (MP) 2 DA also exists in an unstable modification which melts between 18.2 to 18.4°C 3 1.3875 @ 50°C 3 9.1(calculated) 1.79 x 10-2 @ 50°C (extrapolated) 3 2.36 x 102 @ 50°C (calculated from vapor pressure) 3 15.1 (calculated from Clausius Clapeyron equation which assumes constant heat of vaporization as a function of temperature) 3 350°C 1 300 to 350°C 2 Solubility in water is 0.078 g/L @ 37°C; 4 soluble in acetone, ether, 5 ethanol, benzene, carbon tetrachloride, ethylene chloride, chloroform, and dichloroethylene
2, 5

Slow in bulk but rapid when finely divided 2 Diphenylarsenious oxide and hydrogen chloride 2 Stable when pure. Stable in steel shells for almost 4 months @ 60°C and for 1 year @ room temperature. 2 None when dry 2 Other Data Irritant 6 Irritant 6 Rapid 7 Protective mask 8 If symptoms persist, the eyes, mouth, and skin may be washed with water. Do not swallow water. 9 Previously used as “mask breaker” 6

III-10

Table III-10. DA (Continued)
NOTES ¹Lau, T.M.K., Brief Evaluation of the Possibilities of Using Arsenicals as Incapacitating Agents, CRDEC-TR-87061, USA Chemical Research, Development and Engineering Center, Aberdeen Proving Ground, MD, July 1987, UNCLASSIFIED Report (ADB114319). 2 Macy, R., Constants and Physiological Action of Chemical Warfare Agents, EATR 78, Chemical Warfare Service Edgewood Arsenal, MD, July 1932, UNCLASSIFIED Report (ADB956574). ³Owens, R., Diphenylcyanoarsine: Part V – The Physical Properties of M.A., D.A. T.A., and D.C., SO/R 492, Sutton Oak, England, December 1940, UNCLASSIFIED Report. 4 Carter, R.H., and Knight, H.C., Fundamental Study of Toxicity: Solubility of Certain Toxics in Water and in Olive Oil, EACD 445, Chemical Warfare Service, Edgewood Arsenal, MD, May 1928, UNCLASSIFIED Report (ADB955216). 5 Lide, D.R, CRC Handbook of Chemistry and Physics, 82nd, ed., p. 3-15, CRC Press, Washington, DC 2001. 6 Sharon Reutter, et al., Review and Recommendations for Human Toxicity Estimates for FM 3-11.9, ECBC-TR-349, September 2003. 7 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report, February 2000. 8 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11, Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries, 22 December 1995. 9 FM 8-9/NAVMED P-3059/AFJMAN 49-151, NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B), 1 February 1996.

c. DA Toxicity Estimates (Table III-11). No toxicity estimates are recommended for lethal exposure. The existing estimates could not be substantiated.
Table III-11. DA Toxicity Estimates5
Endpoint Lethality Intolerable
a

Toxicity (mg min/m3) LCt50: NR ECt50 : 12a

MV (L) N/A 15

Exposure Duration N/A 2 min

ROE Inhalation/Ocular Inhalation/Ocular NOTES

Probit Slope Unknown Unknown

TLE Unknown Unknown

ROD Unknown Unknown

DOC N/A Low

Based on secondary human data.

d. DC (see Table III-12 [page III-12]). The Germans introduced DC in 1918 as an improvement over DA, which is readily hydrolyzed by water. DC causes irritation of the nose and throat, salivation, and profuse secretion from the eyes and nose. There is a feeling of suffocation and headache. Symptoms last for 30 minutes to 1 hour, except the headache may last for several hours.5 See Table III-13 (page III-13) for DC toxicity estimates.

III-11

Table III-12. DC
Alternate Designations: CLARK II (German); Clark 2 (German); Blue Cross (German), Sternite (French) Chemical Name: Diphenylcyanoarsine Synonyms: Diphenylarsinous cyanide; Diphenylarsinecarbonitrile; Arsinous cyanide, diphenyl-; Arsinecarbonitrle, diphenylCAS Registry Number: 23525-22-6 RTECS Number: Data not available Physical and Chemical Properties Structural Formula:

N C As

Molecular Formula: C13H10AsN Molecular Weight: 255.15 Physical state Odor Boiling point FP/MP Liquid density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m3) Latent heat of vaporization (kcal/mol) Flash point Decomposition temperatures Solubility Rate of hydrolysis Hydrolysis products Stability in storage Action on metals or other material Skin and eye toxicity Inhalation toxicity Rate of action Protection required Decontamination Use Colorless crystalline solid 1 Similar to garlic and bitter almonds 1 341°C (extrapolated) decomposes 2 31.2°C (FP) 2 1.3338 @ 35°C 2 8.8 (calculated) 7.2 x 10-4 @ 35°C (extrapolated) 2 9.56 @ 35°C (calculated from vapor pressure) 2 17.1 (calculated from Clausius Clapeyron equation which assumes constant heat of vaporization as a function of temperature) 2 Low 1 Above 240°C 2 Solubility in water is 0.021 mg/L @ 37°C; 3 soluble in chloroform and other organic solvents4 Very slow 1 Hydrogen cyanide and diphenylarsenious oxide 1 Stable at all ordinary temperatures 1 None on metals 4 Other Data Irritant 5 Irritant 5 Rapid 6 Protective mask 7 If symptoms persist, the eyes, mouth and skin may be washed with water. Do not swallow water. 8 Previously used as “mask breaker” 5

III-12

Table III-12. DC (Continued)
NOTES Lau, T.M.K., Brief Evaluation of the Possibilities of Using Arsenicals as Incapacitating Agents, CRDEC-TR-87061, USA Chemical Research Development and Engineering Center, Aberdeen Proving Ground, MD, July 1987, UNCLASSIFIED Report (ADB114319). 2 Owens, R., Diphenylcyanoarsine: Part V – The Physical Properties of M.A., D.A. T.A., and D.C., SO/R 492, Sutton Oak, England, December 1940, UNCLASSIFIED Report. 3 Carter, R.H., and Knight, H.C., Fundamental Study of Toxicity: Solubility of Certain Toxics in Water and in Olive Oil, EACD 445, Chemical Warfare Service, Edgewood Arsenal, MD, May 1928, UNCLASSIFIED Report (ADB955216). 4 Franke, S., Manual of Military Chemistry Volume I- Chemistry of Chemical Warfare Agents, ACSI-J-3890, Chemie der Kampfstoffe, East Berlin, April 1968, UNCLASSIFIED Technical Manual (AD849866). 5 Sharon Reutter, et al., Review and Recommendations for Human Toxicity Estimates for FM 3-11.9, ECBC-TR-349, September 2003. 6 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report, February 2000. 7 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11, Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries, 22 December 1995. 8 FM 8-9/NAVMED P-3059/AFJMAN 49-151, NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B), 1 February 1996.
1

Table III-13. DC Toxicity Estimates5
Endpoint Lethality Severe effects; incapacitation Toxicity (mg min/m3) LCT50: NR ECt50 : NR MV (L) N/A N/A Exposure Duration N/A N/A ROE Inhalation/ Ocular Inhalation/ Ocular Probit Slope Unknown Unknown TLE Unknown Unknown ROD Unknown Unknown DOC N/A N/A

e. Chlorine (Cl₂) (see Table III-14). Chlorine causes spasm of the larynx muscles; burning of the eyes, nose, and throat;, bronchitis; and asphyxiation.5 Rapid evaporation of the liquid may cause frostbite.7 Chlorine has been classified as a lung injurant,5 as a choking agent,4 and as a TIC.8 See Table III-15 (page III-14) for toxicity estimates.
Table III-14. Cl2
Alternate Designations: Bertholite Chemical Name: Chlorine Synonyms: Chloor (Dutch); Chlor (German); Chlore (French); Chlorine mol.; Cloro (Italian); Molecular chlorine CAS Registry Number: 7782-50-5 RTECS Number: FO2100000 Physical and Chemical Properties Structural Formula: Molecular Formula: Cl2 Molecular Weight: 70.91 Physical state Odor Boiling point MP/FP Liquid density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m3) Latent heat of vaporization (kcal/mol) Flash point Decomposition temperature

Cl

Cl

Greenish-yellow diatomic gas 1 Disagreeable and suffocating; irritating to the nose and throat 2 -34.7oC 3, 4 -101.6oC (FP) 5 Liquefied chlorine: 1.393 @ 25oC; 1.468 @ 0oC 4 2.4 (calculated) 5.75 x 103 @ 25oC; 2.73 x 103 @ 0oC 3, 4 2.19 x 107 @ 25oC; 1.14 x 107 @ 0oC (calculated from vapor pressure) 3, 4 4.86 @ 25oC; 4.80 @ 0oC (calculated from vapor pressure) 3, 4 Nonflammable 2 Above 600oC 5

III-13

Solubility in water is 0.63 g/100 g water @ 25oC; solubility in carbon tetrachloride is 3.5% @ ambient temperature 5 Rate of hydrolysis Slow 6 Hydrolysis products HCl and HOCl 5 Stability in storage Stable when dry 5 Action on metals or other materials None if chlorine is dry. Vigorous action with metals when chlorine is moist due to the presence of hypochlorous acid. 5 Other Data Skin and eye toxicity Irritant 7 Inhalation toxicity Can cause pulmonary edema 7 Rate of action Like choking agents, pulmonary edema does not manifest until hours have passed and are aggravated by physical effort 7 Protection required Protective mask 8 Decontamination Inhalation - fresh air and rest. Eyes and skin - rinse with plenty of water. 7 Use Not authorized for military use NOTES ¹The Merck Index: An Encyclopedia of Chemicals, Drugs, and Biologicals, 13th ed., p. 5225, Merck & Company, Inc., Whitehouse Station, NJ, 2001. ²Yaws, C.L., Matheson Gas Data Book, 7th ed., p. 162, McGraw-Hill Companies, New York, NY, 2001. ³Abercrombie, P., ECBC Notebook # NB 98-0079, p. 32 (U). 4 Beebe, C.H, Important Constants of Fourteen Common Chemical Warfare Agents, EACD 328, Chemical Warfare Service, Edgewood Arsenal, Edgewood, MD, December 1924, UNCLASSIFIED Report (ADB958296). 5 Macy, R., Constants and Physiological Action of Chemical Warfare Agents, EATR 78, Chemical Warfare Service, Edgewood Arsenal, MD July 1932, UNCLASSIFIED Report (ADB956574). 6 TM 3-215/AFM 355-7, Military Chemistry and Chemical Agents, December 1963, UNCLASSIFIED Technical Manual (ADA292141). 7 ICSC 0126, “Chlorine (Cl2).” 8 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11, Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries, 22 December 1995. Solubility

Table III-14. Cl2 (Continued)

f. Cl2 Toxicity Estimates. Toxicity estimates for lethal and severe effects are recommended. Existing estimates could not be substantiated.
Table III-15. Cl2 Toxicity Estimates5
Endpoint Lethality Severe effects, incapacitation Threshold effects, odor
a

Toxicity (mg min/m3) LCt50: NR ECt50 : NR ECt50 : 10a

MV (L) N/A N/A N/A

Exposure Duration N/A N/A Seconds

ROE Inhalation/Ocular Inhalation/Ocular Inhalation/Ocular NOTES

Probit Slope Unknown Unknown Unknown

TLE Unknown Unknown N/A

ROD Unknown Unknown Unknown

DOC N/A N/A Low

Based on human secondary data and TM 3-215 (1952).

4. Obsolete Riot Control Agents
The following RCAs are considered obsolete for military employment. The following is primarily of academic and historical interest. a. Chloroacetophenone (CN) (see Table III-16). The symbol CN identifies the RCA popularly known as tear gas or mace. The USA replaced CN with CS in 1959.3 Inhalation of CN causes a burning sensation, cough, sore throat, nausea, and shortness of breath. Exposure to skin causes redness and pain. Eye exposure causes redness, pain, and blurred vision. CN can cause pulmonary edema.9 High concentrations can cause blisters to form, and CN is a potent skin sensitizer. The indiscriminate use of large amounts of CN in confined spaces has caused injuries requiring medical attention and death.3

III-14

Table III-16. CN
Chemical name: 2-Chloracetophenone
1

Synonyms: alpha-Chloroacetophenone, 2-Chloro-1-pheylethanone, Chloromethyl phenyl ketone, Mace®, Phenacyl chloride, Phenyl chloromethyl ketone, Tear Gas 2 CAS Registry Number: 532-27-4 1 RTECS Number: AM6300000 1 Physical and Chemical Properties Molecular formula Molecular weight Physical state Odor Boiling point FP/MP Density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m3) Latent heat of vaporization (kcal/mol) Flash point Decomposition temperature Solubility Rate of hydrolysis Hydrolysis products Stability in storage Action on metals and other materials Skin and eye toxicity Inhalation toxicity Rate of action Protection required Decontamination Use
1 2

C8H7ClO 1 154.6 1 Colorless to gray crystalline solid 3 Sharp, irritating odor 3 244°C (472°F) 3 57°C (134°F) (MP) 3 1.3 1 5.3 (calculated) 0.005 @ 20°C (68°F) 3 Data not available Data not available 118°C (244°F) 3 Data not available 1.64 g/100 mL @ 25°C, 1 soluble in carbon disulfide, ether, and benzene 2 Slow 2 HCl 2 Sensitive to moisture; incompatible with bases, amines, alcohols, water, and steam
2

Reacts slowly with metals, causing mild corrosions 2 Other Data Irritant 1 Irritant 1 Instantaneous 4
5

Protective mask and ordinary field clothing secured at the neck, wrists, and ankles

Move to fresh air. If necessary, wash with water.6 Skin decontaminants containing bleach should not be used. 7 Previous RCA still in use by police in some countries 6 NOTES

ISCS 0128, “2-Chloroacetophenone.” National Toxicity Program, “NTP Chemical Repository: Chloroacetophenone.” 3 NIOSH Pocket Guide to Chemical Hazards, “a-Chloroacetophenone,” CAS 532-27-4. 4 NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report, February 2000. 5 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11, Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries, 22 December 1995. 6 FM 8-9/NAVMED P-5059/AFJMAN 44-151, NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP6(B), 1 February 1996. 7 BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare, Office of the Surgeon General, 1997, Chap. 12, “Riot Control Agents.”

b. Chloroacetophenone Mixtures. Different CN mixtures were produced to include CN in chloroform (CNC), CN in benzene and carbon tetrachloride (CNB), and CN with PS

III-15

in chloroform (CNS). Fog oils are nonhygroscopic and depend upon vaporization techniques to produce extremely small diameter droplets to scatter light rays. early collapse and death. and it was the most potent. they absorb water vapor from the atmosphere. The toxicity of this chemical compound is generally attributed to zinc chloride (ZnCl2) (see Table III-17). (1) Hexachloroethane (HC). the object cannot be seen. ethyl tetrachloride. hexachlorobenzene. and cough. carbon tetrachloride and chloroform are suspected carcinogens. CS proved more effective and less toxic than any of the CN series and largely has replaced them. and fog oil smoke. smoke has long been employed as a means of concealing battlefield targets. but the three basic types of screening smokes are hexachloroethane (HC) smoke.13 III-16 .11 5.10 c. Smokes and Obscurants. obscurants. However.12 Most smokes are not hazardous in concentrations that are useful for obscuring purposes. Bromobenzylcyanide (CA). symptoms include tightness in the chest. sore throat or hoarseness. thus reducing visibility. hydrogen chloride.4 Exposures to very high doses of HC smoke commonly result in sudden. Obscurants. the reaction products are zinc chloride and 10 percent phosgene. obscurants. On combustion. hexachloroethane.6 White phosphorous (WP) and HC are hygroscopic. carbon tetrachloride. For example. and Incendiaries Smokes. a. chlorine. is not chemically stable in storage.12 Many types and combinations of smokes are used.13 Immediately after exposure.12 This section contains the physical and chemical properties of selected smokes. CA was the last irritating agent introduced by the Allies in World War I (WWI).4 CAUTION The protective mask must be worn when operating in or around smoke material. The more humid the air. The protective mask gives the respiratory tract and the eyes adequate protection against all smokes. Smokes. Their use provides tactical advantages for offensive and defensive operations. However. the more dense the HC smoke. Fire damage causes casualties and material damage and can impact psychologically. CAUTION Benzene is a known carcinogen. and incendiaries are combat multipliers. When the density or amount of smoke material between the observer and the object to be screened exceeds a certain minimum threshold value.3 CA is too toxic for use as an RCA and is considered obsolete. These particles scatter or absorb the light. CA irritates the eyes and causes lacrimation. This increases their diameters and makes them more efficient at reflecting light rays. phosphorous smoke. with approximately 7 percent grained aluminum. and incendiaries. Smoke is an aerosol that owes its ability to conceal or obscure to its composition of many small particles suspended in the air. and is sensitive to heat—all the characteristics that made it unsuitable for storage and use in artillery shells. any smoke can be hazardous to health if the concentration is sufficient or if the exposure is long enough. The ZnCl2 reacts with the moisture in the air to form a grayish white smoke. HC is a pyrotechnic containing an equal amount of hexachloroethane and zinc oxide. It corrodes iron and steel. and carbon monoxide.

white smoke composed of particles of phosphorous pentoxide.14 (a) White Phosphorous (WP) (see Table III-18 [page III-18]). Smoke Operations NOTES ¹NIOSH Pocket Guide to Chemical Hazards. and wear protective mask when making smoke.7 (calculated) Approximately 0 @ 20°C (68°F) 1 Data not available 2. Phosphorous occurs in three allotropic forms: white. The military uses white and red phosphorous.: 7646-85-7 1 RTECS Number. 432 g/100 mL at 25°C 2 Decomposes upon heating. “Zinc Chloride. Launder clothing following exposure. 2 Other Data Skin and eye toxicity Corrosive to the eyes and the skin 2 Inhalation toxicity Irritant. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. ZnCl2 Chemical name: Zinc Dichloride Synonyms: Zinc Dichloride Flume 1 CAS Registry No. which are converted by moist air into phosphoric acid.” ³FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. 22 December 1995.CAUTION Hexachloroethane is a suspected carcinogen.4 WP is a very active chemical that will III-17 . “Zinc Chloride fume. producing toxic fumes of hydrogen chloride and zinc oxide 2 Action on metals or other materials The solution in water is a medium-strong acid.3 1 Physical state Odor Boiling point FP/MP Liquid density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m3) Specific gravity (water = 1 @ 4°C) Flash point Decomposition temperature Solubility Stability in storage Cl — Zn — Cl Hygroscopic white solid 2 Data not available 732°C (1350°F) 1 290°C (554°F) (MP) 1 Data not available 4. and black.91 @ 25°C 1 Data not available Data not available In water. ²ICSC 1064.” CAS 7646-85-7. inhalation of fumes may cause lung edema 2 Protection required Try to remain out of smoke/obscurant clouds. red. Personnel can reduce exposure to smoke by rolling down their sleeves and showering after exposure. dense. (2) Phosphorous.10 Table III-17. WP produces a hot. Soldiers must wear respiratory protection. 3 Use See FM 3-50. 3 Decontamination Remove contaminated clothing and shoes.: ZH1400000 1 Physical and Chemical Properties Structural Formula: Molecular Formula: ZnCl2 1 Molecular Weight: 136. CAUTION Phosphorous smoke produces phosphoric acid.

13 It is used primarily as a smoke agent and can also function as an antipersonnel flame compound capable of causing serious burns. Construction Engineering Research Laboratory. Obscurants. ²NIOSH Pocket Guide to Chemical Hazards. Office of the Surgeon General. Table III-18. “Phosphorus.: 7723-14-0 Physical and Chemical Properties Chemical formula P4 2 Molecular weight 124. 1997. Exolit-LPKN. WP/F. Keep the WP covered with the wet material to exclude air until the particles can be removed. soft waxy solid 2 Odor Garlic-like 1 Boiling point 280°C (536°F) 2 FP/MP 44°C (111°F) (MP) 2 Density (g/mL) 1.82 @ 20°C 2 Flash point (mg/m3) 20°C 4 Decomposition temperature Data not available Solubility Insoluble in water. et al. USACERL Technical Report 99/56. 4: Chemical Analytical Methods. 5 Inhalation toxicity At room temperature may produce a toxic inhalational injury 6 Protection required Protective mask. Smoke Operations NOTES ¹Spectrum Chemical Fact Sheet.” 5 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. Smoke causes irritation to the eyes. Exolit VPK-n 361. Phosphore-Blanc (French). 4 Action on metals or other materials Incompatible with sulfur. 2 yellow phosphorus. oil of turpentine. 22 December 1995.” 7 FM 3-50. even at room temperature. Complete submersion in water is the only way to extinguish the flames. white phosphorus.0 2 Physical state White to yellow. (eds). 4 December 1990. As oxidation occurs.” CAS 7723-14-0. Chapter 9. and Riot-control Agents on Threatened and Endangered Species. or mud. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. 5 Use See FM 3-50. If burning WP strikes the skin.03 at 20°C 2 Volatility (relative to air) Data not available Specific Gravity (water = 1 @ 4°C) 1. “Phosphorus (yellow). WP Chemical name: Phosphorus Synonyms: Bonide-Blue-Death-Rat-Killer. soluble in carbon disulfide 1 Rate of hydrolysis Data not available Hydrolysis products Data not available Stability in storage Darkens on exposure to light. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries.readily combine with oxygen in the air. WP.” CAS 7723-14-0. Forforo-Bianco (Italian). smother the flame with water. 3 USA Corps of Engineers.83 4 Vapor density 4. July 1999. Particles on skin continue to burn unless deprived of atmospheric oxygen. “Toxic Inhalational Injury. 1 elemental phosphorus. Willie Peter3 CAS Registry No. 6 BG Russ Zajtchuk. Methods for Field Studies of the Effects of Military Smokes. iodine. 7 Do not handle the charred wedges on the ground without protective covering. “Phosphorus (Yellow). and throat.28 (calculated) Vapor pressure (torr) 0. Vol. a wet cloth. III-18 . 4 ISCS 0628. deep and variable in size. nose. WP becomes luminous and bursts into flames within minutes. Smoke Operations. This substance spontaneously ignites on contact with air producing toxic fumes. and potassium chlorate 1 Other Data Skin and eye toxicity Burns on skin are usually multiple. Gelber-Phosphor (German). 5 Decontamination Flush skin with water.

1 Titanium Oxide. potassium. TiO2 Chemical name: Titanium Dioxide Synonyms: Titanium (IV) Oxide. Violent or incandescent reaction may also occur with other metals such as aluminum. Titanium White. hydrogen fluoride. white smoke results from the decomposition of FM smoke into hydrochloric acid.871 Physical state White Powder1 Odor Odorless1 Boiling point 2500 .6 Table III-19. is essentially nontoxic. and is easier and safer to handle than WP. It is soluble in hot concentrated sulfuric acid. nitric acid.15 RP is produced by heating WP to 270 to 300 degrees C in the absence of air. therefore. the temperature can reach 900°C. The grenades consist of a 95:5 mixture of RP and butyl rubber.13 TiO2 is the major component of training smoke grenade XM82 and is also used in conjunction with HC in the production of white screening smoke. Exposure to liquid may create burns similar to those of mineral acids on conjunctiva or skin. and zinc. When RP is heated. FM smoke is a corrosive substance typically dispersed by spray or explosive munitions. A dense. 1 Other Data Skin and eye toxicity May cause mild irritation and redness 1 Inhalation toxicity May cause mild irritation 1 Protection required Protective mask 4 Decontamination Flush with water 4 Use See FM 3-50.14 (3) Titanium Tetrachloride (FM Smoke).(b) Red Phosphorous (RP). calcium. and titanium dioxide (TiO2) (see Table III-19). Brookite2 CAS Number: 13463-67-71 Physical and Chemical Properties Molecular formula TiO21 Molecular weight 79. and alcohol. RP smoke is deployed explosively from grenades and mortar shells. RP is more dense. 3 Rate of Hydrolysis Data not available Hydrolysis Products Data not available Stability in storage Stable under ordinary conditions of use and storage1 Action on metals or other materials Violent reaction with lithium occurs around 200°C with a flash of light.3000°C (4532 .75 (calculated) Vapor pressure (torr) Data not available 3 Volatility (mg/m ) Data not available Specific gravity (H2O = 1) 4. magnesium. sodium. Smoke Operations 1 III-19 . is much less reactive. WP molecules sublime from the solid.1 Insoluble in hydrochloric acid.16 RP will not ignite spontaneously and.5432°F) 1 FP/MP 1855°C (3371°F) (MP) 1 Solid density (g/mL) 4. has a higher melting point. titanium oxychloride. Titania. requires ignition to burn and make smoke.261 Flashpoint Data not available Decomposition temperature Data not available Solubility Insoluble in water. and alkali. It is extremely irritating and corrosive in both liquid and smoke formulations.17 2 Vapor density (relative to air) 2.

“Titanium Dioxide. 22 December 1995. 3 NRC. Toxicity of Military Smokes and Obscurants. strong bases. 4 FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. oxides of silicon.. colorless gas. silica. cyanides. Graphite exists naturally and synthetically and is chemically inert. most common metals. TiO2 (Continued) NOTES Mallinckroct Baker. It can cause severe burns that may not be immediately painful or visible. rubber.” effective date: 15 February 1998. it could yield toxic fumes of fluorides. Handle and transfer in a manner that avoids excessive dusting. exercise caution when handling graphite in areas where contact with electrical circuitry is possible.25 g/mL2 N/A1 N/A1 Data not available 2. It reacts with silica to produce silicon tetrafluoride. Vol. 4: Chemical Analytical Methods. near-. colorless.and far-infrared (IR) bands as well as a combination of visible. a hazardous. Vol.20 – 2. phosphorus pentoxide. eyes. vinyl acetate. It is extremely hazardous in liquid and vapor form.18 Inhalation of dust can cause nose and/or throat irritation and shortness of breath. and the respiratory tract.19 Table III-20.19 CAUTION Graphite is electrically conductive. It can also cause bone damage. and water. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. sulfuric acid.7°C2 N/A1 2. Graphite is used as an obscurant to screen electromagnetic tracking and targeting systems. hydrogen fluoride. and fluorine. carbonates. It is incompatible with arsenic trioxide. Graphite flakes perform well in obscuring mid. 2 USA Corps of Engineers. On heating to decomposition. sulfides. and Riot-control Agents on Threatened and Endangered Species. July 1999. 1 (4) Tantalum (Ta). Ta is a clear.Table III-19. Obscurants.6 It consists primarily of carbon. It is stable at 68 degrees F when stored and used under proper conditions. National Academy Press. It is a mixture of tantalum pentachloride.261 III-20 . Liquid and vapor can burn skin. odorless liquid. and especially glass. organic materials. Construction Engineering Research Laboratory. with trace impurities totaling less than one percent of the total weight. alkalis. USACERL Technical Report 99/56. acetic anhydride. 1999. 2. sodium hydroxide. MSDS Number T3627. water. Inc. ammonia. It can be fatal if swallowed or inhaled. leather. and far-IR bands. mid-. It is a corrosive poison. ethylenediamine. It attacks glass and other silicon-containing compounds.17 (5) Synthetic Graphite (see Table III-20). concrete. calcium oxide. Synthetic Graphite Chemical name: Synthetic Graphite1 Synonyms: Crystalline carbon1 CAS Number: N/A2 Molecular formula Molecular weight Physical state Odor Boiling point FP/MP Density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m3) Specific gravity (H2O = 1) Physical and Chemical Properties Carbon 12 Grey to Black1 Odorless1 3337. Methods for Field Studies of the Effects of Military Smokes.

but the predominant class of chemicals is aliphatic hydrocarbons with very low levels of noncarcinogenic aromatic hydrocarbons. The CAS numbers may vary from contract to contract. Table III-21. Smoke Operations NOTES 1 Asbury Graphite Mils. Fog oil is a low-viscosity petroleum oil used to generate screening smokes. and laser target designators as well as to provide protection for armored vehicles. thermal surveillance systems. January 2003. “Synthetic Graphite. 2 Graphite obscurant materials are purchased from manufacturers in accordance with a specification that have specific purity and performance requirements. MSDS. Smoke munitions containing metal flakes or powders are used to screen against range finders..1 Data not available Other Data Skin and eye toxicity Minor 1 Inhalation toxicity Cases of pulmonary fibrosis. 7782-42-5. Fog oil is composed of many different types of chemicals.” CAS No.Table III-20. Incompatible with oxidizing agents. rinse eyes with water1 Use See FM 3-50. SGF-2 Chemical name: Mineral Oil 1 Synonyms: SGF-2. rinse skin with soap and water. Smoke screens containing brass performed the best against far-IR bands but did poorly on visible light bands. Synthetic Graphite (Continued) Data not available Data not available Insoluble in water1 Data not available Data not available This material is stable and will not polymerize. Brass is a metal alloy composed mostly of copper (70 percent) and zinc (30 percent) with approximately 1 percent contamination of trace metals. Inc. Fog Oil 1 CAS Number: N/A 2 Molecular formula Molecular weight Physical state Odor Boiling point FP/MP Liquid density (g/mL) Vapor density (relative to air) Vapor pressure (torr) Volatility (mg/m3) Specific gravity (H2O = 1) Flashpoint Physical and Chemical Properties N/A N/A Lube Oil 1 Hydrocarbon odor 1 600°F (316°C) 1 Data not available Data not available > 11 < 11 Data not available 0.6 Fog oil is the overhead fraction of petroleum. These specifications do not contain CAS number requirements. and corpulmonale may result from prolonged inhalation of dust1 Protection required Protective mask 1 Decontamination Move to fresh air.9 Data not available III-21 .20 Fog oil is commonly called smoke generator fuel number 2 (SGF-2) (see Table III-21). It contains no additives and is not refined. The fog is generated by evaporating the hydrocarbons in the oil. Brass in flake or powder form is one of the components of screening smoke grenade M76. emphysema.6 (7) Fog Oil (SGF-2). Flashpoint Decomposition temperature Solubility Rate of hydrolysis Hydrolysis products Stability in storage Action on metals or other materials (6) Brass.

Table III-21. heart beat irregularities. When explosive charges have been added. drowsiness. Incendiaries. The purpose of incendiaries is to cause maximum fire damage on flammable materials and objects and to illuminate.” 2 Fog oil obscurant materials are purchased from manufacturers in accordance with a specification that has specific purity and performance requirements. nausea. These specifications do not contain CAS number requirements. Healing is slow unless these particles are removed quickly. slurred speech. It is an exothermic reaction in which the III-22 . dizziness. or the spreading and continuing of fires started by the incendiary may destroy them. defatting. weakness. DF-1 is clear or straw-colored liquid when undyed and low-sulfur diesel is red. lung damage. and dermatitis. The initial action of the incendiary munition may destroy these materials.22 (10) Jet Fuel Grade (JP-8).21 (9) Diesel Fuel No. headache. 1 Diesel Fuel (DF-1). Magnesium is a soft metal. defatting. anesthesia. negligible1 Data not available Data not available Avoid extreme heat and strong oxidants. which when raised to its ignition temperature. producing irritating or toxic fumes. Smoke Operations NOTES 1 Defense General Supply Center. vomiting. 1 Inhalation toxicity May cause irritation1 Protection required Protective mask 1 Decontamination Move to fresh air 1 Use See FM 3-50. dizziness.24 Magnesium (Mg) burns at approximately 2000 degrees C with a scattering effect. confusion. and loss of coordination. Overexposure by inhalation can produce symptoms of intoxication such as headache. Eyes: May cause irritation. The CAS numbers may vary from contract to contract. These smokes are produced by explosive dissemination of dyes. dizziness. 1 Data not available Other Data Skin and eye toxicity Skin: Prolonged/repeated contact may cause dryness. causing headaches. and death. “SGF-2 Type. A thermite reaction occurs when powdered aluminum metal and iron oxide mix.23 (11) Signaling Smokes. unconsciousness. Decomposition temperature Solubility Rate of hydrolysis Hydrolysis products Stability in storage Action on metals or other materials (8) No. SGF-2 (Continued) Data not available In water. causing the localized formation of hydrogen gas and tissue necrosis. upper respiratory tract irritation.4 b. fragments may be embedded deep in the tissues. drying to burns or blistering of skin.4 (2) Thermite and Thermate Incendiaries. spontaneously ignites on contact with air or moisture. MSDS MIL-F-12070C. Chronic exposure of the skin can cause drying.12 (1) Magnesium Incendiaries. and CNS effects. convulsions. vomiting. drowsiness. dermatitis. unconsciousness. Fog Oil. nausea. blurred vision. No hazardous polymerization. There are no reports of ill effects produced by exposure to these smokes. diarrhea. flushed face. 2 (DF-2). Symptoms of overexposure include eye and skin irritation. Its particles produce deep burns. aortic plaques. High vapor concentrations can be irritating to the eyes and respiratory tract. Symptoms of overexposure include redness.

4 (3) Oil and Metal Incendiary Mixtures. Toxicity of Military Smokes and Obscurants. March 18. National Academy Press. 1991. 1. September 2003. 9th ed. Lexington. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. Methods for Field Studies of the Effects of Military Smokes. and Chemical Agents and Defense Equipment. 16Henry III-23 .” 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11.C. 9. Field Behavior of NBC Agents (Including Smoke and Incendiaries).7. 1997. Particles of iron that lodge in the skin produce multiple small. 9ICSC 10US 0128.9. Flame. et al. Reutter. 12. USACERL Technical Report 99/56. “Chlorine (Cl2). Final Report of International Task Force-25: Hazard From Toxic Industrial Chemicals. 19 August 1996 (Renumbered from FM 3-11). Vol. General Chemistry with Qualitative Analysis. “Toxic Inhalational Injury. ECBC-TR-349. 6USA 5Sharon 4FM 3BG 2FM 1USACHPPM 0126. Office of the Surgeon General. MA. December 2001.. 10th Report on Carcinogens. Riot Control Agents and Herbicide Operations. 11FM 8-9/NAVMED P-5059/AFJMAN 44-151. 7ICSC 8A. Construction Engineering Research Laboratory. Office of the Surgeon General.” 3-50. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. The particles should be cooled immediately with water and removed. 1 February 1996. 1996. 22 December 1995. causing the aluminum and iron to become a liquid. et al. 3-11. July 1999. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. “2-Chloroacetophenone. 4 December 1990. Vol.K. 14FM 15NRC. “Riot Control Agents.. et al. Heath and Company. 1997. Review and Recommendations for Human Toxicity Estimates for FM 3-11. Lung damage from heat and irritating gases may be complications added to the injuries from incendiaries.11/MCRP 3-3. 4: Chemical Analytical Methods. (eds).16 Explosive charges are frequently added. et al. Russ Zajtchuk et al (eds). Corps of Engineers.4 NOTES TG 204. Chap. Holtzclaw.2. National Toxicology Program. 13BG 12FM Russ Zajtchuk.. Smoke Operations. Obscurants.” HHS. Glossary of Terms for Nuclear. deep burns. 3-6/FMFM 7-11-H/AFM 105-7. Biological. and Riot-control Agents on Threatened and Endangered Species.” Steumpfle. 1997. D. Public Health Service.temperature rises to about 3000 degrees C. Jr... 3 November 1986. December 2002. Chap. especially in confined spaces. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B). F.

“Diesel fuel 2. 1 Diesel Fuel. 17Mallinckrodt Toxicity of Military Smokes and Obscurants. 18NRC.. Vol. MSDS Number T0080. 1. 1999. Inc. MSDS.000 µg/mL or 10. MSDS.Baker.” Company. “No.” 0701. “Synthetic Graphite. Graphite Mills. 27020-00079.” effective date 29 October 2001. “SGF-2 Type. Fog Oil..” III-24 . “Tantalum.000 µg/mL. Inc. “Magnesium (Pellets). 2..” Corporation.” 19Asbury 2003. No. January General Supply Center. MSDS MIL-F-12070C. 1 Fuel Oil. 7782-42-5. Inc. MSDS. “Jet Fuel Grade JP-8. MSDS. National Academy Press. 20Defense 21Conoco 22Costal 23Exxon 24ICSC International.” CAS No.

See Table IV-1 (page IV-2) for the list of potential biological agents. Background The military application of biological agents concerns those microorganisms that may be deliberately employed in weapon systems to cause disease or death to man. 2. See Appendix J for more detailed information on animal pathogens. NOTES: 1.Chapter IV BIOLOGICAL AGENTS AND THEIR PROPERTIES 1. See Appendix K for more detailed information on plant pathogens. See Appendix I for the properties of selected biological agents. 5. See Table IV-2 (page IV-3) for the list of animal and plant pathogens with potential biological agent applications. 6. animals. or plants. and viruses) and toxins. See Appendix L for information on the dissemination of biological agents IV-1 . 4. rickettsiae. 3. Biological agents consist of microorganisms such as pathogens (which include disease-causing bacteria.

formerly Pseudomonas pseudomallei (Melioidosis) Salmonella typhi (Typhoid Fever) Shigella dysenteriae (Shigellosis) Vibrio cholerae (Cholera and other Vibrioses) Yersinia pestis (Plague) IV-2 . however. formerly Rochalimaea quintana or Rickettsia quintana (Trench Fever) Rickettsia prowasecki (Typhus Fever) Rickettsia rickettsii (Rocky Mountain Spotted Fever) NOTE: Trichothecene mycotoxin is not on the list of BW agents listed in the reference. Tetrodotoxin Verotoxin Microcystin Trichothecene mycotoxin (see Note) Toxins Bacteria Bacillus anthracis (Anthrax) Brucella abortus (Brucellosis) Brucella melitensis (Brucellosis) Brucella suis (Brucellosis) Chlamydia psittaci (Psittacosis) Clostridium botulinum (Botulism) Francisella tularensis (Tularemia) Burkholderia mallei. List of Potential BW Agents26 Viruses Chikungunya virus Crimean-Congo hemorrhagic fever virus Dengue fever virus Eastern equine encephalitis virus Ebola virus Hantaan virus Junin virus Lassa virus Lymphocytic choriomeningitis virus Machupo virus Marburg virus Monkeypox Rift Valley Fever virus Tick-borne encephalitis virus (Russian Spring-Summer encephalitis virus) Variola virus Venezuelan equine encephalitis virus Western equine encephalitis virus Yellow fever virus Japanese encephalitis virus Botulinum toxins Clostidium perfringens toxins Conotoxin Ricin Saxitoxin Shiga toxin Staphylococcus aureus toxins Rickettsia Coxiella burnetii (Q Fever) Bart quintana.Table IV-1. formerly Pseudomonas mallei (Glanders) Burkholderia pseudomallei. mycotoxins were alleged to have been used in Southwest Asia in the mid-1980s.

citri Plant Pathogens for Export Control Bacteria a. soil. Provides information on where the disease is known to be prevalent and/or in what population groups it is most likely to occur. Phoma Tracjeo[jo. Moniliophtora rorei) Items for Inclusions in Awareness-Raising Guidelines Barley Yellow Dwarf Virus Virus Cochiliobolus miyabeans (Helminthosporium oryzae) Microcylus ulei (syn. The biological agents addressed in this chapter are presented in a standard format that includes the following information: (1) Infectious Agent.a) Monlia rorei (syn. Puccinia graminis fsp. oryzae Xylella fastidiosa Fungi Deutrrerophoma tracheiphila (syn. Tritici) Puccinia striformis (syn. and toxins. animal. (2) Occurrence. arthropod. b. Identifies the specific pathogen that causes the disease. rickettsiae. plant. classifies the pathogen.Table IV-2. viruses. and where it reproduces itself in such a manner that it can be transmitted to a susceptible host. Puccinia glumarium) Pyricularia grisea/Pyricularia oryzae Fungi Colletorichum coffeanum var Xanthomonas albilineans Xanthomonas campestris pv. Dothidella ulei) Puccinia graminis (syn. (3) Reservoir. IV-3 . or substance (or a combination of these) in which an infectious agent normally lives and multiplies. on which it depends primarily for survival. Animal and Plant Pathogens with Potential BW Applications26 Animal Pathogens for Export Control Viruses African swine fever virus Highly pathogenic Avian influenza virus (synonym: fowl plague) Bluetongue virus Foot and mouth disease virus Goat pox virus Herpes virus (Aujeszky’s disease) Hog cholera virus (synonym: Swine fever virus) Lyssa virus Newcastle disease virus Peste des petits ruminants virus Porcine enterovirus type-9 (synonym: Swine vesicular disease virus) Rinderpest virus (synonym: Cattle plague Sheep pox virus Teschen disease virus Vesicular stomatitis virus Bacteria Bacteria Mycoplasma mycoides Other Animal Diseases/Pathogens of Concern Contagious bovine pleuropneumonia Contagious Equine Metritis Heartwater (Cowdria) Screwworm Myiasis (synonym: Blowfly Cochliomyia hominivorax) Swine vesicular disease Banana bunchy top virus Virus Xanthomonas campestris pv. Indicates the ultimate and/or intermediate human. and may indicate any of its important characteristics. The information presented in this chapter provides descriptions of selected bacteria.

(8) (9) Prevention. or talking (usually limited to a distance of about 1 meter or less). (7) Communicability. coughing. 2. (a) Direct transmission can be by direct contact (such as touching or biting). Vector-borne transmission can be mechanical or biological. few bacteria are of military significance. (1) Infectious Agent. weeks. The spores are extremely hardy and can survive extremes of temperature. Describes the most likely means to disseminate the agent. Anthrax. Delivery. Worldwide. transmittable from animals to humans. (c) Airborne transmission is the dissemination of microbial aerosols to a suitable portal of entry—usually the respiratory tract. nose.1 Describes the mechanisms by which an infectious agent is spread to humans. or months) during which an infectious agent may be transmitted. Vehicle-borne transmission is when contaminated inanimate materials or objects (e. Of several thousand identified species. spitting. (5) Symptoms. effective exposure to an infectious organism and the first appearance of symptoms of the infection. Zoonotic organisms include anthrax. Describes prophylaxis measures. tularemia.(4) Transmission.. or by passage of organisms through its GI tract. Microbial aerosols are suspensions of particles in the air consisting partially or wholly of microorganisms. directly or indirectly. and flooding. Biological means that the propagation (multiplication). indirect. soiled clothes. An incubation period is required following infection before the arthropod becomes infective. These unicellular forms outnumber all other forms of microorganisms. a.2 Some bacteria that infect man are selective human parasites. or mouth during sneezing. singing. or food) serve as an intermediate means by which an infectious agent is transported and introduced into a susceptible host through a suitable portal of entry. Bacteria have primary military potential as antipersonnel agents. Describes the time (days. This does not require multiplication or development of the organism. This organism forms a protective spore under adverse environmental conditions or upon exposure to air. only about 100 are known to be pathogenic. water. (6) Incubation period. Bacillus anthracis. and airborne. or a combination of these is required before the arthropod can transmit the infective form of the agent to humans. days. Describes the symptoms of the disease. However. but many are zoonotic.g. microscopic organisms.3 IV-4 . When conditions improve. or by the direct projection (droplet spread) of droplet spray onto the conjunctiva or onto the mucous membranes of the eye. Mechanical includes simple mechanical carriage by a crawling or flying insect through soiling of its feet or proboscis. cyclic development. or weeks) between initial. (b) Indirect transmission can be vehicle. Such mechanisms include direct. from an infected person to another person or from an infected animal to humans. cooking or eating utensils.or vector-borne.3 (2) Occurrence. the spores germinate to produce vegetative bacteria. and brucellosis. They may remain suspended in the air for long periods of time. dryness. Bacterial Agents of Potential Concern Bacteria are single-celled. Identifies the interval (in hours.

3 (c) Initial symptoms of inhalation anthrax are mild and nonspecific and may include fever.3 (5) Symptoms. Cattle. caribou. Brucella suis. swine. Brucellosis.2 Incubation periods up to 60 days are possible. or irregular fever of variable duration. loss of appetite. or other products). bomblets. Worldwide. and possibly massive abdominal swelling may follow.1 (b) Ingestion causes oropharyngeal and GI anthrax. and vomiting. The disease may last for IV-5 . sheep.(3) Reservoir. Hours to 7 days. swine. and some species of deer. with death occurring shortly thereafter. bloody diarrhea. In both cases. and generalized aching.3 b. and mild cough or chest discomfort. Brucella melitensis.3 (5) Symptoms. A bacterial disease with sudden or insidious onset. Initial symptoms of oropharyngeal anthrax are fever.1 (6) Incubation period. contact with infected animals (their hides. weakness. severe pain in a joint.2 (9) Delivery. and difficulty swallowing. Initial symptoms of GI anthrax include fever. headache. horses. Transmission from person to person is very rare. weight loss. goats. and swine) serve as reservoirs. profuse sweating. (1) Infectious Agent. Anthrax vaccine is available. septic shock and death may follow. especially one not inflammatory in character. Infection may occur in bison. The soil and domestic and wild animals (primarily herbivores. swelling of neck tissues. and abnormal enlargement of the lymph nodes. Brucella abortus.3 Untreated cutaneous anthrax has a case-fatality rate between 5 and 20 percent. Acute symptoms include ulcer or scab involving the hard palate or tonsils. fatigue. cattle. sheep. Articles and soil contaminated with spores may remain infective for decades. wool. The disease is transmitted by the inhalation of aerosols or dusts that contain organisms.1 Dogs and coyotes have been found to be infected. Brucella canis. although most cases occur within 48 hours post-exposure.4 (4) Transmission. or ingestion of contaminated meat. humans do not contract anthrax directly from the soil. and shock follow. intermittent. characterized by continued. acute symptoms of respiratory distress.1 (3) Reservoir. camels. chills. Symptoms of anthrax depend upon the method of transmission. Missiles. including goats.3 (2) Occurrence.1 (7) Communicability. Abdominal pain. (a) Cutaneous anthrax features a painless.1 (8) Prevention. Contamination of food and water could also be used. goats. Humans can contract anthrax from the inhalation of aerosolized spores. bloody vomiting. necrotic ulcer with a black scab and local swelling. ingestion of unpasteurized dairy products and contaminated meat. artillery fires. or inoculation of abraded skin or mucosal surfaces. (4) Transmission. fever. sore throat. malaise. point release. nausea. or airborne line release may deliver aerosolized spores. depression. Usually. cattle. and sheep serve as reservoirs. elk. dogs and coyotes.

Worldwide. and donkeys serve as reservoirs. but could be executed. Personnel must avoid consuming unpasteurized dairy products or uncooked foods containing the dairy products and avoid contact with suspect infected animals. The untreated case-fatality rate is 2 percent or less. The cases have been among workers with jobs that involve horses. Varies from 5 days to 8 weeks.1 (5) Symptoms. Transmission is negligible from person to person. Burkholderia mallei (formerly Pseudomonas mallei).3 (9) Delivery. The primary threat is by aerosol release. and circulatory collapse.3 (2) Occurrence. The primary threat is from contamination of food and water supplies and secondly by aerosol spray.1 (8) Prevention. Vibrio cholerae1 Occurrence. Africa.3 Communicability. (1) Infectious Agent. This disease is not communicable from person to (3) Reservoir. acidosis. Glanders. Humans and some strains of bacteria found in aquatic environments. Ingestion of raw or undercooked seafood from polluted waters has caused outbreaks.5 d.3 IV-6 . (1) (2) Infectious Agent. oral.3 c. and (in untreated cases) rapid dehydration.1 (7) Communicability. Vaccines are not currently available for human use. From a few hours to 5 days. Horses. by inhaling into the lungs.1 (4) Transmission. Do not eat raw seafood. donkeys. or mules and laboratory workers. watery stools. The disease is not widespread.6 (3) Reservoir.several days.1 (6) Incubation period. A food-borne brucellosis attack is unlikely. nausea and vomiting.3 (4) Transmission. The organism is transmitted from animals to humans by invading the nasal. and Central and South America. Cholera and other Vibrioses. and by invading abraded or lacerated skin.3 Cases continue to occur in Asia. Through ingestion of food or water contaminated directly or indirectly with feces or vomit of infected persons. In severe untreated cases death may occur within a few hours and the case-fatality rate may exceed 50 percent. the Middle East.6 Occasionally the carrier state may persist for several months. or occasionally a year or more if not adequately treated.1 Incubation period.1 (6) (7) person. particularly brackish waters.3 (8) Prevention. usually 2 to 8 weeks. usually 2 to 3 days. Following proper field sanitation and personal hygiene are useful preventive measures. Some of the original syndrome may reappear as relapses. mules. but usually only a few days after recovery. Symptoms include profuse painless. months. A vaccine is available.1 (9) Delivery. and mucous membranes around the eyes.

The casefatality rate for acute septicemic disease exceeds 90 percent. There is no evidence that animals are important reservoirs except that they spread the agent to new soil and water. rabbits. horses. Yersinia pestis. goats. 10 to 14 days following inhalation. Worldwide.3 (7) Communicability.3 (3) Reservoir. Person-to-person transmission has not been proven. headache. Other symptoms may include fever (over 102 degrees F). muscle pain. Laboratory acquired infections are uncommon.3 (4) Transmission. Acute pulmonary disease can progress into a rapidly fatal septicemic disease. plague would be IV-7 . but do occur.3 Incubation period. Cases of person-to-person transmission have been Melioidosis.3 Delivery.3 (8) (9) f. The disease is transmitted from infected fleas—either from rodents to humans. Symptoms include fever. The primary reservoir is wild rodents (especially ground squirrels). from dogs or cats to humans. Melioidosis will most likely present as an acute pulmonary infection ranging from mild bronchitis to severe pneumonia.3 Infectious Agent. Contact with contaminated soil or water through gross or unapparent skin lesions.3 (2) Occurrence. wild carnivores. loss of appetite.1 In the most likely BW scenario. The primary threat is aerosol release. aspiration or ingestion of contaminated water. and hares can also transmit plague to humans. and rodents. In countries between 20 degrees north and south latitudes. Several animals including sheep.1 Plague.3 Mortality rate is over 50 percent despite antibiotic treatment.7 (6) (7) reported. and pain in one or more muscles. and generalized papular/pustular eruptions. especially if procedures produce aerosols. No vaccines are available. or inhalation of contaminated dust. or from person to person—and by handling tissues of infected animals. pleuritis.6 (8) (9) e. (1) Infectious Agent.8 Plague continues to be a threat because of vast areas of persistent wild rodent infection.(5) Symptoms.3 Delivery. rigors. (1) Prevention. swine.1 (3) Reservoir. headache. chest pain.3 (6) Incubation period. Soil and water are the reservoirs. can become infected.1 (4) Transmission. Domestic cats. (2) Occurrence.3 Communicability. monkeys. sweating. The primary threat is aerosol release. Burkholderia pseudomallei (formerly Pseudomonas pseudomallei). 10 to 14 days after inhalation.3 (5) Symptoms. Prevention. No vaccine is available.

3 g. headache. secretions. Modern therapy markedly reduces fatality from bubonic plague. muscular pain. Respiratory symptoms are mild when compared with the extensive pneumonia confirmed by X-ray. fever. maybe a few days longer for an immunized individual. ducks. The primary threat is by aerosol release or by contamination of food and water. From 1 to 7 days. and duck farms and in poultry processing plants. malaise. and other birds serve as reservoirs. usually short. and tender and may form or discharge pus. and upper or lower respiratory tract disease are common. Fever is usually present.1 (6) Incubation period. sore throat. overcrowding facilitates transmission. Initial signs and symptoms may be nonspecific with fever. chills. particularly when subjected to the stresses of crowding and shipping. pneumonic and septicemic plagues also respond if recognized and treated early. (1) (2) Infectious Agent. followed by turkey. and can survive 6 months without a feeding. exhaustion. A vaccine is available to prevent bubonic plague. patients who do not receive adequate therapy for primary pneumonic plague within 18 hours after onset of respiratory symptoms are not likely to survive. This is bubonic plague.1 (7) Communicability. Pneumonic plague may be highly communicable under appropriate climatic conditions. Fleas may remain infective for months under suitable conditions of temperature and humidity. approved for human use. and dust from infected feathers of birds.spread via aerosol. Worldwide. pigeons.3 (9) Delivery. parrots. psittaci).1 (5) Symptoms. Untreated bubonic plague has a case-fatality rate of about 50 to 60 percent. For primary plague pneumonia.1 Occurrence. chills.1 IV-8 . In humans. usually psittacine birds. Untreated primary septicemic plague and pneumonic plague are invariably fatal. will provide a level of protection from bites by infected fleas. The involved nodes become swollen.9 (6) Incubation period. and it occurs more often in lymph nodes.1 Fleas flourish at humidity just above 65 percent and temperatures between 20 to 26 degrees C. turkeys.1 (3) Reservoir. nausea. psittaci infection were reported to have died. muscle pain. Apparently healthy birds can be carriers and occasionally shed the infectious agent. squab. Infection is acquired by inhaling dried droppings.1 Before antimicrobial agents were available.8 Cat bites or scratches may also transmit plague. Chlamydia psittaci (c. rash. 1 to 4 days. Household birds. and headache. are the most frequent source of exposure. 15 to 20 percent of persons with C. Parakeets. Psittacosis.1 (4) Transmission. A rapidly person-to-person spread of fulminant pneumonia would occur. inflamed. From 1 to 4 weeks. Bubonic plague is not usually transmitted directly from person to person unless there is contact with pus from suppurating buboes. However. Use of insect repellents.8 (8) Prevention.1 (5) Symptoms.

some outbreaks have occurred in primate IV-9 .1 (8) (9) h. Ten virulent organisms injected subcutaneously and 10 to 50 organisms given by aerosol can cause infection in humans.3 There are two biovars: Jellison type A (F. No vaccine is available.1 The type A strain is highly virulent.1 (2) (3) colonies. S. Dysenteriae 1. During acute infection and until the infectious agent is no longer present in the feces. (1) Infectious Agent. Francisella tularensis (F.1 (9) supplies. many cases present with a watery diarrhea. vomiting. usually within 4 weeks after illness. dysenteriae 1 is often associated with serious disease.1 (7) Communicability. however. S. characterized by diarrhea accompanied by fever. Case-fatality rates have been as high as 20 percent among hospitalized cases even in recent years. Group B. In typical cases. tularensis biovar palaerctica). for weeks or months. the former Soviet Union. cramps. China. Worldwide. Rare person-to-person transmission has been reported. Symptoms involve the large and distal small intestine. S.(7) Communicability. and Group D. and sometimes continuously. The primary threat is from aerosol release. dysenteriae.5 Delivery. the stools contain blood.1 (4) Transmission. flexneri. Man.) is comprised of four species: Group A. Tularemia. sonnei. (1) Infectious Agent. and mucus (dysentery). S. i.1 Prevention.5 Shigellosis (Bacillary dysentery). Prevention. They may then spread infection to others directly by physical contact or indirectly by contaminating food. Diseased as well as seemingly healthy birds may shed the agent intermittently. Water and milk transmission may occur as the result of direct fecal contamination.1 (6) Incubation period. flies can transfer organisms from latrines to uncovered food items. Group C.1 (5) Symptoms. Follow proper personal hygiene and field sanitation Delivery.10 (2) Occurrence. and tenesmus. Individuals primarily responsible for transmission are those who fail to clean hands and under fingernails thoroughly after defecation.1 (8) procedures. S. tularensis biovar tularensis) and type B (F. however.1 Reservoir. tularensis). Transmission is mainly by direct or indirect fecal-oral transmission from a patient or carrier. nausea. boydii. The primary threat would be contamination of food and water Occurrence. The genus Shigella (S. Infection may occur after the ingestion of very few (10 to 100) organisms. and Japan. From 12 to 96 hours (usually 1 to 3 days) up to 1 week for S. Tularemia occurs throughout North America and in many parts of continental Europe. and sometimes toxemia.

a relative bradycardia. The protective mask provides protection of the respiratory tract from exposure to aerosol organisms. Inhalation of infectious material may be followed by pneumonic involvement with a 30 to 60 percent case-fatality rate if untreated. Salmonella typhi. Type A has a 5 to 15 percent untreated case-fatality rate. and ingestion of contaminated food or water. Ingestion of organisms in contaminated food or water may produce painful pharyngitis. Not directly transmitted from person to person. Flies may infect foods where the organisms then multiply and achieve an infective dose. but only one or more enlarged and painful lymph nodes.3 In addition. This bacterial disease has a variety of clinical manifestations related to the route of introduction and the virulence of the disease agent.3 j. hares. nonproductive cough.1 (8) Prevention. the infectious agent may be found in the blood during the first 2 weeks of disease and in lesions for a month. and rodents) and tick reservoirs.(3) Reservoir. abdominal pain. aerosols generated by skinning/processing infected animals. Finland. and type B produces few fatalities even without treatment. enlargement of the spleen.1 IV-10 .3 (5) Symptoms. All food must be thoroughly cooked to kill any organisms before consumption. (1) Infectious Agent. rose spots on the trunk. This organism is maintained in numerous and diverse mammalian (rabbits.1 (4) Transmission. Worldwide. A live attenuated vaccine is available. also mosquitoes in Sweden. sometimes longer. Transmission is by food and water contaminated by feces and urine of patients and carriers. vegetables fertilized by human excrement and eaten raw. severe headache. the range is 1 to 14 days (usually 3 to 5 days). Transmission is through the bite of arthropods (ticks and deerflies. Rabbit meat frozen at –15 degrees C (5 degrees F) has remained infective longer than 3 years.1 (5) Symptoms.1 (4) Transmission.3 (9) Delivery. There may be no apparent primary ulcer. Water must be thoroughly disinfected before consumption.1 (3) Reservoir. and Russia). direct contact with infected animals. loss of appetite. The primary threat is by aerosol release or by contamination of food or water supplies. raw fruits. Prior to antibiotics the case-fatality rate was 10 to 20 percent.1 (6) Incubation period. Most often it presents itself as an ulcer at the site of introduction of the organism. Typhoid Fever. and constipation. malaise. Unless treated. and vomiting. Man. Systemic bacterial diseases characterized by insidious onset of sustained fever. Related to virulence of infecting strain and to size of inoculum. together with swelling of the regional lymph nodes. Important vehicles in some parts of the world include shellfish taken from sewage-contaminated beds (particularly oysters). The annual incidence of typhoid fever is estimated at about 17 million cases with approximately 600 thousand deaths. diarrhea. a rodentmosquito cycle has been described.1 (7) Communicability.1 (2) Occurrence. and contaminated milk and milk products. Flies can be infective for 14 days and ticks throughout their lifetime (about 2 years).

there is a sporelike form of the organism that is extremely resistant to heat. by aerosol. Airborne particles containing organisms may be carried downwind for a considerable distance (one-half mile or more). also by direct contact with infected animals and other contaminated materials such as wool. secondly. lice. sweats. Coxiella burnetii (C. some wild mammals. and laundry. Most rickettsiae are parasites. Person-to-person transmission is possible. Infected animals usually do not develop the disease. chills.1 (9) Delivery. Query (Q) Fever. they are considered parasites. burnetii is unable to grow or replicate outside host cells. Rickettsiae of Potential Concern The rickettsiae are intracellular.11 (2) Occurrence. a. Rickettsiae are transmitted to man and animals by vectors such as ticks.3 It is commonly transmitted by airborne dissemination of coxiellae in dust from premises contaminated by placental tissues. They resemble the bacteria in their shape and resemble the viruses in their strict growth requirements for living host cells. fatigue. cats. this allows the organism to persist in the environment for long periods (weeks or months) under harsh conditions. Despite the fact that C. primarily of lower animals and arthropods. (1) Infectious Agent. The incubation period depends on the size of the infecting dose. birds. Following proper field sanitation and personal hygiene are useful preventive measures. straw. dogs.(6) Incubation period. dehydration. and 2 to 5 percent become permanent carriers. Sheep. About 10 percent of untreated typhoid fever patients will discharge bacilli for 3 months after the onset of symptoms. The period of communicability is as long as the bacilli appear in excreta.1 (8) Prevention. As they require living tissue for reproduction. but shed large numbers of organism in placental tissues and body fluids. cattle. and severe headache in 75 percent of cases. muscular pain. fleas.1 (7) Communicability. A vaccine is available. The rickettsiae have a selective affinity for specific types of cells of the human and animal bodies. they are easily killed by heat. A single viable organism is enough to cause infection in humans. goats.2 Usually. Worldwide. Direct transmission by blood or marrow transfusion has been reported. The primary threat is from the sabotage of food and water supplies and.3 The case-fatality rate in untreated acute cases is usually less than 1 percent. in establishments processing infected animals or their byproducts. The organism is highly communicable by aerosol.1 (5) Symptoms. variable thereafter. Symptoms include fever. but has been reported as high as 2. or disinfectants. and excreta of infected animals. and in necropsy rooms.3 (3) Reservoir.1 IV-11 . and many standard antiseptic compounds.1 (4) Transmission.5 3. fertilizer. pressure. desiccation. and mites. burnetii). and ticks serve as reservoirs. parasitic microorganisms that are considered intermediate in size between the bacteria and viruses. birth fluids. usually from the first week throughout convalescence. but this has not been proven. range is from 3 days to 1 month and usually between 8 to 14 days. Raw milk from infected cows contains organisms and may be responsible for some cases.4 percent.

1 (5) Symptoms.1 (7) Communicability. This disease is characterized by sudden onset of moderate to high fever (which ordinarily persists 2 to 3 weeks in untreated cases). Infection has been documented throughout the US. From 3 to about 14 days. Epidemics occurred in Europe during World Wars I and II among troops and prisoners of war living in crowded. Maintained in nature in ticks. Rickettsia rickettsii. commonly as long as 18 months.1 (6) Incubation period.1 (4) Transmission.1 Delivery. (1) Infectious Agent. western and central Mexico. Colombia. Varies from 10 to 40 days and depends on the size of the infecting dose.1 Delivery. in Canada.3 b. The primary threat would be from aerosol or from infected (2) Occurrence. Measures that can be taken to reduce the opportunity for exposure include good field sanitation and use of insect repellents.11 (9) food. and chills. significant malaise. However. Disease in rodents and dogs have been observed. Panama. Argentina. various rodents. No vaccine is available. Bartonella quintana (formerly Rochalimaea Quintana). Contamination of breaks in the skin or mucous membranes with crushed tissues or feces of the tick may also lead to infection. The military protective mask provides protection from aerosols. An investigational vaccine is being tested. unhygienic conditions. and heat all foods sufficiently to destroy the organisms (see TB MED 530 for food preparation guidelines). severe headache.11 (8) Prevention. (1) Infectious Agent. if ever. and Brazil. and other animals. At least 4 to 6 hours of attachment and feeding on blood by the tick are required before the rickettsiae become reactivated and infectious for people. Consume only pasteurized dairy products.(6) Incubation period. Transmission is ordinarily from the bite of an infected tick. The rickettsiae can be transmitted to dogs. Costa Rica. The fatality rate ranges between 13 to 25 percent in the absence of specific therapy. Not directly transmitted from person to person.5 c. this soon includes the palms and soles and spreads rapidly to much of the body.1 IV-12 . deep muscle pain.1 (3) Reservoir. Direct transmission from person to person occurs rarely. Trench Fever. A rash generally appears on the extremities on about the third to fifth day. The organism probably can be found wherever the human body louse exists.11 (7) Communicability. The tick remains infective for life.1 (9) vectors.1 (8) Prevention.1 Coxiella organisms may persist in the environment and produce infection for weeks or months. Rocky Mountain Spotted Fever. The primary threat is by aerosol or through contamination of (2) Occurrence. contaminated clothing may be a source of infection.

A macular eruption appears on the fifth to sixth day.1 (3) Reservoir. months. Infected lice pass rickettsiae in their feces within 2 to 6 days after the IV-13 . The body louse is infected by feeding on the blood of an infected patient. or years and may recur with or without symptoms. is infected by feeding on the blood of a patient with acute typhus fever. The case-fatality rate increases with age and varies from 10 to 40 percent in the absence of specific therapy. palms. commonly 12 days.1 Washing sheets and clothing in hot water will eliminate the louse. People are infected by rubbing feces or crushed lice into the bite or into superficial abrasions.1 (7) Communicability. Dust clothing and body with an effective insecticide. Symptoms have variable onsets. often are sudden. Pediculus humanus corporis.1 (6) Incubation period. initially on the upper trunk. It is characterized by headache. Onset is either sudden or slow. Humans are the reservoirs and are responsible for maintaining the infection between epidemic periods. typhoid-like. Inhalation of infective louse feces in dust may account for some infections. Infectious Agent. Good hygiene will help prevent this condition. fever.1 (5) Symptoms.1 (6) Incubation period. Humans serve as reservoirs. Pediculus humanus corporis. enormous and explosive epidemics may occur during war and famine.(3) Reservoir. The organism multiplies extracellularly in the gut lumen for the duration of the insect’s life. and are marked by headache. (1) Delivery.1 (7) Communicability. exhaustion. From 1 to 2 weeks. bacterial disease varying in manifestations and severity. the intermediate host and vector is the body louse. The primary threat would be by aerosol release or infected vector. Patients are infective for lice during the febrile illness and possibly for 2 to 3 days after the temperature returns to normal.1 (4) Transmission.1 Typhus Fever (Epidemic Louse-Borne Typhus Fever). and pain and tenderness—especially on the shins.1 (4) Transmission. malaise. Rickettsia prowazekii. followed by spreading to the entire body (but usually not to the face. (9) d. with a fever that may be relapsing. No direct person-to-person transmission. Generally 7 to 30 days. Organisms may circulate in the blood (by which lice are infected) for weeks. (2) Occurrence. Infected lice excrete rickettsiae in their feces and usually defecate at the time of feeding. In colder areas where people may live under unhygienic conditions and are louse-infested. Trench Fever is typically a nonfatal. or limited to a single episode lasting for several days. The infected louse excrete rickettsiae in their feces and usually defecate at the time of feeding. Delousing procedures will destroy the vector and prevent transmission to man. Not directly transmitted from person to person. chills. which is approximately 5 weeks after hatching. people are infected by rubbing feces or crushed lice into the bite or into superficial abrasions. and general pains. or soles).1 (5) Symptoms.1 (8) Prevention. The body louse.

The reservoir is unknown for most viruses. hares. India. The louse invariably dies within 2 weeks after infection. and South Africa. transformation to a nonfunctioning state.1 (2) Occurrence. IV-14 . and the Philippine Islands. it is infective earlier if crushed.5 Washing sheets and clothing in hot water will eliminate the louse. The likely method of dissemination is aerosol. (9) vectors.blood meal. Iraq. especially one not inflammatory) or arthritis. western China. No direct person-to-person transmission. tropical Africa. Crimean-Congo HFV.1 Crimean-Congo Hemorrhagic Fever Virus (HFV). Cells infected with viruses show one of the following responses: degeneration and death.1 No vaccine is available. Chikungunya Virus Disease. This virus is found in Africa.1 Communicability.1 (5) Symptoms. The primary threat would be by aerosol release or infected 4. and small joints of the extremities. primarily in the wrist. Rashes are common. An insect (mosquito) reservoir is a possibility.1 (8) Prevention. In nature. birds and ticks in Eurasia and South Africa are believed to be reservoirs. or survival without transformation but with the evidence of the presence of one or more viral components. rickettsiae may remain viable in the dead louse for weeks. Minor hemorrhages have been attributed to this virus. ankle. southeast Asia.2 Viruses have primary military potential as antipersonnel agents.1 (4) Transmission.1 (3) Reservoir. which lasts from days to months.5 Infectious Agent.5 Delivery. Pakistan. reservoir hosts remain undefined in tropical Africa. Diseases of viral origin do not respond to treatment with antibiotics. but ticks. Once a virus enters a living cell.1 (6) (7) Incubation period: From 3 to 11 days. Dust clothing and body with an effective insecticide. (1) Delivery. Chikungunya Virus (alphavirus). knee. genus Nairovirus. a.1 (3) Reservoir. (1) Infectious Agent. Polyarthritis is a characteristic feature. Viruses cause about 60 percent of all infectious diseases.1 (8) Prevention. Viral Agents of Potential Concern The groups of microorganisms called viruses are all parasites that live in the cells of their selected hosts. Mosquitoes transmit the virus. the Arabian Peninsula. Insecticides and proper field sanitation are examples of preventive measures.1 An experimental vaccine is being tested. Bulgaria. Observed in regions of Russia as well as in Albania and Bosnia-Herzogovina. it is capable of replicating itself by taking over the metabolic processes of the invaded cell. (2) Occurrence.5 (9) b. The usual onset of symptoms is characterized by arthalgia (severe pain in a joint. Good hygiene will help prevent this condition.

and Dengue-4.1 An experimental vaccine is available. headache. and intestine. and cattle) may act as amplifying hosts. usually 1 to 3 days. Range is from 1 to 12 days.5 (8) Prevention.1 (4) Transmission. and rodents may be involved. commonly 4 to 7 days. This is a disease with sudden onset of fever. An acute febrile viral disease that is characterized by sudden onset. protective clothing. and marked anorexia. retro-orbital pain. Africa. uterus. Domestic animals (sheep. Aerosol is the likely method of dissemination. They are all flaviviruses. (1) Infectious Agent. Not directly transmitted from person to person. Vomiting. and rash. Epidemics are explosive. From 3 to 14 days. Dengue-1. irritability. lungs.5 d. There may be some bleeding from gums. Insecticides and proper field sanitation are examples of preventive measures. and the (3) Reservoir. goats.1 (4) Transmission. IV-15 . fever for 3 to 5 days.insectivores.1 An experimental vaccine is available. Transmission from patients to medical workers after exposure to blood and secretions has been important in recent outbreaks. Minor bleeding may occur. Use screening. severe pain in limbs and loins. Flush on face and chest develops early. Eastern and Western Equine Encephalitis (EEE and WEE).1 Communicability. Infection is also associated with butchering infected animals. myalgia. intense headache. The reported case fatality rate ranges from 2 to 50 percent. The viruses are maintained in a human mosquito cycle in tropical urban centers. Patients are infective for mosquitoes from shortly before to the end of the febrile period.5 Dengue Fever.1 (5) Symptoms. Fever is constantly elevated for 5 to 12 days. The primary threat is delivery by aerosol release. a monkey mosquito cycle serves as a reservoir in southest Asia and west Africa.1 (5) Symptoms.5 (9) c.1 (8) Prevention. nose.5 (9) Delivery. Moderate person-to-person transmission.1 (6) Incubation period. but in large amounts only in serious or fatal cases.1 Occurrence. Most countries in the tropics. Saudi Arabia. Dengue-3. and repellents and try to eliminate breeding grounds. weakness. but fatalities in the absence of dengue hemorrhagic fever are rare.1 (6) (7) Incubation period. By the bite of infective mosquitoes. Delivery.1 (2) Americas. Dengue-2. usually a period of 3 to 5 days. abdominal pain. and diarrhea occur occasionally. anorexia.1 (7) Communicability. malaise. arthralgia. Immature ticks are believed to acquire infection from the animal hosts and by transovarian transmission. Japanese Encephalitis (JE). GI disturbances. Transmission is by a bite of infective adult ticks. The mosquito becomes infective 8 to 12 days after the viremic blood meal and remains so for life.

Canada. Canada.1 (9) e. secretions. and pharyngitis.1 (2) Occurrence. Person-to-person transmission occurs by direct contact with infected blood. or it survives in mosquito eggs or adult mosquitoes. organs. Kenya. rodents. Symptoms of these diseases are similar. and the Democratic Republic of the Congo. Humans and horses are uncommon sources of mosquito infection. (1) Infectious Agent. but may be prolonged in bats. Delivery. protective clothing. A specific virus causes each disease. Approximately 25 percent of reported primary cases of Marburg virus infection have been fatal. The true reservoir or means of winter carryover for these viruses is unknown—possibly birds.1 (2) Occurrence. The primary threat would be delivery from aerosol release.13 Marburg disease was found in Germany and Yugoslavia after exposure to green monkeys from Uganda. Transmission is from the bite of infective mosquitoes. Zimbabwe. The EEE is recognized in eastern and north central US.1 (8) Prevention. tremors. diarrhea. fever. and try to eliminate breeding grounds. stupor. and hemorrhagic diathesis. and amphibians. particularly if interrupted by hibernation. disorientation. and/or amphibians. Virus is not usually demonstrable in the blood of humans after onset of the disease. case-fatality rates of Ebola infections have ranged from 50 to nearly 90 percent. Uganda.12 Severe infections are usually marked by acute onset. Gabon. and repellents. A large percentage of patients with vector-borne infections are either asymptomatic or present with a nonspecific febrile illness or aseptic meningitis. Viremia in birds usually lasts 2 to 5 days. headache. Vaccines are available. The Ebola virus and the Marburg virus are in the Filoviridea group. Use screening.1 (4) Transmission. Central and South America. WEE occurs in western and central US. and the Caribbean islands. and the Republic of the Congo. These diseases are usually characterized by sudden onset with malaise. but vary in severity and rate of progress.1 (6) Incubation period. coma.3 to 60 percent (JE and EEE among the highest). or semen. myalgia. high fever. bats.1 (5) Symptoms.6 Ebola Viral Hemorrhagic Fever (VHF) and Marburg Viral Disease. Sudan.1 (3) Reservoir. occasional convulsions. with the mechanisms probably differing in each virus.(1) Infectious Agent. Confirmed cases of Ebola VHF have been reported in the Democratic Republic of the Congo.1 (5) Symptoms. Usually 5 to 15 days. reptiles. Mosquitoes remain infective for life.1 (3) Reservoir. Unknown despite extensive studies.1 (7) Communicability.1 IV-16 . The JE occurs in western Pacific islands from Japan to the Philippines. the Ivory Coast.1 (4) Transmission. reptiles. Not directly transmitted from person to person. Casefatality rates range from 0. EEE and WEE are caused by alphaviruses and JE by a flavivirus. headache. rash. followed by vomiting. and parts of South America. and spastic (but rarely flaccid) paralysis.

or birds serve as sources of tick infections. Delivery. Ebola—2 to 21 days. No direct person-to-person transmission. up to 7 to 10 days. Field rodents. and insect control. WEE.1 (6) Incubation period.6 (9) g.1 A vaccine is available. Preventive measures can include effective personal hygiene. By the bite of infective ticks or by consumption of milk from certain infected animals. field sanitation. but generally ranges from 5 to 15 percent.1 (4) Transmission. varying degrees of hemorrhagic manifestations. The likely method of dissemination is aerosol or through milk.1 The prototype virus from this group. and JE). other parts of eastern and central Europe.5 Hantaviral Disease (Korean Hemorrhagic Fever [KHF]). An acute viral disease characterized by an abrupt onset of fever. (1) Prevention. Rodents. Marburg—3 to 9 days. Ticks. Virus is present in urine. The primary threat would be delivery from aerosol release.1 (7) Communicability. Worldwide. Hantaan. This is a viral disease clinically resembling the mosquito-borne encephalitides (EEE.1 (7) Communicability. man is an accidental host.1 (5) Symptoms.1 Reservoir. a genus of the Bunyaviridae family. Aerosol transmission from rodent excreta is presumed (aerosol infectivity has been demonstrated experimentally). Person-to-person transmission is possible as long as blood and secretions contain the virus. lower back pain. No vaccines are available. appear to be the true reservoir.1 (8) Prevention. (2) Occurrence. Usually 7 to 14 days.1 (4) Transmission. The disease is distributed spottily over much of the former Soviet Union. The case fatality rate is variable. Symptoms also include focal epilepsy and flaccid paralysis (particularly of the shoulder girdle).(6) Incubation period. is the cause of the KHF.5 Infectious Agent.1 (8) (9) f. Areas of highest incidence are those where humans have intimate association with large numbers of infected ticks. or ticks and mammals in combination.14 (2) (3) Occurrence. Viremia in a variety of vertebrates may last for several days. highest virus concentration is found in the lungs. A tick infected at any stage remains infective for life.1 (5) Symptoms. (1) Infectious Agent. other mammals. and saliva of persistently infected rodents.5 Delivery.1 IV-17 . and the United Kingdom (UK).1 (3) Reservoir. A complex within the flaviviruses. in humans. Hantaviruses.1 Far Eastern Tick-Borne Encephalitis (Russian Spring-Summer Encephalitis). but also in some urban populations. generally in rural or forested areas. feces. and renal involvement. Scandinavia.

(1) Infectious Agent. retro-orbital pain. Infectious Agent. Junin Hemorrhagic Fever (Argentine Disease) and Machupo Hemorrhagic Fever (Bolivian Disease). followed by prostration. Case fatality rates range from 15 to 30 percent or more. Experimental vaccine is Communicability.5 h.1 (4) Transmission.1 (6) Incubation period. Onset is gradual with malaise. Person-to-person transmission is (8) Prevention. seizures. nausea. Follow rodent control procedures. both saliva and excreta of infected rodents contain the virus. vomiting. or in food and water. (4) Transmission. A live-attenuated vaccine is currently in field trials (unlicensed in the US). Wild rodents. Africa. As short as a few days. Primarily through aerosol or direct contact with excreta of infected rodents deposited on surfaces such as floors. headache. Follow rodent control procedures. Acute febrile viral illnesses. The primary threat would be delivery from aerosol release. Lassa fever is an acute viral illness of 1 to 4 weeks duration.1 (6) (7) Incubation period: Usually 7 to 16 days. pharyngeal secretions. beds. hemorrhage.1 Occurrence.1 Occurrence.1 (3) Reservoir. Not often directly transmitted from person to person.1 (2) Bolivia.1 (7) rare.1 (5) Symptoms.1 (8) available. Rodents. sustained fever. Airborne transmission may occur via dust contaminated with infected rodent excreta. sore throat. diarrhea.1 Lassa Fever. Lassa virus. The onset is gradual with malaise. as long as nearly 2 months. Junin virus for the Argentine disease and closely related Machupo virus for the Bolivian disease.1 IV-18 . fever. In severe cases.5 (9) Delivery.1 (9) i. Person-toperson and laboratory infections occur by direct contact with blood. Fever is persistent or intermittently spiking. myalgia. but usually 2 to 4 weeks. Commonly 6 to 21 days. Not well-defined. or by sexual contact. and sweats. Junin virus in Argentina and Machupo virus in northeastern Prevention.(6) Incubation period. or urine. The primary threat would be delivery from an aerosol release. headache. The Case-fatality rate is about 15 percent among hospitalized cases. Abraded skin may also be a portal of entry for infection. and chest and abdominal pain.1 Communicability. (1) (2) (3) Delivery. and edema of the face and neck are frequent. cough.1 (5) Symptoms.1 Reservoir.

The acute course is usually short. transmissible to humans. and feces of infected animals—usually mice. with a marked diversity of clinical manifestations. 15 to 21 days until meningeal symptoms appear. and rabbits can get monkeypox. especially in patients presenting with cough.17 Occurrence.1 (5) Symptoms. Studies suggest several species of squirrels and Gambian rats in Africa16 and pet prairie dogs in the US may be animal reservoirs.1 (9) Prevention. especially mice. and the cowpox virus.16 Rats.5 (9) j. food.13 (4) Transmission. Field hygiene and personal hygiene are effective individual Delivery. Airborne transmission cannot be excluded.1 No vaccine is (4) Transmission. Transmission to humans is probably through oral or respiratory contact with virus-contaminated excreta. The rain forest countries of central and western Africa and the IV-19 .1 (6) Incubation period.1 Reservoir.1 (7) Communicability. Lymphocytic choriomeningitis virus. very rarely fatal.1 Occurrence.15 Other animals may be possible reservoirs.1 (8) measures.5 Infectious Agent. The infected house mouse is the natural reservoir. which includes the smallpox virus (variola). an arenavirus. Transmission from person to person has not been demonstrated and is unlikely. Virus is excreted in urine. Person-to-person transmission is believed to occur primarily through direct contact and also by respiratory droplet spread. Monkeypox. saliva.1 Lymphocytic Choriomeningitis. The virus may be excreted in the urine of patients for 3 to 9 weeks from onset of illness. the virus used in the smallpox vaccine (vaccinia). k. Probably 8 to 13 days. The primary threat would be delivery from an aerosol release. (1) Infectious Agent. with myalgia and headache. it belongs to the genus orthopoxvirus. Person-to-person transmission spread may occur during the acute febrile phase when the virus is present in the throat. The primary threat would be delivery from aerosol release. Not uncommon in Europe and the Americas. (1) (2) (3) Delivery. At times. Infected female mice transmit infection to the offspring. or dust or by contamination of skin lesions or cuts. there may be influenza-like symptoms.16 (3) Reservoir. mice. This disease is a viral infection of animals. Follow specific rodent control procedures. Monkeypox virus.(7) Communicability.1 (8) available. Limited data on the transmission of monkeypox virus are available from studies conducted in Africa. Prevention.15 (2) US. which become asymptomatic persistent viral shedders.

The World Health Organization (WHO) reaffirmed that destruction of all the remaining virus stocks is still the organization’s ultimate goal and will appoint a group of experts to consider what research needs to be carried out before the virus can be destroyed. (1) (2) (3) Delivery. and generally some conjunctivitis and photophobia. Infectious Agent. The WHO will also set up an inspection schedule for the two laboratories where the official stocks are kept to make sure that they are secure and that research can be carried out safely.1 Occurrence. The lesions usually develop through several stages before crusting and falling off. About 12 days.1 Reservoir. the smallpox vaccine can protect people from getting monkeypox as well as smallpox. field sanitation. Encephalitis. often first on the face. headache. The likely method of dissemination is an aerosol release. Because the monkeypox virus is related to the virus that causes smallpox. a general feeling of discomfort.1 Rift Valley Fever (RVF). In humans.17 (8) Prevention. Unknown. Smallpox.15 (7) Communicability. muscle aches. The usual onset is fever. The illness begins with fever. The likely method of dissemination is aerosol or through infected IV-20 . backache. arthralgia.15 (6) Incubation period. Mosquitoes transmit the virus. occasional nausea and vomiting. swollen lymph nodes. (4) Transmission. The Centers for Disease Control and Prevention (CDC) suggests there is a relatively low risk of person-to-person transmission. In Africa. In response to concerns that variola stocks may by needed for counterterrorism research in the event that clandestine stocks held by other countries fall into terrorist hands.5 (9) vectors. Mechanical transmission by flies and transmission by aerosols or contact with highly infective blood may contribute to the explosive nature of RVF outbreaks.1 Delivery. authorized that the virus be held at laboratories in the US and Russia until no later than 2002. Infected mosquitoes probably transmit the virus throughout life.1 (8) Prevention. but usually milder. No direct person-to-person transmission. headache. myalgia. Usually 3 to 12 days.1 (6) Incubation period.1 A vaccine is available. the symptoms are similar to those of smallpox. Many human infections of RVF are associated with handling infective material of animal tissues during autopsy and butchering. and personal hygiene are examples of preventive measures. Epidemics may involve thousands of people.18 (9) l.1 (5) Symptoms.(5) Symptoms. and exhaustion. RVF Virus (RVF is a phlebovirus). Precautions in the care and handling of infected animals and their products are important.1 (7) Communicability. or retinitis may develop. hemorrhage.5 m. the World Health Assembly (WHA). malaise. Insecticides. the reported case-fatality rate is 10 percent. A papular rash develops. in May 1999. This virus is found in Africa.

The primary threat is delivery by aerosol release. From 7 to 19 days. or with contaminated objects. All known variola virus stocks are held under security at the CDC. and Central Venezuelan Equine Encephalitis. laboratory infections by aerosol are common. occasionally as late as the second week. There are no routine immunizations of US forces for smallpox. After 2 to 4 days. papules. or the State Research Center (SRC) of Virology and Biotechnology.1 (3) Reservoir. VEE virus is transmitted in a cycle involving horses—which serve as the major source of the virus—to mosquitoes. The patient is most contagious during the pre-eruptive period by aerosol droplets from lesions. Georgia. Onset was sudden.1 (4) Transmission. and occasional abdominal pain and vomiting—a clinical picture that resembled influenza. a species of Orthopoxvirus. IV-21 .1 (8) Prevention. and variola major (ordinary) with a fatality rate among unvaccinated populations of 20 to 40 percent or more. smallpox was a worldwide disease.3 (4) Transmission. airborne transmission (longdistance) also occurred. and crusted scabs. Koltsovo. prostration. Formerly.1 (7) Communicability. Smallpox is very contagious from the time of development of the earliest lesions to disappearance of all scabs—about 3 weeks. Humans also serve as hosts in a human-to-mosquito-to-human transmission cycle. The last naturally acquired case of smallpox occurred in October 1977 in Somalia. headache. By the bite of an infected mosquito.3 Infectious Agent. malaise. Smallpox was also transmitted by direct contact with skin lesions or drainage. When the threat indicates. senior leadership may direct vaccination of personnel with vaccinia.1 Delivery.1 (6) Incubation period.3 Occurrence. the fever began to fall and a deepseated rash developed in which individual lesions containing infectious virus progressed through successive stages of macules. The lesions were first evident on the face and extremities and subsequently on the trunk. global eradication was certified two years later by the WHO and sanctioned by the WHA in May 1980. Usually by respiratory droplet transmission. commonly 10 to 14 days to onset of illness and 2 to 4 days more to onset of rash. Fatalities normally occurred in 5 to 7 days. Although uncommon. Humans were the only natural reservoir of variola. which in turn infect humans. Present in northern South America. Russian Federation (RF). Two epidemiologic types of smallpox were recognized during the twentieth century: variola minor (alastrim). Variola virus. Novosibirsk Region. following close face-to-face contact. Atlanta. pustules. which had a case-fatality rate of less than 1 percent.1 (2) Occurrence. which fell off after 3 to 4 weeks.3 (9) n.1 (3) Reservoir. vesicles.3 (5) Symptoms. During outbreaks. VEE virus (alphavirus). Smallpox was a systemic viral disease that generally presented with a characteristic skin eruption. Trinidad. (1) (2) America.(1) Infectious Agent. with fever. severe backache.

1 Delivery. Use general mosquito control procedures. (1) Infectious Agent.1 (3) Reservoir. The likely method of dissemination is aerosol. Their effects on the human body range from minor illness to death. The spores are ubiquitous. mosquitoes remain so for life. Typical attacks are characterized by a sudden onset of fever. Jaundice is moderate early in the disease and is intensified later. and Trinidad. with symptoms lasting from 3 to 5 days. Toxins of Potential Concern Toxins are poisonous byproducts of living organisms.1 (6) Incubation period.1 (7) Communicability. with an abrupt onset of severe headache. From 3 to 6 days.5 Delivery. Sylvatic: vertebrates other than humans—mainly monkeys. nausea. can be as short as 1 day. Once infected. A vaccine is available.5 Infected humans and horses are infectious for mosquitoes for up to 72 hours. No person-to-person transmission. and vomiting. and death. they germinate to give rise to IV-22 . paralysis.5 (9) vectors. Usually 2 to 6 days.1 (8) (9) Prevention. The incubation period in mosquitoes is commonly 9 to 12 days at the usual tropical temperatures. retro-orbital pain. possibly marsupials. coma. convulsions. infected mosquitoes probably transmit the virus throughout life.1 (8) available. and vomiting. chills. Sylvatic type: tropical regions of Africa and Latin America.(5) Symptoms. Clinical manifestations of this viral infection are influenza-like. and South America.1 (5) Symptoms. generalized muscle pain. Some toxins are susceptible to heat. Urban: from the bite of an infective mosquito. chills. while others are heat-stable. Botulinum Toxins.1 (7) Communicability. Central. headache.5 5. Urban: humans and mosquitoes. Botulinum toxins are a group of seven toxins produced by Clostridium (C.1 (6) Incubation period. backache. or introduced into the body by any other means.5 Blood of patients is infective for mosquitoes shortly before onset of fever and for the first 3 to 5 days of illness. Most infections are relatively mild. nausea. They are very stable and produce severe illness when ingested. The disease is highly communicable where many susceptible people and abundant vector mosquitoes co-exist. and mosquitoes. The primary threat is by aerosol release or through infected Prevention. Urban type: North. Yellow Fever.) botulinum. (1) Toxin Origin.3 a.1 (4) Transmission. prostration. There may be CNS involvement ranging from somnolence to disorientation. inhaled. Low risk of person-to-person transmission.1 Vaccine is (2) Occurrence. fever. Sylvatic: from infective monkey to mosquito to man.5 o. myalgia. Yellow Fever Virus of the genus Flavivirus.

3 (2) Occurrence. Dilated pupils occur in approximately 50 percent of cases. The organisms can be recovered from honey and other agriculture products. but vomiting and fever are usually absent.3 The case-fatality rate in the US for food-borne botulism is 5 to 10 percent. Generally. slow cooling.1 (3) Reservoir. respiratory failure may occur. or inadequate rewarming. ileus. infantile.1 Gas gangrene results from wound contamination with soil containing spores. Transmission is by the ingestion of food that was contaminated by soil or feces and then held under conditions that permit multiplication of the organism. Symptoms usually begin 12 to 36 hours following intoxication. The autonomic features of botulism are typical anticholinergic signs and symptoms: dry mouth. one day or less. Clostridium Perfringens (C. Industrial-scale fermentation can produce large quantities of toxins for use as a BW agent. Almost all outbreaks are associated with inadequately heated or reheated meats. The reservoirs are soil and the GI tract of healthy people and IV-23 .3 Food poisoning is an intestinal disorder characterized by sudden onset of colic followed by diarrhea. There are three forms of naturally occurring botulism—food-borne. The reservoirs are soil. Worldwide. The incubation period for food-borne botulism is usually 24 to 36 hours.1 (6) Incubation period.3 (4) Transmission. High-risk foods are primarily improperly canned foods and dried meat or fish. The vaccine currently available is used under Investigational New Drug (IND) status. Gas gangrene features pathological death of skeletal muscles and overlying soft tissue and constitutes a surgical emergency.3 Reservoir. The motor complications of botulism feature a descending paralysis leading to blurred vision and.3 (5) Symptoms. Spores survive cooking and then germinate and multiply in storage at ambient temperatures. and fish. Nausea and vomiting can occur.6 (8) Prevention. nausea is common. constipation. for wound botulism it is usually 3 or more days. Botulinum toxin is the most potent neurotoxin known. perfringens) Toxins.19 (9) Delivery.3 (4) Transmission. and rarely fatal in healthy persons.3 (2) (3) animals. The primary threats are by sabotage of food and water supply and by aerosol release. perfringens is a common anaerobic bacillus that produces at least 12 toxins. No person-to-person transmission.3 (7) Communicability. and wound. Worldwide.1 (5) Symptoms. and urinary retention. Transmission is from consumption of contaminated food or contamination of a wound by ground-in soil or gravel. time can vary according to the amount of toxin absorbed and could be reduced to hours following a BW attack.vegetative bacteria that produce toxins during anaerobic incubation.1 Occurrence. eventually. (1) Toxin Origin. C. it is a mild disease of short duration.5 b. animals.

Conotoxins. coli O157:H7.1 (2) Occurrence.20 (2) Occurrence. Symptoms begin immediately. This category of diarrheogenic E. coli [VTEC]). The toxin may also be delivered in combination with other toxins to produce a variety of effects. deep. altered level of consciousness. and paralysis. The main EHEC serotype in North America is E. Neurological effects may include impaired coordination. Cone snails.3 Communicability. coli O157:H7. (1) Toxin Origin. Cattle are the most important reservoir. and Australia. followed by numbness and swelling at the point of envenomation. E.20 Transmission. diminished or absent reflexes. There is increasing evidence in North America that deer may also serve as a reservoir. Verotoxin-producing E.3 c. east to Hawaii. No person-to-person transmission. These infections are now recognized to be an important problem in North America.20 (3) (4) Reservoir. however. vastly different from the naturally occurring diseases associated with C.000 different conotoxins present in the venoms of species in the genus Conus. IV-24 .17 (5) Symptoms. No specific antivenom exists.1 (3) Reservoir. and south to New Zealand and Australia.1 No vaccine is available.5 Prevention. difficulty swallowing. Japan.5 (9) Delivery. It is most often due to inadequately cooked beef (especially ground beef). vomiting. Transmission occurs mainly by ingestion of contaminated food.20 (9) Delivery. There are potentially over 50. Pain results immediately. These cone snails live in intertidal regions of the Indian and Pacific Oceans. triangular puncture wound. Europe.20 Communicability. South Africa. decreased visual acuity. Nausea. South America. Previously. ranging from mild to severe. Paralysis of the respiratory muscles might cause the airway to collapse. The sting produces a small. Diarrhea Caused by Enterohemorrhagic (EHEC) Strains (Shiga toxin-producing E. and weakness may occur. No person-to-person transmission.20 (6) (7) (8) Incubation period. The incubation period is 1 to 6 hours. Prevention. Conotoxins are a neurotoxin from the mollusks of the genus Conus. coli produces cytotoxins. This would result in pulmonary disease. commonly known as cone snails. perfringens alpha toxin as an aerosol to the respiratory tract. The untreated case-fatality rate is 70 percent. The primary threat is delivery of C. perfringens. humans may also serve as a reservoir for person-to-person transmission. (1) Toxin Origin. coli [STEC].1 (4) Transmission.(6) (7) (8) Incubation period. The heart may beat irregularly. Educate food handlers. Conotoxins are injected by the sting of a cone snail. malaise. The likely dissemination is by respirable aerosols or contamination of food or water supply.19 d. raw milk. north to Japan. these toxins were called Verotoxins 1 and 2 or Shiga-like toxins I and II.

1 (6) Incubation period. Nostoc. the tissue damage to the liver is so severe that therapy may have little or no value.1 (5) Symptoms. Microcystin cause gastroenteritis. When this happens. Field sanitation and personal hygiene are useful tools to help prevent exposure. (1) Toxin Origin. with a median of 3 to 4 days. The diarrhea may range from mild and nonbloody to stools that are virtually all blood but no fecal leukocytes. The likely method of dissemination is by respirable aerosols or contamination of food or water supply.22 Microcystin is extremely stable and resistant to chemical hydrolysis or oxidation and remain potent even after boiling. Very limited available information suggests that inhalation in aerosols may be an equally important route of exposure. Transmission also occurs directly from person to person. Worldwide. Prolonged carriage is uncommon. The likely method of dissemination is by respirable aerosol or contamination of food and water supply. Blue-green algae.”21 For microcystin.22 (4) Transmission. irreversible damage to the organ occurs within 15 to 60 minutes after exposure to a lethal dose. Ricin. (1) Toxin Origin. Freshwater cyanobacteria accumulate in surface water supplies and appear as blue-green “scums. unlike most toxins. f. Person-to-person transmission is possible. Their structural class is cyanobacteria.19 e.23 (5) Symptoms. Oscillatoria. Unless uptake of the toxin by the liver is blocked.1 (9) Delivery. The duration of excretion of the pathogen is typically a week or less in adults. Ricin toxins are potent inhibitors of DNA replication and protein synthesis.1 (8) Prevention. and Microcystic. Data not available. Hapalosiphon.1 (7) Communicability. microcystins may persist for months or years. (9) Delivery.23 (8) Prevention.22 (6) Incubation period. Data not available. Microcystin. Common species of the blue-green algae that produce microcystins include Anabaena. Drinking or swimming in contaminated water. Ranges from 2 to 8 days.23 (2) (3) Occurrence. (7) Communicability.3 IV-25 . no matter what the route of exposure. Ricin is a potent cytotoxin derived from the beans of the castor plant (Ricinus communis). Large quantities of ricin are easily and inexpensively produced.and fruit or vegetables contaminated with ruminant feces.20 It is a membranedamaging toxin. Approximately 2 to 7 percent of subjects develop hemolytic uremic syndrome. the toxicity is the same. Waterborne transmission has been documented. In natural waters and in the dark.23 Reservoir.

(9) Delivery. Symptoms begin as early as 10 minutes to several hours after ingestion.3 (5) Symptoms. Prevention. Communicability. and pathological manifestations of ricin toxicity vary with the dose and the route of exposure. Reservoir. Transmission has been by inhalation of organism during industrial operations and ingestion of castor bean meal. tongue. A large quantity is required to cover a significant area on a battlefield. life-threatening neuromuscular condition. memory loss. and fingertips followed by numbness of the neck and extremities and motor incoordination. Initial symptoms include numbness and tingling of the lips. Castor beans. The clinical signs. IV-26 . (2) (3) Occurrence.24 (6) (7) (8) Incubation period. Supportive care is essential. N/A. Saxitoxin may also be delivered by projectiles or by contamination of food and water. No person-to-person transmission. (6) (7) (8) Incubation period. which accumulate dinoflagellates during filter feeding.3 (4) Transmission. No person-to-person transmission. Inhalation results in respiratory distress and airway and pulmonary lesions. symptoms. dizziness. N/A.3 (9) Delivery.3 (1) Toxin Origin. Other symptoms may include lightheadedness. Saxitoxin is rapidly absorbed from the GI tract following ingestion of contaminated shellfish. No vaccine is available. From 18 to 24 hours. however. and headache. ingestion causes GI signs and GI hemorrhage with necrosis of liver. it can be used for small-scale operations. Saxitoxin. Saxitoxin is the parent compound of a group of related neurotoxins produced by marine dinoflagellates of the genus Gonyaulax. The agent may also be delivered through contamination of food and water supplies. Shellfish. spleen. (5) Symptoms. depending on the ingested dose and host factors. Minutes to hours. Saxitoxin is transmitted to humans by ingesting bivalve mollusks.3 Prevention. and moderate involvement of the visceral organs. and kidneys.(2) (3) Occurrence. The primary threat is delivery by aerosol release. Flaccid paralysis and respiratory failure are life-threatening complications and occur within 2 to 12 hours after ingestion.3 Communicability. (4) Transmission. Reservoir. Candidate vaccines are under development. Paralytic shellfish poisoning (PSP) is a severe. and intramuscular intoxication causes severe localized pain. The primary threat is delivery by aerosol release. weakness.3 g. h. Staphylococcal Enterotoxin B. confusion. muscle and regional lymph node necrosis.

No vaccine is available.20 Avoid ingesting any of the fish or amphibians that produce tetrodotoxin.5 i.20 newt. There is no specific antidote available.3 (6) (7) Incubation period. Majority of cases occur in Japan where puffer fish is a traditional delicacy. and ataxia.1 (4) Transmission.1 Protecting food and water supplies from contamination and avoiding potentially contaminated food and water will protect individuals from the effects of ingested toxins. 4 to 10 hours for GI illness. The primary threat is SEB aerosol release. or milk products containing preformed toxin.20 (8) Prevention. The case-fatality rate approaches 60 percent. California porcupine fish.17 (2) Occurrence. ocean sunfish. Trichothecene Mycotoxins.3 (5) Symptoms. Variable.3 Communicability.3 (9) Delivery. The likely method of dissemination is by respirable aerosols or contamination of food or water supply. Symptoms may also occur in the GI tract due to inadvertent swallowing of SEB delivered via aerosol and deposited in the upper aero-digestive tract. aureus are humans and contaminated milk and milk products.20 (5) Symptoms. Staphylococcal enterotoxin B (SEB) is one of numerous exotoxins produced by Staphylococcus (S.20 (7) Communicability. Worldwide and relatively frequent. Puffer fish poisoning is characterized by onset of paresthesias. No person-to-person transmission. Ingestion of food. GI symptoms.(1) Toxin Origin. Symptoms include the acute onset of fever. aureus. The SEB toxin is heat-stable and is the second most common source of outbreaks of food poisoning. a heat-stable. The reservoirs of S. Symptoms can appear 20 minutes to 3 hours after toxin is introduced.1 (3) Reservoir.22 j.1 (9) Delivery. Death can occur 4 to 6 hours after introduction. nausea. A variety of marine species—notably the puffer fish. milk. (1) Toxin Origin. vomiting. The SEB may also be employed by sabotage contamination of food and/or water supplies. IV-27 . The causative toxin is tetrodotoxin. and species of newts and salamanders.3 (2) Occurrence.1 (6) Incubation period. The SEB is usually produced in foods contaminated with S. dizziness. nonprotein neurotoxin1 that even in small amounts can cause rapid and violent death in humans.3 (8) Prevention. and diarrhea within hours of intoxication. Poisoning results from consuming tetrodotoxin. Illness due to inhalation will result in respiratory tract disease not encountered in the endemic disease. Tetrodotoxin (Puffer Fish Poisoning).20 (3) Reservoir. which often progresses rapidly to paralysis and death within several hours after eating.) aureus. No person-to-person transmission.3 (4) Transmission. Follow strict food hygiene and sanitation controls.

3 (8) Prevention.3 Communicability.3 Transmission. these compounds are stable when exposed to air. rhinorrhea. The incubation period is minutes after exposure.25 (9) Delivery. The toxin may be delivered by aerosol release or through the contamination of food and water supplies. blistering. These toxins inhibit protein and DNA synthesis and mitochondrial respiration and alter cell membrane structure and function.3 (6) (7) Incubation period. or both. and progression to skin necrosis with eschar formation and sloughing. Moldy grain. Respiratory exposure may result in nasal itching with pain.3 (2) Occurrence.3 (5) Symptoms. As a pre-exposure prophylaxis. They are not inactivated by autoclaving but require heating at 900 degrees F for 10 minutes or 500 degrees F for 30 minutes for complete inactivation. wheezing. Mycotoxins are highly cytotoxic and have effects similar to vesicants. No person-to-person transmission. Naturally occurring mycotoxicosis occurs in livestock following ingestion of grains contaminated with molds. When maintained as either crystalline powders or liquid solutions.(1) Toxin Origin. the use of topical antivesicant cream or ointment may provide limited protection of skin surfaces. A 3 to 5 percent solution of bleach is an effective inactivation agent for them. Delivery to the skin may cause a burning skin pain.3 Washing the exposed skin areas with soap and water will decrease absorption through the skin. redness.25 (3) (4) Reservoir. sneezing. These toxins are the agents allegedly delivered via aerosol during the “Yellow Rain” attacks in Afghanistan and Southeast Asia during 1970s and 1980s. Trichothecene (T-2) mycotoxins are a diverse group of over 40 compounds produced by molds of the genus Fusarium. light. Food and water contaminated with mycotoxins must not be consumed. and cough. Worldwide. tenderness. especially mustard agents.3 IV-28 . The T-2 mycotoxins are the only potential BW agents that can harm and be absorbed through the intact skin. Ingestion of moldy grains.

Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. Hutin (CDC). “Fact Sheet: Basic Information About Monkeypox. 7. 1997.gov/ncidod/dbmd/diseaseinfo/glanders_g. No.” Russ Zajtchuk. Chapter 28. N0.” Emerging Infectious Diseases.gov/ncidod/dvrd/spb/mnpages/dispages/ebola. Baltimore. Control of Communicable Diseases Manual. “Plague. (eds). “Ebola Hemorrhagic Fever. Vol. Chap. 1997. 2 September 2003. 17 July 2000. 11 August 2003. et al.gov/ncidod/dbmd/diseaseinfo/glanders_t. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B). (eds). “Disease Information: Glanders (Technical Information). et al. et. Division of Bacterial and Mycotic Diseases. et al. Office of the Surgeon General. Office of the Surgeon General. United Book Press. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. 7 March 2003. al.” Morbidity and Mortality Weekly Report.” 8-9/NAVMED P-5059/AFJMAN 44-151. “Compendium of Measures to Control Chlamydia psittaci Infection Among Humans (Psittacosis) and Pet Birds (Avian Chlamydiosis). 20 June 2001. <http://www. “Disease Information: Glanders (General Information).NOTES Chin (ed. 3. 1997. 2TM 3FM 1James 3-216/AFM 355-6. Division of Bacterial and Mycotic Diseases.” Russ Zajtchuk. et al. Chapter 24. Chapter 26. “Updated Interim Infection Control and Exposure Management Guidance in the Health-Care and Community Setting for Patients with possible Monkeypox 17CDC. Technical Aspects of Biological Defense. Office of the Surgeon General. http://www. et al. (eds). CDC.gov/ncidod/monkeypox/factsheet.htm>. 47. Monkeypox. 16Yvan IV-29 .. J. Monkeypox. Inc.cdc. Russ Zajtchuk. 23. May-June 2001. Democratic Republic of Congo. “Viral Hemorrhagic Fevers. 1998. 12 January 1971. Office of the Surgeon General. “Q Fever.” 11BG 12BG 13CDC. 1997. 1996-1997.” 15CDC. 14BG Russ Zajtchuk. Chapter 29.1C. 17th ed. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare.cdc. (eds). MD. 1 February 1996. <http://www.. Russ Zajtchuk.cdc. 6CDC. 1997. http://www. 1997. et al. Chap. 29 August 2003.cdc. Special Pathogens Branch.). Vol.htm. “Viral Encephalitides. 2000.htm>. 5 FM 4BG Russ Zajtchuk. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. 2 September 2003. “Tularemia. 10BG 9US 8BG 7CDC.. Office of the Surgeon General. “Anthrax. (eds).F. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. RR-10. Office of the Surgeon General. “Research: Outbreak of Human Monkeypox.” 12 June 2003. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. (eds). 10 July 1998.htm. 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11. 22.” 6 August 2003. Treatment of Biological Warfare Agent Casualties.” HHS.

” Chorus and Jamie Bartram ed. “Botulinum Toxins.Virus Infection. Office of the Surgeon General.” of the US President. “Defense Against Toxin Weapons.” Russ Zajtchuk. 1999. et al.” HHS.” 18 July 2003. Cancer Institute (NCI) Nomination Submitted to the National Toxicity Program (NTP).” September 2000.” 9 December 2002. 1997. 32. Monkeypox. (eds). 1997. Chap. The Biological and Chemical Warfare Threat. 30. 25BG 26Office IV-30 . “Regulatory Impact Analysis: 42 CFR Part 73: Select Biological Agents and Toxins. 1997. Office of the Surgeon General. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. 22BG 21National 20CDC. 34. WHO. 18CDC.” 9 July 2003. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. Chap.gov/ncidod/monkeypox/smallpoxvaccine_mpox. 24BG 23Ingrid Russ Zajtchuk. (eds). (eds). 1997.cdc. et al. Russ Zajtchuk. Toxic Cyanobacteria in Water: A guide to their public health consequences.gov/ncidod/monkeypox/infectioncontrol. http://www. “Blue-Green Algae. Office of the Surgeon General. 19BG Russ Zajtchuk. et al. (eds). Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. “Ricin Toxin. 2 September 2003. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. 1999. Interim Final Rule (Draft). “Trichothecene Mycotoxins. Geneva.htm. 2 September 2003. monitoring and management.. Chapter 33. “Fact Sheet: Smallpox Vaccine and Monkeypox.cdc. Office of the Surgeon General. et al.htm. Chap. http://www.

A number of hazards are associated with a release of TIC. (5) Determining the exposure level that constitutes a hazard for the individual is often difficult due to the variances of susceptibility among individuals. c. must become aware of and plan for defense against the potential release of TIC in their AO.000 became casualties. In future operations. The US troops—through the deliberate release. India. or surface contact with the material. Personnel or equipment that have been contaminated with TIC can be decontaminated by washing with large amounts of cold. Characteristics. hydrogen cyanide. These forces must be able to safely operate. are not detectable by current military equipment. phosgene.1 a. and sustain operations in those instances where they may be exposed to toxic industrial hazards. Military personnel are trained to operate in an environment in which CW weapons may be used. and treatment difficult. (4) Symptoms are often difficult to trace back to a specific chemical. In Bhopal. It is estimated that up to 5. soapy water. or as a result of collateral damage—could encounter TIC. other gases were used against the Allies in other periods during this war. in many cases. in December 1984. Protection. disruption of operations. ingestion. failure to properly plan for the release of TIC may result in significant casualties. The military field protective mask can provide limited protection and should only be used to escape the hazard area. However. diagnosis. Background In April 1915. (2) Exposure can be through several routes. these gases were first developed for industrial purposes. b. V-1 . accidental release. Commanders have direct responsibility for protecting their forces against these threats and. survive. therefore. It is important that commanders and troops be aware that the best defense against TIC is to escape the path of the TIC immediately. Arsine. In addition to chlorine. and hydrogen sulfide were used during WWI. (3) Many of these chemicals cause a variety of immediate and delayed symptoms that make detection. Some key factors are— (1) Certain chemicals have the ability to bypass or penetrate current military protective equipment and.Chapter V TOXIC INDUSTRIAL CHEMICALS AND THEIR PROPERTIES 1. the potential hazards of TIC are a relatively new threat. but the potential of these chemicals as war gases was recognized.000 allied soldiers were killed and 20. and mission degradation. cyanogen chloride. including inhalation. Potential Hazard. an accidental release of methyl isocyanate from a production facility killed an estimated 2. the Germans released 150 tons of a TIC (chlorine gas) across a 4-mile front in one of the first gas attacks of WWI. In most cases.500 persons and left many thousands injured. Contaminated clothing should be immediately removed and disposed of in a safe manner.

under US federal regulations. propane.gov/gydebook. 10 thousand evacuated or deprived of water. police. and these properties cause many chemical injuries and damage annually. or $10 million US damages to third parties. (2) Consideration of a chemical’s many hazardous properties is reinforced by the criteria governing the US chemical manufacturing Risk Management Program (RMP). For example. 125 injured. Of these processes. cyanides. The RMP. Other Information Sources Multiple data sources are available to support the need for data and information to support the military decision-making process (MDMP).d.. Columbia. Croatia Yes – Jovan. that were involved. It is primarily a guide to aid first responders in quickly identifying the specific or generic classification of the material(s) involved in the incident. and protecting themselves and the general public during this initial response phase of the incident. liquid fuel. Guatemala. phosgene. flammability. The ERG is updated every 3 years to accommodate new products and technology. metals NA (1) As shown.828 facilities containing 20. See Table V-1 for a listing of the hazardous substances. The TIC have important physical properties (such as reactivity.htm). Transport Canada. The ERG 2000 incorporates V-2 . including precursors 3 • PCBs (slow onset) 2 • Fertilizers 2 • Dusts (e. fuel gases. petrochemicals. (1) The US DOT. or corrosivity). explosives. instituted in June 1999. the United Nations Environmental Protection Organization (UNEPO) developed a list of accidents (1970-98) involving hazardous substances in which there were at least 25 deaths. and the Secretariat of Communications and Transportation (SCT) of Mexico developed the Emergency Response Guide (ERG) 2000 jointly for use by firefighters.dot.210 chemical processes. primarily TIC. Kuwait Yes – Kutina. TIC of Concern. and flammable mixtures are present in nearly 70 percent of all RMP processes. requires certain chemical facilities to implement chemical accident prevention and preparedness measures and to submit summary reports to the government every 5 years. grain elevator) 1 • Radiation 1 • Other Chemicals 13 • Not specified 5 Ever used as a weapon? Yes – Columbia. The RMP database contains information on 14. and other emergency services personnel who may be the first to arrive at the scene of a transportation incident involving a hazardous material. and oil account for nearly 50 percent of the incidents. These sources include— a. Accidents Involving Hazardous Substances Chemical Class Frequency % • Fuel gases 15 • Explosives 12 • Liquid fuels 8 • Petrochemicals 8 • Chlorine 8 • Oil 7 • Ammonia 6 • Acids & bases 6 • Plastics manufacture 3 • Pesticides. Croatia Yes –Texas. 17.529 contain at least one TIC and 8. Chemicals such as anhydrous ammonia. 2. chlorine.107 contain at least one flammable chemical. 2000 Yes – Oklahoma City bomb Yes – animal rights and environmental arson Yes – Kutina. North American Emergency Response Guidebook (NAERG) 2000 (http:// hazmat.g. Croatia Yes – abortion clinics No Yes – Bhopal (sabotage) No Yes – Oklahoma City bomb Yes – IEDs Yes – RDDs (Moscow) Yes – arsenic. Table V-1.

cdc. more than 7 million copies have been distributed without charge to the emergency responder community. and peer-reviewed by V-3 . contact the Canadian Transport.gc. (2) An ICSC summarizes essential health and safety information on TIC. (1) The RTECS provides toxicological information with citations on over 140.000 chemical substances.gov/niosh/npg/npg. The industrial hygiene information found in the pocket guide should help users recognize and control occupational chemical hazards. c. The ICSCs are not legally binding documents. analytical methods. The chemicals or substances contained in this revision include all substances for which the NIOSH has recommended exposure limits (RELs) and those with permissible exposure limits (PELs) as found in the Occupational Safety and Health Administration (OSHA) General Industry Air Contaminants Standard (29 Code of Federal Regulations [CFR] 1910. (2) The data are compiled into substance records for ease of use. measurement methods. Registry of Toxic Effects of Chemical Substances (RTECS) (http:// www. synonyms.cdc. references to US standards and regulations. In Mexico.) that are found in the work environment. mainly summarizing health and safety information collected. international workplace exposure limits. verified. d. exposure limits. identification codes. chemical and physical properties.html). The NPG presents key information and data in abbreviated tabular form for 677 chemicals or substance groupings (e. and occupational health professionals. manganese compounds.ca for information. In Canada. etc. call SCT at 52-5-684-1275. but consist of a series of standard phrases. b. and exposure and hazard survey data. inorganic tin compounds. To date. and procedures for emergency treatment.1000). and the WHO. (2) The DOT goal is to place one ERG 2000 in each emergency service vehicle. respirator selections.cdc. nationwide. incompatibilities and reactivities. (1) The International Program on Chemical Safety (IPCS) is a joint activity of three cooperating International Organizations: the United Nations Environment Program (UNEP). the International Labor Office (ILO).. These detailed profiles include toxicological data and reviews. International Chemical Safety Cards (ICSCs) (http:// www. through distribution to state and local public safety authorities. signs and symptoms of exposure.g. Copies are made available free of charge to public emergency responders through the state coordinators (US only). (2) The information in the NPG includes chemical structures and formulas.html). Emergency Centre (CANUTEC) at 613-992-4624 or e-mail canutec@tc. (1) The NPG is intended as a source of general industrial hygiene information for workers. and updated data are fully integrated. NIOSH Pocket Guide (NPG) to Chemical Hazards (http://www. The main objective of the IPCS is to carry out and disseminate evaluations of the hazards posed by chemicals to human health and the environment.gov/niosh/ipcs/icstart.dangerous goods lists from the most recent United Nations (UN) recommendations as well as from other international and national regulations. tellurium compounds. employers.html).gov/niosh/rtecs.

safety and handling. (1) The HSDB is a nonbibliographic data bank created and maintained by the National Library of Medicine (NLM) in the US. g. In addition. information useful for emergency response situations—such as health. manufacturing.nih.21 for additional resources. Reach-back should be conducted using established unit protocols. (1) The CHRIS database is a comprehensive source of emergency response information for those involved in the transport of hazardous materials (HAZMAT). Technical reach-back is the ability to contact technical subject matter experts (SMEs) when a technical issue exceeds the on-scene SME’s capability. 3. and observable characteristics. (3) The first aid guide provides signs and symptoms of poisoning and emergency treatment for first responders. use. and analytical determinations of chemical substances. hazard labels. Chemical Hazard Response Information System (CHRIS) (http:// www. reactivity data. first aid. (3) HSDB information is organized into chemical records. chemical and physical properties. Extremely Hazardous Substance (EHS) Chemical Profiles and Emergency First Aid Guides.com). Chemical Abstracts Service (CAS) numbers.html). (2) Each chemical profile includes physical/chemical properties. At printing. e.gov/swercepp/ehs/ehslist. Each record for a HAZMAT contains key identification data. regulations.internationally recognized experts.500 chemical substances. National Response Center (NRC). Reach-Back Capability2 a. The NRC mans the hotline service and serves as an emergency resource for first responders to request technical assistance during an V-4 .nlm. Hazardous Substances Data Bank (HSDB) (http: www. and physical and chemical properties—is included in each record.html). this site does not yet have an electronic version of CHRIS available. and protective equipment of emergency situations. fire and explosion hazards. pharmacology. (2) The data bank provides extensive information on identification. f. with records for over 4. health hazards. human and nonhuman toxicity.300 HAZMAT are provided in English. shipping and hazard classifications. environmental fate and exposure. fire and reactivity hazards.chrismanual. (1) This guide contains information on over 300 EHSs currently listed as part of Section 302 of the Emergency Planning and Community Right-to-Know Act. See FM 311. General. precautions for safe handling and use. b. (2) Records for more than 1. Many of the reach-back resources have other primary missions and are not specifically resourced for reach-back. taking into account advice from manufacturers and poison control centers.gov/pubs/factsheets/hsdbfs. water pollution. The database is based upon the text of the United States Coast Guard (USCG) CHRIS manual. (http://www. such as synonyms.epa. The chemical profiles and first aid guides may be accessed from either the CAS number or alphabetical list of EHSs.

Federal Bureau of Investigation (FBI). (1) The USCG operates the NRC. (3) Use the local established policies and procedures for requesting federal assistance before contacting the CB hot line. Hazard prediction models. and emergency medical technicians [EMTs]) who arrive at the scene of a CB terrorist incident. Federal response assets. These and other federal agencies can be accessed within a few minutes to provide technical assistance during a potential CB incident. Other potential users may include the state emergency operations centers (EOCs) and hospitals that may treat victims of agent exposure. Department of Health and Human Services (DHHS). If the situation warrants. NRC duty officers take reports of actual or potential domestic terrorism and link emergency calls with applicable SMEs (such as United States Army Soldier and Biological Chemical Command [SBCCOM] and United States Army Medical Research Institute of Chemical Defense [USAMRICD]) for technical assistance and with the FBI for federal response actions. and trained operators staff the hotline 7 days a week. Treatment of exposure to CB agents. Personal protective equipment (PPE). EPA. The NRC receives basic incident information and links the caller to the DOD and FBI CB and terrorism experts. The intended users include trained emergency personnel (such as emergency operators) and first responders (such as firefighters. Medical symptoms from exposure to CB agents. and the DOD. Physical properties of CB agents. Federal Emergency Management Agency (FEMA). Applicable laws and regulations. V-5 .incident. (2) The CB hotline is a joint effort of the USCG. Specialty areas include the following: (a) (b) (c) (d) (e) (f) (g) (h) (i) (j) Detection equipment. a federal response action may be initiated. State and local officials can access the hotline in emergency circumstances by calling 1-800-424-8802. Toxicology information. police. The NRC also provides reports and notifications to other federal agencies as necessary. Decontamination systems and methods. The NRC is the entry point for the CB hotline. 24 hours a day.

March 18. 1996. Techniques. Final Report of International Task Force-25: Hazard From Toxic Industrial Chemicals. 2 1A. et al.NOTES Steumpfle. and Procedures. 6 June 2003. FM 3-11.K..22. V-6 . Weapons of Mass Destruction Civil Support Team Tactics.

000001 10-9 = 0.000000001 10-12 = 0.609 meter 0.9144 meter 5.6214 miles Volume 1 gallon (US) = 4 quarts (liquid) 1 gallon (US) = 3.546 liters 1 liter = 1.000000000001 Factor 106 = 1.540 centimeters 0.Appendix A TABLE OF EQUIVALENTS Table A-1.001 10-6 = 0.01 10-3 = 0. Table of Equivalents1 Distance 2.237 miles per hour Latent Heat of Vaporization 1 kcal/mol = (1000 / MW) cal/gram *avdp = avoirdupois (Avoirdupois weight is the US system of weights and is based on a pound containing 16 ounces or 7.280 feet = 1. Table of Commonly Used Prefixes1 Prefix mega kilo hecto deca deci centi milli micro nano pico Symbol M k h da d c m µ n p 103 = 1.3937 inch 3.) 1 inch 1 foot 1 yard 1 mile 1 millimeter 1 centimeter 1 meter 1 kilometer = = = = = = = = Table A-2.057 quart (liquid) 1 milliliter = 1.281 feet 0.349527 grams 1 pound (avdp*) = 16 ounces (avdp*) 1 pound (avdp*) = 0.03937 inch 0.4536 kilogram 1 kilogram = 2.785 liters 1 gallon (UK) = 4.000 grains.0 cm3 Weight 1 ounce (avdp*) = 28.205 pounds (avdp*) Pressure 1 torr = 1 millimeter of mercury (mm Hg) 1 atmosphere (atm) = 760 mm Hg Wind Speed 1 meter per second (m/s) = 2.000 A-1 .3048 meter 0.000.000 102 = 100 101 = 10 10-1 = 0.1 10-2 = 0.

NOTES Merck Index: An Encyclopedia of Chemicals. 1996. 12th ed. Drugs. Whitehouse Station. 1The A-2 .. NJ. and Biologicals. Merck Research Laboratories.

or use Table B-1 as a quick reference.Appendix B TEMPERATURE CONVERSIONS To convert degrees C to degrees F or degrees F to degrees C. • • To convert C to F.8 (°C) + 32 To convert F to C. use the following formulas. Temperature Conversions °C -60 -55 -50 -45 -40 -35 -30 -25 -20 -15 -10 -5 0 2 4 6 8 10 12 14 16 18 20 22 24 °F -76 -67 -58 -49 -40 -31 -22 -13 -4 5 14 23 32 36 39 43 46 50 54 57 61 64 68 72 75 °C 26 28 30 32 34 36 38 40 45 50 55 60 65 70 75 80 85 90 95 100 105 110 115 120 125 °F 79 82 86 90 93 97 100 104 113 122 131 140 149 158 167 176 185 194 203 212 221 230 239 248 257 °C 130 135 140 145 150 155 160 165 170 175 180 185 190 195 200 205 210 215 220 225 230 235 240 245 250 °F 266 275 284 293 302 311 320 329 338 347 356 365 374 383 392 401 410 419 428 437 446 455 464 473 482 B-1 . use this formula: °C = (°F – 32)/1. use this formula: °F = 1.8 Table B-1.

1996. 1The B-2 . Drugs. Whitehouse Station.NOTES Merck Index: An Encyclopedia of Chemicals.. NJ. Merck Research Laboratories. 12th ed. and Biologicals.

Periodic Table of the Elements1 Inert C-1 .Appendix C PERIODIC TABLE OF THE ELEMENTS Table C-1.

Chemical Elements and Symbols Chemical Element Actinium Aluminum Americium Antimony Argon Arsenic Astatine Barium Berkelium Beryllium Bismuth Bohrium Boron Bromine Cadmium Calcium Californium Carbon Cerium Cesium Chlorine Chromium Cobalt Copper Curium Darmstadtium Dubnium Dysprosium Einsteinium Erbium Europium Fermium Fluorine Francium Gadolinium Gallium Germanium Gold Hafnium Hassium Helium Holmium Hydrogen Indium Iodine Iridium Iron Krypton Lanthanum Lawrencium Lead Lithium Lutetium Magnesium Manganese Meitnerium Mendelevium Mercury Symbol Ac Al Am Sb Ar As At Ba Bk Be Bi Bh B Br Cd Ca Cf C Ce Cs Cl Cr Co Cu Cm DS Db Dy Es Er Eu Fm F Fr Gd Ga Ge Au Hf Hs He Ho H In I Ir Fe Kr La Lr Pb Li Lu Mg Mn Mt Md Hg Chemical Element Molybdenum Neodymium Neon Neptunium Nickel Niobium Nitrogen Nobelium Osmium Oxygen Palladium Phosphorus Platinum Plutonium Polonium Potassium Praseodymium Promethium Protactinium Radium Radon Rhenium Rhodium Rubidium Ruthenium Rutherfordium Samarium Scandium Seaborgium Selenium Silicon Silver Sodium Strontium Sulfur Tantalum Technetium Tellurium Terbium Thallium Thorium Thulium Tin Titanium Tungsten Uranium Vanadium Xenon Ytterbium Yttrium Zinc Zirconium Symbol Mo Nd Ne Np Ni Nb N No Os O Pd P Pt Pu Po K Pr Pm Pa Ra Rn Re Rh Rb Ru Rf Sm Sc Sg Se Si Ag Na Sr S Ta Tc Te Tb Tl Th Tm Sn Ti W U V Xe Yb Y Zn Zr C-2 .Table C-2.

23 December 2002. C-3 .ac.chemgmw. http://chemlab.html.pc. 20 May 2004.uk/uipac/atwt/>.NOTES 1 Chris Heilman. http://www.edu/periodic/default. The pictorial Periodic Table. 2 IUPAC Commission on Atomic Weights and Isotopic Abundances: Atomic Weights of the Elements 2001. 25 May 2004.maricopa.

Soman: O-Pinacolyl methylphosphonofluoridate O-Alkyl (≤ C10. including cycloalkyl) alkyl (Me. Et. including cycloalkyl) S-2-dialkyl (Me. 2 AND 3 CHEMICALS Table D-1.g. Et.Appendix D CHEMICAL WEAPONS CONVENTION SCHEDULE 1. or i-Pr)-aminoethyl alkyl (Me.2-Bis(2-chloroethylthio)ethane 1. CWC Schedule 1 Chemicals1 Substance Toxic Chemicals O-Alkyl (< C10. Et. Sarin: O-Isopropyl methylphosphonofluoridate e.5-Bis(2-chloroethylthio)-n-pentane Bis(2-chloroethylthiomethyl)ether O-Mustard: Bis(2-chloroethylthioethyl)ether Lewisites Lewisite 1: 2-Chlorovinyldichloroarsine Lewisite 2: Bis(2-chlorovinyl)chloroarsine Lewisite 3: Tris(2-chlorovinyl)arsine Nitrogen mustards HN1: Bis(2-chloroethyl)ethylamine HN2: Bis(2-chloroethyl)methylamine HN3: Tris(2-chloroethyl)amine Saxitoxin Ricin 538-07-8 51-75-2 555-77-1 35523-89-8 9009-86-3 541-25-3 40334-69-8 40334-70-1 50782-69-9 2625-76-5 505-60-2 63869-13-6 3563-36-8 63905-10-2 142868-93-7 142868-94-8 63918-90-1 63918-89-8 77-81-6 107-44-8 96-64-0 CAS Registry Number D-1 . n-Pr or I-Pr)-phosphonofluoridates e. N-dimethyl phosphoramidocyanidate O-Alkyl (H or ≤ C10. VX: O-ethyl S-2-diisopropylaminoethyl methyl phosphonothiolate Sulphur mustards: 2-Chlorethychloromethylsulfide Mustard gas: Bis(2-chloroethyl)sulfide Bis(2-chloroethylthio)methane Sesquimustard: 1.4-Bis(2-chloroethylthio)-n-butane 1. Tabun: O-Ethyl N.g.g. n-Pr.g. n-Pr.3-Bis(2-chloroethylthio)-n-propane 1. or i-Pr)-phosphonothiolates and corresponding alkylated or protonated salts e.N-dialkyl (Me. Et. including cycloalkyl) N. n-Pr or i-Pr)phosphoramidocyanidates e.

1. n-Pr or i-Pr) aminoethyl-2-chlorides and corresponding protonated salts N. n-Pr or i-Pr) aminoethane-2-thiols and corresponding protonated salts Thiodiglycol: Bis(2-hydroxyethyl)sulfide Pinacolyl alcohol: 3. Et.g. or i-Pr) phosphonyldifluorides e.N-dialkyl (Me. Methylphosphonyl dichloride e. or propyl (normal or iso) group but not further carbon atoms e. n-Pr or i-Pr) aminoethane-2-ols and corresponding protonated salts Exemptions: N.3. Et.g. including cycloalkyl) O-2-dialkyl (Me.Table D-1. Et.N-Dimethylaminoethanol and corresponding protonated salts N. Et. CWC Schedule 1 Chemicals1 (Continued) Precursors Alkyl (Me. except for those listed in Schedule 1. n-Pr or i-Pr) phosphoramidic dihalides Diakyl (Me. DF: Methylphosphonyldifluoride O-Alkyl (H or <C10. O-Diethyl S-[2-(diethylamino) ethyl] phosphorothiolate and corresponding alkylated or protonated salts PFIB: 1.N-Dialkyl (Me. QL: O-Ethyl O-2-diisopropylaminoethyl methylphosphonite Chlorosarin: O-Isopropyl methylphosphonochloridate Chlorosoman: O-Pinacolyl methylphosphonochloridate 57856-11-8 1445-76-7 7040-57-5 676-99-3 Table D-2.N-Dialkyl (Me. n-Pr or i-Pr) N. as specified in Part VII of the Verification Annex of the CWC.N-Dialkyl (Me.g. Et.3-Pentafluoro-2-(trifluoromethyl)-1-propene BZ: 3-Quinuclidinyl benzilate* Precursors Chemicals. containing a phosphorous atom to which is bonded one methyl.N-Dialkyl (Me. n-Pr. Et. n-Pr or i-Pr)-phosphoramidates Arsenic trichloride 2.2-Diphenyl-2-hydroxyacetic acid Quinuclidine-3-ol N. CWC Schedule 2 Chemicals1 Substance Toxic Chemicals Amiton: O. Et. 111-48-8 464-07-3 108-01-0 100-37-8 7784-34-1 76-93-7 1619-34-7 676-97-1 756-79-6 944-22-9 78-53-5 382-21-8 6581-06-2 CAS Registry Number D-2 . Et.N-Diethylaminoethanol and corresponding protonated salts N.3-Dimethylbutane-2-ol NOTES *Subject to special thresholds for declaration and verification.3. n-Pr or i-Pr) phosphonites and corresponding alkylated or protonated salts e.g. Et. ethyl. n-Pr or i-Pr)-aminoethyl alkyl (Me. Dimethyl methylphosphonate Exemption: Fonofos: O-Ethyl S-phenyl ethylphosphonothiolothionate N.

Table D-3. CWC Schedule 3 Chemicals1 Substance Toxic Chemicals Phosgene: Carbonyl dichloride Cyanogen chloride Hydrogen cyanide Chloropicrin: Trichloronitromethane Precursors Phosphorus oxychloride Phosphorus trichloride Phosphorus pentachloride Trimethyl phosphite Triethyl phosphite Dimethyl phosphite Diethyl phosphite Sulfur monochloride Sulfur dichloride Thionyl chloride Ethyldiethanolamine Methyldiethanolamine Triethanolamine 10025-87-3 7719-12-2 10026-13-8 121-45-9 122-52-1 868-85-9 762-04-9 10025-67-9 10545-99-0 7719-09-7 139-87-7 105-59-9 102-71-6 75-44-5 506-77-4 74-90-8 76-06-2 CAS Registry Number D-3 .

D-4 .NOTES 1Office of the US President. The Biological and Chemical Warfare Threat. 1999.

80 1. Phosphorus trichloride 7719-12-2 Organic synthesis Specific uses not identified Organic synthesis Specific uses not identified Organic synthesis Lubricant additive Organic synthesis Insecticides Gasoline additives Plasticizers Surfactants Dyestuffs Sarin (GB) Soman (GD) Cyclosarin (GF) Sarin (GB) Soman (GD) Cyclosarin (GF) Sarin (GB) Soman (GD) Cyclosarin (GF) Sarin (GB) Soman (GD) Cyclosarin (GF) Amiton (VG) Tabun (GA) Sarin (GB) Salt process Rearrangement process Soman (GD) Salt process Rearrangement process Cyclosarin (GF) Salt process Rearrangement process 1.31 (0.35 1.65 1.36 1.44) b 1.95 1.32 (0.82 1. Methylphosphonyl dichloride 676-97-1 6.44) b 1. Dimethyl phosphite 868-85-9 7. Thiodiglygol 111-48-8 Civil Uses Organic synthesis Carrier for dyes in textile industry Lubricant additives Manufacturing plastics Organic synthesis Plasticizers Gasoline additives Hydraulic fluids Insecticides Dopant for semiconductors grade silicon Flame retardants Flame retardant CW Agent Production Sulfur mustard (HD) Units of Agent per Unit of Precursora 1.34) b 1.32/(0.40 1.02/(0.02 (0.18 1.Appendix E CHEMICAL WARFARE AGENT PRECURSOR CHEMICALS: USES AND EQUIVALENTS Table E-1.79 1.88) b 1. Phosphorus oxychloride 10025-87-3 3. Methylphosphonyl difluoride 676-99-3 5. CW Agent Precursor Chemicals: Uses and Equivalents1 Precursor Chemical/CAS Registry Number 1.27 1.87) b E-1 .45 1.3 Sesqui mustard (Q) Tabun (GA) 1.68) b 1.31/(0. Dimethyl methylphosphonate (DMMP) 756-79-6 4.65 1.05 2.05 1.12 1.

61 Ethyl sarin (GE) 0.64 1.18 1.65 Organic Synthesis 15.06 Tabun (GA) 3. Trimethyl phosphite 121-45-9 9. 3-Hydroxy-1-methylpiperidine 3554-74-3 11.99 0.145 Organic synthesis 10. probably used in pharmaceutical industry Organic Synthesis 1.51 1. 3-Quinuclidinol 1619-34-7 14.53 1. 2-Chloroethanol 107-07-3 16.714 0.14 3. could be used in the synthesis of psychoactive compounds such as BZ VX VS VX VS BZ Units of Agent per Unit of Precursora See dimethyl methylphosphonate 1. Potassium fluoride 7789-23-3 Chlorinating agent Catalyst Pesticides Engineering plastics Specific uses not identified. dairy. N.655 1.Table E-1.N-diisopropylaminoethanethiol 5842-07-9 13.34 1. Thionyl chlorideb 7719-09-7 Could serve as chlorinating agent in all of these processes—other chlorinating agents could be substituted Civil Uses Organic synthesis CW Agent Production Used to make dimethyl methylphosphonate (DMMP)—molecular rearrangement Sarin (GB) Soman (GD) Cyclosarin (GF) Sulfur mustard (HD) Sesqui mustard (Q) Nitrogen mustard (HN-1) Nitrogen mustard (HN-2) Nitrogen mustard (HN-3) Nonidentified.99 1. N.N-diisopropyl-(beta)aminoethyl chloride 96-79-7 12.10 0.41 3.66 1. CW Agent Precursor Chemicals: Uses and Equivalents (Continued) Precursor Chemical/CAS Registry Number 8.93 E-2 .84 0. Diethyl ethylphosphonate 78-38-6 Hypotensive agent Probably used in synthesis of pharmaceuticals Fluorination of organic compounds Cleaning and disinfecting brewery. and other food processing equipment Glass and porcelain manufacturing Organic synthesis Manufacturing of ethylene oxide and ethylene-glycol Insecticides Solvent Organic synthesis Pharmaceuticals Detergents Pesticides Gasoline additive Missile fuels Vulcanization of rubber Heavy metal extraction Gasoline additive Antifoam agent Plasticizer Sarin (GB) Soman (GD) Cyclosarin (GF) Sulfur mustard (HD) Sesqui mustard (Q) Nitrogen mustard (HN-1) 2.75 2.72 1. Dimethylamine 124-40-3 17.

02 1.90 20.10 Ethyl sarin (GE) 2.14 Organic synthesis Plasticizers Lubricant additives Amiton (VG) 1.30 1. pesticides.7 9.99 21. 57856-11-8 30.Table E-1.N-dimethyl phosphoramidate 2404-03-7 19. Diethyl phosphite 762-04-9 Civil Uses Organic synthesis Specific uses not identified.N-diisopropyl-(beta)aminoethanol 96-80-0 28.62 E-3 .0 9.18 22. Hydrogen fluoride 7664-39-3 Ethyl sarin (GE) 2. Pinacolyl alcohol 464-07-3 29.2-diisopropyl aminoethyl methyl-phosphonate (QL). Methyl benzilate 76-89-1 26. Organic synthesis Specific uses not identified.01 1. gas additives.84 25.93 2.32 1. Ethylphosphonyl difluoride 753-98-0 24. N. Organic synthesis Paint solvent Lubricant additive Organic synthesis Pharmaceuticals Surfactants Pesticides Gasoline additives Organic synthesis Specific uses not identified but could be used in manufacturing of flame retardants. etc.28 1. Dimethylamine HCl 506-59-2 Amiton (VG) Sarin (GB) Soman (GD) Cyclosarin (GF) Tabun (GA) Catalyst 1.39 2.79 1. see ethylphosphonous dichloride Fluorinating agent in chemical reactions Catalyst in alkylation and polymerization reactions Additives to liquid rocket fuels Uranium refining Organic synthesis Tranquilizers Organic synthesis Organic synthesis Specific uses not identified Specific uses not identified Specific uses not identified CW Agent Production Tabun (GA) Units of Agent per Unit of Precursora 0.70 Sarin (GB) Soman (GD) Ethyl sarin (GE) Cyclosarin (GF) BZ VX VX 7. see ethylphosphonous dichloride Organic synthesis Specific uses not identified.11 7. Methylphosphonous dichloride 676-83-5 27. CW Agent Precursor Chemicals: Uses and Equivalents (Continued) Precursor Chemical/CAS Registry Number 18. Diethyl N. O-ethyl.14 1. Ethylphosphonyl dichloride 1066-50-8 23. surfactants. Triethyl phosphite 122-52-1 Soman (GD) VX 1. Ethylphosphonous dichloride 1498-40-4 VE VS Ethyl sarin (GE) 1.

57 3. Benzilic acid 76-93-7 33. Ammonium bifluoride 1341-49-7 Sarin (GB) Soman (GD) Cyclosarin (GF) Sarin (GB) Soman (GD) Cyclosarin (GF) 2.58 1.15 2.97 1. Diethyl methylphosphonite 15715-41-0 34.34 4.43 1. Phosphorous pentachloride 10026-13-8 39.25 Hydrogen cyanide (AC) Sarin (GB) Soman (GD) Cyclosarin (GF) 0.16 3. Potassium cyanide 151-50-8 Same as 3-Quinuclidinol3quinuclidinol Organic synthesis Pesticides Plastics Specific uses not identified Extraction of gold and silver from ores Pesticide Fumigant Electroplating Fluorine production Catalyst in alkylation Treatment of coal to reduce slag formation Fluid in silver solder Ceramics Disinfectant for food equipment Electroplating Etching glass Pesticide Disinfectant Dental prophylaxis Glass and steel manufacturing Soman (GD) Tabun (GA) 1.65 0. Methylphosphonous difluoride 753-59-3 37. Potassium bifluoride 7789-29-9 42.20 3. CW Agent Precursor Chemicals: Uses and Equivalents (Continued) Precursor Chemical/CAS Registry Number 31. Ethylphosphonous difluoride 430-78-4 36.31 41.Table E-1. Pinacolone 75-97-8 40.33 4.17 2. Sodium fluoride 7681-49-4 E-4 .45 1.12 2.29 43.53 1.14 1.48 1.41 1.82 1.18 2.78 32.84 1. Dimethyl ethylphosphonate 6163-75-3 35. Arsenic trichloride 7784-34-1 Civil Uses Organic synthesis Pharmaceuticals Insecticides Ceramics Organic synthesis Organic synthesis Organic synthesis Organic synthesis Organic synthesis CW Agent Production Arsine (SA) Lewisite (L) Adamsite (DM) Diphenylchloroarsine (DA) BZ VX Ethyl sarin (GE) VE Ethyl sarin (GE) VX VM Sarin (GB) Soman (GD) Cyclosarin (GF) BZ Tabun (GA) Units of Agent per Unit of Precursora 0.67 2. 3-Quinuclidone 1619-34-7 38.33 2.79 2.46 3.

Phosphorus pentasulfide 1314-80-3 Amiton (VG) VX 1.54 E-5 .94 2.91 1. Sodium bifluoride 1333-83-1 45.65 2. Sodium sulfide 1313-82-2 Sulfur mustard (HD) 2.21 1.30 2. CW Agent Precursor Chemicals: Uses and Equivalents (Continued) Precursor Chemical/CAS Registry Number 44.18 52. Diethylaminoethanol 100-37-8 VX Amiton (VG) VM 3.25 46.65 0. Sodium cyanide 143-33-9 Civil Uses Antiseptic Neutralizer in laundry operations Tin plate production Extraction from gold and silver ores Fumigant Manufacturing dyes and pigments Core hardening of metals Nylon production Organic synthesis Detergents Cosmetics Corrosion inhibitor Plasticizer Rubber accelerator Organic synthesis Insecticide Mitocides Lubricant oil additives Pyrotechnics Organic synthesis Specific uses not identified Organic synthesis Anticorrosion compositions Pharmaceuticals Textile softeners Paper manufacturing Rubber manufacturing Metal refining Dye manufacturing Organic synthesis Pharmaceuticals Sulfur dyes Insecticides Rubber vulcanization Polymerization catalyst Hardening of soft woods Extraction of gold from ores Organic synthesis Rubber vulcanizing Insecticides Vulcanizing oils Chlorinating agents CW Agent Production Sarin (GB) Soman (GD) Cyclosarin (GF) Tabun (GA) Hydrogen cyanide (AC) Cyanogen chloride (CK) Units of Agent per Unit of Precursora 2. Triethanolamine 102-71-6 Nitrogen mustard (HN-3) 1.05 50. Diisopropylamine 108-18-9 49.Table E-1.20 48.55 1.26 2.37 47. Sulfur dichloride 10545-99-0 Sulfur mustard (HD) 1.04 51. Sulfur monochloride sulfur chloride 10025-67-9 Sulfur mustard (HD) 1.

The Biological and Chemical Warfare Threat. E-6 .34 NOTES 1Office of the US President. CW Agent Precursor Chemicals: Uses and Equivalents (Continued) Precursor Chemical/CAS Registry Number 53. 1999.N-diisopropyl-2-aminoethyl VX chloride hydrochloride 4261-68-1 Notes: a Assumes quantitative reaction yields b Figures in parentheses are based on the use of PCl3 as a chlorine donator in the reaction.Table E-1. N. 1.10 54. Triethanolamine hydrochloride 637-39-8 Civil Uses Organic synthesis Insecticides Surface active agents Waxes and polishes Textile specialties Lubricants Toiletries Cement additive Petroleum demulsifier Synthetic resin Organic synthesis CW Agent Production Nitrogen mustard (HN) Units of Agent per Unit of Precursora 1.

f)-1:4-oxazepine Capsaicin Diphenylchloroarsine Diphenylcyanoarsine Adamsite Chlorine Symbol CG DP PS GA GB GD GF GE VX Vx VE VG VM VS AC CK SA H/HD HN-1. HN-2.Appendix F CHEMICAL WARFARE AGENTS AND OTHER MILITARY CHEMICAL COMPOUNDS Table F-1. Symbols for CW Agents and Military Chemical Compounds Agent Class Choking Agents Agent Phosgene Diphosgene Chloropicrin Tabun Sarin Soman Cyclosarin Ethyl Sarin VX Vx VE Amiton VM VS Hydrogen Cyanide Cyanogen Chloride Arsine Distilled Mustard Nitrogen Mustard Mustard-T Mixture Sesqui Mustard Lewisite Mustard-Lewisite Mixture Phenyldichloroarsine Ethyldichloroarsine Methyldichloroarsine Phosgene Oxime 3-Quinuclidinyl benzilate O-Chlorobenzylidene Malononitrile Dibenz(b. HN-3 HT Q L HL PD ED MD CX BZ CS CR OC DA DC DM Cl2 Nerve Agents Blood Agents Blister Agents Incapacitating Agent Riot Control Agents Respiratory Irritants F-1 .

Appendix G PROPERTIES OF CHEMICAL WARFARE AGENTS AND MILITARY CHEMICAL COMPOUNDS Tables G-1 through G-6 (pages G-2 through G-18) and Figures G-1 through G-7 (pages G-19 through G-25) provide a ready source of data for key CW agents and military chemical compounds. The data were compiled from the detailed data presented for each agent described in Chapters II and III. G-1 .

Physical Properties of Choking.41 (20°C).0820 (0°C) 0. 0. 1.222 (0°C) 1.00673 (25°C). 1.00978 (0°C) 0.420 (0°C) Munitions grade: 1. AC Cyanogen chloride.0222 (25°C). GD Cyclosarin. 265 (0°C) 760 (12. 0.Choking Agents Nerve Agents Blood Agents G-2 Table G-1. 0.9 (FP) 2.7 . camphor when impure None when pure 198 -42 (MP) 6. 12 (MP) Below -51 (FP).0999 (0°C) Pure: 1.060 (25°C). 1. SA 211. Symbol Phosgene.202 (10°C).1182 (0°C) 1.0456 (0°C) 1. C4H10FO2P. none when pure None when pure 248 -50 (FP) 5.2 267. 39 to –60 (FP) Data not available 6.4 Vapor Pressure (torr) 1400 (25°C). COCl2.656 (20°C). Nerve. C5H11N2O2P.734 (100°C) Vapor Density (Air=1) 3.17 Colorless liquid when pure Colorless liquid Fruity.8 162. AsH3. GB Soman.8 -6.8°C).95 Colorless gas -62. and Blood Agents Agents Chemical Agent. HCN.00475 (0°C) 248 (25°C).3 180.13 Colorless to brown liquid Colorless liquid Faintly fruity. CK Arsine.47 Colorless gas 12.2 -116 (MP) 2. 0.8°C). Formula.687 (0°C) 1.667 (-75°C). 746 (25. 1.0083 (25°C). 0. GA Sarin. 1. C7H16FO2P.7162 (0°C) 1.6 140.0209 (0°C) 1. GF VX. 680 (10°C).6797 (25°C).9 (-100°C) 197.5 -13. 1.3 27. C7H14FO2P. 0.360 (25°C). 0. 0.8 182. 1.0496 (0°C) 0. 1.0000422 (0°C) 0.914 (0°C) 0.00057 (0°C) 760 (25.03 Colorless liquid Bitter almonds. 1.09 150 -56 (FP) 4.1276 (25°C).37 Colorless liquid when pure Liquid Odorless when pure Odorless 292 9. DP Tabun.1525 (0°C) 1.401 (25°C).83 127 -57 (MP) 6.0570 (25°C). CNCl.0756 (25°C).2 “V-Sub X”.402 (7. 86. peach kernels Lacrimatory and irritating Disagreeable. 48 (0°C) 400 (-75°C).92 State at 20°C Colorless gas that is readily liquefied Colorless oily liquid Odor Musty hay or rotting fruit Musty hay Boiling Point (°C) 7.0°C).0927 (25°C).93 61. 760 (7.1 77. 1.0887 (25°C). C2Cl4O2 .3 (MP) 0.000878 (25°C).5°C). garlic-like 25. C7H18NO2PS. CG Diphosgene. 1.8 FP/MP (°C) -128 (MP) Liquid Density (g/mL) 1. C11H26NO2PS Molecular Weight 98. 560 (0°C) 4.16 228 -30 to -50 (FP).410 (0°C) 0. Vx Hydrogen cyanide.26 256 7.8°C).

0.7 (0°C) 31.44 (0°C) 4.00560 (0°C) 0.0°C). 5.8 (0°C) 19.00590 (25.8°C). 0.17 Viscosity (cP) Viscosity of Vapor (cP) Data Not Available in Samuel. 7. 2. 0. 16.00615 (25.9 (25.8°C).0°C).72 (25.789 (0°C) 5. 28.5 (25. 1.620. reference 0. reference Data Not Available in Samuel.370.02 (0°C) 1.0°C).0°C).95 (7.4 (25. et al.40 (12.00556 (25.0°C).5°C).397 (25.2 (25°C).71 (0°C) 6.000 (0°C) 2.7 (0°C) 11.0 (0°C) 25.7 (0°C) 13.4 (25°C). reference Nonflammable DP None GA 78°C GB Nonflammable Nerve Agents GD 121°C GF 32.00620 (25.5°C).460.628 (25. 627.662 (0°C) 76.0°C). et al. reference Data Not Available in Samuel.000 (25.620. 15. reference Data Not Available in Samuel. 6.277 (25.2 (0°C) 18.530.320 (0°C) 1. 6. reference Surface Tension (dynes/cm) Data Not Available in Samuel.00463 (0°C) 0. reference 127°C Vx Data not available AC Blood Agents -18°C. reference Data Not Available in Samuel.3 (25. et al.0°C). 531 (0°C) 898 (25°C).00555 (0°C) 0. 420.0°C).8 (0°C) 15. and Blood Agents (Continued) Agents Volatility 3 (mg/m ) CG 7.Table G-1. 45. reference 2.000 (0°C) 47. 1. 6.583 (0°C) 3.5°C) 94°C VX 31.431 (25.167(25.3 (25. et al. forms explosive mixtures with air G-3 .8°C).5 (26.0°C). 20.2 (20°C). et al.0°C). 0.000 (-100°C) Latent Heat of Vaporization (kcal/mol) 5. 14. Physical Properties of Choking.600 (0°C) 497 (25°C).370 (0°C) 3. reference Data Not Available in Samuel. et al. 2. 37.6 (25°C). 103 (0°C) 12. 11.000 (7.00513 (25.700 (20°C). 0.000 (25°C).532 (0°C) 5.1 (0°C) 16. 16. reference Data Not Available in Samuel.00719 (25.0°C).41 (10°C).00651 (0°C) 0.290.0 (25°C).0°C).7 (0°C) Data Not Available in Samuel. 0. et al.041 (25. reference Data Not Available in Samuel. 6. 3. et al.000 (-75°C).0°C). 35.0°C).5°C) Flash Point Choking Agents Data Not Available in Samuel.5 (25°C). reference Data Not Available in Samuel.0°C). 6. 5. et al.0°C). 13.0°C).2 (25°C).92 (25°C). 0. 3.000 (10°C).100. 14.000 (0°C) 2. et al.3 (25°C).930 (25°C). et al. et al.000 (12.72 (25. et al. et al. can ignite when explosively disseminated Nonflammable CK SA Flammable. 34.0°C).1 (0°C) 6. et al. 4.8 (0°C) 24.550.335 (0°C) Data Not Available in Samuel.080.700 (25°C).00502 (0°C) Data Not Available in Samuel. 12.8°C). Nerve. reference Data Not Available in Samuel.6 (25°C). 33. reference 32. 4.762 (0°C) 10.96 (0°C) 12.00533 (0°C) 0.8 (0°C) 14.000 (25. 10.

pH 7) Rapid in light. HF GF HF and another product VX EMPA. t1/2 = 60 hrs (pH 10). t1/2 = 60 hrs (pure water) Rate coefficient is 0. soluble in common organic solvents In water. very soluble in organic solvents In water. 5. t1/2 = 80 hrs (pH 7). t½ = 180 hrs (ambient temperature. t½ = 1. 7. t1/2 = 3 hrs (pH 2). t1/2 = 45 hrs (pH 6. pH 7). 3. halogen alkanes. t1/2 = 0. Nerve. miscible with common organic solvents. t1/2 = 34.003M GF (distilled water). and HCN In water. t1/2 = 27 min (pH 1).2 g GA/100 g (20°C). soluble in common organic solvents.0078 hrs-1 Hydrolysis Products HCl(aq)1. sulfur mustard. t1/2 = 5.5 hrs (150°C). CO2 GA 150°C (3 to 3¼ hrs) HCN and other products GB 150°C (2½ hrs) HF. IMPA. unstabilized: 130°C (4 hrs) 150°C (2 hrs) t1/2 = 502 days (71°C). fairly rapid with strong acids and alkalis with self-buffering (pH 4 to 5) At 20°C.8 min (1. soluble in common organic solvents Soluble in organic solvents. 44. t½ = 31 min (0.Choking Agents Nerve Agents Blood Agents G-4 Table G-1.5°C. t1/2 = 3½ hrs (pH 2). < 5 min in 5% NaOH3 solution 0. readily soluble in common organic solvents Completely miscible with water and common organic solvents In water. EA 2192. t1/2 = 36 sec (295°C) Data not available PMPA. t1/2 = 41 days (100°C). does not react quickly with water vapor but does with liquid water Slow at ambient temperature and fairly rapid at 100°C t1/2 = 8.7 g GF/100 g (20°C).5 hrs (20°C. slow in water.1 g GF/100 g (0°C) Water solubility = 5% (21. Physical Properties of Choking. MPA. and Blood Agents (Continued) Agents CG Decomposition Temperature Complete @ 800°C Solubility Limited in water. slow in absence of light and air (15.10M NaOH).5°C). IPA GD > 150°C. t½ = 10.25M NaOH).65).4 g/L (20°C). MFPA. and lubricating oil In water. hydrocarbons. forms explosive polymer on standing ≈ 149°C Miscible with water and common organic solvents including alcohol and ether Liquefied CK in water.25 sec (13°C). 3.4 min (pH 10).25M NaOH). 2. 0.4 g GD/100 g (0°C).6 min (pH 11) 0. slightly soluble in water Rate of Hydrolysis t½ = 0. miscible with water below 9.003M2 GD at 25°C. soluble in alkalis.8 min (0. pH 7). CNOH SA 300°C Arsenic (toxic) . 66% in 24 hrs NH3 and other products CK HCl.1 g GD/100 g solution (20°C). rapid with traces of base or basic salts With tap water. CO2 DP 300 to 350°C HCl. and other products Ethanol and other toxic products Vx AC Stabilized: >65. 71.8 g GA/100 g (0°C).6 g DP/L (20°C). and benzene Slow under acidic conditions. t1/2 = 42 hrs (25°C) At 22°C. stabilized: 130°C (200 hrs). 9.028 g/100 g (20°C).5°C.4°C. petroleum. 32% hydrolyzed in 5 hrs.

liquid penetrates skin Extremely toxic by skin and eye absorption Extremely toxic by skin and eye absorption None Primarily inhalation hazard GB Most toxic route of exposure Nerve Agents GD Most toxic route of exposure GF Most toxic route of exposure VX Extremely potent Vx Extremely potent AC Blood Agents Pure: unstable on storage.Table G-1. copper. only 9 weeks (60°C). 3 months (65°C) Stabilized GB: Stable in steel for 5-10 years (ambient temperatures).000034 in/month (65°C) At 71°C. Data not available Action on Metals None when dry. purified VX is stable in glass and steel. stable in steel for 1 year at ambient temperatures. chromium steel. and 1 year in steel and aluminum containers Stable at ambient temperature. inconel. and lead None if dry. stabilized GD: 6 months (71°C) in glass. Nerve. greater through eyes than through skin. and lead. stability decreases as temperature increases. acidic and corrosive when moist Metals act as catalyzers in conversion to CG. unstabilized CK slowly polymerizes in steel and other common metals (elevated temperatures) Corrosive to most metals Can cause death within minutes CK Irritation to eyes similar to RCAs Can cause death within minutes SA Exposure to liquid causes frostbite Acute toxicity is high G-5 . attacks rubber. greater through eyes than through skin. stabilized CK: long periods (up to 100°C) Unstable in most metal containers. and Blood Agents (Continued) Agents CG Stability In Storage If dry. steel. slight to severe corrosion on aluminum Corrosion rate on steel is 0. brass. K-monel. stabilized AC: may be stored in metal containers for long periods (65°C) Stable in glass for long periods and elevated temperatures. metals catalyze decomposition on exposure to light.00001 in/month (65°C) Corrosion rate on steel is 0. stable in steel for 1 year at ambient temperatures. converts to CG Stabilized GA: stable in steel for several years (ambient temperatures). liquid penetrates skin Very high toxicity. unstabilized VX (95% purity) decomposes 5% a month (71°C). 6 months (50°C). greater through eyes than through skin. steel. Physical Properties of Choking.000053 in/month (65°C) Negligible on brass. slightly corrosive on steel. At elevated temperatures up to 71°C storage life decreases slightly Relatively stable in glass 5½ months (ambient temperature). stability decreases as temperature increases Unstable. slight corrosion with copper Data not available Skin and Eye Toxicity Initial effects resemble those of tear gas Inhalation Toxicity Causes pulmonary edema Choking Agents DP Lacrimator Causes pulmonary edema GA Very high toxicity. liquid penetrates skin Very high toxicity. greater through eyes than through skin. and aluminum. cast iron. and cement Corrosion rate of steel on crude GA (520% chlorobenene) is 0. liquid penetrates skin Very high toxicity. cork. moist arsine decomposes quickly Corrodes iron. and aluminum containers Stabilized GF (71°C): 6 months in glass.

CAM/ICAM. M8. M21. M22. M21. AN/KAS-1. IEDK. AN/KAS-1. M272. M90. M8. M21. MM1. IPDS. MM1. M9. MM1. Nerve. MM1 Protective mask Not required under field conditions SA MM1 Protective mask Not required under field conditions NOTES: 1 Hydrochloric acid. M18A3 M256A1. M21. CAM/ICAM. IPDS. MM1 Protection Required Protective mask Decontamination Not required in field except in very cold climates Not required in field except in very cold climates SDK. M90. AN/KAS-1. M18A2. M21. M272. M8. CAPDS. M9. STB GD Rapid MOPP4 SDK. STB VX Rapid MOPP4 SDK. MM1. M272. M8. M8A1. HCl (aq) 2 M = molarity. M18A2. M90. CAPDS. IPDS. IEDK. AN/KAS-1. STB. M272. CAPDS. M18A3. M18A2. IEDK. MM1 Protective mask CK Rapid 1-24 hours (dependent on concentration and exposure duration) M256A1. CAPDS. AN/KAS-1. M272. household bleach SDK. IPDS. STB Use Delayed-action casualty agent Quick-acting casualty agent Quick-acting casualty agent Quick-acting casualty agent Quick-acting casualty agent Quick-acting casualty agent Quick-acting casualty agent Quick-acting casualty agent Quick-acting casualty agent Quick-acting casualty agent Delayed-action casualty agent CG DP MM1 Protective mask GA Rapid M256A1. M272. STB. IEDK. IPDS. M8A1. M22. IPDS. M90. and Blood Agents (Continued) Agents Rate of Action Immediate to 3 hours depending on concentration Immediate to 3 hours Means of Detection M18A2. M18A2. CAM/ICAM. M8A1. M90. M9. M8A1. IEDK. CAM/ICAM. CAPDS. molarity is a term for concentration and means moles per liter. Physical Properties of Choking. STB GF Rapid MOPP4 SDK. household bleach Not required under field conditions Vx Rapid MOPP4 AC Rapid M256A1. M18A2. M18A3 M256A1. M18A3. M272. M22. M8. M22. M9. MM1. M22. M8A1. . HTH. HTH. M8A1. MM1. M18A3 M256A1. CAM/ICAM MOPP4 GB Rapid MOPP4 SDK. M9. M9. M18A3 M256A1. IEDK. M18A3 M8. M18A2. CAM/ICAM. M18A2. M18A2.Choking Agents Nerve Agents Blood Agents G-6 Table G-1.

colorless when pure Colorless liquid when pure Oily dark liquid.5 (FP) 6.Table G-2. biting. HD Nitrogen mustard.42 412 167.106 (25°C) 170. 0.7 to -1.0021 (00C) 2. 1.39 (average) 222. C2H5AsCl2.110 (0°C) 1.416 (25°C).3 (50°C) 113. C5H11Cl2N. deliquescent solid when pure White crystalline solid 129. 1. C6H12Cl3N.07 State at 20°C Pale yellow to dark brown oily liquid.8 (FP) 1.372 (0°C). Symbol Distilled mustard.6 (25°C).4 Colorless to yellow liquid Colorless liquid None 233 1.063 (0°C) 24. crystalline. .5 Vapor Pressure (torr) 0. Solid Density: 1.1 34.6383 (20°C) 7.32 None Constant 196 1. 1.022 (250C).74 x 10-13 (0°C) G-7 . C12H23NO3 337. 1. 4. C4H8Cl2S. HN-3 Mustard-T Mixture.08 Faint. 0. 0.51 Crystal: 1.86 Colorless liquid Extremely irritating.2685 (25°C). 63% L.9 0. and irritating 156 < -65 (MP) 6. 1.363 (25°C). ED Methyldichloroarsine CH3AsCl2.2596 (0°C) 1.29 (21. HT Lewisite.1 Blister Agents 188. less pronounced than mustard Geranium-like. 39 (MP) 3.118 (25°C). 1.2 (MP) 5. colorless when pure Pale yellow to brown liquid Brown liquid. none if pure Garlic-like. C6H13Cl2N.244 (25°C).7 174.8793 (25°C).5 7. 1. colorless when pure Liquid Odor Garlic-like or horseradish Boiling Point (°C) 218 FP/MP (°C) 14.593 (20°C).53 Geranium-like. 2.96 (average) 207.2352 (25°C).33 11.9 Incapacitating Agents BZ.645 (25°C). L Mustard-lewisite. colorless when pure Dark oily liquid. 60% HD. MD Phosgene Oxime CHCl2NO.0271 (0°C) 0.333 (10°C) 1.011 (25°C) 0.50C) 186. Physical Properties of Blister Agents and Incapacitating Agents Agents Chemical Agent.93 200 Pure: -25.839 (20°C).8 (FP) 1.1425 (0°C) 1.0332 (0°C) 0.00092 (0°C) 0. fishy or soapy 192 -34.6 1.45 (FP) Liquid Density (g/mL) 1.677 (0°C) 1.74 (MP) 7. 40% T. 0.0570 (°C) 0.4 204. 37% HD. none when pure Unpleasant and irritating.3 (MP) 6. HL Phenyldichloroarsine C6H5AsCl2.5 (MP) Solid Density: (g/cm3) Bulk: 0.93 Colorless.742 (14°C) 7.5 -44. C2H2AsCl3.0493 (0°C) 0.05 Fishy or soapy 177 -70 (FP) 5.9210 (0°C) 1.4 (FP) Munitions: -42 (FP) -22.4 x 10-10 (25°C).89 Fruity.875 (0°C) Data not available 5. none if pure Garlic-like (HD) 257 -3. Formula.6 -54. HN-2 Nitrogen mustard.077 (25°C) 156. PD Ethyldichloroarsine.0 160.086 (25°C). low concentrations resembles new-mown hay None 132. HN-1 Nitrogen mustard.263 (20°C) Vapor Density (Air=1) 5. CX Molecular Weight 159.

00770 (0°C) Data Not Available in Samuel. et al.18 Data not available 66.0°C).5 (25. 522 (0°C) 120 (25°C). et al. reference Surface Tension (dynes/cm) 42. et al. reference Data Not Available in Samuel.00600 (0°C) Data Not Available in Samuel. 13. reference 0.00597 (25.00000260 (25°) 0. et al. et al. 0. et al. reference 40. et al. et al.9 (25°C). reference 0.746 (0°C) Data Not Available in Samuel. 0.073 (25.0°C).053 (25. 44. reference 0. reference Data Not Available in Samuel. 12.5 (20°C).521 (0°C) Data Not Available in Samuel.0°C). reference Data Not Available in Samuel. et al. et al. 331 (0°C) 3. 7.0 (25°C). reference Data Not Available in Samuel.0°C). et al. reference Viscosity of Vapor (cP) 0. 23 (0°C) 21. reference Data Not Available in Samuel. 11 (0°C) 783 (25°C) 13. reference Data Not Available in Samuel. et al. reference Data Not Available in Samuel.2 Data Not Available in Samuel. 10.0°C). et al.8 (25°C).5 (25°C) 17.640 (25°C). 12.1 (0°C) 15. 3.9 (25.000 (50°C) 10.8 (25°C). flashing on static detonation Data not available Data not available 109 to 115°C 3. reference Data Not Available in Samuel.8 (0°C) 15. reference Data Not Available in Samuel.0 (0°C) Data not available Data not available.860 (25C). 539 (0°C) 264 (25°C). et al.1 (25. et al. 19.9 (0°C) 12. 0. reference Data Not Available in Samuel. 0. 16.2 (50°C) Data not available Data not available 0. 44.800 (20°C). reference Data Not Available in Samuel. reference Flash Point 105°C 2. et al. reference 41. et al. 330 (0°C) 3.490 (25°C).Blister Agents Incapacitating Agents G-8 Agents HD HN-1 HN-2 HN-3 HT L HL PD ED MD CX BZ Table G-2. et al.2 (0°C) Data Not Available in Samuel. See HD Data not available 9.2 (0°C) 11. reference Data Not Available in Samuel. reference Data Not Available in Samuel. et al. Physical Properties of Blister Agents and Incapacitating Agents (Continued) Volatility 3 (mg/m ) 906 (25°C) Latent Heat of Vaporization (kcal/mol) 15.0°C). reference Data Not Available in Samuel.500 (0°C) 137. et al. et al. 45. et al.0°C).1 Nonflammable Data not available.9 (0°C) Data Not Available in Samuel. reference Munitions: 220°C Pure: 246°C . et al.5 (°C) 12. reference 2. et al. reference Data Not Available in Samuel.00597 (25.900 (20°C) 15.0 (25°C) Viscosity (cP) 3. et al.0000000090 (0°C) 21. reference Data Not Available in Samuel.177 (0°C) Data Not Available in Samuel.00538 (0°C) Data Not Available in Samuel. reference Data Not Available in Samuel.0°C).1 (0°C) Data Not Available in Samuel. et al. et al.230 (25°C).00853 (25.0°C).951 (25.

kerosene.5 hrs (100°C. miscible with common organic solvents In water. 5% within 6 days (ambient temperature).8 min (25°C. and olive oil Immediately with water.4 hrs (50°C.7 hrs (25°C. oils and CW agents Probably soluble in most organic solvents. soluble in common organic solvents (ambient temperatures) Very soluble in both water and common organic solvents Rate of Hydrolysis t1/2 = 5 min (25°C). slightly soluble in water Immediately with water. acetone. t1/2 = 12 min (37°C. see HD and L PD Stable to normal boiling point Very rapid ED Stable to boiling point Very rapid HCl(aq). t1/2 = 3-4 wks (25°C. acetone. HCl. pH 12). slow except where alkali is present. most organic solvents and CW agents In water. soluble in most organic solvents Immediately with water to form Lewisite oxide. on or under water only if dissolved. methylarsenic oxide CO2. prolonged heating at ≈170°C (purity and temperature dependent) In water. alcohol.7% at 149°C and >99% at 426°C Below boiling point. miscible with common organic solvents In water. phenylarsine oxide (toxic) HN-1 For HN-1٠HCl: 12. petroleum. soluble in common organic solvents. t1/2 = 1. 4g HN-1/L (ambient temperature). soluble in dilute acids and common organic solvents such as alcohol and chloroform. sulfonium CVAA. soluble in ethyl chloride. pH 0). pH 8. insoluble in aqueous alkali t1/2 = 6.18 g/mL. and cyclohexane Immediately with water. pH 7 and moist air). ethylarsine oxide (toxic) HCl. freely soluble in fats and oils. remains stable when explosively disseminated 165 to 180°C HN-2 t1/2 = 4 min (25°C). slightly soluble in water. Physical Properties of Blister Agents and Incapacitating Agents (Continued) Agents HD Decomposition Temperature 180°C Solubility In distilled water.08 g HN-3/L (ambient temperature). polymerizes with heat (can cause explosion) >150°C. thiodiglycol. hydroxylmine MD Stable to boiling point Very rapid.5). 13 g HN-2/L (ambient temperature. acids slow down hydrolysis. pH 13). miscible with common organic solvents Slightly soluble in water. t1/2 = 1.99% at 493°C > 100°C HL t1/2 = 5 min (25°C). HCl(aq) See HD and L HCl(aq). t1/2 = 9. and other products HCl(aq). basic solutions react violently Incapacitating Agents BZ Stable to melting point. not complete after several days unless alkali is present By prolonged boiling with water or treatment with caustic alkalis Rapid HN-3 HT Blister Agents L 5% at 149°C > 99.8). gasoline. which dissolves very slowly. kerosene. benzene. kerosene. 1. thiodiglycol. EtDEA. t1/2 = 60 min (25°C) (salt water). lewisite oxide. ether. < 2 min (25°C) in dilute solution CX < 129°C Slow in water. 0. ether. dimerizes fairly rapidly in water Very slow. benzene. and other products HCl and other products HCl. TEA. 3-Quinuclidinol and benzylic acid G-9 . t1/2 = 1.3 min (25°C) in aqueous solution Hydrolysis Products HCl. miscible with alcohol.Table G-2. sulfonium ion HCl(aq). 0.92 g HD/100 g (22°C). pH 9. aqueous solution).

Causes pain. Physical Properties of Blister Agents and Incapacitating Agents (Continued) Stability In Storage Stable in steel for over 50 years (slight degradation) Action on Metals Very little when pure. skin absorption requires higher concentrations Eyes very susceptible to low concentrations. if dry Pressure develops in steel Fairly stable in steel and glass. especially upon heating Slight pitting of aluminum and stainless steel occurs after 2 yrs (71°C) Fairly potent vesicant and lacrimator Primarily a lung irritant Toxic lung injurant and respiratory irritant Can cause pulmonary edema Stable in steel for 15 weeks (60°C). immediate burning sensation on skin Equal to L in vesication action. eye and skin irritant Causes pain. both H and L are irritating to the eyes. skin absorption requires higher concentrations Extremely irritating to the eyes and produces copious tearing. Satisfactory with steel for 1 yr (ambient temperature). stable in glass @ 65°C Data not available No serious affects on mild steel and cast iron None on steel when pure. corrosive penetration on steel is 1x10-5 to 5x10-5 in/month (65°C). corrodes steel at a rate of 1x10-5 to 5x10-5 in/month (65°C) Very little when pure. noncorrosive toward iron (<50°C) when ED is dry. slight at ambient temperatures but increases at temperatures > 50°C None on steel and brass If dry.0001 in/month (65°C) Corrosion on steel is 1x10-5 to 5x10-5 in/month (65°C) Skin and Eye Toxicity Eyes very susceptible to low concentrations. conjunctivitis and inflammation of the cornea of the eye. skin absorption requires higher concentrations Eyes very susceptible to low concentrations. irritation and severe tissue damage on skin. crude pitting within 15 weeks (60°C) Metals especially iron causes rapid decomposition of CX.00007 in/month (65°C) None if dry. no attack on iron. Canadian HT corrodes steel at a rate of 0. indefinitely (-20°C). skin absorption requires higher concentrations Eyes very susceptible to low concentrations. attacks rubber. skin absorption requires higher concentrations Eyes very susceptible to low concentrations. Fairly potent vesicant Inhalation Toxicity Most toxic route of exposure Most toxic route of exposure Most toxic route of exposure Most toxic route of exposure Most toxic route of exposure Most toxic route of exposure Most toxic route of exposure Toxic lung irritant Polymerizes in steel. alkalis decompose L at ambient temperatures Stable in lacquered steel for 3 months (65°C). 1 year (ambient temperatures) Pure unstabilized CX decomposes at ambient temperatures. extremely corrosive towards aluminum and aluminum alloys If dry. unstable in presence of impurities such as metals Stable in aluminum and stainless steel for at least 2 years (71°C) Blistering action less than that of HD and L. attacks brass (50°C) and is destructive to rubber and plastics. little or none Relatively stable in steel. iron chloride may cause explosive decomposition. >1 yr (ambient temperatures). 6 months (50°C). uncoated: less stable (>50°C). for munitions grade. the corrosion rate on steel is 0.Blister Agents Incapacitating Agents G-10 Agents HD HN-1 HN-2 Unstable HN-3 HT L HL PD ED Stable MD CX BZ Table G-2. decomposes considerably upon detonation. Can cause blurred vision and dilation of pupils Primary route of exposure .

M256A1. MM1 M9. MM1 MOPP4 HTH. M18A3. household bleach Delayed-action casualty agent HN-3 Delayed . MM1 MOPP4 HTH. delayed blistering CAM/ICAM.12 hrs or longer M8. household bleach Quick-acting casualty agent HL Prompt stinging. household bleach Delayed-action casualty agent PD M18A2. household bleach Delayed-action casualty agent HN-2 Delayed . CAM/ICAM. M9.Table G-2. household bleach Quick-acting casualty agent Incapacitating Agents BZ Delayed action – 1 to 4 hrs. household bleach Delayed-action casualty agent HT No data available Blister Agents M8. MM1 MOPP4 Household bleach Delayed-action casualty agent MD Immediate irritation. M18A3. blistering delayed about 12 hrs Immediate eye effect. HTH. Physical Properties of Blister Agents and Incapacitating Agents (Continued) Agents HD Rate of Action Delayed – hrs to days Means of Detection M8. M22. skin effects delayed @ 1 hr Immediate irritation. delayed blistering M18A1. M9. M18A3. M22. M21. M9. CAM/ICAM. M18A2. M256A1. M9. MM1 M8. M18A3. M256A1. MM1 MOPP4 SDK or large amounts of water. MM1 MOPP4 Household bleach Delayed-action casualty agent ED M18A2. SDK if soap and water are not available Delayed-action incapacitating agent G-11 . M18A2. IEDK. M256A1. CAM/ICAM. MM1 Protection MOPP4 Decontamination SDK. CAM/ICAM. M21. M256A1. MM1 MOPP4 HTH. M18A3. HTH. M18A2. M90. CAM/ICAM. M18A3.12 hrs or longer M8. M18A3. MM1 MOPP4 Household bleach Delayed-action casualty agent CX Almost instantaneous M256A1. household bleach Delayed-action casualty agent L Rapid MOPP4 STB. M272. M256A1. depending on exposure MM1 MOPP4 Soap and water. MM1 MOPP4 HTH. Use Delayed-action casualty agent HN-1 Delayed – 12 hrs or longer MOPP4 HTH. M256A1. M272. M9. household bleach.

24-0. DC Chlorine.8 70.5 195.672 (0°C) 1.4 . C10H5ClN2. DM Diphenylchloroarsine C12H10AsCl DA Diphenylcyanoarsine C13H10AsN.5 277. C13H9NO.3338 (35°C) 8.6 State at 20°C White crystalline solid Odor Pepper-like Boiling Point (°C) 310 to 315 FP/MP (°C) 95 to 96 (MP) Liquid Density (g/mL) Solid Density Bulk: 0. CR Capsaicin C18H27N03 OC Adamsite.58 Light yellow to green crystals Colorless crystalline solid when pure Colorless crystalline solid 410 195 (MP).f)-1. Cl2 Molecular Weight 188.22 Pale yellow crystalline solid Pepper-like Data not available 340.15 Garlic and bitter almonds Disagreeable and suffocating 341 1.04 Data not available Vapor Density (Air=1) 6.6 (FP) Liquefied: 1. Symbol O-Chlorobenylidene malononitrile.393 (25°C).2 (FP) 9. 1.7 305.4 73 (MP) 6. 1.7 -101.3. irritating None.1 255. CS Dibenz-(b. Crystal: 1.26.91 Greenish-yellow diatomic gas -34. Formula. irritating 65 (FP) Data not available 10. Physical Properties of RCAs and Respiratory Irritants Agents Chemical Agent. 39 to 44 (MP) 31.648 (20°C). C12H9AsClN.4-oxazepine.6 264.Riot Control Agents Respiratory Irritants G-12 Table G-3.468 (0°C) 2.3875 (50°C) 9.42 Colorless Pungent. Solid Density 1.59 None 383 37.

2 (410°C) Nonflammable Respiratory Irritants DA 0.000 (0°C) 4.1 350°C DC 0. 4. Physical Properties of RCAs and Respiratory Irritants (Continued) Agents Riot Control Agents CS Vapor Pressure (torr) 0.Table G-3.71 (25°C) Volatility 3 (mg/m ) Latent Heat of Vaporization (kcal/mol) Data not available Flash Point Data not available CR Data not available Data not available Data not available Data not available OC 0.000 (25°C).86 (25°C). 11.4 Depends on delivery system DM Negligible @ ambient temperatures Negligible @ ambient temperatures 14.0179 (50°C) 236 (50°C) 15.00034 (20°C) 0.750 (25°C).900.56 (35°C) 17.80 (0°C) Nonflammable G-13 .00072 (35°C) 9. 2.1 Low Cl2 5.00000015 (65°C) 0.730 (0°C) 21.0022 (65°C) 33.400.

ethylene chloride. 0.slowly when covered with water. ether. 0. Physical Properties of RCAs and Respiratory Irritants (Continued) Agents CS Decomposition Temperature Data not available Solubility Insoluble in water. 0. and dichloroethylene In water. ethanol. soluble in chloroform and other organic solvents In water. soluble in alcohol. aromatic solvents.090 g/L @ 37°C.Riot Control Agents Respiratory Irritants G-14 Table G-3. 0. ketones and aqueous alkali. carbon tetrachloride.02% per min @ 200°C.15% per min @ 250°C 300 to 350 Solid DM . carbon tetrachloride. acidic solutions prevent hydrolysis Slow in bulk but rapid when finely divided DA DC > 240 Very slow HCN and Diphenylarsenious oxide Cl2 > 600°C Slow HCl and HOCl . tetrachoethane In water. slightly soluble in benzene exylene. ether. 0. moderate in alcohol. soluble in acetone. acetone.63 g/100 g water @25°C. HCl. 0. carbon disulfide. benzene. solubility in carbon tetrachloride is 3. chloroform. conc. HCl (aq) Diphenylarsenious oxide and HCl OC DM Slight at 195°C. 0. finely divided – rapidly. ethylacetate and benzene Sparingly soluble in water in water.5% @ ambient temperatures Rate of Hydrolysis Data not available Hydrolysis Products Data not available CR Data not available > 150 Not hydrolyzed in aqueous solutions Data not available Data not available Alkaline hydrolysis yields vanilylamine and isomeric decenoic acid Diphenylaminearsenious oxide.021 g/L @ 37°C. and good in acetone.044 g/L @ 37°C.078 g/L @ 37°C. alcohols. chloroform. methylene dichloride. hydrocarbons. In water. chloroform.

incompatible with strong oxiders. munitions grade. corrodes iron.Table G-3. primary skin irritant Irritant. Containers may explode when heater. bronze. vesication. and brass None when dry Causes eye irritation and burning DA Irritant DC None on metals Irritant Irritant Cl2 Stable when dry None if dry. stable for at least 1 year @ room temperature and in aluminum and stainless steel 2 yrs @ 71°C. may burn but does not ignite readily. Physical Properties of RCAs and Respiratory Irritants (Continued) Agents CS Stability In Storage Combustible material. Stable in organic solutions Action on Metals Contact with metals may evolve flammable hydrogen gas. vigorous action with metals if moist Irritant Can cause pulmonary edema G-15 . or contact sensitization Powerful irritant and lacrimator Inhalation Toxicity Causes sensation of choking Riot Control Agents CR Causes almost no effects in the lower airways and lungs Causes bronchoconstriction and edema Primary action on upper respiratory tract Irritant OC Data not available Data not available DM Respiratory Irritants f pure. however. CR does not induce inflammatory cell infiltration. Data not available Skin and Eye Toxicity Burning and irritation to eyes. stable for 6 months Stable when pure. stable in steel shells for almost 4 months at 60°C and for 1 year at room temperature Stable at all ordinary temperatures After 3 months causes extensive corrosion on aluminum and stainless steel @ 71°C.

and gloves Protective mask and clothing secured at neck. Physical Properties of RCAs and Respiratory Irritants (Continued) Agents CS Rate of Action Instantaneous Protection Required Protective mask and dry field clothing. do not use any form of bleach Move to fresh air. do not use any form of bleach Use Training and RCA CR Instantaneous RCA OC Almost immediate Incapacitating violent or threatening subjects. do not use any form of bleach Move to fresh air. and ankles Decontamination Move to fresh air. SF stability and support operations Former RCA and mask breaker DM Rapid Protective mask Move to fresh air DA Rapid Protective mask Move to fresh air Previously used as mask breaker DC Rapid Protective mask Move to fresh air Previously used as mask breaker Cl2 Delayed (pulmonary edema) Protective mask Move to fresh air Not authorized for military use . wrists.Riot Control Agents Respiratory Irritants G-16 Table G-3. and ankles Protective mask and field clothing secured at neck. personnel handling/loading bulk CS should wear protective clothing. wrists. masks.

6 – 1 S 8S 2S 1 (1) 1 (1) < 1 (1) 1P (10) Ocular 3 (mg-min/m ) Severe (ECt50) 75 (2-360) 75P (2) 75P (2) 75P (2-360) 75P (2-360) 75P (2-360) 75P (2-360) Mild (ECt50) 25 (2-360) 25P (2) 25P (2) 25P (2-360) 25P (2-360) 25P (2-360) 25P (2-360) Lethal (LCt50) Moderate Hot 15. G-17 .000 (30-360) 2.500P (2) 1.4 (2) 0.000P (30-360) 4.000 (30-360) 150 (30-360) 10.000P (30-360) 1. S = Seconds.000 200 200 2 Inhalation/Ocular 3 (mg-min/m ) Lethal (LCt50) 1.200 (30-360) 300 (30-360) 300 (30-360) 10 (30-360) 50 (30) 50P (30) 50P (30-360) 50P (30-360) 50P (30-360) 50P (30-360) 50P (30-360) 1. Exposure duration given in minutes except when specified.500P (30-360) 6.000P (2-360) 1.000 (30-360) 12.000P (30-360) N/R NR - Percutaneous Vapor 3 (mg-min/m ) Severe (ECt50) Moderate Hot 12.000P (30-360) 10.000 (30-360) 3.500P (10-60) 70 (2) 35 (2) 35 (2) 35 (2) 15 (2-360) 2860P (2) NR 7.000P (2-360) 2600P (2-360) NR NR 3200P (10) Severe (ECt50) 50 (2) 25 (2) 25 (2) 25 (2) 10 (2-360) NR NR 5-10 (1) 25P (1) 16 (1-2) 3P (1) Mild (ECt50) 0.000 (30-360) 3. Toxicity Estimates for CW Agents ROE Endpoints Liquid (mg/70 kg man) Lethal (LD50) 1.000P (2) 1.000P (30-360) 5.1 (2-360) Inhalation 3 (mg/m ) Odor Detection (EC50) 6S 4S 34 S 12 S 0.000P (30-360) 5.000P (30-360) - Nerve Agents Blood Agent Blister Agents Incapacitating Agents AC CK SA HD HN-1 HN-2 HN-3 HT L HL PD ED MD CX BZ - - NR 100P (<5) - NR - - - - - - - - NOTES: P = Provisional.000P (30) 5. NR = None Recommended.000P (30-360) 5.000P (2-360) 1.000P (30) 10.2 (2) 0.000P (30-360) 10.500 (2-60) 1.000P (30-360) 5.000P (30-360) 1. The existing estimates are not supported by the available data Toxicity estimates are followed by exposure duration in parentheses.000P (30-360) 2.000 (30-360) 10.000P (30-360) 1.500 .500P (30-360) 75P (30-360) 5.Table G-4.000P (30) 10.000P (30-360) 600P (30-360) 150P (30-360) 150P (30-360) 5 (30-360) 25 (30) 25P (30) 25P (30-360) 25P (30-360) 25P (30-360) 25P (30-360) 25P (30-360) - Choking Agents CG DP GA GB GD GF VX Vx 7.000 (30-360) 25 (30-360) 500 (30-360) 500P (30) 500P (30-360) 500P (30-360) 500P (30-360) 500P (30-360) 500P (30-360) 200-500P (30-50) 6.000 (2) 1.500 1.000 (30-360) 2.000 (30-360) 1.500P (30-360) 1.000 (30-360) 8.000P (30-360) 12P (30-360) 200 (30-360) 200P (30) 200P (30-360) 200P (30-360) 200P (30-360) 200P (30-360) 200P (30-360) Threshold (ECt50) Moderate Hot 2.4 (2) 0.2 (2) 0.000 .000P (2-360) 1.10.5.700 350 350 5 NR 1400 1400P 1400P 1400P 1400P 1400P 1400P NR 600 600P 600P 600P 600P 600P 600P NR Severe (ED50) 900 1.000P (2) 1.000P (30) 5.

(JP 102) Note: In general.000-61.3 Nonpersistent Nonpersistent Nonpersistent Nonpersistent Nonpersistent Nonpersistent Persistent Persistent Nonpersistent Nonpersistent Nonpersistent Persistent Persistent Persistent Persistent Persistent Persistent Persistent Persistent Persistent Persistent Nonpersistent Nonpersistent NOTES 1 Persistent Agent: A chemical agent that.002 – 0. CW Agents CG DP GA GB GD GF VX Vx AC CK SA HD HN-1 HN-2 HN-3 HT L HL PD ED MD CX BZ G-18 .15 (1 minute) 22 – 150P (1 minutes) 12 (2 minutes) Threshold (ECt50) 0.2. Toxicity estimates are followed by exposure duration in parenthesis.Table G-5. Persistency of Selected CW Agents Persistency1. as temperature increases.000P (2-240 minutes) None Recommended None Recommended None Recommended Inhalation/Ocular Severe (ECt50) None Recommended None Recommended NOTES Intolerable (ECt50) 7 (1 minute) 0.004 (1 minute) <1 (1 minute) 10 (seconds) Riot Control Agents CS CR OC DM DA DC Cl2 P = Provisional The existing estimates are not supported by the available data. Toxicity Estimates (Exposure Duration) for Military Chemical Compounds ROE Lethal (LCt50) 52. remains able to cause casualties for more than 24 hours to several days or weeks. Respiratory Irritants Table G-6. when released. persistency decreases.000P (5-90 minutes) None Recommended 11. (JP 1-02) 2 Nonpersistent Agent: A chemical agent that when released dissipates and/or loses its ability to cause casualties after 10 to 15 minutes.

1 -30 -10 10 30 50 o 70 90 110 130 Temperature ( C) Figure G-1.Choking Agents 10000 1000 CG Water DP Pressure (torr) 100 10 1 0. Vapor Pressure of Choking Agents1 G-19 .

Vapor Pressure of Nerve Agents1 .01 0.Pressure (torr) G-20 Nerve Agents 1000 100 10 Water GB GD GF GA EA 1699 VX 1 0.001 -40 -20 0 20 40 60 80 100 120 o 140 160 180 200 220 240 Temperature ( C) Figure G-2.1 0.

Vapor Pressure of Blood Agents1 G-21 .Blood Agents 1000 SA CK AC Water 100 Pressure (torr) 10 1 -120 -100 -80 -60 -40 -20 0 20 40 60 80 100 120 Temperature (oC) Figure G-3.

01 -20 0 20 40 60 80 100 120 140 160 180 200 Temperature (oC) Figure G-4. Vapor Pressure of Blister Agents1 .1 HT HL 0.Pressure (torr) G-22 Blister Agents 1000 100 Water MD CX L HD 10 ED HN-1 1 HN-2 PD HN-3 0.

1 BZ 0.Incapacitating Agent (BZ) 1000 100 Water 10 Pressure (torr) 1 0.001 0 20 40 60 80 100 120 140 160 180 Temperature (oC) Figure G-5.01 0. Vapor Pressure of Incapacitating Agent (BZ)1 G-23 .

Pressure (torr) G-24 Riot Control Agent (Capsaicin) 1000 100 Water 10 1 0. Vapor Pressure of Riot Control Agent (Capsaicin)1 .1 Capsaicin 0.01 0.001 -20 0 20 40 60 80 100 120 140 160 180 200 Temperature (oC) Figure G-6.

Respiratory Irritants 10000 Chlorine 1000 Water Pressure (torr) 100 DA 10 DC DM 1 0.1 -50 -25 0 25 50 75 100 125 150 175 200 225 250 275 Temperature (oC) Figure G-7. Vapor Pressure of Respiratory Irritants1 G-25 .

NOTES 1Patrice L. September 2003. G-26 . Abercombie. Physical Property Data Review of Selected Chemical Agents and Related Compounds.

0 3. (1) Table H-3 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to GA. CG Profile Estimates (Lethal Dose. GA Profile. Nerve Agents a. Choking Agents a.6 2. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 12 LCt50 (mg-min/m ) 70 120 170 220 270 345 395 3 MV Profile (2-Minute Exposure) Concentration (mg/m ) 35 12 6. DP Profile. Table H-2. Background This appendix gives the Ct profile estimates and the MV profile estimates (when available) for selected CW agents. Table H-1. Table H-2 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to DP. GA Profile Estimates (Lethal Dose.5 DOC: Moderate H-1 . DP Profile Estimates (Lethal Dose.3 1. 2. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 Probit Slope: Unknown LCt50 (mg-min/m ) 1500 1500 1500 1500 3 MV Profile (2-Minute Exposure) Concentration (mg/m ) 750 150 50 25 DOC: Low 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 2250 1500 750 450 3 Selected Toxicology Information TLE: 1 (Assumed) 3.1 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 100 70 35 20 3 Selected Toxicology Information TLE: 1. Table H-3. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 Probit Slope: Unknown LCt50 (mg-min/m ) 1500 1500 1500 1500 TLE: 1 3 MV Profile (2-Minute Exposure) Concentration (mg/m ) 750 150 50 25 3 MV (L) 10 15 30 50 DOC: Moderate LCt50 (mg-min/m ) 2250 1500 750 450 3 Selected Toxicology Information b.4 1.Appendix H TOXICITY PROFILE ESTIMATES 1. CG Profile. Table H-1 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to CG.

000 12.000 12.8 3 MV (L) 10 15 30 50 ECt50 (mg-min/m ) 75 50 25 15 3 Selected Toxicology Information TLE: 1. GA Profile Estimates (Severe Effects.000 12.6 1.000 12. Personnel are masked with bare skin.6 1.000 15.000 15. Table H-4. Table H-5.000 15. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 10 ECt50 (mg-min/m ) 50 85 120 155 200 250 280 3 MV Profile (2-Minute Exposure) Concentration (mg/m ) 25 8.000 12.000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 7500 1500 500 250 125 60 40 DOC: Low Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 Hot Temperatures LCt50 3 (mg-min/m ) 7500 7500 7500 7500 7500 7500 7500 TLE: 1 (Assumed) Concentration 3 (mg/m ) 3750 750 250 125 60 30 20 DOC: Low Selected Toxicology Information (3) Table H-5 provides toxicity estimates for severe effects from an inhalation/ocular vapor exposure to GA. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 ECt50 3 (mg-min/m ) 12.1 2. Personnel are masked with bare skin.(2) Table H-4 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to GA. Table H-6.5 DOC: Moderate (4) Table H-6 provides toxicity estimates for severe effects from a percutaneous vapor exposure to GA.000 15.000 12. GA Profile Estimates (Lethal Dose.000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 6000 1200 400 200 100 50 35 DOC: Low Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 Hot Temperatures ECt50 3 (mg-min/m ) 6000 6000 6000 6000 6000 6000 6000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 3000 600 200 100 50 25 15 DOC: Low Selected Toxicology Information H-2 . GA Profile Estimates (Severe Effects.000 15.000 15. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 LCt50 3 (mg-min/m ) 15.5 4.0 0.

07 0.9 1.007 0. Table H-7. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 ECt50 3 (mg-min/m ) 2000 2000 2000 2000 2000 2000 2000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 1000 200 65 30 15 10 5 DOC: Moderate Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 Hot Temperatures ECt50 3 (mg-min/m ) 1000 1000 1000 1000 1000 1000 1000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 500 100 30 15 10 5 2. Mild effects include miosis and rhinorrhea. Inhalation/Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 10 ECt50 (mg-min/m ) 0. Personnel are masked with bare skin.005 DOC: Low 3 Selected Toxicology Information TLE: 1.4 0. GA Profile Estimates (Mild Effects.1 1.03 0.5 DOC: Moderate Selected Toxicology Information (6) Table H-8 provides toxicity estimates for mild effects from an inhalation/ocular vapor exposure to GA. Concentration-Time (mg-min/m3) Ct (mg-min/m3) 100 Upper Band: LCt16 and LCt84 Region 10 Line: ECt16 (Severe) [roughly LCt01] Lower Band: ECt16 and ECt84 Region for miosis (pupil shrinkage) 1 0.5 (7) Figure H-1 is a graphical representation of GA vapor Ct profile for dosage from an inhalation/ocular exposure.1 1 10 100 Extrapolation Beyond 10 minutes: Based on experimental data out to 120 minutes.01 0. GA Vapor: Dosage versus Exposure Duration H-3 .0 3 Concentration (mg/m ) 0. Time (minutes) Time (minutes) Figure H-1.02 0.4 1.6 0.7 2. GA Profile Estimates (Threshold Effects.(5) Table H-7 provides toxicity estimates for threshold effects from a percutaneous vapor exposure to GA.16 0. Table H-8.

Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 12 LCt50 (mg-min/m ) 35 60 86 110 140 175 200 3 MV Profile (2-Minute Exposure) Concentration (mg/m ) 17. GB Profile.5 6.1 0.5 DOC: Moderate H-4 . GB Profile Estimates (Lethal Dose. (1) Table H-9 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to GB. Vapor Concentration (mg/m3) 10 1 0.0 3.001 1 Extrapolation Beyond 10 minutes: Based on experimental data out to 120 minutes. GA Vapor: Concentration versus Exposure Duration b.8 1.6 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 50 35 17 10 3 Selected Toxicology Information TLE: 1. 10 100 Time (minutes) Figure H-2.(8) Figure H-2 is a graphical representation of GA vapor Ct profile for concentration from an inhalation/ocular exposure.1 0.7 0. Table H-9.0 1.01 Upper Band: LCt16 and LCt84 Region Line: ECt16 (Severe) [roughly LCt01] Lower Band: ECt16 and ECt84 Region for miosis (pupil shrinkage) 0.

Table H-11. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 12 ECt50 (mg-min/m ) 25 45 60 80 100 125 140 3 MV Profile (2-Minute Exposure) Concentration (mg/m ) 12. GB Profile Estimates (Severe Effects. Personnel are masked with bare skin.(2) Table H-10 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to GB.000 12.3 2.1 1. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 ECt50 3 (mg-min/m ) 8000 8000 8000 8000 8000 8000 8000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 4000 800 250 130 65 30 20 DOC: Low Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 Hot Temperatures ECt50 3 (mg-min/m ) 4000 4000 4000 4000 4000 4000 4000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 2000 400 125 65 30 15 10 DOC: Low Selected Toxicology Information H-5 .000 12.000 12.4 3 MV (L) 10 15 30 50 ECt50 (mg-min/m ) 37 25 12 7. Table H-10.5 3 Selected Toxicology Information TLE: 1.5 DOC: Moderate (4) Table H-12 provides toxicity estimates for severe effects from a percutaneous vapor exposure to GB.8 0. GB Profile Estimates (Lethal Dose. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 LCt50 3 (mg-min/m ) 12. Table H-12.000 12.3 0.000 12.5 4.5 0.000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 6000 1200 400 200 100 50 30 DOC: Low Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 Hot Temperatures LCt50 3 (mg-min/m ) 6000 6000 6000 6000 6000 6000 6000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 3000 600 200 100 50 25 15 DOC: Low Selected Toxicology Information (3) Table H-11 provides toxicity estimates for severe effects from an inhalation/ocular vapor exposure to GB. GB Profile Estimates (Severe Effects.000 12. and personnel are masked with bare skin.

0 3 Concentration (mg/m ) 0. Personnel are masked with bare skin.5 (7) Figure H-3 is a graphical representation of GB vapor Ct profile for dosage from an inhalation/ocular exposure.5 1.4 1. GB Profile Estimates (Threshold Effects.007 0.03 0. Time (minutes) Figure H-3.7 2.5 DOC: Low Selected Toxicology Information (6) Table H-14 provides toxicity estimates for mild effects from an inhalation/ocular vapor exposure to GB.1 1 10 100 Extrapolation Beyond 10 minutes: Based on experimental data out to 360 minutes. Table H-13. Concentration-Time (mg-min/m3) 100 Ct (mg-min/m ) 3 10 Upper Band: LCt16 and LCt84 Region Line: ECt16 (Severe)[roughly LCt01} Lower Band: ECt16 and ECt84 Region for miosis (pupil shrinkage) 1 0.01 0. GB Vapor: Dosage versus Exposure Duration H-6 .005 DOC: Moderate 3 Selected Toxicology Information TLE: 1. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 ECt50 3 (mg-min/m ) 1200 1200 1200 1200 1200 1200 1200 TLE: 1 (Assumed) Concentration 3 (mg/m ) 600 120 40 20 10 5 3 DOC: Moderate Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 Hot Temperatures ECt50 3 (mg-min/m ) 600 600 600 600 600 600 600 TLE: 1 (Assumed) Concentration 3 (mg/m ) 300 60 20 10 5 2.(5) Table H-13 provides toxicity estimates for threshold effects from a percutaneous vapor exposure to GB.9 1.18 0. GB Profile Estimates (Mild Effects.06 0.02 0.6 0. Table H-14. Inhalation/Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 10 ECt50 (mg-min/m ) 0.4 0.1 1.

5 4.4 0. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 12 LCt50 (mg-min/m ) 35 50 60 70 80 90 100 3 MV Profile (2-Minute Exposure) Concentration (mg/m ) 17.(8) Figure H-4 is a graphical representation of GB vapor Ct profile for concentration from an inhalation/ocular exposure.01 Upper Band: LCt16 and LCt84 Region Line: ECt16 (Severe) [roughly LCt01] Lower Band: ECt16 and ECt84 Region for miosis (pupil shrinkage) 0. Vapor Concentration (mg/m3) 10 1 0. (1) Table H-15 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to GD.2 0.1 0. GB Vapor: Concentration versus Exposure Duration c. GD Profile.001 1 Extrapolation Beyond 10 minutes: Based on experimental data out to 360 minutes.8 2.25 H-7 . GD Profile Estimates (Lethal Dose. Table H-15.3 DOC: Low 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 50 35 15 10 3 Selected Toxicology Information TLE: 1.7 0. 10 100 Time (minutes) Figure H-4.0 1.

5 0.4 0. Table H-18.5 3.5 5 2. Personnel are masked with bare skin.5 DOC: Low Selected Toxicology Information H-8 . GD Profile Estimates (Severe Effects.25 (4) Table H-18 provides toxicity estimates for severe effects from a percutaneous vapor exposure to GD.(2) Table H-16 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to GD. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 12 MV Profile (2-Minute Exposure) Concentration (mg/m ) 12. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 6 Hot Temperatures Concentration 3 (mg/m ) 1500 300 100 50 25 12 5 DOC: Low LCt50 3 (mg-min/m ) 3000 3000 3000 3000 3000 3000 3000 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 6 LCt50 3 (mg-min/m ) 1500 1500 1500 1500 1500 1500 1500 TLE: 1 (Assumed) Concentration 3 (mg/m ) 750 375 150 25 12 5 2 DOC: Low Selected Toxicology Information (3) Table H-17 provides toxicity estimates for severe effects from an inhalation/ocular vapor exposure to GD.2 DOC: Low 3 ECt50 (mg-min/m ) 25 35 45 50 55 65 70 3 MV (L) 10 15 30 50 ECt50 (mg-min/m ) 35 25 10 7.5 3 Selected Toxicology Information TLE: 1.5 1. GD Profile Estimates (Severe Effects. Table H-17.3 0. Personnel are masked with bare skin.5 5 DOC: Low ECt50 3 (mg-min/m ) 2000 2000 2000 2000 2000 2000 2000 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 6 ECt50 3 (mg-min/m ) 1000 1000 1000 1000 1000 1000 1000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 500 100 30 15 7. Table H-16. GD Profile Estimates (Lethal Dose. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 6 Hot Temperatures Concentration 3 (mg/m ) 1000 200 60 30 15 7.8 0.

3 0. GD Profile Estimates (Mild Effects.0025 DOC: Low 3 Selected Toxicology Information TLE: 1. Time (minutes) Figure H-5.5 1.005 0.2 0.8 0.6 DOC: Low ECt50 3 (mg-min/m ) 300 300 300 300 300 300 300 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 6 ECt50 3 (mg-min/m ) 150 150 150 150 150 150 150 TLE: 1 (Assumed) Concentration 3 (mg/m ) 75 15 5 2.6 0.25 0. Inhalation/Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 10 ECt50 (mg-min/m ) 0.003 0. GD Profile Estimates (Threshold Effects.5 0.25 0. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 6 Hot Temperatures Concentration 3 (mg/m ) 150 30 10 5 2. Ct (mg-min/m ) Concentration-Time (mg-min/m3) 100 3 10 Upper Band: LCt16 and LCt84 Region Line: ECt16 (Severe) [roughly LCt01] Lower Band: ECt16 and ECt84 Region for miosis (pupil shrinkage) 1 0.4 0.1 0.No experimental data available. Table H-19.(5) Table H-19 provides toxicity estimates for threshold effects from a percutaneous vapor exposure to GD.009 0.4 (7) Figure H-5 is a graphical representation of Ct profile for GD vapor dosage from an inhalation/ocular exposure.9 3 Concentration (mg/m ) 0. Table H-20.5 0. GD Vapor: Dosage versus Exposure Duration H-9 .5 1.01 0. Personnel are masked with bare skin.3 DOC: Low Selected Toxicology Information (6) Table H-20 provides a toxicity estimate given for mild effects from an inhalation/ocular vapor exposure to GD.1 1 10 100 Extrapolation Beyond 10 minutes: Based on n for GF .03 0.

GF Profile Estimates (Lethal Dose. GD Vapor: Concentration versus Exposure Duration d. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 12 MV Profile (2-Minute Exposure) Concentration (mg/m ) 17. (1) Table H-21 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to GF.01 Upper Band: LCt16 and LCt84 Region Line: ECt16 (Severe)[roughly LCt01] Lower Band: ECt16 and ECt84 Region for miosis (pupil shrinkage). GF Profile Estimates (Lethal Dose. Personnel are masked with bare skin.1 0. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 Hot Temperatures Concentration 3 (mg/m ) 1500 300 100 50 25 12 5 DOC: Low LCt50 3 (mg-min/m ) 3000 3000 3000 3000 3000 3000 3000 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 5 LCt50 3 (mg-min/m ) 1500 1500 1500 1500 1500 1500 1500 TLE: 1 (Assumed) Concentration 3 (mg/m ) 7500 375 150 25 12 5 2 DOC: Low Selected Toxicology Information H-10 .0 0. Time (minutes) Figure H-6. 0. GF Profile. Table H-21.4 0.001 1 10 100 Extrapolation Beyond 10 minutes: No experimental data available – based on n for GF.0 1.7 0.5 4.8 2.25 DOC: Moderate (2) Table H-22 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to GF. 10 Vapor Concentration (mg/m3) 1 0. Table H-22.(8) Figure H-6 is a graphical representation of Ct profile for GD vapor concentration from an inhalation/ocular exposure.3 3 LCt50 (mg-min/m ) 35 48 60 69 79 91 99 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 50 35 17 10 3 Selected Toxicology Information TLE: 1.

(3) Table H-23 provides toxicity estimates for severe effects from an inhalation/ocular vapor exposure to GF.
Table H-23. GF Profile Estimates (Severe Effects, Inhalation/Ocular)1
Ct Profile (15L MV)
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 12

MV Profile (2-Minute Exposure)
Concentration (mg/m ) 12.5 3.5 1.5 0.8 0.4 0.3 0.2
3

ECt50 (mg-min/m ) 25 35 45 50 55 65 70

3

MV (L) 10 15 30 50

ECt50 (mg-min/m ) 35 25 10 7.5

3

Selected Toxicology Information
TLE: 1.25 DOC: Moderate

(4) Table H-24 provides toxicity estimates for severe effects from a percutaneous vapor exposure to GF. Personnel are masked with bare skin.
Table H-24. GF Profile Estimates (Severe Effects, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 5

Hot Temperatures
Concentration 3 (mg/m ) 1000 200 60 30 15 7.5 5
DOC: Low

ECt50 3 (mg-min/m ) 2000 2000 2000 2000 2000 2000 2000
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 5

ECt50 3 (mg-min/m ) 1000 1000 1000 1000 1000 1000 1000
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 500 100 30 15 7.5 5 2.5
DOC: Low

Selected Toxicology Information

(5) Table H-25 provides toxicity estimates for threshold effects from a percutaneous vapor exposure to GF. Personnel are masked with bare skin.
Table H-25. GF Profile Estimates (Threshold Effects, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 6

Hot Temperatures
Concentration 3 (mg/m ) 150 30 10 5 2.5 1.25 0.6
DOC: Low

ECt50 3 (mg-min/m ) 300 300 300 300 300 300 300
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 6

ECt50 3 (mg-min/m ) 150 150 150 150 150 150 150
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 75 15 5 2.5 1.25 0.5 0.3
DOC: Low

Selected Toxicology Information

H-11

(6) Table H-26 provides toxicity estimates for mild effects from an inhalation/ocular vapor exposure to GF.
Table H-26. GF Profile Estimates (Mild Effects, Inhalation/Ocular)1
Ct Profile
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 10

ECt50 (mg-min/m ) 0.2 0.3 0.4 0.5 0.6 0.8 0.9

3

Concentration (mg/m ) 0.1 0.03 0.01 0.009 0.005 0.003 0.0025
DOC: Low

3

Selected Toxicology Information
TLE: 1.4

(7) Figure H-7 is a graphical representation Ct profile for GF vapor dosage from an inhalation/ocular exposure.
Concentration-Time (mg-min/m3)

100

10

Upper Band: LCt16 and LCt84 Region Line: ECt16 (Severe) [roughly LCt01] Lower Band: ECt16 and ECt84 Region for miosis (pupil shrinkage)

1

0.1

1

10

100

Extrapolation Beyond 10 minutes: Based on experimental data to 240 minutes.

Time (minutes)

Figure H-7. GF Vapor: Dosage versus Exposure Duration

H-12

(8) Figure H-8 is a graphical representation of Ct profile for GF vapor concentration from an inhalation/ocular exposure.
Upper Band: LCt16 and LCt84 Region

Vapor Concentration (mg/m3)

10

Line: ECt16 (Severe) {roughly LCt01) Lower Band: ECt16 and ECt84 Region for miosis (pupil shrinkage)

1

0.1

0.01

0.00 1 10 100
Extrapolation Beyond 10 minutes: Based on experimental data to 240 minutes.

Time (minutes)

Figure H-8. GF Vapor: Concentration versus Exposure Duration

e.

VX Profile.

(1) Table H-27 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to VX.
Table H-27. VX Profile Estimates (Lethal Dose, Inhalation/Ocular)1
Ct Profile (15L MV)
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 6

MV Profile (2-Minute Exposure)
Concentration (mg/m ) 7.50 1.50 0.50 0.25 0.12 0.06 0.04
3

LCt50 (mg-min/m ) 15 15 15 15 15 15 15
TLE: 1

3

MV (L) 10 15 30 50

LCt50 (mg-min/m ) 20 15 5 4

3

Selected Toxicology Information
DOC: Low (LCt50 could be less)

H-13

(2) Table H-28 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to VX. Personnel are masked with bare skin.
Table H-28. VX Profile Estimates (Lethal Dose, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 6

Hot Temperatures
Concentration 3 (mg/m ) 75 15 5 2.5 1.25 0.6 0.4
DOC: Low

LCt50 3 (mg-min/m ) 150 150 150 150 150 150 150
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 5

LCt50 3 (mg-min/m ) 75 75 75 75 75 75 75
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 38 7.5 2.5 1.3 0.6 0.3 0.2
DOC: Low

Selected Toxicology Data

(3) Table H-29 provides toxicity estimates for severe effects from an inhalation/ocular vapor exposure to VX.
Table H-29. VX Profile Estimates (Severe Effects, Inhalation/Ocular)1
Ct Profile (15L MV)
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 6

MV Profile (2-Minute Exposure)
Concentration (mg/m ) 5 1 0.3 0.2 0.1 0.04 0.03
TLE: 1
3

ECt50 (mg-min/m ) 10 10 10 10 10 10 10

3

MV (L) 10 15 30 50

ECt50 (mg-min/m ) 15 10 5 3

3

Selected Toxicology Estimates
DOC: Low (ECt50 could be less)

(4) Table H-30 provides toxicity estimates for severe effects from a percutaneous vapor exposure to VX. Personnel are masked with bare skin.
Table H-30. VX Profile Estimates (Severe Effects, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 6

Hot Temperatures
Concentration 3 (mg/m ) 12.5 2.5 1.25 0.63 0.30 0.16 0.07 Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 6

ECt50 3 (mg-min/m ) 25 25 25 25 25 25 25
TLE: 1 (Assumed)

ECt50 3 (mg-min/m ) 12 12 12 12 12 12 12
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 2.5 1.25 0.63 0.30 0.16 0.07 0.04
DOC: Low

Selected Toxicology Information
DOC: Moderate

H-14

(5) Table H-31 provides toxicity estimates for threshold effects from a percutaneous vapor exposure to VX. Personnel are masked with bare skin.
Table H-31. VX Profile Estimates (Threshold Effects, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 6

Hot Temperatures
Concentration 3 (mg/m ) 5 1 0.3 0.15 0.08 0.04 0.03 Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 6

ECt50 3 (mg-min/m ) 10 10 10 10 10 10 10
TLE: 1 (Assumed)

ECt50 3 (mg-min/m ) 5 5 5 5 5 5 5
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 2.5 0.5 0.15 0.08 0.04 0.02 0.01
DOC: Low

Selected Toxicology Information
DOC: Moderate

(6) Table H-32 provides toxicity estimates for mild effects from an inhalation/ocular vapor exposure to VX.
Table H-32. VX Profile Estimates (Mild Effects, Inhalation/Ocular)1
Ct Profile
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: 4

ECt50 (mg-min/m ) 0.1 0.1 0.1 0.1 0.1 0.1 0.1

3

Concentration (mg/m ) 0.05 0.01 0.003 0.002 0.001 0.0004 0.0003
DOC: Low

3

Selected Toxicology Information
TLE: 1 (Assumed)

(7) Figure H-9 is a graphical representation of Ct profile for VX vapor dosage from an inhalation/ocular exposure.
Concentration-Time (mg-min/m3)

10
Upper Band: LCt16 and LCt84 Region Line: ECt16 (Severe) [roughly LCt01]

1

Lower Band: ECt16 and ECt84 Region for miosis (pupil shrinkage)

0.1

0.0

1

10

100

Extrapolation Beyond 10 minutes: From poor experimental data to 360 minutes, n=1.

Time (minutes)

Figure H-9. VX Vapor: Dosage versus Exposure Duration

H-15

(8) Figure H-10 is a graphical representation of Ct profile for VX vapor concentration from an inhalation/ocular exposure.
Upper Band: LCt16 and LCt84 Region

10

Line: ECt16 (Severe) [roughly LCt01] Lower Band: ECt16 and ECt84 Region for miosis (pupil shrinkage)

Vapor Concentration (mg/m3)

1

0.1

0.01

0.001

0.0001 1
Extrapolation Beyond 10 minutes: From poor experimental data to 360 minutes, n=1.

10

100

Time (minutes)

Figure H-10. VX Vapor: Concentration versus Exposure Duration

4.

Blood Agents

a. AC Profile. Table H-33 provides provisional toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to AC.
Table H-33. AC Profile Estimates (Lethal Dose, Inhalation/Ocular)1
Ct Profile (15L MV)
Exposure Duration (min) 2 10 30
Probit Slope: 10

MV Profile (2-Minute Exposure)
Concentration (mg/m ) 1430 607 685
DOC: Low
3

LCt50 (mg-min/m ) 2860 6070 20,630

3

MV (L) 10 15 30 50

LCt50 (mg-min/m ) 4290 2860 1430 858

3

Selected Toxicology Inforamtion
TLE: 1.85

b. SA Profile. Table H-34 provides provisional toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to SA.
Table H-34. SA Profile Estimates (Lethal Dose, Inhalation/Ocular)1
Ct Profile (15L MV)
Exposure Duration (min) 1 2 5 10 20 30 60 120 240
Probit Slope: Not Calculated

MV Profile (2-Minute Exposure)
Concentration (mg/m ) 6000 3750 1900 1150 700 530 325 195 120
DOC: Low
3

LCt50 (mg-min/m ) 6000 7500 9500 11,500 14,000 16,000 19,500 23,500 26,500

3

MV (L) 10 15 30 50

LCt50 (mg-min/m ) 11,250 7500 3750 2250

3

Selected Toxicology Information
TLE: 1.4

H-16

5 (2) Table H-36 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to HD. HD Profile Estimates (Lethal Dose.000 10. Blister Agents a.000 10.4 DOC: Moderate Selected Toxicology Information Probit Slope: 3 TLE: 1 (Assumed) True human ECt50 may be lower.000 10.000 10. (1) Table H-35 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to HD. Table H-35. HD Profile.8 0. Personnel are masked with clothed skin.6 DOC: Moderate ECt50 3 (mg-min/m ) 500 500 500 500 500 500 500 TLE: 1 (Assumed) Concentration 3 (mg/m ) 250 50 15 10 5 2 1. HD Profile Estimates (Lethal Dose. Personnel are masked with clothed skin.000 Concentration 3 (mg/m ) 5000 1000 330 165 85 40 30 DOC: Low Hot Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 7 LCt50 3 (mg-min/m ) 5000 5000 5000 5000 5000 5000 5000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 2500 500 165 85 40 20 15 DOC: Low Selected Toxicology Information Probit Slope: 7 TLE: 1 (Assumed) True human LCt50 may be lower. (3) Table H-37 provides toxicity estimates for severe effects (vesication) from a percutaneous vapor exposure to HD. Table H-36. H-17 . Table H-37.000 10.5. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 3 Hot Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 ECt50 3 (mg-min/m ) 200 200 200 200 200 200 200 Concentration 3 (mg/m ) 100 20 5 3 1. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 LCt50 3 (mg-min/m ) 10. HD Profile Estimates (Severe Effects. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 6 MV Profile (2-Minute Exposure) Concentration (mg/m ) 500 170 80 50 30 20 15 DOC: Low 3 LCt50 (mg-min/m ) 1000 1710 2466 3107 3915 4932 5646 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 1500 1000 500 300 3 Selected Toxicology Information TLE: 1.000 10.7 0.

Table H-39. Table H-38. Table H-40.4 0.(4) Table H-38 provides toxicity estimates for severe effects (eyes) from an ocular vapor exposure to HD.5 2.7 0.2 0. Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 3 ECt50 (mg-min/m ) 25 25 25 25 25 25 25 3 Concentration (mg/m ) 12.31 0.5 0. HD Profile Estimates (Mild Effects.21 DOC: High 3 Selected Toxicology Information TLE: 1 (5) Table H-39 provides toxicity estimates for mild effects from a percutaneous vapor exposure to HD. HD Profile Estimates (Mild Effects. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 3 Hot Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 3 ECt50 3 (mg-min/m ) 50 50 50 50 50 50 50 TLE: 1 Concentration 3 (mg/m ) 25 5 1. HD Profile Estimates (Severe Effects.25 0.2 0. Personnel are masked with clothed skin.5 0. Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: 3 ECt50 (mg-min/m ) 75 75 75 75 75 75 75 3 Concentration (mg/m ) 37.1 DOC: Moderate ECt50 3 (mg-min/m ) 25 25 25 25 25 25 25 TLE: 1 Concentration 3 (mg/m ) 12.5 7.5 2.07 DOC: Moderate Selected Toxicology Information (6) Table H-40 provides toxicity estimates for mild effects (eyes) from an ocular vapor exposure to HD.5 1.8 0.2 0.8 0.63 0.8 0.1 0.5 2.4 0.4 0.1 0.07 DOC: High 3 Selected Toxicology Information TLE: 1 H-18 .

HD Vapor: Dosage versus Exposure Duration (8) Figure H-12 is a graphical representation of Ct profile for HD vapor concentration for inhalation/ocular exposure. PC Severe Region (Middle Band) should be shifted downward by a factor of 3. 10000 For hot conditions. Ct (mg-min/m ) Concentration-Time (mg-min/m3) 3 1000 100 Upper Band: LCt16 and LCt84 (IH) Middle Band: ECt16 and ECt84 (PC severe) Lower Band: ECt16 and ECt84 (OC severe) Extrapolation Beyond 10 minutes: Based on experimental data to 360 minutes.(7) Figure H-11 is a graphical representation of Ct profile for HD vapor dosage from an inhalation/ocular exposure. 10 1 10 100 Time (minutes) Time (minutes) Figure H-11. Vapor Concentration (mg/m3) 100 10 1 Upper Band: LCt16 and LCt84 (IH) Middle Band: ECt16 and ECt84 (PC severe) Lower Band: ECt16 and ECt84 (OC severe) 0. 10 100 Time (minutes) Figure H-12. HD Vapor: Concentration versus Exposure Duration H-19 . 1000 For hot conditions. PC Severe Region (middle band) should be shifted downward by a factor of 3.1 1 Extrapolation Beyond 10 minutes: Based Extrapolation Beyond 10 Minutes: Based on experimental data to to minutes on experimental data360360 minutes.

b.

HN-1 Profile.

(1) Table H-41 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to HN-1.
Table H-41. HN-1 Profile Estimates (Lethal Dose, Inhalation/Ocular)1
Ct Profile (15L MV)
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

MV Profile (2-Minute Exposure)
Concentration (mg/m ) 500 100 35 15 10 5 2.5
DOC: Low
3

LCt50 (mg-min/m ) 1000 1000 1000 1000 1000 1000 1000

3

MV (L) 10 15 30 50

LCt50 (mg-min/m ) 1500 1000 500 300

3

Selected Toxicology Information
TLE: 1 (Assumed)

(2) Table H-42 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to HN-1. Personnel are masked.
Table H-42. HN-1 Profile Estimates (Lethal Dose, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

Hot Temperatures
Concentration 3 (mg/m ) 5000 1000 330 165 85 40 30
DOC: Low

LCt50 3 (mg-min/m ) 10,000 10,000 10,000 10,000 10,000 10,000 10,000
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

LCt50 3 (mg-min/m ) 5000 5000 5000 5000 5000 5000 5000
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 2500 500 165 85 40 20 15
DOC: Low

Selected Toxicology Information

(3) Table H-43 provides toxicity estimates for severe effects (vesication) from a percutaneous vapor exposure to HN-1. Personnel are masked.
Table H-43. HN-1 Profile Estimates (Severe Effects, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

Hot Temperatures
Concentration 3 (mg/m ) 250 50 15 10 5 2 1.4
DOC: Low

ECt50 3 (mg-min/m ) 500 500 500 500 500 500 500
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 3 (mg-min/m ) 200 200 200 200 200 200 200
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 100 20 5 3 1.7 0.8 0.6
DOC: Low

Selected Toxicology Information

H-20

(4) Table H-44 provides toxicity estimates for severe effects on eyes from an ocular vapor exposure to HN-1.
Table H-44. HN-1 Profile Estimates (Severe Effects, Ocular)1
Ct Profile
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 (mg-min/m ) 75 75 75 75 75 75 75

3

Concentration (mg/m ) 37.5 7.5 2.5 1.25 0.63 0.31 0.21
DOC: Low

3

Selected Toxicology Information
TLE: 1 (Assumed)

(5) Table H-45 provides toxicity estimates for mild effects from a percutaneous vapor exposure to HN-1. Personnel are masked.
Table H-45. HN-1 Profile Estimates (Mild Effects, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

Hot Temperatures
Concentration 3 (mg/m ) 25 5 1.7 0.8 0.4 0.2 0.1
DOC: Low

ECt50 3 (mg-min/m ) 50 50 50 50 50 50 50
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 3 (mg-min/m ) 25 25 25 25 25 25 25
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 12.5 2.5 0.8 0.4 0.2 0.1 0.07
DOC: Low

Selected Toxicology Information

(6) Table H-46 provides toxicity estimates for mild effects on eyes from an ocular vapor exposure to HN-1.
Table H-46. HN-1 Profile Estimates (Mild Effects, Ocular)1
Ct Profile
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 (mg-min/m ) 25 25 25 25 25 25 25

3

Concentration (mg/m ) 12.5 2.5 0.8 0.4 0.2 0.1 0.07
DOC: Low

3

Selected Toxicology Information
TLE: 1 (Assumed)

H-21

c.

HN-2 Profile.

(1) Table H-47 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to HN-2.
Table H-47. HN-2 Profile Estimates (Lethal Dose, Inhalation/Ocular)1
Ct Profile (15L MV)
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

MV Profile (2-Minute Exposure)
Concentration (mg/m ) 500 100 35 15 10 5 2.5
DOC: Low
3

LCt50 (mg-min/m ) 1000 1000 1000 1000 1000 1000 1000

3

MV (L) 10 15 30 50

LCt50 (mg-min/m ) 1500 1000 500 300

3

Selected Toxicology Information
TLE: Unknown

(2) Table H-48 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to HN-2. Personnel are masked.
Table H-48. HN-2 Profile Estimates (Lethal Dose, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

Hot Temperatures
Concentration 3 (mg/m ) 5000 1000 330 165 85 40 30
DOC: Low

LCt50 3 (mg-min/m ) 10,000 10,000 10,000 10,000 10,000 10,000 10,000
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

LCt50 3 (mg-min/m ) 5000 5000 5000 5000 5000 5000 5000
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 2500 500 165 85 40 20 15
DOC: Low

Selected Toxicology Information

(3) Table H-49 provides toxicity estimates for severe effects (vesication) for exposure to HN-2. Personnel are masked.
Table H-49. HN-2 Profile Estimates (Severe Effects, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

Hot Temperatures
Concentration 3 (mg/m ) 250 50 15 10 5 2 1.4
DOC: Low

ECt50 3 (mg-min/m ) 500 500 500 500 500 500 500
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 3 (mg-min/m ) 200 200 200 200 200 200 200
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 100 20 5 3 1.7 0.8 0.6
DOC: Low

Selected Toxicology Information

H-22

(4) Table H-50 provides toxicity estimates for severe effects on eyes from an ocular vapor exposure to HN-2.
Table H-50. HN-2 Profile Estimates (Severe Effects, Ocular)1
Ct Profile
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 (mg-min/m3) 75 75 75 75 75 75 75

Concentration (mg/m3) 37.5 7.5 2.5 1.25 0.63 0.31 0.21
DOC: Low

Selected Toxicology Information
TLE: 1 (Assumed)

(5) Table H-51 provides toxicity estimates for mild effects from a percutaneous vapor exposure to HN-2. Mild effects include erythema, itching and some pain. Personnel are masked.
Table H-51. HN-2 Profile Estimates (Mild Effects, Percutaneous)1
Ct Profiles
Moderate Temperatures Exposure Duration ECt50 3 (min) (mg-min/m ) 2 50 10 50 30 50 60 50 120 50 240 50 360 50
Probit Slope: Unknown TLE: 1 (Assumed)

Concentration 3 (mg/m ) 25 5 1.7 0.8 0.4 0.2 0.1
DOC: Low

Hot Temperatures Exposure Duration ECt50 3 (min) (mg-min/m ) 2 25 10 25 30 25 60 25 120 25 240 25 360 25
Probit Slope: Unknown TLE: 1 (Assumed)

Concentration 3 (mg/m ) 12.5 2.5 0.8 0.4 0.2 0.1 0.07
DOC: Low

Selected Toxicology Information

(6) Table H-52 provides toxicity estimates for mild effects on eyes from an ocular vapor exposure to HN-2.
Table H-52. HN-2 Profile Estimates (Mild Effects, Ocular)1
Ct Profile
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 (mg-min/m ) 25 25 25 25 25 25 25

3

Concentration (mg/m ) 12.5 2.5 0.8 0.4 0.2 0.1 0.07
DOC: Low

3

Selected Toxicology Information
TLE: 1 (Assumed)

H-23

d.

HN-3 Profile.

(1) Table H-53 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to HN-3.
Table H-53. HN-3 Profile Estimates (Lethal Dose, Inhalation/Ocular)1
Ct Profile (15L MV)
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

MV Profile (2-Minute Exposure)
Concentration (mg/m ) 500 100 35 15 10 5 2.5
DOC: Low
3

LCt50 (mg-min/m ) 1000 1000 1000 1000 1000 1000 1000

3

MV (L) 10 15 30 50

LCt50 (mg-min/m ) 1500 1000 500 300

3

Selected Toxicology Information
TLE: 1 (Assumed)

(2) Table H-54 provides toxicity estimates given for a lethal dose from a percutaneous vapor exposure to HN-3. Personnel are masked.
Table H-54. HN-3 Profile Estimates (Lethal Dose, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

Hot Temperatures
Concentration 3 (mg/m ) 5000 1000 330 165 85 40 30
DOC: Low

LCt50 3 (mg-min/m ) 10,000 10,000 10,000 10,000 10,000 10,000 10,000
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

LCt50 3 (mg-min/m ) 5000 5000 5000 5000 5000 5000 5000
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 2500 500 165 85 40 20 15
DOC: Low

Selected Toxicology Information

(3) Table H-55 provides toxicity estimates for severe effects (vesication) from a percutaneous vapor exposure to HN-3. Personnel are masked.
Table H-55. HN-3 Profile Estimates (Severe Effects, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

Hot Temperatures
Concentration 3 (mg/m ) 250 50 15 10 5 2 1.4
DOC: Low

ECt50 3 (mg-min/m ) 500 500 500 500 500 500 500
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 3 (mg-min/m ) 200 200 200 200 200 200 200
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 100 20 5 3 1.7 0.8 0.6
DOC: Low

Selected Toxicology Information

H-24

(4) Table H-56 provides toxicity estimates given for severe effects on eyes from an ocular vapor exposure to HN-3.
Table H-56. HN-3 Profile Estimates (Severe Effects, Ocular)1
Ct Profile
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 (mg-min/m ) 75 75 75 75 75 75 75

3

Concentration (mg/m ) 37.5 7.5 2.5 1.25 0.63 0.31 0.21
DOC: Low

3

Selected Toxicology Information
TLE: 1 (Assumed)

(5) Table H-57 provides toxicity estimates for mild effects from a percutaneous vapor exposure to HN-3. Personnel are masked.
Table H-57. HN-3 Profile Estimates (Mild Effects, Percutaneous)1
Ct Profiles Moderate Temperatures
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

Hot Temperatures
Concentration 3 (mg/m ) 25 5 1.7 0.8 0.4 0.2 0.1
DOC: Low

ECt50 3 (mg-min/m ) 50 50 50 50 50 50 50
TLE: 1 (Assumed)

Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 3 (mg-min/m ) 25 25 25 25 25 25 25
TLE: 1 (Assumed)

Concentration 3 (mg/m ) 12.5 2.5 0.8 0.4 0.2 0.1 0.07
DOC: Low

Selected Toxicology Information

(6) Table H-58 provides toxicity estimates for mild effects on eyes from an ocular vapor exposure to HN-3.
Table H-58. HN-3 Profile Estimates (Mild Effects, Ocular)1
Ct Profile
Exposure Duration (min) 2 10 30 60 120 240 360
Probit Slope: Unknown

ECt50 (mg-min/m ) 25 25 25 25 25 25 25

3

Concentration (mg/m ) 12.5 2.5 0.8 0.4 0.2 0.1 0.07
DOC: Low

3

Selected Toxicology Information
TLE: 1 (Assumed)

H-25

8 0.000 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown LCt50 3 (mg-min/m ) 5000 5000 5000 5000 5000 5000 5000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 2500 500 165 85 40 20 15 DOC: Low Selected Toxicology Information (3) Table H-61 provides toxicity estimates for severe effects (vesication) from a percutaneous vapor exposure to HT. HT Profile Estimates (Severe Effects. HT Profile Estimates (Lethal Dose. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown Hot Temperatures Concentration 3 (mg/m ) 5000 1000 330 165 85 40 30 DOC: Low LCt50 3 (mg-min/m ) 10. HT Profile. Personnel are masked.5 DOC: Low 3 LCt50 (mg-min/m ) 1000 1000 1000 1000 1000 1000 1000 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 1500 1000 500 300 3 Selected Toxicology Information TLE: 1 (Assumed) (2) Table H-60 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to HT.000 10.000 10. (1) Table H-59 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to HT.000 10. Table H-61. Table H-60.000 10.4 DOC: Low ECt50 3 (mg-min/m ) 500 500 500 500 500 500 500 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 3 (mg-min/m ) 200 200 200 200 200 200 200 TLE: 1 (Assumed) Concentration 3 (mg/m ) 100 20 5 3 1.7 0.e.6 DOC: Low Selected Toxicology Information H-26 .000 10. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown MV Profile (2-Minute Exposure) Concentration (mg/m ) 500 100 35 15 10 5 2. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown Hot Temperatures Concentration 3 (mg/m ) 250 50 15 10 5 2 1.000 10. HT Profile Estimates (Lethal Dose. Table H-59. Personnel are masked.

Table H-64. Table H-63.21 DOC: Low 3 Selected Toxicology Information TLE: 1 (Assumed) (5) Table H-63 provides toxicity estimates for mild effects from a percutaneous vapor exposure to HT. HT Profile Estimates (Mild Effects.1 0.4 0.2 0.5 1.8 0.31 0.8 0.25 0. Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 (mg-min/m ) 25 25 25 25 25 25 25 3 Concentration (mg/m ) 12.5 2. Table H-62. HT Profile Estimates (Mild Effects. HT Profile Estimates (Severe Effects.07 DOC: Low Selected Toxicology Information (6) Table H-64 provides toxicity estimates for mild effects on eyes from an ocular vapor exposure to HT.(4) Table H-62 provides toxicity estimates for severe effects on eyes from an ocular vapor exposure to HT.5 0. Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 (mg-min/m ) 75 75 75 75 75 75 75 3 Concentration (mg/m ) 37.5 7. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown Hot Temperatures Concentration 3 (mg/m ) 25 5 1.4 0.4 0. Personnel are masked.7 0.07 DOC: Low 3 Selected Toxicology Information TLE: 1 (Assumed) H-27 .5 0.8 0.1 DOC: Low ECt50 3 (mg-min/m ) 50 50 50 50 50 50 50 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 3 (mg-min/m ) 25 25 25 25 25 25 25 TLE: 1 (Assumed) Concentration 3 (mg/m ) 12.2 0.63 0.1 0.5 2.2 0.5 2.

Probit Slope: Unknown TLE: 1 (Assumed) True human LCt50 may be lower. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 LCt50 3 (mg-min/m ) 5000-10. (3) Table H-67 provides toxicity estimates for severe effects (vesication) from a percutaneous vapor exposure to L. L Profile Estimates (Lethal Dose. Table H-65. Personnel are masked.000 5000-10.000 5000-10.000 5000-10.8 0.4 DOC: Low ECt50 3 (mg-min/m ) 500 500 500 500 500 500 500 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 3 (mg-min/m ) 200 200 200 200 200 200 200 TLE: 1 (Assumed) Concentration 3 (mg/m ) 100 20 5 3 1.7 0. Table H-66.000 Concentration 3 (mg/m ) 2500-5000 500-1000 165-330 85-165 40-85 20-40 15-30 DOC: Low Hot Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 LCt50 3 (mg-min/m ) 2500-5000 2500-5000 2500-5000 2500-5000 2500-5000 2500-5000 2500-5000 Concentration 3 (mg/m ) 1260-2500 250-500 85-165 40-85 20-40 10-20 5-15 DOC: Low Selected Toxicology Information Probit Slope: Unknown TLE: 1 (Assumed) True human LCt50 may be lower. L Profile Estimates (Lethal Dose. L Profile. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown Hot Temperatures Concentration 3 (mg/m ) 250 50 15 10 5 2 1. Personnel are masked.000 5000-10. L Profile Estimates (Severe Effects. Table H-67.000 5000-10. (1) Table H-65 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to L.f. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown MV Profile (2-Minute Exposure) Concentration (mg/m ) 700 140 45 25 10 5 4 DOC: Low 3 LCT50 (mg-min/m ) 1000 1000 1000 1000 1000 1000 1000 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 1500 1000 500 300 3 Selected Toxicology Information TLE: 1 (Assumed) (2) Table H-66 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to L.6 DOC: Low Selected Toxicology Information H-28 .000 5000-10.

5 0.(4) Table H-68 provides toxicity estimates for severe effects on eyes from an ocular vapor exposure to L. Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 (mg-min/m ) 75 75 75 75 75 75 75 3 Concentration (mg/m ) 37.5 2. Table H-70. Table H-69. Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 (mg-min/m ) 25 25 25 25 25 25 25 3 Concentration (mg/m ) 12. L Profile Estimates (Mild Effects.1 DOC: Low ECt50 3 (mg-min/m ) 50 50 50 50 50 50 50 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 3 (mg-min/m ) 25 25 25 25 25 25 25 TLE: 1 (Assumed) Concentration 3 (mg/m ) 12.5 0.8 0.07 DOC: Low 3 Selected Toxicology Information TLE: 1 (Assumed) H-29 .2 0. Table H-68.4 0. Personnel are masked.1 0.4 0.7 0.1 0.25 0. L Profile Estimates (Mild Effects. L Profile Estimates (Severe Effects.5 7.07 DOC: Low Selected Toxicology Information (6) Table H-70 provides toxicity estimates for mild effects on eyes from an ocular vapor exposure to L.63 0.2 0. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown Hot Temperatures Concentration 3 (mg/m ) 25 5 1.21 DOC: Low 3 Selected Toxicology Information TLE: 1 (Assumed) (5) Table H-69 provides toxicity estimates for mild effects from a percutaneous vapor exposure to L.4 0.5 2.8 0.5 1.31 0.2 0.5 2.8 0.

(1) Table H-71 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to HL. Personnel are masked.000 10.7 0. HL Profile Estimates (Lethal Dose. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown MV Profile (2-Minute Exposure) Concentration (mg/m ) 500 170 80 50 30 20 15 DOC: Low 3 LCt50 (mg-min/m ) 1000 1000 1000 1000 1000 1000 1000 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 1500 1000 500 300 3 Selected Toxicology Information TLE: 1 (Assumed) (2) Table H-72 provides toxicity estimates for a lethal dose from a percutaneous vapor exposure to HL. HL Profile Estimates (Severe Effects.g. HL Profile. Table H-73. HL Profile Estimates (Lethal Dose.000 10.4 DOC: Low ECt50 3 (mg-min/m ) 500 500 500 500 500 500 500 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 3 (mg-min/m ) 200 200 200 200 200 200 200 TLE: 1 (Assumed) Concentration 3 (mg/m ) 100 20 5 3 1. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown Hot Temperatures Concentration 3 (mg/m ) 5000 1000 330 165 85 40 30 DOC: Low LCt50 3 (mg-min/m ) 10. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown Hot Temperatures Concentration 3 (mg/m ) 250 50 15 10 5 2 1.6 DOC: Low Selected Toxicology Information H-30 . Table H-72.000 10.000 10.000 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown LCt50 3 (mg-min/m ) 5000 5000 5000 5000 5000 5000 5000 TLE: 1 (Assumed) Concentration 3 (mg/m ) 2500 500 165 85 40 20 15 DOC: Low Selected Toxicology Information (3) Table H-73 provides toxicity estimates for severe effects (vesication) from a percutaneous vapor exposure to HL. Personnel are masked. Table H-71.8 0.000 10.000 10.

HL Profile Estimates (Mild Effects.8 0. Percutaneous)1 Ct Profiles Moderate Temperatures Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown Hot Temperatures Concentration 3 (mg/m ) 25 5 1.4 0.5 0.4 0.2 0.5 0.2 0.2 0.07 DOC: Low Selected Toxicology Information (6) Table H-76 provides toxicity estimates for mild effects on eyes from an ocular vapor exposure to HL.5 7.31 0.8 0.(4) Table H-74 provides toxicity estimates for severe effects on eyes from an ocular vapor exposure to HL.5 2.07 DOC: Low 3 Selected Toxicology Information TLE: 1 (Assumed) H-31 .5 1.4 0.8 0. Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 (mg-min/m ) 25 25 25 25 25 25 25 3 Concentration (mg/m ) 12.5 2.1 0.25 0.63 0.1 DOC: Low ECt50 3 (mg-min/m ) 50 50 50 50 50 50 50 TLE: 1 (Assumed) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 3 (mg-min/m ) 25 25 25 25 25 25 25 TLE: 1 (Assumed) Concentration 3 (mg/m ) 12.5 2.1 0. Table H-74. HL Profile Estimates (Severe Effects. Personnel are masked.21 DOC: Low 3 Selected Toxicology Information TLE: 1 (Assumed) (5) Table H-75 provides toxicity estimates for mild effects from a percutaneous vapor exposure to HL. Ocular)1 Ct Profile Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown ECt50 (mg-min/m ) 75 75 75 75 75 75 75 3 Concentration (mg/m ) 37. Table H-75. HL Profile Estimates (Mild Effects.7 0. Table H-76.

PD Profile. Table H-78 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to CX. Table H-77. ECBC-TR-349.000 5500 3300 3 Selected Toxicology Information TLE: 1 (Assumed) DOC: Low NOTES 1Sharon Reutter. September 2003.000 11.000 11.000 11. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 Probit Slope: Unknown MV Profile (2-Minute Exposure) Concentration (mg/m ) 5500 1100 365 185 90 45 3 LCt50 (mg-min/m ) 11..h. H-32 .000 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 16.000 11. Review and Recommendations for Human Toxicity Estimates for FM 311.000 11.9. Table H-78. Table H-77 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to PD. CX Profile Estimates (Lethal Dose. Respiratory Irritants Table H-79 provides toxicity estimates for a lethal dose from an inhalation/ocular vapor exposure to DM. DM Profile Estimates (Lethal Dose. PD Profile Estimates (Lethal Dose.500 11. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown MV Profile (2-Minute Exposure) Concentration (mg/m ) 1600 320 105 55 25 15 10 3 LCt50 (mg-min/m ) 3200 3200 3200 3200 3200 3200 3200 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 4800 3200 1600 960 3 Selected Toxicology Information TLE: 1 (Assumed) DOC: Low 6. et al. CX Profile. Inhalation/Ocular)1 Ct Profile (15L MV) Exposure Duration (min) 2 10 30 60 120 240 360 Probit Slope: Unknown MV Profile (2-Minute Exposure) Concentration (mg/m ) 1300 260 85 45 20 10 5 3 LCt50 (mg-min/m ) 2600 2600 2600 2600 2600 2600 2600 3 MV (L) 10 15 30 50 LCt50 (mg-min/m ) 3900 2600 1300 780 3 Selected Toxicology Information TLE: 1 (Assumed) DOC: Low i. Table H-79.

I-1 .Appendix I PROPERTIES OF SELECTED BIOLOGICAL AGENTS This appendix provides information on the properties of selected biological agents.

Sabotage (food supply) 1. Aerosol 2. Milk Aerosol Aerosol Table I-1. more so in polluted water DNA Stable Less important because of high transmissibility Stable DNA Not very stable Unknown Stable Not very stable DNA Not very stable Relatively stable Relatively stable Relatively unstable Relatively unstable Relatively unstable Relatively unstable Relatively unstable Relatively stable DNA Moderate to high DNA Variable Very high Very low DNA Moderate if untreated Moderate if untreated Very low High Low High Very low High Low High Low High Moderate Moderate DNA Aerosol Infected Vectors Sabotage (Food/Water Supply) 1.I-2 BW Agents1 Anthrax (Inhalation) Brucellosis Cholera Glanders Melioidosis Plague (Pneumonic) Psittacosis Shigellosis Tularemia Typhoid Fever Q Fever Rocky Mountain Spotted Fever Trench Fever Typhus Fever Chikungunya Crimean-Congo Hemorrhagic Fever Dengue Fever Eastern Equine Encephalitis Western Equine Encephalitis Ebola Fever Far Eastern Tick-borne Encephalitis Hantaan Virus (Korean HFV) Juinn Hemorrhagic Fever Aerosol Aerosol 1. Aerosol 2. Aerosol 1. Sabotage (food supply) 1. Aerosol Aerosol 1. 2. Aerosol 2. Aerosol 2. Infected Vectors 1. Infected vectors . Sabotage (food/water supply) 2. Sabotage (food/water supply) 2. Aerosol 2. Properties of Selected Biological Agents Likely Methods of Dissemination Spores in aerosols 1. Aerosol 2. Aerosol Transmissibility Person-to-Person None None Negligible DNA Negligible High Negligible DNA Negligible Negligible None None None None None Moderate None None None Moderate None None DNA Infectivity Moderate High Low DNA High High Moderate DNA High Moderate High High DNA High High High High High High High High High DNA High Low Lethality 2 Stability2 Spores are highly stable Long persistence in wet soil and food Unstable in aerosol and pure water. Vector Aerosol Aerosol Aerosol Aerosol Aerosol Aerosol 1.

Sabotage 2. Aerosol 2. Sabotage 1. Aerosol Aerosol Transmissibility Person-to-Person DNA Low to moderate None DNA Low High Low None None None None DNA None None None None None None Infectivity DNA High DNA High High High High N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A DNA Lethality 2 Stability2 DNA Relatively stable DNA Relatively stable Stable Relatively unstable Relatively unstable Stable Stable DNa DNA DNA Stable Stable Stable Stable Stable Machuo Hemorrhagic Fever Lassa Fever Lymphocytic Choriomeningitis Monkeypox Rift Valley Fever Smallpox Venezuelan Equine Encephalitis Yellow Fever Botulinum Toxin Clostridium Perfringens Toxins Conotoxins Shigatoxins Microcystin Ricin Saxitoxin Staphylococcal Enterotoxin B Tetrodotoxin Trichothecene Mycotoxins Unknown Low Low High Low High High Low High DNA DNA High High Low High High I-3 . Sabotage (food/water) Aerosol 1. Aerosol 2. Aerosol 2. Sabotage 2. Aerosol 2. Sabotage (food/water) 1. Aerosol 1. Aerosol 1. Properties of Selected Biological Agents (Continued) BW Agents 1 Likely Methods of Dissemination Aerosol Aerosol Aerosol Aerosol 1. Aerosol 1. Sabotage 2. Sabotage (food/water supply) 2. Sabotage (food/water) 1. Infected vectors Aerosol 1. Infected vectors Aerosol 1.Table I-1. Aerosol 2. Aerosol 2.

2Lethality 1FM I-4 . and stability information is based on studies of natural. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B).NOTES 8-9/NAVMED P-5059/AFJMAN 44-151. There is potential that the lethality and/or stability of some agents may be changed through various laboratory alterations and/or the use of stabilizing chemicals. 1 February 1996. endemic strains of these agents.

The information generally addressed in this appendix provides descriptions. and the brief descriptions provided furnish an awareness of the agents that could be used. moderate anorexia. (2) There is no treatment available. and control measures. high fever. and the possibility exists that they could be involved in the development. England. Animal Diseases a. J-1 . (2) The practice of accepted sanitation and biosecurity procedures in the rearing of the poultry is of utmost importance.1 (1) ASF is a tick-borne and contagious disease of swine caused by a virus and characterized by hemorrhages of internal organs. Mexico. Pakistan. widespread testing and elimination of all seropositive animals. especially migratory waterfowl. frequently within 48 hours. The military role. treatment. Human beings are not susceptible to ASF. or can be delayed for as long as a week. Death may occur within 24 hours of first signs of disease. In areas where waterfowl. and good herd isolation and sanitary practices can accomplish control and eradication of ASF in developed countries. and other avian species. fatal disease of chickens. would likely be in a consequence management support role. Mortality rates may reach 100 percent. It occurs in Africa and on the island of Sardinia. guinea fowls. contact the Army Medical Department (AMEDD). It is generally accepted belief that waterfowl. Avian Influenza (AI) (Fowl Plague). (3) Control. through genetic reassortment. Scotland. Ireland. African Swine Fever (ASF). or sea birds are prevalent. turkeys. For further information. and leukopia. Cleaning and disinfection procedures are critical. 2. shore birds. Background This appendix provides summaries of animal diseases listed in The Biological and Chemical Warfare Threat (1999). of new mammalian strains. the rearing of poultry on open range is incompatible with a sound AI prevention program. There is no vaccine. and the US. (4) b. sea birds. if any. South Africa. Slaughter and disposal of all acutely infected pigs.2 (1) AI is a disease of viral etiology that ranges from a mild or even asymptomatic infection to an acute.Appendix J SELECTED ANIMAL PATHOGENS 1. The infection and deaths of 6 of 18 humans infected with an AI virus in Hong Kong in 1997 has resulted in a reconsideration of the role that the avian species have on the epidemiology of human influenza. Highly pathogenic AI viruses have periodically occurred in recent years in Australia. (3) The AI viruses are Type A influenza viruses. or shore birds are generally responsible for introducing the virus into poultry.

4 (1) FMD is a highly contagious disease of cloven-footed domestic and wild animals caused by a virus. cattle. debilitation. including those prepared in cell cultures containing the appropriate types or subtypes. Sheep Pox and Goat Pox. a policy of quarantine and slaughter is usually practiced with the goal of complete eradication. and the possibility exists that they could be involved in the development. FMD occurs in many major livestock-producing countries. mastitis. Bluetongue (Sore Muzzle). Vaccination of susceptible animals on premises surrounding the infected flock should be considered. the area should be quarantined. Africa.3 (1) Bluetongue is an acute. and that was a laboratory J-2 . the Indian subcontinent. Great economic loss results from the effects of the disease. There is no conclusive evidence that SGPV infects humans. the Middle East. he reported that. Foot-and-Mouth Disease (FMD). (2) The only applicable treatment available is to minimize animal stress and administer broad-spectrum antibiotics to combat secondary infections. (3) When a new case is confirmed. goats. The morbidity is essentially 100 percent. in fully susceptible animals. The diseases are endemic in Africa. Treatment to prevent and cope with secondary infection may be necessary. The duration of immunity may be as short as 4 months. and the mortality is less than 1 percent. Cattle and goats with inapparent infections are important reservoirs of the virus. There is only one documented human infection. FMD is not considered to be a public health problem. (2) A number of inactivated vaccines. and much of Asia. Transmission is by direct and indirect contact. and the viruses can survive on contaminated premises for many months. Aujeszky’s Disease (AJD) (Pseudorabies). e. insect-borne disease of sheep. since 1921. Bauer in 1997. through genetic reassortment. (4) In a review of the zoonotic aspects of FMD by K. d. (4) f. are used in countries where the disease is endemic. (2) There is no treatment available. noncontagious. Occurrence is probably worldwide.6 A live attenuated vaccine is available for use in sheep in the US. the FMD virus has been isolated and typed from slightly over 40 human cases. and South America. are highly contagious and often fatal diseases caused by a capripoxvirus and characterized by fever and pox. which include lameness. weight loss. Because infection is uncommon. (3) In countries free of FMD. and wild ruminants caused by a virus. and the premises cleaned and disinfected. (3) (4) worker. The cases occurred on three continents: Europe. and abortion. of new mammalian strains.(4) The AI viruses are Type A influenza viruses. infected and exposed animals should be slaughtered.5 (1) Sheep pox and goat pox. c. low milk production.

(4) h. nonbite transmission of the disease from this source has been reported in a number of animal species. J-3 . In about 25 to 50 percent of cases. It has been eradicated in Australia. and the US. and the Pacific Islands are free of rabies. AJD is highly contagious and is principally spread via the respiratory route. will attack almost anything. This behavior may suddenly change. As the disease progresses. It is endemic in the swine of many countries. parts of Scandinavia. Africa. followed by progressive paralysis. the dog may try repeatedly to lick the hands and face of its owner or handler. usually terminating in death within 7 days of the onset of symptoms. Pigs are the main host. Rabies is present in most of Europe. cats. The UK. sheep. throughout Africa.” in which there is an early progressive paralysis. It occurs frequently in the US. (2) There is no treatment available. Australia. Ireland. The disease generally takes one of two forms: “furious. dogs with rabies develop the furious form of the disease.” with sporadic episodes of rage. and rodents. foxes. is caused by a virus and is characterized in fully susceptible pigs by high mortality. Lyssa Virus (Rabies). and Asia. indicating the onset of paralysis. including humans. horses. for example. goats. (3) A strict regimen of vaccination will reduce the number of outbreaks to a level at which complete eradication by sanitary measure alone will be feasible. At this stage. New Zealand. may become anorexic. apparently as a result of limbic lobe dysfunction. Papua New Guinea. There is no transmission to humans. but not in Canada and Australia. and during paroxysms of rage. withdrawn.8 (1) Rabies infections are usually established following introduction of virusinfected saliva into a bite or scratch. irritable. Human beings are not susceptible to Hog Cholera infection. the animal may appear to have difficulty swallowing. as if a bone were caught in its throat. Singapore. (2) There is no treatment available. A normally lively and sociable dog. Hog Cholera (Swine Fever). and most of Asia and the Americas. although animals can also be infected by the oral and nasal (olfactory) routes. or restless.7 (1) Hog cholera. the Middle East. or “dumb. (3) Live attenuated and inactivated virus vaccines are available to reduce losses in herds in which the disease is a continuing problem. Any attempt to alleviate the problem manually exposes the handler to considerable risk.(1) AJD is caused by porcine herpesvirus-1. The dog’s bark becomes high pitched and hoarse. but sporadic cases have occurred in cattle. Both forms almost invariably result in death. (4) g. Vaccination does not necessarily prevent infection or shedding of the virus. Convulsive seizures and muscular incoordination become apparent. dogs. either through a bite or the deposition of virus-infected saliva on mucous membranes or minor scratches. (2) There is no treatment available. Bat-infested caves may result in infectious aerosols. Canada. Affected animals may eat abnormal objects. Japan. The disease occurs in many countries of Europe. The disease is spread by direct and indirect contact. The animal drools saliva. a highly contagious disease. with the animal becoming highly affectionate.

destruction of all infected and exposed birds followed by thorough cleaning. however. VND virus has been recovered from effluent water for as long as 21 days and from carcasses for 7 days when the daytime temperatures were over 90 degrees. In chickens it is characterized by morbidity rates near 100 percent and mortality rates as high as 90 percent in susceptible chickens. Eradication J-4 . This disease. and disinfection of the premises are the main actions necessary for eradication of VND virus. Drugs that control bacterial and parasitic complications may decrease mortality.(3) Once a virulent strain of rabies virus has established itself in the CNS of an infected animal. No instance of transmission to humans through handling or consuming of poultry products is known. and restrictions on importation of sheep and goats from affected areas. Swine Vesicular Disease (SVD). Infections have occurred mostly in laboratory workers and vaccinating crews. i. and the Indian subcontinent. This disease produces lesions that are grossly indistinguishable from those of FMD. Velogenic Newcastle Disease (VND) (Exotic Newcastle Disease. (2) The establishment of a strict quarantine. in most countries. does not occur in North America. (4) All warm blooded animals. (3) Although people may become infected with VND virus. as soon as it is recognized.11 (1) SVD is a contagious disease of swine. The mortality. PPR is not infectious to humans. with rare cases in poultry handlers. Individuals with conjunctivitis from VND virus should not enter poultry premises or come in contact with live avian species. and proper disposal of carcasses and contact fomites. and transmission requires close contact. which has been reported from several European countries and Asia. varies form 50 to 80 percent. (2) There is no specific treatment for PPR. however. the pigs are slaughtered. Asiatic Newcastle disease). slaughter. the Middle East. j. The disease is not contagious. (2) There is no treatment available. depending on the form. including humans. Peste Des Petits Ruminants (PPR) (Pest of Small Ruminants). decontamination. the prognosis is favorable. are susceptible. and the virus is no longer present in eye fluids after 4 to 7 days. Methods should include quarantine. The disease has been reported from west and central Africa. In the natural disease.10 (1) PPR is an acute or subacute disease of sheep and goats caused by a virus. (3) Preventive measures include control of animals imported from infected areas and sanitary disposal of garbage from international aircraft and ships. the resulting disease is typically limited to conjunctivitis. the only ways of preventing rabies are by preexposure immunization. At a practical level. the outcome is almost always death. (4) k.9 (1) VND is likely the most serious disease of poultry throughout the world. Recovery is usually rapid. (3) Eradication is recommended when PPR appears in new areas.

l. Madagascar. and Uganda. and Chandipura) are much more infectious for man. infected and exposed animals slaughtered and buried or burned.15 J-5 . and some species of wildlife. (3) Infected and exposed animals should be quarantined. (4) Vesicular stomitis (New Jersey and Indiana) infection frequently occurs in man and causes influenza-like symptoms. Transmission is by direct and indirect contact. stiffness. and direct contact. The disease occurs in North and Central America and the northern part of South America. and cleaning and disinfecting infected premises. domestic buffalo. swill feeding. horses. strict import regulations must be followed for Teschen disease. and ring vaccination considered. (3) Live attenuated and inactivated vaccines are effective in controlling the disease.14 (1) Vesicular stomatitis is a contagious disease of cattle. and sub-Saharan Africa. Rinderpest. A vaccine is available in some countries. and fomites spread the disease rapidly. and fomites. Quarantine and hygienic measures should be applied.13 (1) These diseases are caused by several closely related enteroviruses. The highly virulent strain (Teschen Disease) has a mortality rate of 70 to 90 percent. Isfahan. Enterovirus Encephalomyelitis (Porcine Polioencephalomyelitis. (4) There are no reports of Rinderpest infection in humans.12 (1) Rinderpest is a contagious viral disease of cattle. (4) n. The disease is found only in the Indian subcontinent. (2) There is no treatment available. Near East. the area should be quarantined. (4) Human infection has been reported in laboratory personnel working with the virus. Transmission is made by direct or indirect contact. (2) There is no treatment except the use of mild antiseptics and astringents on the mucosa of the mouth. biting insects. Aerosol transmission is not a significant means of transmission except in confined areas and over short distances. Teschen disease is found in central and eastern Europe. o. m. (3) If an outbreak occurs. but rarely results in vesicles. Vesicular Stomatitis.measures consist of quarantining infected farms and areas. In the US. They occur in pigs of all ages and are characterized by a fever and convulsions. The incubation period is usually 24 hours. Humans may be infected by contact and by aerosol. Caution should be taken when working with infected material. In fully susceptible cattle. and pigs. slaughtering and disposing of infected and exposed pigs. spasms. Contagious Bovine Pleuropneumonia (CBPP). Talfan Disease). Teschen Disease. and paralysis. Other vesicular stomitis viruses (Piry. Pigs are the only susceptible species. the mortality may approach 100 percent with some virulent strains. (2) There is no treatment available for this pathogen.

It occurs in Africa. with occasional outbreaks in Europe. Japan. (3) Preventive measures include control of ticks. Switzerland. Norway. feed on the host’s dead or living tissue.17 There is no evidence to indicate that humans are susceptible to this (1) Heartwater is a disease of ruminants caused by rickettsia and transmitted by ticks. p. (2) Treatments are generally ineffective for this pathogen. even though the disease-causing organism is generally susceptible to antibiotics. Quarantine or isolation with attempts to eliminate actively infected animals and positive carriers is generally used. animals must be inspected at least every 3 to 4 days to discover and treat cases of screwworm myiasis. (3) This is a reportable disease in North America. The disease has been eradicated from the US. (4) r. Belgium. and goats are affected. Contagious Equine Metritis (CEM). Humans are not known to be affected by Heartwater. liquid body substances. (4) q. Enterovirus Infections of Swine (Virus Infection of Swine). Simultaneous infection with infectious blood and treatment with tetracyclines provides protection against some strains.16 (1) CEM is a highly contagious disease of horses. (4) s. It has been reported from Australia. and other islands of the Caribbean. Screwworm Myiasis. (4) disease.19 J-6 . and indigenous breeds are more resistant than imported ones. or ingested food. (3) Where screwworm is endemic. Netherlands. A live attenuated vaccine is employed in areas where eradication is not feasible. Guadeloupe. Heartwater (Cowdriosis).18 (1) Myiasis is the infestation of live vertebrate animals with larvae. Madagascar. (3) CBPP is a notifiable disease in most countries. a number of European countries. The principal mode of infection is by inhalation. (2) Treatment of mares with antimicrobial drugs is not always effective. Denmark.(1) CBPP is caused by Mycoplasma mycoides and primarily affects cattle. Sweden. sheep. Ireland. Cattle. Humans are susceptible to screwworm myiasis. There is no evidence that man is affected by the CEM. Screwworm larvae penetrate deeply into a wound of a warm-blooded animal and feed on living tissue and body fluid. and Luxembourg. (2) Screwworm myiasis is treated with topical application of an approved larvacide directly into the infested wound. which for at least a certain period. (2) Treatment involves administering tetracyclines. The disease occurs in Africa and some regions of Asia (especially India and China).

HTM (1 April 2003).vet.W.vet.uga. colera porcina.” Foreign Animal Diseases “The Gray Book”.htm (31 March 2003). Foreign Animal Diseases “The Gray Book”.edu/vpp/gray_book/FAD/hoc.int/rahs/Manual/Porcine/AUJESZKYSE. 1998 ed. (Developed by G. 17 December 2002. 5 James 4 James A.edu/vpp/gray_book/FAD/asf. fiebre porcina Africana..” Foreign Animal Diseases “The Gray Book”.vet.spc..edu/vpp/gray_book/FAD/fmd. NOTES 1 C. Fiebra aftosa. 1998 ed. 17 December 2002. stomatitispneumoenteritis complex or syndrome pseudorinderpest of small ruminants and kata [Pidgin English for catarrh]).int/rahs/Manual/Multiple_Species/RABIESE. http://www. 1998 ed. Virusschweinepest).edu/vpp/gray_book/FAD/vnd. 1998 ed. pseudo foot-andmouth disease.vet.vet. J-7 . Fievre aphteuse. embryonic death.uga. House and C.spc. http://www. (2) There is no treatment for this virus.. “African Swine Fever (Peste porcine Africaine. http://www. http://www. maladie de Montgomer). W.htm (31 March 2003). http://www.. http://www. “Bluetongue and Epizootic Hemorrhagic Disease (Sore muzzle. Beard.” Foreign Animal Diseases “The Gray Book”.uga.L 2 C. “Hog Cholera (Classical swine fever. 1998 ed..uga. 1998 ed.edu/vpp/gray_book/FAD/avi.” Manual for the Recognition of Exotic Diseases of Livestock.” Foreign Animal Diseases “The Gray Book”.uga. Mebus.” Foreign Animal Diseases “The Gray Book”.HTM (31 March 2003)..(1) This virus causes stillbirths. C. Stott. (3) Enterovirus can be controlled by comingling new replacement boars or gilts by fence-line contact or exchange of manure for 30 days before breeding begins. Maul-und-Klauenseuche). http://www.uga. http://www. Beard. “Velogenic Newcastle Disease (Exotic Newcastle disease. 10 J.. 1998 ed.htm (31 March 2003). 9 Charles 8 Alexandre 7 Gilles 6 Alexandre Saliki. peste du porc..A.” Foreign Animal Diseases “The Gray Book”. “Foot-and-Mouth Disease (Afta epizootica. 1998 ed.” Manual for the Recognition of Exotic Diseases of Livestock.htm (31 March 2003).T. http://www. 3 O. mummification.htm (31 March 2003). muzzle disease). Garner and Peter Saville). Fediaevsky. and infertility.” Foreign Animal Diseases “The Gray Book”. Mebus. Fediaevsky.uga.vet.htm (31 March 2003).edu/vpp/gray_book/FAD/blt.vet.edu/vpp/gray_book/FAD/sgp. Dulac. “Avian Influenza (Fowl Plague). These infections can be widespread where swine are raised intensively. “Peste Des Petits Ruminants (Pest of Small Ruminants.htm (31 March 2003). (Developed by G. “B052-Aujeszky’s Disease. “B058-Rabies. “Sheep and Goat Pox”. http://www.htm (31 March 2003).edu/vpp/gray_book/FAD/pdp. House. Asiatic Newcastle disease). Bek-en-klouseer.A. Garner and Peter Saville).vet.uga.

12 C. Swerczek.. J-8 .” Foreign Animal Diseases “The Gray Book”. 16 T.htm (8 April 2003). http://www.htm (31 March 2003). Mosca Verde. 15 Corrie Brown. John Mare.” Foreign Animal Diseases “The Gray Book”.” Foreign Animal Diseases “The Gray Book”.uga.edu/vpp/gray_book/FAD/cem. Novy.edu/vpp/gray_book/FAD/SCM. 1998 ed. http://www.spc.HTML (1 April 2003)..uga.vet.htm (31 March 2003). 13 Alexandre Mebus.vet.edu/vpp/gray_book/FAD/CBP. “Vesicular Stomatitis.edu/vpp/gray_book/FAD/svd.W. http://www. Gusaneras). February 1997.” Manual for the Recognition of Exotic Diseases of Livestock.” NebGuide. 1998 ed. “Contagious Equine Metritis. “Swine Reproductive Problems: Infectious Causes).htm (31 March 2003). http://www.uga.vet. http://www.A.edu/vpp/gray_book/FAD/vst..” Foreign Animal Diseases “The Gray Book”.edu/vpp/gray_book/FAD/hea.edu/pubs/swine/g926.vet. 14 C. “Screwworm Myiasis (Gusanos. Mebus.vet.int/rahs/Manual/Porcine/PEVE.htm (8 April 2003). 1998 ed.uga.A.” Foreign Animal Diseases “The Gray Book”.uga. http://www. http://www. http://www.edu/vpp/gray_book/FAD/rin. 1998 ed.A. E. 1998 ed.. 19 Alex Hogg and Donald G Levis.. “Rinderpest. http://www..uga.vet.(Developed by G.. “Heartwater (Cowdriosis).ianr.htm (31 March 2003). “Contagious Bovine Pleuropneumonia.” Foreign Animal Diseases “The Gray Book”. 18 James 17 C.htm (31 March 2003). 1998 ed. 17 December 2002.vet. Garner and Peter Saville). Gusano barrendor. 1998 ed.unl. Fediaevsky. Mebus.uga. “Swine Vesicular Disease. “B256-Enterovirus Encephalomyelitis (Previsously Teschen Disease).11 C.htm (31 March 2003).” Foreign Animal Diseases “The Gray Book”.

Xanthomonas campestris pv. Xanthomonas albilineans.Appendix K SELECTED PLANT PATHOGENS 1. 2. contact AMEDD. Specific Bacteria. c. Bacterium-Xanthomonas campestris pv. the disease is kept out of production areas through quarantine of varieties introduced from other areas. The lesions are often similarly sized. citrus-producing areas. citri. Additionally. control is attempted by burning all infected and adjacent trees to prevent the spread of the pathogen. In canker-free. citri.1 (1) (2) Description. The disease can be spread aerially in windblown rain. Specific Bacteria.2 (1) (2) Description. Citrus Canker (citrus plants). Background The purpose of this appendix is to provide a brief summary of select plant diseases listed in The Biological and Chemical Warfare Threat (1999). The initial characteristic symptom is one or more narrow. white “pencil lines” running longitudinally down the leaf blade into the sheath. strict quarantine measures are practiced. Later. oryzae. (4) Transmission. overhead irrigation. and brief descriptions are provided to furnish an awareness of these agents. Citrus canker seems to be much more severe in areas in which the periods of high rainfall coincide with the period of high mean temperature (such as Florida and other Gulf Coast states). Leaf Scald (Sugar Cane). (4) Transmission.to 10-mm circular spots. Sunken craters are noticeable on fruits. Xanthomonas campestris pv. The bacterium lives from year to year in infected plants. When the canker bacterium is found in such an area. 2. Xanthomonas albilineans. For further information. and contaminated equipment. On leaves. b.3 K-1 . (3) Symptom. (3) Symptom. It is spread by the harvester and possibly by other cultivation practices that cause plant wounding. (5) Control Measures. Under severe disease conditions. The main control measures are use of disease-free or treated seed and crop rotation. (5) Control Measures. The bacterium is spread primarily by wind-driven rain. The pustules darken and thicken into tan to brown corky cankers. Bacterial Diseases a. Defoliation occurs on severely infected trees. first appearance is as oily-Looking. entire plants may die. they become white or yellow spongy pustules. The military could potentially be involved in a consequence management support role.

wilt. Bacterium-Xylella fastidiosa. Specific Bacteria. oryzae. maple. Since CBD is limited to Africa. Colletotrichum Coffeanum. Bacterium-Xanthomonas campestris pv. and plum. Xylella fastidiosa (grapevines). Specific Fungi. CBD attacks the green tissues at the beginning stage of berry development. Cochiliobolus miyabeans (Helminthosporium oryzae). Colletotrichum Coffeanum. Bacterial Leaf Blight (rice). (3) Symptom. systemic seed-borne inoculum could easily infect the bark of young seedlings and become established in mature orchards.5 (1) (2) Description. d. The first symptom of the disease is a water-soaked lesion on the edges of the leaf blades near the leaf tip. There is no practical control of Pierce’s disease of grapes in the field. (3) Symptom. (4) Transmission. Fungal Diseases a. symptoms appear as a sudden drying and scorching of much of the margin area of the leaf while the rest of the leaf is still green. Infected berries are the major source of transmission. Grape clusters on vines with leaf symptoms stop growing. The bacterium also causes leaf scorching in the American elm. b. (5) Control Measures. precautions should be taken with coffee seeds from this region. (5) Control Measures. (5) Control Measures. (4) Transmission. Specific Fungi. K-2 . All commercial grape varieties are susceptible to the disease. and dry up. (3) Symptom. often penetrating into the interior of the berry and destroying the bean. The pathogen is transmitted by certain kinds of leafhoppers known as sharpshooters. Specific Bacteria.4 (1) (2) Description. Windblown rain also results in local dispersal from tree to tree or over relatively short distances. High rainfall and strong winds are thought to provide conditions for the bacteria to multiply and enter the leaf through injured tissue. If an infected seed is planted.6 (1) (2) Description. Coffee Berry Disease (CBD) (coffee).(1) (2) Description. Fall plowing or rolling of stubble to hasten decay of the rice debris should help to manage the disease by destroying the tissue in which the bacterium is maintained. Brown Spot (rice). The leafhopper vectors transmit the bacteria from diseased to healthy plants. In grapes. In the peach and alfalfa plants. mulberry. Cochliobolus miyabeanus (Helminthosporium oryzae). Rain is also a major factor responsible for spreading spores. the bacterium slows and stunts growth. (4) Transmission. 3. Pierce’s disease (PD) (grapevines).

Leaf spots are observed throughout the growing season and can vary in size. Virtually all of the stem rust infections come by way of spores blown in from infected fields of other regions. slightly colored hypertrophic deformations are visible 3 to 4 days after inoculation. on young leaves up to 10 days old. d. wild barley. and cereal rye). Leaf spots initially appear as small circular to oval spots on the first seedling leaves. Severely infected leaves will produce lightweight or chalky kernels. Wheat stem rust is encountered during growing season and may occur on any aboveground parts. Leaves must be continuously wet for 8 to 24 hours for infection to occur. c. Disease development is favored by high relative humidity (86 to 100 percent) and temperatures between 68 and 78 degrees F. Plant-resistant wheat varieties are available.8 (1) Disease. Older spots may have a bright yellow halo surrounding the lesion. the rust pustules darken because of the production of dark brown spores that are the over-wintering stage of the rust. The disease threatens the rubber cultivation in the tropical regions of the globe. and vivid orange-red in color. reddish-brown or gray center surrounded by a dark to reddish-brown margin. Microcyclus ulei (M. South American Leaf Blight (Hevea species only. Puccinia graminis. can occasionally infect barley. and goat grass).(3) Symptom. circular or elongated. Rust spots are very small. Specific Fungi. and rye. and color.9 (1) Disease. ulei because leaves are only susceptible when they are less than 10 to 15 days old. (4) Transmission. Fungicidal seed treatment has proven very effective in reducing seedling brown spot disease. Plants older than 4 to 5 years normally change leaves once a year at the onset of the dry season. (2) Specific Fungi. Puccinia graminis tritici. (5) Control Measures. ulei).7 (1) (2) Disease. This change behavior is very important for an epidemic of M. triticale. (3) Symptom. (4) Transmission. K-3 . The disease spreads from plant to plant in the field by airborne spores. shape. Puccinia striiformis. Later in the year. If necessary. (3) Symptom. yields latex). (5) Control Measures. The symptoms vary with the age of the leaves. (4) Transmission. some varieties of barley. The spores of M. The best management strategy is balanced nutrition because plants that grow in soils with nutritional deficiencies or in soils where nutrient uptake is hindered are more susceptible to infection. however. (5) Control Measures. Small spots are dark brown to reddish brown while large spots have a light. e. oats. Microcyclus ulei. Stripe Rust of Wheat (mainly wheat. apply a foliar fungicide at the very early stage of disease development. Wheat Stem Rust (wheat. ulei are disseminated mainly by rain splash or wind.

The first symptoms appear in the spring. Stripe rust spores can be spread on contaminated clothing. (4) Transmission. (3) Symptom. The disease is favored by long periods of free moisture. Resistant varieties are available. Specific Fungi. (5) h. fungal strands called “conidiophores” grow and produce spores called “conidia. Specific Fungi. As the crop matures. (5) Control Measures. Prunings containing affected twigs or branches can be a source of inoculum for several weeks. Leaf wetness from dew or other sources is required for infection. Shortly after the fungus infects and produces a lesion on rice. Moniliophthora roreri. little or no wind at night. Pyricularia grisea. Avoid field drainage. especially for extended periods because it allows the formation of nitrate and may cause drought stress. f. Continuous flooding is recommended to limit blast development. and wind. Monilia Pod Rot (cocoa). Infected leaves develop yellow-orange spore masses (pustules) in long stripes on the leaves. (5) Control Measures. (4) Transmission.10 (1) (2) Disease. the spore masses turn from yellow to black stripes. Disease. hail. and night temperatures between 63 and 73 degrees F. develops from spores blown in from other wheat-growing areas. Initially. The fungus can survive within infected twigs in the soil for more than 4 months. Dissemination by birds and contaminated insects is also suspected. Puccinia striiformis. high humidity.(2) Specific Fungi. g. (3) Symptom. Panicle lesions are usually brown. the pathogen affects the entire tree. Pyricularia grisea. (3) Symptom. Resistant varieties can be selected if this disease becomes serious. Rice Blast (rice). like leaf rust. Resistant varieties of lemon trees are available. Lesions that occur on the leaf are usually diamond-shaped with a gray or white center and brown or reddish brown border. but rarely on the stems and heads.12 K-4 . Moniliophthora roreri.11 (1) (2) Disease. (1) (2) Control Measures. Foliar fungicides also are labeled for stripe rust. Deuterophoma tracheiphila. Gradually. but may also be black. Deuterophoma tracheiphila. Citrus. The disease can also be transmitted by rain. small areas 1 to 10 meters in diameter will appear as yellow patches in paddocks. (4) Transmission. Specific Fungi.” These conidia are dispersed in the air. Sporulation is greatest when relative humidity is above 93 percent. followed by a dieback of twigs and branches. The disease. and it eventually dies.

Transmission. and have yellow leaf margins. Detection of cocoa-infected pods and their removal is the real and only key to pest management. are narrower than normal. avoid very early or very late planting dates during active aphid populations. K-5 . BYD (wheat.13 (1) (2) Disease. or purple. Barley Yellow Dwarf (BYD) Virus. There will be conspicuous bumpy swellings on the pod surfaces. Sporulation begins over the pod causing a tan discoloration within 12 days after pod swellings. Symptoms include uneven. (3) Symptom. Specific Virus. Good surface drainage and removal of weeds should be practiced on a regular basis. and wheat are susceptible to BYD. A number of varieties have been found or developed that show some tolerance or resistance to BYD. Banana Bunchy Top Virus (BBTV).to 10-day schedules. and oat). which disperses spores throughout the trees during rainy periods. progressing from leaf tip to base and margin to midrib. “sanitation sweeps” are made through the planting after pod set and should be continued on 7. They appear to be “bunched” at the top of the plant.(3) Symptom. corn leaf (3) Symptom. Transmitted by more than 20 aphid species (e. barley. To monitor for Moniliophthora Pod Rot. The most striking symptoms occur on older leaves Wheat and barley leaves usually turn yellow. 4. (5) Control Measures. Most of the commercial varieties of oats. (5) Control Measures. Specific Virus. On mature plants. are wavy rather than flat. red.14 (1) (2) Disease. (5) Control Measures. blotchy leaf discoloration in various shades of yellow.. The most important factors in controlling this disease are killing the aphid vector and removing and destroying infected banana plants. The main hope of control of BYD is the use of resistant varieties. BBTV. Moniliophthora roreri completes its entire life cycle on the pods in the tree. (4) aphid). BYD. (4) Transmission. BBTV (bananas). This is well within infected pod surface sporulation. BBTV is transmitted from plant to plant by aphids and transmitted from place to place by people transporting planting materials obtained from infected plants. New leaves of infected plants develop dark green streaks. b. (4) Transmission. while oat leaves are more red. new leaves emerge with difficulty. barley.g. Also. but some are less susceptible than others. Viral Diseases a.

au/agency/Pubns/factsheets/2002/fs002_2002.ifas. of Tropical Agriculture & Human Resources.” University of California Statewide Integrated Pest Management Program.sp. et al.ctahr. “Rice: Rice Blast. 9Department 8J.gov. “Small Grains: Barley Yellow Dwarf.rtf (8 April 2003).cosave.H.html (31 March 2003).htm (1 April 2003).htm (April 1.biotech.htm (1 April 2003). http://plantpathology.html (8 April 2003). “Bacterial Leaf Blight Symptoms on Rice. 14College 13R. “Stripe Rust of Wheat: Puccinia striiformis f.edu/PlantContainment/canker. K-6 . December 1997.tamu. “South American Leaf Blight. 1997.” UC Pest Management Guidelines.berkeley. “Colletrotrichum Coffeanum.ufl.edu/PMG/r682100611. http://plantpath.edu/xylella/page2. International Rubber Research and Development Board.ucdavis. of Agriculture-Western Australia. Ferreira and Rebecca A.agric.edu/cocoa/monilia. Datnoff and Richard S.” University of Nebraska-Lincoln. http://www. Lentini. Gabriel.K.edu/Texlab/Grains/Rice/riceblb. 6Lawrence 5Stephen 4A. 2001. University of Hawaii. Boley.irrdb.. http://www. November 1999.edu/oc/freepubs/pdf/PD-12.com/irrdb/NaturalRubber/Diseases/salb.htm (1 April 2003).ipm. http://edis.ohio-state. Oryzae (Ishiyama) Dye. 2Dean W.” Xylella Fastidiosa Web Site.” Crop Knowledge Master.wa.” http://www. “Banana Bunchy Top Virus.html (31 March 2003).hawaii.lsuagcenter. 5 August 2002. 2003).extento. 3Texas E. November 1991.” http://www. http://www.” July 1999.htm (31 March 2003).skp/agron/wheat/WhStRst. July 2000.edu/PMG/r730101911.ufl. Sheets on Organisms Cuarentenarios for the Paises Members of the Cosave Card Cuarentenaria. http://www. “Brown Spot in Florida Rice.pdf (8 April 2003).html (1 April 2003).oardc.unl.NOTES 1Kenneth Witam. Partridge.edu/peartree/homer/disease. 10R. http://www.” May 1994.” August 2002. “Field Crops: Sugarcane” 2001 Plant Disease Control Guide.ipm.com/Subjects/guides/plantdisease/01disease. Citrus Canker Disease. “Monilia (Moniliophthora roreri).cnr. Department of Plant Pathology. “Xanthomonas campestris (Pammel) Dowson pv.edu/BODY_RH007 (2 April 2003). http://www.html (8 April 2003). tritici.M.hawaii. “Stem Rust of Wheat.edu/kbase/crop/Type/c_coffee. Extension Plant Pathologists. http://www.org. Purcell. December 2002. A. “An Introduction to Pierce’s Disease. http://www2. 7The Webster.html (2 April 2003).” Plant Disease. 12 11Data Davis.ucdavis.” February 1996. http://www.E.py/lpcdeuterophomatracheiphila.

This increases the probability of contacting an airborne organism. (4) Increased Severity and Mortality Rate. therefore. such as the flu. An aerosol is comprised of finely divided particles. (3) Difficulty of Diagnosis. and smoke. b. (1) Difficulty of Detection. Personnel might be exposed to massive overdoses of an agent through the use of an aerosol. Man has a constant requirement for oxygen. (6) Increased Susceptibility. a. A biological agent aerosol is defined as an airborne suspension of particles containing biological agents. A biological agent aerosol in field concentrations cannot be detected by the physical senses. For the biological agent aerosol to be effective. he is breathing continually. the acquired immunities of target personnel might be overcome by the use of selected agents. (5) Massive Overdoses. (2) Capability of Penetration. Background The term “dissemination” refers to the intentional release of a biological agent by an adversary so that it will reach the portals of entry of target personnel in a viable and virulent state. certain methods of dissemination are feasible for biological attacks. Characteristics of Aerosol Dissemination. This would be accomplished by disseminating the agent as an aerosol. Inhalation or Aerosol Route of Entry The primary route of exposure to biological agents is through the respiratory tract. the characteristics of agents used.1 These routes of entry are inhalation. Particle Size.Appendix L DISSEMINATION OF BIOLOGICAL AGENTS 1. Particles in the size range from 1 to 5 microns are much more capable of passing through the defensive barriers of the L-1 . This is the result of the organism diffusing directly into the bloodstream and being carried by the blood directly to the body tissues. Thus. The classical symptoms of a disease associated with a particular agent can mimic the symptoms of diseases. percutaneous. Dissemination methods are related to the routes of entry through which pathogens may be introduced into the body to establish infection. Based on the portals of entry. fog. and oral. and the results desired. either liquid or solid. The effectiveness of these methods is determined by physical and environmental factors that limit the ability of the agent to establish infection. Aerosol particles tend to diffuse in much the same manner as a gas. Examples of common aerosols are dust. The aerosol cloud travels with the wind and is capable of diffusing into nonairtight structures that are not equipped with adequate filtering devices. Certain diseases have altered incubation periods and incapacitation times and increased mortality rates when the agent enters the body through the respiratory tract. it must reach target personnel. Particle size is a critical factor in lung infections. suspended in a gaseous medium. 2.

From the instant an aerosol is created. These determine the direction in which the aerosol cloud will travel and the size of the area that it will cover. Size control of solid particles (dry form of agent) can be achieved by presizing before dissemination. The terminal velocity of a 1. certain physical and environmental factors affect its stability. Biological agents can be disseminated by explosive means. There are three general methods of forming biological agent aerosols— (1) Generator. However. the size of the orifices. (5) Relative Humidity and Evaporation. Formation of Aerosol Particles. Aerosols of biological agents with a high decay rate can be employed effectively at high wind speeds (8 to 18 knots). Some of the factors that determine aerosol stability are— (1) Settling.to 5-micron particles to be negligible. The UV radiation in sunlight kills microorganisms. The decay rate differs from agent to agent and for meteorological conditions. d. Agent Aerosol Stability. Low wind speeds decrease downwind travel. which reduces area coverage. Aerosols eventually diffuse and become too dilute to be effective. The total volume and agent concentration will support low efficiencies and still produce aerosols that result in adequate area coverage with high infective dose concentrations. particles within the cloud strike and stick to objects in their path. environmental conditions cause the agent in the aerosol to gradually lose its ability to establish infection. Liquid particles in a biological aerosol may be reduced in size by evaporation. low wind speeds also tend to lengthen the time the aerosol is on the target and thereby increase the inhaled dose in target personnel. and the relative humidity determine particle size. c. (4) Wind Direction and Speed. As the aerosol cloud moves downwind from its release point. This can be accomplished by release through a nozzle or a spray or by an explosive force.upper respiratory tract and of being retained in the lungs than those below or above this size range. (2) Impaction. the aerosol may be carried over extensive areas during the agent’s survival period. (3) UV Radiation. its killing effect for most pathogens is complete and takes place in a relatively short period of time upon direct contact. the overall effect is negligible. The amount of pressure.” which is usually expressed as percent decay (death) of microorganisms per minute.to 5-micron particle is relatively small (5 inches per hour for a 1micron-diameter particle in still air). A decrease in the amount of liquid in the particle creates a corresponding increase in the percentage of salts remaining in the liquid L-2 . Releasing the agent in slurry form into a high-velocity air stream can produce aerosol particles in the proper size range. the viscosity of the agent. The rate of fall of the particle is directly related to its size. The use of an explosive means for aerosol production is feasible because large numbers of organisms can be packaged in a munition. This decline in aerosol effectiveness is called the “aerosol decay rate. In spite of the low penetrating power of UV radiation. (2) Spray. While a number of particles will impact. This slow settling rate and the presence of convection currents within the target area cause fallout of 1. Particles in the proper size range can be formed by physically breaking up a substance. Particles can be formed by forcing the wet (slurry form) agent through a nozzle at a regulated pressure. At these speeds. (3) Explosive Force.

Soil will have an effect only as related to heat absorption and reflection. Indirectly. which in turn influences the vertical diffusion of the aerosol cloud. The virus of yellow fever is transmitted from man to man by the bite of a mosquito. but those few that have mouthparts capable of piercing the skin of man or animals carry pathogens that cause some of the most feared human diseases. Most varieties of true flies have sucking mouthparts. which tends to draw fluids out through the cell membrane and results in dehydration of the living microorganisms. Some examples of vectors and the pathogens that they have shown to be capable of transmitting are as follows: (1) Mosquitoes. inversion. injection.surrounding the agent. High temperatures (170 to 180 degrees F) tend to kill most vegetative bacteria as well as the viral and rickettsiae agents. Heavy and prolonged precipitation will substantially reduce the number of agent particles in the air. Disseminating the agents affected during conditions of high relative humidity reduces the rate of evaporation. or absorption. e. Terrain affects cloud travel of biological agent aerosols in the same general manner as it affects chemical agent clouds. These insects are capable of transferring pathogens to man through breaks in the skin. Temperature has little direct effect on the living portion of a biological aerosol. This results in increased osmotic pressure. Turbulence. The rate of evaporation is dependent upon the relative humidity and the temperature in the environment surrounding the particle. (2) Flies. Inversion and neutral conditions are most effective for aerosol travel because the cloud is kept at a height conducive to inhalation by target personnel. Penetration of the skin can be accomplished by the bite of an arthropod vector (carrier). The ground contour of rough terrain creates wind turbulence. The spread of pathogens by arthropod vectors to man is wellestablished in history. the definition of “vector” is limited to the arthropods. which aid in determining temperature gradients. The high relative humidity associated with very light rain makes it less important in aerosol effectiveness than the rainout effect of heavy rainfall. will cause vertical diffusion of the cloud with a resulting loss of agent to higher altitudes and a reduction of area coverage. however. (6) Temperature. an increase in temperature is normally followed by an increase in evaporation rate. The temperature gradient conditions of lapse. Low relative humidity is conducive to the stability of some biological agents. Effects of Terrain on Cloud Travel. Percutaneous Route of Entry A second portal of entry that can be utilized for biological agent employment is the skin. which occurs during lapse conditions. (8) Precipitation. The sucking flies introduce pathogens L-3 . For the purpose of this manual. Arthropod Vector. and neutral affect the biological agent aerosol in much the same manner as they affect a chemical agent cloud. these temperatures are not normally encountered under field conditions. 3. These agents would be disseminated during conditions of low relative humidity. Other important mosquito-borne viral diseases are dengue fever and several types of encephalitis. (7) Air Stability. however. This freezing tends to preserve the agent and decrease its rate of decay. a. Subfreezing temperatures tend to freeze the aerosol (if it is in liquid form) after its dissemination.

the variety of potential agents. a bacterial disease of man and wild animals. Fleas are small.2 A Flechette is another penetrating device. Lice are sucking. Oral Route of Entry Another possibility is through the oral route by ingestion of contaminated food or water supplies. is known to transmit to man the rickettsia of Rocky Mountain spotted fever. Biological agents may be absorbed through the skin or placed on the skin to do damage to the integument. (4) Fleas. c. Typhoid fever. Covert Dissemination1 a. lakes. which contained Ricin. Covert use of biological agents might be aimed primarily at the respiratory tract and secondly at the digestive tract. the ways they might be employed. and the virus of Colorado tick fever. and the small amounts of materials required to cause infection. Pathogens transported by the biting flies include those that cause the dreaded African sleeping sickness—an infection of man. by a person. Biological agents lend themselves well to covert or hidden operations because of detection difficulties. is sometimes transmitted by the deer fly. was attacked in London. Characteristics. Pediculis humanus. and they have mouthparts for piercing the skin. domestic animals. the bacterium of tularemia. Xenopsylla cheopis.through previously injured body surfaces or mechanically transport them on their body surfaces to exposed food and water. Certain mites transport the causative organism of scrub typhus. L-4 . Tularemia. and Asiatic cholera are examples of diseases that may be spread mechanically by nonbiting flies. dorsoventrally flattened. bacillary and amoebic dysentery. Sabotage is the direct application. Since many pathogens are spread naturally in food and water. It is generally covert in nature. of material to the target. The human body louse. The wood tick. The pellet. b. Bulgarian exile Georgi Markov. The weapon discharged a tiny pellet in the subcutaneous tissue of his leg while he was waiting for a bus. when hungry they will attack any warm-blooded animal. The respiratory tract is an excellent target for the small-scale employment of a biological antipersonnel agent aerosol. they possess eight legs while insects have six. b. Contamination with toxins of chlorinated water. or reservoirs would be difficult because of dilution effects. but a few are important disease vectors. This habit increases their potential to transmit disease to man. In 1978. The common rat flea. is the vector of endemic typhus. England. (5) Ticks and Mites. As adults. Biological agents can be injected through the skin. Most of these are merely parasitic skin pests of land vertebrate animals. wingless insect parasites of the skin of mammals and birds. with a device disguised as an umbrella. and wild game. is the vector for the rickettsiae that cause epidemic typhus and trench fever. While different species show preferences for certain hosts. indigenous to the western US. (3) Lice. Absorption. was found during autopsy. wingless insect parasites of the skin of mammals and birds. 4. these provide proven vehicles in which the saboteur could employ an agent. Targets. He died days later. Injection. Dermacentor andersoni. rivers.5 5. These arthropod vectors are known as acarids and are not true insects. Their bodies are flattened laterally. The vector responsible for this disease is the tsetse fly (Glossina morsitans).

Office of the Surgeon General. Office of the Surgeon General. Russ Zajtchuk et al.” 3BG 4BG Russ Zajtchuk et al.NOTES 1TM 2BG 3-216/AFM 355-6. Chapter 32. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare.” Russ Zajtchuk et al. 1997. (eds). “Defense Against Toxic Weapons. Chapter 20. Chapter 30. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. (eds). January 1971. 1997. Chapter 28. Office of the Surgeon General. “Ricin Toxin. “Viral Encephalitides. (eds). Office of the Surgeon General. 1997. Technical Aspects of Biological Defense. “Use of Biological Weapons. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare.” Russ Zajtchuk et al. 1997.” 21BG L-5 . (eds).

and Procedures for Nuclear.11/MCRP 3-3. Treatment of Biological Warfare Agent Casualties. 11 July 2000. FM 8-9/NAVMED P-5059/AFJMAN 44-151. as amended through 05 September 2003. Joint Joint Publication 1-02. 12 December 2001. 2 June 2003. January 2001. 1 February 1996. Vol. April 2002.3. FM 3-11. Vol. Department of Defense DOD Chemical and Biological Defense Program Annual Report to Congress. Proliferation: Threat and Response. and Procedures for Nuclear. Office of the Secretary of Defense.2. I. Techniques.21/MCRP 3-37. Multiservice Tactics. I.2/NTTP 3-11.2C/NTTP 3-11. FM 3-11. The Biological and Chemical Warfare Threat. FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11. and Chemical Aspects of Consequence Management. November 1997.REFERENCES Office of the US President Office of the US President. Joint Doctrine for Operations in Nuclear. 28 July 2000. and Chemical (NBC) Environments. April 2003. 1999.46. Proliferation: Threat and Response. and Chemical (NBC) Protection. Flame. ISBN: 0-16-0427274. Joint Publication 3-11. 19 August 1996 (Renumbered from FM 3-11). Multiservice Tactics.24/AFTTP (I) 3-2. FM 3-6/FMFM 7-11-H/AFM 105-7. DOD Chemical and Biological Defense Program Annual Report to Congress.1C. Field Behavior of NBC Agents (Including Smoke and Incendiaries).4/MCWP 3-37. Biological. Techniques. 17 July 2000. Riot Control Agent and Herbicide Operations. Multiservice FM 3-5/MCWP 3-37.37. References-1 . Office of the Secretary of Defense. NBC Decontamination. NATO Handbook on the Medical Aspects of NBC Defense Operations AMEDP-6(B). 3 November 1986. Biological. FM 3-11.7. US Government Printing Office. Department of Defense Dictionary of Military and Associated Terms. US Government Printing Office.27/AFTTP (I) 3-2. Biological.

Purcell. July 1999. 1997. MD.FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11. Techniques. and Engineering Center. 6 June 2003. DA Pam 40-173. http://www. and Riot-control Agents on Threatened and Endangered Species.edu/xylella/page2. P. UNCLASSIFIED Report (ADA350462). USACHPPM TG 204. Military Chemistry and Chemical Agents. Abercrombie. A. 4 December 1990. Smoke Operations. and Chemical Agents and Defense Equipment. 3 June 2003. GB.cnr. USA Corps of Engineers.. Guide 153. FM 3-11. AND VX. Obscurants. Office of the Surgeon General. 29 May 2003. ”An Introduction to Pierce’s Disease. Substances-Toxic and/or Corrosive (Combustible). Occupational Health Guidelines for the Evaluation and Control of Occupational Exposure to Nerve Agents GA. (eds). TM 3-216/AFM 355-6. Other Sources 2000 Emergency Response Guidebook. FM 3-50. Air Force AFMAN 10-2602. UNCLASSIFIED Technical Manual (ADA292141). DA Form 12-99-R. Initial Distribution (ID) Requirements for Publications (LRA). Construction Engineering Research Laboratory. Army BG Russ Zajtchuk. Occupational Health Guidelines for the Evaluation and Control of Occupational Exposure to Mustard Agents H. Abercrombie. December 2001. Biological. Washington. GD. and Procedures. July 1998. 4: Chemical Analytical Methods. Army Edgewood Research.S. 1 April 1996.berkeley. and Butrow. P. Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. Reference-2 . and Conventional (NBCC) Defense Operations and Standards (Operations). Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare. et al. December 1963. Chemical.B. ERDEC-TR-450. Aberdeen Proving Ground. ECBC Notebook # NB 98-0079 (U). L. Vol. November 1999. USACERL Technical Report 99/56.. Biological.” Xylella Fastidiosa Web Site.22. Methods for Field Studies of the Effects of Military Smokes. TM 3-215/AFM 355-7. Development. DA Pam 40-8.H. Selected Physical Properties of Ton Container HD (Mustard) and VX. 22 December 1995. 12 January 1971. Technical Aspects of Biological Defense. Nuclear. Glossary of Terms for Nuclear. 4 December 1990.html (31 March 2003). DC. HD. AND HT. Weapons of Mass Destruction Civil Support Team Tactics. U.. A.

March 18.H. Aberdeen Proving Ground. 1921. C. ECTR-75032. Grace and Company. W. 1949.. http://www. References-3 .. ASTM Method D 167. Final Report of International Task Force-25: Hazard From Toxic Industrial Chemicals.. E. October 1977. Compatibility and Other Physicochemical Studies (U). Vol. Belkin. SO/R/576. K. G. Bodenstein. UNCLASSIFIED Report (ADA206000). et al. “The Preparation and Physical Properties of Carbonyl Chloride. Baskerville. April 1945. R. Beebe. G.E. MD. Edgewood. January 2003. EACD 328. 1908. MD.” Z. Final Report – Task I.K..” CAS No. The Relationship Between Oxygen Index and the Flashing Propensity of Explosively Disseminated Liquids.” J.C. “Solvents for Phosgene.H. P. Chem. 13. Edgewood Arsenal. Inc.W. 61. et al. Chemical Defence Experimental Establishment. Chemical Warfare Service. UNCLASSIFIED Report. Eng. Edgewood Arsenal. Bartlett. UNCLASSIFIED Report (ADA045976). Important Constants of Fourteen Common Chemical Warfare Agents. Great Britain.J. 117... The Kinetics of the Hydrolysis of Vesicants Part II. UNCLASSIFIED Report (ADB042888). Brooks. Determination of Lewisite Contamination in Environmental Waters by High Performance Liquid Chromatography. England... Aberdeen Proving Ground.. October 1979. MD. Brooks.. Determination of the Vapor Pressure of T. May 1964. and Durant. Corrosion. et al. ARCSL-TR-79040.. January 1989. 1996. Physik. Soc. UNCLASSIFIED Report. Vol. Washington Research Center. Balson. MD. March 1942.. Chem..edu/pubs/swine/g926... Military Intelligence Division.W. Military Intelligence Division. UNCLASSIFIED Report (ADA010666). M. Soc.G.D.ianr. A. Chem. Allan.2104.R... Steumpfle et al. C. C. Atkinson.. Asbury Graphite Mills. M.A.. Porton. December 1924. Chemical Systems Laboratory. MSDS. Vapor Pressure Measurements of Some Chemical Agents Using Differential Thermal Analysis. UNCLASSIFIED Report (AD350755). H. Standard Test Method for Apparent and True Specific Gravity and Porosity of Lump Coke. Vol. Incineration/Pyrolysis of Several Agents and Related Chemical Materials Contained in Identification Sets.. C. 1920. USA Chemical Research Development and Engineering Center. MD. F. “Synthetic Graphite.–2:2’Dichlorodiethylsulphide (H).A. Aberdeen Proving Ground. and Parker.. et al.A..3804/3.” NebGuide. Bossle.” J. and Brown. Vol. June 1975. P. USA Armament Research and Development Command. February 1997. Ind. and Cohen. P. ARCSL-TR-77061. 71. CRDEC-TR-042.. “Swine Reproductive Problems: Infectious Causes). 7782-42-5.htm (8 April 2003). E.” J. “Kinetics of Hydrolyisis and Displacement Reactions of β β’-(Dichlorodiethyl Sulfide (Mustard Gas) and of β -Chloro.β’-hyroxidediethyl Sulfide (Mustard Chlorohydrin). Chem... Alex Hogg and Donald G Levis. M.R. Brookfield. “Die Dissociation des Kohlenoxychlorids. Part III. UNCLASSIFIED Report (ADB958296). Clarksville. DA18-108-CML-6602 (A).unl. and Swain.

J. Buswell. MD. Brown. H. May 1991.H. Compatibility and Other Physicochemical Studies (U). Final Report – Task VII. Edgewood Arsenal. B. By-Products. Chemical Corps Chemical and Radiological Laboratories.F. Buckles. The Hydrolysis Rate of G Agents. Washington Research Center.. MD. CDC. Chemical Corps Technical Command. UNCLASSSIFIED Report (AD352753). UNCLASSIFIED Report (ADA186083). ECBC-TR-068. USA Chemical Research and Development Laboratories..B. Reference-4 . K. Final Report – Task VII RES-6486.. Fundamental Study of Toxicity: Solubility of Certain Toxics in Water and in Olive Oil.M. Modified NM: An Improved Liquid Binary VX Reactant (U). UNCLASSIFIED Report (ADB955216). et al. MD.. UNCLASSIFIED Report (ADB155651). Buchi. K. The Chemistry of Certain Arsenical Chemical Warfare Agents as Water Contaminants. Buckles. Division of Bacterial and Mycotic Diseases. MD. M.. May 1956. December 1947. Army Chemical Center. November 1999..gov/ncidod/dbmd/diseaseinfo/glanders_t... CRDEC-TR-076. <http://www. A. MD. R. “Disease Information: Glanders (Technical Information).. Chemical Research and Development Center Notebook #NB 83-0155 (U). UNCLASSIFIED Report (ADB966236). Butrow. USA Chemical Research Development and Engineering Center. Edgewood Arsenal. UNCLASSIFIED Report (ADA371297). M. USA Armament Command. H. and DF.. Chemical Warfare Service. Buchanan. ECBC Notebook # NB 97-0109 (C)..gov/ncidod/dbmd/diseaseinfo/glanders_g.C.M. EACD 445.Brooks. Jr.C. 11 August 2003. Vapor Pressure of VX.. ECBC Notebook # NB 03-0025 (U). UNCLASSIFIED Report (ADB966291). UNCLASSIFIED Report. Contract DA18-108-CML-6602 (A). Aberdeen Proving Ground. Environmental Overview of Intermediates.H.cdc.C. et al. Special Report CRLR 542. USA Chemical Research Development and Engineering Center. Clarksville.. Aberdeen Proving Ground. June 1944. W. CDC. Maryland. “Disease Information: Glanders (General Information). Environmental Overview of Common Industrial Chemicals with Potential Application in the Binary Munitions Program. T. and Q (U). L. 7 March 2003. EC-TR76075.M.E. Aberdeen Proving Ground. L. Division of Bacterial and Mycotic Diseases.. MD. and Products in the Production of QL.htm>. A. A. June 1964. Butrow.. May 1928.A. July 1987. <http://www.. MD. 20 June 2001. DC. CRDEC-TR-87041. March 1947. MD. Butrow. Grace & Co. TCIR 393. OSRD 4193. Corrosion. UNCLASSIFIED Report (ADC008561). Buckles. Army Chemical Center. USA Soldier and Biological Chemical Command. The Hydrolysis Rate of GD. 29 August 2003. November 1976. Carter..htm>. CW Vesicants: Selected Values for the Physical Properties of H. UNCLASSIFIED Report (AD108272). TCIR 373.. and Knight. et al.cdc. R. Buchi. Division 9 National Defense Research Committee of the Office of Scientific Research and Development. Army Chemical Center. et al. Aberdeen Proving Ground.

MD. Aberdeen Proving Ground.gas/. http://chemlab. http://www2. Chris Heilman. December 1997.pc. “Fact Sheet: Basic Information About Monkeypox. Part Three: Agents GD and GF (U). Monkeypox. The pictorial Periodic Table.N.htm. 2 September 2003.com. Documentation for Immediately Dangerous to Life or Health Concentrations./World. Edgewood Arsenal. College of Tropical Agriculture & Human Resources.pdf (8 April 2003). “Fact Sheet: Smallpox Vaccine and Monkeypox. Special Pathogens Branch. Edgewood Arsenal Special Report EO-SR-74002.cnn. CNN.... “Updated Interim Infection Control and Exposure Management Guidance in the Health-Care and Community Setting for Patients with possible Monkeypox Virus Infection. December 1974. 19 August 2003. UNCLASSIFIED Report (ADB028222). “Banana Bunchy Top Virus. 20 May 2004.cdc. CDC.ctahr. CDC. OH. References-5 . Chemical Agent Data Sheets Volume I. 27 August 2003. USA Dugway Proving Ground. SECRET Report (ADC032927).cdc. II. 2 September 2003. Cheicante. Interim Final Rule (Draft). “Investigation for the Determination of Nitrogen Mustard and Related Compounds in Air by Gas Chromatography Using Solid Sorbent Collection and Thermal Desorption. December 1974.gov/ncidod/monkeypox/infectioncontrol. Battelle. Aberdeen Proving Ground. CDC. NIOSH. “Russia names Moscow siege gas.gov/OD/OHS/BIOSFTY/bmb14/bmbl4s7d. MD. Clark.cdc. MD. Volume III.maricopa. http://www. K.htm. OHS. UNCLASSIFIED Report (ADA213287).” 18 July 2003. “Ebola Hemorrhagic Fever. 2 September 2003. R. UNCLASSFIED Paper. et al. July 1999.html. Review of Reactions of Chemical Agents in Water.” 30 October 2002. http://www. Chinn.” In Proceedings of the 1998 ERDEC Scientific Conference on Chemical and Biological Defense Research 17-20 November 1998.htm. PB-94-195047. 2 September 2003. CDC.cdc.gov/ncidod/monkeypox/factsheet.CDC. USA Edgewood Chemical Biological Center. January 1989. Chemical Agent Data Sheets Vol. University of Hawaii.” 9 December 2002. August 1983.L.com/2002/WORLD/europe/10/30/moscow. Monkeypox.” 17 June 1999. “BMBL Section VII: Agent Summary Statements.htm. May 1994.htm. USA Armament Command.gov/ncidod/dvrd/spb/mnpages/dispages/ebola.edu/periodic/default. D. HHS. Edgewood Arsenal. Aberdeen Proving Ground.hawaii.cdc.” 6 August 2003. Utah. Section VII-D: Prions. Final Report to USA Biomedical Research and Development Laboratory.” 12 June 2003. DPG-TR-82-004. http://www. G Nerve Agents. CDC. Joint CB Technical Data Source Book. CONFIDENTIAL Report (AD000020). S. NTIS Publication No. Edgewood Arsenal Special Report EO-SR-74001. 23 December 2002.” Plant Disease. http://www..gov/ncidod/monkeypox/smallpoxvaccine_mpox. ERDEC-SP-004. http://www. “Regulatory Impact Analysis: 42 CFR Part 73: Select Biological Agents and Toxins. http://www. CDC. UNCLASSFIED Report (ADA375171). Kenneth. Columbus.” 9 July 2003. Monkeypox.edu/oc/freepubs/pdf/PD-12.

P. Chem.B. Edgewood Arsenal. Aberdeen Proving Ground. A Memorandum Report: New Compounds Bis(B-Chloroethylthioethyl) Ether (T) and its Mixtures with Mustard (HT). TDMR 534.. Conoco International. MD. MSDS.. Davies.Coates.. T. USA Dugway Proving Ground. MD. Army Chemical Center. 1946. CRDEC-CR-86049. “Certain Physical Properties of Cyanogen and its Halides. M.. Inc.” J. Army Chemical Center. June 1986. Costal Corporation. 1 Fuel Oil. T. Physical Constants of Thirteen V Agents.. C. et al. Code of Federal Regulations Comparison of GA and GB as Chemical Warfare Agents (U). November 1957. R. N. A Memorandum Report New Compounds 2. C. September 1942.. Oleoresin Capsicum: An Effective Less-Than Lethal Riot Control Agent. and Witten. Army Chemical Center. UNCLASSFIED Report (ADB960467)...py/lpcdeuterophomatracheiphila.” J. http://www.P. Bis (2-chloroethyl) methylamine. “The Density and Thermal Expansion of Liquid Phosgene. and Davies. 1 Diesel Fuel. December 1959.H. Technical Division Memorandum Report 552. Soc. Phys.. Soc. CWLR 2346. N. “Xanthomonas campestris (Pammel) Dowson pv. Acute Toxicity of Methylphosphonic Difluoride (DF) Methylphosphonic Dichloride (DC) and their Hydrolysis Products by Inhalation and other Routes in Mice. DPG/JCP-097-002... UNCLASSIFIED Report..” J. Technical Division Memorandum Report 442. and Robinson. Chemical Warfare Center. Dawson.” Coulter.E. Part XVIII. and Stability. UNCLASSIFIED Report (ADB960651). et al. et al. USA Chemical Research and Development Laboratories. UNCLASSIFIED Report.. USA Chemical Warfare Laboratories. Chemical Biological Defense. Literature.P. USA Chemical Research and Development Laboratories. Army Chemical Center. 1950. “No.A.htm (1 April 2003). Dawson. T. Oryzae (Ishiyama) Dye.. A.” July 1999.M. UT. and Witten. Army Chemical Center.... February 1943. Rats and Guinea Pigs. J. MSDS. “Diesel fuel 2. P. MD. HQ & HT Review of British & U.L. UNCLASSIFIED Report (ADB225032). UNCLASSIFIED Report (AD314520). February 1943. B.. MD. Vol.P.cosave.. USA Chemical Research and Development Laboratories.org. R. and Roviller. TDMR 575.” Cook.2’ Dichlorotriethylamine. Chem. Data Sheets on Organisms Cuarentenarios for the Paises Members of the Cosave Card Cuarentenaria. USA Chemical Research Development and Engineering Center. B. Reference-6 . UNCLASSIFIED Report (ADB105158). January 1997. Preparation. Dawson. No. Chem. MD. MD. Daroff. Dahl. Cone.S. MD.. “Studies on Hydrogen Cyanide. Some Physical Properties of Anhydrous Hydrogen Cyanide. USA Chemical Warfare Laboratories. CWL-PS-1. UNCLASSIFIED Report (ADB960331). P. January 1943. 1935. Decontamination. 14.R..

Chem. 25B.” December 30. Quarterly Status Report (March through May 1972). D. Eakle.. Department of Commerce.edu/PlantContainment/canker. Fielder. Final Rule. J. Purification. Fog Oil. Aberdeen Proving Ground... February 1959. Defense General Supply Center. MD. Resistance of Various Materials of Construction in Contact with Transester Process. and Sauer. Manual for the Recognition of Exotic Diseases of Livestock. Last Updated 12 December 2002. 1999. Ellzy. S.O. Fort Douglas. Chemical Warfare Laboratories. USA Chemical Warfare Laboratories Notebook # NB 6695 (C). References-7 . MSDS MIL-F-12070C. Chemical Agent GF (U). “The Melting Point of Mustard Gas. Exxon Company. 5 August 2002. DAAA15-71C-0478-QSR 3. 1948. Secretariat of the Pacific Community..” J.Dawson. Gabriel. (1947). Effect of pH and Temperature on Hydrolysis Rates.. B. Dean W. CONFIDENTAL Report. Technical Study 69-C4. CRDL-SP-4-28. UNCLASSIFIED Report (ADB154752). Chemical Warfare Service. CWL Technical Memorandum 31-73.. Difluor (DF) – Flooring Compatibility Studies. et al..A. Utah. Edgewood Arsenal.sp. M. Douglas. Vol.. http://www. USA Chemical Research and Development Laboratories. “SGF-2 Type. UNCLASSIFIED Report (ADB963125). MSDS. Food & Agriculture Organization of the United Nations. UNCLASSIFIED Report. MDR 132. February 1973.. May 1991. Edgewood Arsenal. et al. “Stripe Rust of Wheat: Puccinia striiformis f.. March 1961. MD. Amer. W. Army Chemical Center.htm (31 March 2003). Army Chemical Center. tritici.. “The Preparation.. T. Epstein.int/rahs/Manual).P.wa.” Federal Register. Bureau of Export Administration. January 1969. Army Chemical Center. USA Chemical Research and Development Laboratories. Vol.agric. Report No. and Winkler. USA Deseret Test Center. USA Chemical Laboratories. Citrus Canker Disease. M. November 1941. III.. MD. D. Research. EA 2277 (U): A Summary Report as of 15 March 1961. Physical Properties and Hydrolysis of Cyanogen Chloride. 70. II.spc. Felsing. 27020-00079. Chemical Reactivity of Cyanogen Chloride in Aqueous Solution. MD. J.F. D.R. UNCLASSIFIED Report (ADB957078). MD. MD. Fielder.” August 2002. Chemical Systems Laboratories Notebook #NB-CSL-82-0213 (U). http://www.au/agency/Pubns/factsheets/2002/fs002_2002.A. (http://www.. J. Chemical Weapons Convention Regulations. EATR 325. Observations on Hydrolysis of GB in Sodium Bicarbonate Buffered Waters. Studies on Hydrolysis of GB I.” Ca.gov. Ethyldichloroarsine (ED): Preliminary Investigation (1939). “Jet Fuel Grade JP-8.rtf (8 April 2003).. Edwards. UNCLASSIFIED Report (AD509689).biotech.E. C. “15 CFR Part 710 et al. et al.ufl.” Department of Agriculture-Western Australia. CRDEC-TR-229. Soc. USA Chemical Research Development and Engineering Center.. Eckhaus. UNCLASSIFIED Report (ADA090556). February 1948.

. B. 4. and L. East Berlin. Army Chemical Center. W. F. England.F. and Taylor. Hall. & Chem... Entropy. Furukawa. Grula. 48(5). December 1965. Rsch. February 1976. Soc. Giauque. B.L. Manual of Military Chemistry Volume I. Chem. 1928. et al. Corrosion by Vesicants: Rate of Corrosion of Steel and Other Metals by H. USA Chemical Research and Development Laboratories. USA Armament Command.. USA Chemical Research and Development Laboratories. NBS Phy. Harris. R. UNCLASSIFIED Report. Chemical Defence Experimental Establishment. USA Chemical Research and Development Laboratories. 1964. HQ. 70. UNCLASSIFIED Report (ADB964902). Porton Report 2663. July 1945. Memorandum Report Storage Stability of HL.F. Amer. CRDLR 3342. A.. “The Entropy of Hydrogen Cyanide. Germann. S. UNCLASSIFIED Report. B. and Ruehrwein. MD. 19 December 1944.. Soc. Heat Capacity.L. Technical Division Memorandum Report 1094.Franke. Storage Stability of GD. Heat Capacity.. Comments on Solid Sulfur Dioxide Structures.Chemistry of Chemical Warfare Agents. 68A. Heat of Vaporization and Vapor Pressure. Heats of Fusion and Vaporization. “The Critical Constants and Vapor Tension of Phosgene. MD. USA Chemical Research and Development Laboratories.. Harris. July 1943. and Macy. Technical Division Memorandum Report 706. B.. MD.” J. Harris. Chem. “Carbonyl Chloride. Edgewood Arsenal.. Vol. Physical Constants of MCE.. and Macy R. MD. Edgewood Arsenal.A. et al. Vapor Pressure. Grula. February 1947.M. April 1945. December 1946.” J. USA Chemical Research and Development Laboratories. R. Hydrogen Bond Polymerization of the Gas in Chains of Indefinite Length. Army Chemical Center.” J.T. R. Q. Corrosion Rate of Steel by GA at 65°C.L. Army Chemical Center. and Jones. Aberdeen Proving Ground. W. UNCLASSIFIED Report (ADB962153). Vol. Reference-8 . Army Chemical Center.L. No.. UNCLASSIFIED Report (ADB963161). MD. Am. 1948. Harris. UNCLASSIFIED Report (ADB96498). MD. Amer.. GF and EA 1356 (U).. Mixtures of Mustard and Lewisite.W.O. Mostly at 65°C. Chemie der Kampfstoffe. An Investigation on the Solubility and Rate of Hydrolysis of Phosgene in Water.J. Compatibility Studies with Candidate Binary VX2 Components. Technical Division Memorandum Report 1299. UNCLASSIFIED Report (ADB964103). Vol. ACSI-J-3890.. EC-TM76009. Thickened Vesicants: Storage Stability of Unthickened and Thickened Nitrogen Mustards and Their Mixtures with Levinstein Mustard.S. UNCLASSIFIED Technical Manual (AD849866). G. Porton.L.. MD. R. Soc.. R. HN-1.W.. R. Vol.” J. April 1968.. Technical Division Memorandum Report 1302. Harris.. 61 1939. Chem. and Macy. et al. HN-3. USA Chemical Research and Development Laboratories. W.. Giauque. “Thermodynamic Properties of Some Methylphosphonyl Dihalides From 15 to 335°K. Army Chemical Center. CONFIDENTIAL Report (AD369299).. B. Storage Stability of German GA in Uncoated and Lacquered 75mm Shell at 50°C and 65°C. et al. Technical Division Memorandum Report 1031.

Army Chemical Center.. et al. Heath and Company. Toxic Cyanobacteria in Water: A guide to their public health consequences. Holtzclaw... Jr. 1927. UNCLASSIFIED Report (ADB964759). “Chlorine (Cl2). Heath and Company.).. Jeffrey H. “Zinc Chloride. USA Chemical and Radiological Laboratories. F.. 1991. Hormats. Vol. Aberdeen Proving Ground.” Kolloid Beihefte. A. Corrosion Rate of Steel at 65°C. TDMR 1346. “Uber die Fluchtigkeit und Vernebelung einer Reihe organischer Stoffe.. UNCLASSIFIED Report (ADB959731). MD. Control of Communicable Diseases Manual. Holzclaw. “Superpalite. June 1983.. January 1992. Chem. EACD 11. Hutchcraft.” J. A.P. Special Report: Corrosion Resistance of Metals Toward Isopropyl-Methylphosphonofluoridate (GB). Grotte and Lynn I Yang. Jackson. W. W. Hood. USA Chemical Research Development and Engineering Center. Surveillance Tests on 75 MM. 1998. Long-Term Storability of the M20 DF Canister Used in the M687 Binary Projectile.. June 2001. Chemical Corps Technical Compound. General Chemistry with Qualitative Analysis.J.. March 1948. CRLR 510. ARCSL-TR-83080. H. V. Phys. Inc.. Jr. and Semiatin. CRDC-TR-84104. CONFIDENTIAL Report (ADC033576).. Chemical Warfare Service. MD. 17th ed. 23.. Hyttinen.ac. James Chin (ed. Storage Stability in Steel at 65°C of Pure GD.F. “2-Chloroacetophenone. and Murdock. et al. HHS.M.” ICSC 1064. 2000. January 1985. Army Chemical Center.M.C.J. Henry F. IDA Document D-2176.. NIOSH Recommendations for Occupational Safety and Health: Compendium of Policy Documents and Statements. APG.. Mixed Binary Agents New Approach Toward Meeting Expanded Chemical Munitions Effectiveness Requirements. Report of the Workshop on Chemical Agent Toxicity for Acute Effects: Institute for Defense Analyses..R. Geneva. UNCLASSIFIED Report (ADB092563). May 11-12. MA.. MA. Vol. “Magnesium (Pellets). MD. D. ICSC 0126. 1919. United Book Press.C. 23. et al. 25 May 2004. Baltimore. Herbst. References-9 . H. USA Armament Research and Development Command. College Chemistry with Qualitative Analysis.S. L.uk/uipac/atwt/>. http://www..H...Henley.” ICSC 0701.” Ingrid Chorus and Jamie Bartram ed. MD.chemgmw. IUPAC Commission on Atomic Weights and Isotopic Abundances: Atomic Weights of the Elements 2001. 9th ed.” ISCS 0128. monitoring and management. H. 1999. May 1955. et al. 8th ed. Steel Gas Shell Extending Over a Period of One Year. Lexington.R.. Jr. WHO.. Edgewood Arsenal. 1988. S. D. and Robinson. June 1920. MD. UNCLASSIFIED Report (AD474404). MD.

L. UNCLASSIFIED Report (ADB969725). Kenneth Witam.. P. “Concise International Chemical Assessment Document 47: Arsine: Human Health Aspects. Sax’s Dangerous Properties of Industrial Materials. EATR 58.ufl. Edgewood Arsenal.. Vol. Technical Division Memorandum Report 456. T. Kinkead.F. Soc.” WHO.(2-Diisopropyaminoethyl) Methylphosphonite. Physico Chemical Constants of Diphenylaminochlorarsine. A. Kibler. Volume 2. MD. Summary of Information on Agent GF. W. S.” J.edu/peartree/homer/disease..L.. The Physico Chemical Properties of Methyldichloroarsine and Arsenic Trichloride. http://www.ifas..lsuagcenter. 1937. Army Chemical Center. New York. UNCLASSIFIED Report (ADB955049). CRDEC-TR-87061. Aberdeen Proving Ground. Czerczak.com/Subjects/guides/plantdisease/01disease. John Wiley & Sons. Kay Lau. MD. http://plantpath. Tony Man. Kibler.A. and Stricker. E. Johnson. Klosky. Data on Chemical Warfare. I. Inc.html (8 April 2003). MD. http://edis. “Stem Rust of Wheat. UNCLASSIFIED Report (ADB114319).R. 59. 2001. UNCLASSIFIED Report (ADB969120)..skp/agron/wheat/WhStRst. Edgewood Arsenal..” May 1994. 2001. Fishbein and S. Aberdeen Proving Ground. November 1942. R.” University of Nebraska-Lincoln. EACD459. MD. Partridge. Chem. Chemical Warfare Service. Lentini.E... A. Brief Evaluation of the Possibilities of Using Arsenicals as Incapacitating Agents.L. Lawrence E. and Stricker. Datnoff and Richard S. MD. CRLR 164. 2002. Am. Evaluation of the Acute Toxicity of Four Compounds Associated with the Manufacture of O-Ethyl-O’. 1997. Lewis. MD. USA Chemical Research and Development Laboratories. August 1986..F. March 1954. Edgewood. 1928 UNCLASSIFIED Report (ADB955210). and Pechukas. Development & Engineering Center. Aberdeen Proving Ground. 10th ed. et al. Glass or Polymer Etching Due to the Reaction of Methylphosphonic Difluoride (DF) with Water (U).J.. July 1921. A. August 1921. Chemical Warfare Service Edgewood Arsenal. USA Chemical Research Development and Engineering Center.edu/BODY_RH007 (2 April 2003). Chemical Warfare Center. Klosky. “Hydrogen Compounds of Arsenic.J. S. W. Edgewood Arsenal.unl.K. July 1987. Kaiser. P. Preparation of Arsine in Liquid Ammonia Some Physical Properties of Arsine. USA Chemical Research. EACD 63.. “Brown Spot in Florida Rice. NY. “Field Crops: Sugarcane” 2001 Plant Disease Control Guide. MD. USA Chemical Research Development and Engineering Center. Department of Plant Pathology. UNCLASSIFIED Report (ADB113969). Chemical Warfare Service.html (31 March 2003). June 1987..M.. Lau. UNCLASSIFIED Report (ADB955024). CRDEC-TR-86074. Fundamental Study of Toxicity Miscellaneous Data. MD. CRDEC-CR87077. Reference-10 . CONFIDENTIAL Report (ADC039896).

Lochboehler.M. et al. Technical Division Memorandum Report 1132.. 10th ed.P. NY. UNCLASSIFIED Report. May 1922.” effective date 29 October 2001. Army Chemical Center. Methyldichloroarsine and Methyldifluoroarsine Field Tests.000 µg/mL or 10.stanford. CONFIDENTIAL Report (AD508308). http://palimpsest. MD.A. Thermal Studies on MCE.html (8 April 2003). Chemical Warfare Service Edgewood Arsenal. 1970. C.. UNCLASSIFIED Report (ADB955243). December 1948.. TCIR 512. UNCLASSIFIED Report (ADB964104).. Part XV of the Thermal Decomposition of the Secondary Alkylflurophosphonites. Edgewood Arsenal. MD. Washington. R.edu/don/dt/dt3670. 85 (PTP-85). Freezing Point and Volatilities of Mustard and Lewisite Mixtures. W. Freezing Points of Mixtures of Methyldichloroarsine and Mustard Gas and of Lewisite and Mustard Gas. Mallinckroct Baker. 2001. Mark Davis. “Tantalum. Moelwyn-Hughes.G. UNCLASSIFIED Report. September 1945. MD. UNCLASSIFIED Report (ADB9670444). R. Mallinckroct Baker. 2001. July 1932.. Inc. 2001. et al. Sax’s Dangerous Properties of Industrial Materials. Chemical Warfare Service. EACD 410. England. Inc. Sutton Oak Report 544. EACD 170.” effective date: 15 February 1998. New York. Macy. March 1931. Proton Technical Paper No. MD. East Rutherford. Edgewood. Chemical Research Laboratory.E. MD. MSDS Number T0080. MSDS Number T3627.000 µg/mL. Baseline Study on the Problem of Obsolete Pesticide Stocks. March 1935... John Wiley & Sons. C.. 4th ed. CRC Press. Chemical Defense Experimental Establishment. “Titanium Dioxide. The Molecular Surface Energy and the Parachor of Toxic Compounds and of Certain Chlorides Used in Their Manufacture. England. EASP-100-61. Chemical Warfare Service.. D. Mead. Porton. NJ. Matt T. FAO Pesticide Disposal Series N. Inc. Macy. EATR 78. Kinetics of the Hydrolysis of Ethyl Dimethylamino Cyanophosphonate (and certain other related compounds) in Water. R.” Bookbinding and the Conservation of Books: A Dictionary of Descriptive Terminology. Marsh.9.J. R. 82nd ed. D. USA Munitions Command.R. 1966... “Vapor Density. USA Chemical Research and Development Laboratories. Roberts and Don Etherington. The Physical Properties of the Glycolates (U). Inc. B. Lide. and Owens. CRC Handbook of Chemistry and Physics.J. September 1941. UNCLASSIFIED Report (ADB956574). Edgewood Arsenal. Constants and Physiological Action of Chemical Warfare Agents.. Miller. USA Chemical Research and Development Laboratories.Lewis. 1. Edgewood Arsenal. References-11 . The Matheson Company. DC..... Volume 3. The Surface Tension. Sutton Oak. MD. E. Army Chemical Center. Matheson Gas Data Book. Macintire. UNCLASSIFIED Report (ADB95011). 7 January 2002.

September 2003. Edgewood Arsenal. (Diphenylaminechloroarsine).” CAS 532-27-4. Sutton Oak.” CAS 2698-41-1.E. R.” CAS 7723-14-0. Abercrombie.E..” CAS 7646-85-7.. “Blue-Green Algae.. D. Vol. November 1972. “NTP Chemical Repository: Chloroacetophenone. H.E.. April 1977. UNCLASSIFIED Report.K. 1997. “a-Chloroacetophenone. Soc. Edgewood Arsenal. D. Newman. Newman. Edgewood Arsenal Notebook # NB 9298 (U). UNCLASSIFIED Report (ADB955053).. EATR 4700. NIOSH Pocket Guide to Chemical Hazards. III. 1999. Owens. Development and Engineering Reference-12 . E. et al. Am. NIOSH Pocket Guide to Chemical Hazards. CONFIDENTIAL Report (ADC009719). and Dawson. Chemical Warfare Service. Toxicity of Military Smokes and Obscurants. Edgewood Arsenal.. T.. et al. England.A. Diphenylcyanoarsine: Part V – The Physical Properties of M. ERDEC-TR-043. Vapor Pressure of D.A. NCI Nomination Submitted to the NTP. UNCLASSIFIED Report. “Zinc Chloride fume.M.. The Pungent Principle of Capsicum. J. EACD 124. Penski. Aberdeen Proving Ground.” Owens. National Academy Press.oardc. February 2000. UNCLASSIFIED Report. June 1921. Patten.A. Toxicity of Military Smokes and Obscurants. L. USA Edgewood Research.. EC-TR-77016. MD.“Monilia (Moniliophthora roreri). R. Vol.ohio-state. Chem. USA Chemical Research and Development Laboratories. England.A..A. SO/R 492. and Perry.” September 2000. SO/R 488.. National Academy Press. S.C. Nelson. EATR 46.C. MD. PR-1342. E. March 1923. NRC. Mumford. NIOSH Pocket Guide to Chemical Hazards. National Toxicity Program. G. March 1935. and D. Chemical Properties of Phosgene.. Vapor Pressure Data Review and Analysis.htm (1 April 2003). NIOSH Pocket Guide to Chemical Hazards. Physical Property Data Review of Selected Chemical Agents and Related Compounds. J. T. “Phosphorus (yellow)..edu/cocoa/monilia. Parker. UNCLASSIFIED Report (AD524088). NRC. Diphenylcyanoarsine Part III – The Pope-Turner Process.. Chemical Warfare Service Edgewood Arsenal.H. A New Binary VX Reaction-Two-Liquid System (U).H. Report on Physical Properties of Mixtures of H and Lewisite I..” http://www. 45..” J. “o-Chlorobenzylidene malononitrile. December 1940.1. and Bouder.. “The Constitution of Capsaicin. Vol. USA Munitions Command. MD. MD.M. 2. December 1940.H.. A Thickener for GD (U). NIOSH-DOD-OSHA Sponsored Chemical and Biological Respiratory Protection Workshop Report. MD. Properties of Di-(2-Chloroethyl) Sulfide I. 1923. Sutton Oak. Army Chemical Center. UNCLASSIFIED Report (ADB955133). Nowlin. Patrice L. N.

Vol. Amer. Soc. E. USA Armament Command.. Chem. Aberdeen Proving Ground. Penski. MD.edu/PMG/r682100611. Porton Technical Paper No. Pilot-Scale Operations of Process for Manufacture of VX Binary Intermediate NM (U).. C. R. Petersen. USA Chemical Research and Development Laboratories. References-13 .. Richard J. UNCLASSIFIED Report (ADA265873). OEMCMR114. 62. Chemical Corps Board. C. et al. 1997. England. A. UNCLASSIFIED Report. Edgewood Arsenal. 69. December 1944.. “Rice: Rice Blast. Development. T.. ETF 100-41/Vol-2. The Chemistry of the Alkylfluorophosphonites and Related Compounds. December 1956. Army Chemical Center. MD. USA Chemical and Biological Defense Agency. April 1993.ipm. and Applications.M.. Aberdeen Proving Ground. CR DEC-TR-386. MD. 31 August 1951. MD. UNCLASSIFIED Report (AD-A255090). Army Chemical Center. Aberdeen Proving Ground. Army Chemical Center. The Physical and Chemical Properties of Phosgene and Diphosgene. Agent CX (Phosgene Oxime) Summary Report (U). 258. Properties of War Gases Volume II: Blood and Nettle Gases (U). Porton. Lewis.” Chemische Berichte.html (2 April 2003). M. Hawley’s Condensed Chemical Dictionary. J.. “Trichloronitrosomethane.. CONFIDENTIAL Report (AD108457). ETF 100-41/Vol-3. MD. NY. The Properties of 2-Propyl Methylfluorophosphonate (GB) I.ucdavis. UNCLASSIFIED Report (ADA267059). and Engineering Center. CONFIDENTIAL Report (AD108458). EM-TR-76055. ERDEC-TR-166. ETF 100-41/Vol-4. Vapor Pressure Data Analysis of Dichloroformoxime.. March 1993.. et al. UNCLASSIFED Report (ADB187225). MD. Dichloroformoxime (Phosgene Oxime) and Their Derivatives. Edgewood Arsenal. 1992. Aberdeen Proving Ground. MD. Potts. 1945.. Webster. Penski.” UC Pest Management Guidelines. K. and Sennewald. Vapor Pressure Data Analysis Methodology.K.Center. E. Chemical Research. Aberdeen Proving Ground. Vol. New York. November 1976. Statistics. MD. CRDL Special Publication 7.C. John Wiley & Sons. http://www. ERDEC-TR-042. CONFIDENTIAL Report (AD367890).. Properties of War Gases Volume III: Vomiting & Choking Gases & Lacrimators (U). June 1994. W.G. 1947. Chemical Defense Experimental Establishment. Chemical Corps Board. 13th ed. Vapor Pressure Data Review and Analysis. Chemical Corps Board. Inc. MD. CONFIDENTIAL Report (ADC008383). October 1965.. USA Chemical and Biological Defense Command. Penski. UNCLASSIFIED Report.. December 1956. Price. 1929.. “Hydrolysis and Chlorinolysis of Cyanogen Chloride”.C. Perry.J. Elwin C. CONFIDENTIAL Report (AD108459). Properties of War Gases Volume IV: Vesicants (U). Sr. July 2000. Riordan. Prandtl.B. B.

Salamon. MD. USA Chemical Warfare Laboratories. Aberdeen Proving Ground. Thermal Decomposition of VX. D. MD.K. Detection and Identification of QL Impurities by Electron and Chemical Ionization Gas Chromatography/ Mass Spectrometry. Rosenblatt. USA Chemical Research. December 2002. UNCLASSIFIED Report (ADB013164).edu/PMG/r730101911. 2001. CRDEC-TR88056.B. Rohrbaugh. D. MD.. June 1983. et al. “Small Grains: Barley Yellow Dwarf.H. UNCLASSIFIED Report (ADC033491).K. Albany. and Rubbers. Reference-14 . and Sharp. J.I. Edgewood Arsenal. USA Armament Research and Development Command.ipm. UNCLASSIFIED Report (AD325351). Ed. 8 August 2003.S. Army Chemical Center. USA Chemical Research and Development Laboratories. MD. Development. Evaluation and Synthesis of Chemical Compounds Volume II. et al. “Research in the News: Prions: Puzzling Infectious Proteins. Corrosion Resistance Tables: Metals. Agent VX.. MD. NY. USA Chemical Research. Satu M. USAMBRDL-TR 7710. Rohrbaugh. N.” University of California Statewide Integrated Pest Management Program. Problem Definition Studies on Potential Environmental Pollutants VIII: Chemistry and Toxicology of BZ (3-Quinuclidinyl Benzilate). UNCLASSIFIED Report (ADB136428).R. Plastics. MD. Savage.A.. Somani and James A. EA 5365. Aberdeen Proving Ground. 2nd ed. 3rd ed. Romano. EA 3547. EC-TR-76058. Marcel Dekker.. S. Physical Properties of Standard Agents..html (1 April 2003).. DA-18-108-CML-6673 (A). 1977. CRDLR 3088. MD. Aberdeen Proving Ground. Nonmetallics. August 1961. July 1989. UNCLASSIFIED Report (ADB124301).. INC.. The Vapor Pressure of Chemical Agents GD. http://www. Development and Engineering Center. Sax.. USA Chemical Research Laboratories.gov/nihHTML/ose/snapshots/multimedia/ritn/prions/prions1. ARCSL-SP-83015. EA 3580. UNCLASSIFIED Report. Final Comprehensive Report November 1961 – February 1965. Studies in Support of SUPLECAM (Surveillance Program for Lethal Chemical Agents and Munitions) II..nih. Ruth Levy Guyer.. and Related Compounds at Several Temperatures (U).html.. UNCLASSIFIED Report (ADB030349). D. M. EA2223. May 1988. UNCLASSIFIED Report (ADB253543). Aberdeen Proving Ground...ucdavis. P. J. MD. Candidate Agents. 1986.. 1968. August 1976. February 1965. Chester. June 1959. Fort Detrick. Army Chemical Center. & Engineering Center. Davis. USA Medical Bioengineering Research and Development Laboratory.” http://scienceeducation. Schweitzer. Basic Esters of Glycolic Acids (U): Part III Analysis and Chemical Properties of Microgram and Larger Quantities of EA 2277 and Related Compounds. Chemical Warfare Agents: Toxicity at Low Levels.M. Jr. VX. and EA 5533. H. D.” CRC Press. (eds).. S.K..R. Sass. J.. Rosenberg. et al. et al.. Reinhold Book Corporation. Dangerous Properties of Industrial Materials.. NJ. 1. CWL Special Publication 4-10. and Fielder. Samuel.

Chemical Warfare Service. http://www... UNCLASSIFIED Report (ADB955292). D. USA ECBC. Terminology and Information on Drugs: Part I. Scott. and Simak. P. Siegel. USA Chemical Research Development and Engineering Center.M. MD.L. B. MD. Division for Operations and Analysis.hawaii. Isolation of Capsaicin from Capsicum. (ADB956574).F. Williams & Wilkins. CRDEC-TR-212. Aberdeen Proving Ground. July 1990. et al... Heat of Vaporization. et al. Szafraniec. Chem.J.W. Policy Development and Analysis Branch. D. EACD 188. submitted for publication 2 May 2003. Sumner.. Binary GB: A Compilation of Relevant Data.S. UNCLASSIFIED Report. MD.. H. Heat of Fusion. R. The Corrosive Effect of War Gases on Metals and Materials. 8 August 2003.. et al.” Crop Knowledge Master.. Aberdeen Proving Ground. et al. 2003). Crystallization of GB. EACD 307. November 1991. Steadman. Spectrum Chemical Fact Sheet.M. 25th Ed. Tarantino. Amer. USA Armament Research and Development Command. April 1924. 72. et al.htm (April 1. Vapor Pressure of GF.. L. 1990.A. MD. UNCLASSIFIED Report (AD474404).9.. Electrochemical Corrosion Study of Miscellaneous Metals/Alloys with Methylphosphonic Difluoride. A. November 1949. MD. M. United Nations Office on Drugs and Crime.html. MD. “Opioids: Fentanyls. and Zeffert. Review and Recommendations for Human Toxicity Estimates for FM 3-11. September 2003.extento.org/unodc/report_1998-10-01_1_page016... USA Chemical and Radiological Laboratories.. The Vapour Pressure of Arsenious Chloride and of Lewisite I. USA Chemical Research Laboratories. Sharon Reutter.3-Dithiabutane: Low Temperature Heat Capacity.. Vol. Edgewood Arsenal. UNCLASSIFIED Report (ADA225952). Steadman’s Medical Dictionary. December 1921. Stephen A.. December 1941. June 1922. Army Chemical Center.E. November 1987. 1950. References-15 . On the Stoichiometry of Phosphonothiolate Ester Hydrolysis. CRDEC-TR-88032.. CONFIDENTIAL Report (ADC030931). TCIR-513. Ferreira and Rebecca A. Edgewood Arsenal..Scientific Section (Laboratory). Edgewood Arsenal. USA Chemical Research Laboratories. UNCLASSIFIED Report (ADB955153).” J. Sutton Oak Report 561(SO/R/561). Military Intelligence Division. “2. M. EACD 113. J. Stern.unodc. ”Colletrotrichum Coffeanum.” October 1998. MD. UNCLASSIFIED Report (ADB117574). March 1983. APG.. http://www. ARCSL-TR-82019. UNCLASSIFIED Report (ADB955131). USA Chemical Research Development & Engineering Center. Entropy and Thermodynamic Functions. ECBC-TR-349. Sze. Baltimore. Boley. Vapor Pressure. Tevault. “Phosphorus. UNCLASSIFIED Report. USA Chemical Research and Development Laboratories Notebook # NB 7265 (C). MD. J. Sherrill. Aberdeen Proving Ground. Tannenbaum. MD. R. Great Britain.A.edu/kbase/crop/Type/c_coffee. Investigation of the Synthesis of Capsaicin and Related Compounds..” CAS 7723-14-0. TR-304S. Soc.

and Biologicals. Porton Technical Paper No.. 12th ed. Whitehouse Station. US HHS. EACD 176. The International Rubber Research and Development Board.epa. Physico-Chemical Properties of Phosphorus Esters Part II: Some Constants of Isopropyl methylfluorophosphinate (GB). MD.H. UNCLASSIFIED Report. US Animal Health Association. Determination of the Vapor Pressure of Methyldichloroarsine. Watson.. UNCLASSIFIED Report (ADB096058). Porton. England. USDA. UNCLASSIFIED Report. December 1921. An Encyclopedia of Chemicals.J. UNCLASSIFIED Report (ADB959611). P. September 1985. Porton. R. 13th ed. Army Chemical Center. Revised 1998.irrdb.Texas Extension Plant Pathologists. Cleveland.” Pat Campbell & Associates and Carter Printing Company. 45 (PTP 45).. Whitehouse Station. 47.edu/Texlab/Grains/Rice/riceblb.H. Technical Paper No. May 1922.htm.” 19 May 2003. England. UNCLASSIFIED Report (ADB959625). Wardrop. Edgewood Arsenal.. Chemical Warfare Service. Edgewood.. “The Thermal Decomposition of 2:2’-Dichlorodiethyl Sulphide. http://www. Merck Research Laboratories. Walpole. Soc. OH. Determination of the Flash Points of GA and GB. http://plantpathology.com/irrdb/NaturalRubber/Diseases/salb. 2747 (PR 2747).. Edgewood Arsenal..” February 1996.” Morbidity and Mortality Weekly Report. Watson. March 1948.” 18 June 2001. CRC Handbook of Chemistry and Physics 50th ed. 10 July 1998.. P. Determination of the Vapor Pressure of D.. MJ.” http://www. Williams.. RR-10. A. MD. 1996. March 1952. Chemical Defence Experimental Establishment.R. December 2002. Chemical Warfare Service. “Bacterial Leaf Blight Symptoms on Rice. Inc. N0. 2001.W.M. Thomas.gov/pesticides/health/human. CRDC-CR-85058. Drugs.T. P. CDC. NJ. Public Health Service.. Drugs. MD. National Toxicology program. Research and Development for Candidate Materials for Use as a DF Containment Vessel. Reference-16 .D. Chemical Warfare Laboratories.D. EACD 79. A. UNCLASSIFIED Report. US EPA. MD. US HHS. USA Chemical Research Development and Engineering Center.W. “Pesticides: Health and Safety: Human Health Issues. J. CRC.html (8 April 2003). The Merck Index: An Encyclopedia of Chemicals. 10th Report on Carcinogens. Porton Report No. The Merck Index. Porton. January 1947. 19 August 2003.. Welchman.tamu. 1998. “Protocol for Military Clearance. “South American Leaf Blight. Preliminary Report on the Potential Value of Nerve Gases as C. Chem. Vol. M.htm (1 April 2003).C. 1947. Aberdeen Proving Ground. Foreign Animal Diseases: “The Gray Book (Part IV). 278 (PTP-278). VA. APHIS. R.. Agents.C.A. 1969. Merck & Company. Weast.” J. Richmond. Chemical Defence Experimental Establishment. “Compendium of Measures to Control Chlamydia psittaci Infection Among Humans (Psittacosis) and Pet Birds (Avian Chlamydiosis)..L. and Biologicals. and Bryant..

USA Edgewood Research. DC. EA 1211. ERDEC-SP-048. Matheson Gas Data Book. Zeffert. ERDEC-SP-036. References-17 . MD. UNCLASSFIED Report (ADA334105). Edgewood Arsenal Research Laboratories. Yang. Democratic Republic of Congo. “Hydrolysis of VX with Equimolar Water at Elevated Temperatures: Activation Parameters of VX.R.. and Related Chemical Problems Parts III-VI. Y. Y. Y..” In Proceedings of the 1994 ERDEC Scientific Conference on Chemical Biological Defense Research 15-18 November1994.. UNCLASSIFIED Report (AD234270). et al. In Proceedings of the 1996 ERDEC Scientific Conference on Chemical Biological Defense Research 19-22 November1996. Vol.. “Perhydrolysis of Nerve Agent VX. Chemical Warfare Agents. The Search for Toxic Chemical Agents (U). B.” Emerging Infectious Diseases. UNCLASSIFIED Paper. Technical Division Memorandum Report 1121. Am.L. and Related Chemical Problems Part I-II. Development and Engineering Center. 1992. No. MD. 58. 1996-1997.. NDRC-DIV-9-VOL-1-PT1-2. B. Hutin (CDC). Y. EA 1214.R. and Coulter.. et al. 7. UNCLASSFIED Paper. Vol. Summary Technical Report of Division 9. Vol. Summary Technical Report of Division 9. “Hydrolysis of VX: Activation Energies and Autocatalysis. 1993. Yaws. MD. NDRC Volume 1. Technical Division Memorandum Report 1292. UNCLASSIFIED Report (ADB964102). 82. Aberdeen Proving Ground. UNCLASSIFIED Report (AD234249). Physical Constants of G-Series Compounds: Compounds EA 1210. USA Chemical Research and Development Laboratories. 92. Development and Engineering Center. Benjamin.. et al.” J. Chem. Y. Washington. USA Edgewood Research.. Soc. W. Interaction and Esterification of Methylphosphonic Dihalides. Army Chemical Center. et al. Kirner. 3. August 1945.” J. Zeffert. Witten. 1960. UNCLASSIFIED Report (AD507852).. NDRC Volume 1. ERDEC-SP048. USA Edgewood Research.M. “Properties. The Hydrolysis of MCE. P.. W. Office of Scientific Research and Development Washington. MD. Org.. “Characterization of HD Heels and the Degradation of HD in Ton Containers. et al. et al.M. “Research: Outbreak of Human Monkeypox. October 1997.” In Proceedings of the 1996 ERDEC Scientific Conference on Chemical and Biological Defense Research 19-22 November 1996. Yang. B. C. MD.. USA Chemical Research and Development Laboratories. McGraw-Hill Companies. Yang. Aberdeen Proving Ground.. Yang. et al. Rev.. 1946. EA 1213. Kirner. 1946. UNCLASSIFIED Report (ADB964904). NY. CV and EA 2192”.. UNCLASSIFIED Paper.Witten. Aberdeen Proving Ground.” Chem. May 1996. New York. Vol. Chemical Warfare Agents. July 1947. EA 1212. Chem.B.. Yang.. Yvan J.. 7th ed. Development and Engineering Center. November 1969. Office of Scientific Research and Development. MD. 2001. “Decontamination of Chemical Warfare Agents.. May-June 2001. October 1997. UNCLASSFIED Report (ADA313080). EATR 4210. UNCLASSFIED Report (ADA334105). DC. Army Chemical Center.F.

MD. CRLR-2. B. et al. USA Chemical and Radiological Laboratories. April 1951. Reference-18 ..Zeffert. Slow Fractional Crystallization of GB. UNCLASSIFIED Report (AD498968).M. Army Chemical Center.

GLOSSARY PART I – ABBREVIATIONS AND ACRONYMS AC ACAA ACADA ACh AChE AFJMAN AFM AI AJD AMAD AMEDD AO APHIS ASF ASTM atm ATSDR avdp B BBTV BG BMBL BW BWC BYD BZ C C CA CADK CAM CANA CAPDS CARC CAS CB CBD CBPP CBR CBW Cd CDC CEM A hydrogen cyanide automatic chemical agent alarm automatic chemical agent detector/alarm acetylcholine acetycholinesterase Air Force Joint Manual Air Force Manual area of interest. Avian Influenza (fowl plague) Aujeszky’s disease automatic mustard agent alarm Army Medical Department area of operations Animal and Plant Health Inspection Service African swine fever American Society for Testing and Materials atmosphere Agency for Toxic Substance and Disease Registry avoirdupois weight banana bunchy top virus Brigadier General Biosafety in Microbiological and Biomedical Labs biological warfare Biological Weapons Convention Barley Yellow Dwarf (plant disease) 3-Quinuclidinyl benzilate (an incapacitating agent) Celsius bromobenzylcyanide chemical agent detector kit chemical agent monitor convulsant antidote for nerve agents Chemical Agent Point Detection System chemical agent-resistant coating Chemical Abstract Service chemical-biological coffee berry disease contagious bovine pleuropneumonia chemical. biological. and radiological chemical and biological warfare Cadmium Centers for Disease Control and Prevention contagious equine metritis Glossary-1 .

phosgene cholinesterase US Army Center for Health Promotion and Preventive Medicine Chemical Hazard Response Information System chloroacetophenone in chloroform cyanogen chloride chlorine cyclohexyl methylphosphonafluoridate chloroacetophenone (tear gas or mace) chloroacetophenone-in benzene chloroacetophenenone-in chloroform cyanic acid central nervous system centipoises dibenz (b.CFR CG ChE CHPPM CHRIS CIC CK Cl2 CMPF CN CNB CNC CNOH CNS cP CR CS Ct CW CWA CWC CWDD CX CZ D DA DC DF DM DMDS DNA DOC DOD DOT DP dynes/cm E ECBC ECt ED EEE EHEC EHS EMPA EMT EPA ERG Code of Federal Regulations commanding general. District of Columbia methylphosphonic difluoride diphenylaminochloroarsine (Adamsite) (a vomiting agent) dimethyl disulfide deoxyribonucleic acid degree of confidence Department of Defense Department of Transportation diphosgene dynes per centimeter Edgewood Chemical and Biological Center effective dosage of an aerosol ethyldichloroarsine. effective dose eastern equine encephalitis enterohemorrhagic extremely hazardous substances ethyl methylphosphonate emergency medical technician Environmental Protection Agency Emergency Response Guide Glossary-2 .f)-1:4-oxazepine o-chlorobenzylidene malononitrile (a tear agent) concentration time chemical warfare chemical warfare agent Chemical Weapons Convention Chemical Warfare Directional Detector phosgene oxime combat zone diphenylchloroarsine (a vomiting agent). Department of the Army diphenylcyanoarsine (a vomiting agent).

HN-3) nitric acid hour Hazardous Substance Data Bank mustard-T mixture high test hypochlorite (calcium hypochlorite) improved chemical agent monitor Institute for Defense Analysis immediately dangerous to life and health individual equipment decontamination kit International Labor Office inch(es) investigational new drug intelligence preparation of the battlespace International Program on Chemical Safety improved point detection system Glossary-3 .F F2 FAO FM FMD FMFM FP g GA GB g/cm3 GD GF GI g/ml F Fahrenheit fluorine Food and Agriculture Organization field manual foot and mouth disease Fleet Marine Field Manual freezing point gram(s) tabun (a nerve agent) sarin (a nerve agent) grams per cubic centimeter soman (a nerve agent) cyclosarin (a nerve agent) gastrointestinal grams per milliliter G H H2S H2SO4 HAZMAT HBr HC HCl HCN HD HF HFV H/HD HHS HL HN HNO3 hr HSBD HT HTH I ICAM IDA IDLH IEDK ILO in IND IPB IPCS IPDS H Levinstein mustard (a blister agent) hydrogen sulfide sulphuric acid hazardous material hydrogen bromide hexachloroethane hydrogen chloride hydrogen cyanide distilled mustard (a blister agent) hydrogen fluoride hemorrhagic fever virus sulfur mustards health and human services mustard-lewisite mixture nitrogen mustard (HN-1. HN-2.

and conventional K . biological. biological and chemical nuclear. 4-methylene dioxymethamphetimine (ecstasy) military decision making process methylfluorophosphonic acid milligrams milligrams per kilogram milligram-minute(s) per cubic meter milligram per milliliter military standard requisitioning and issue procedures minute mission oriented protective posture melting point methylposphonic acid Mine Safety and Health Administration minute volume minute volume (in liters) molecular weight not applicable North American Emergency Response Guide North Atlantic Treaty Organization Navy medical nuclear. methyldichloroarsine 3. liters medial lethal dosage of a chemical agent vapor or aerosol lethal dose median lethal dosage of a liquid chemical agent liters per minute d-lysergic acid diethylamide molarity (moles per liter) Massachusetts Marine Corps Combat Development Command Marine Corps Publication Distribution System Marine Corps Reference Publication Maryland. chemical.IR ISBN ISCS ITF JE JP JP-8 kg KHV L L LCt50 LD LD50 L/min LSD M M MA MCCDC MCPDS MCRP MD MDMA MDMP MFPA mg mg/kg mg/m3 mg-min/m3 mg/mL MILSTRIP min MOPP MP MPA MSHA MV MV(L) MW N N/A NAERG NATO NAVMED NBC NBCC Glossary-4 infrared International Standard Book Number International Chemical Safety Cards International Task Force J Japanese encephalitis joint publication jet fuel grade kilogram(s) Korean hemorrhagic fever lewisite.

NCI NCO NE ng NH3 NIOSH NJ NM NPG NPL NR NRC NTIS NTP NWDC NTRP NY OC OCONUS OH OPA OPR OSD OSHA P PB PCB PCl3 PCP PD PEL pH PHS PIC PMPA ppm PPR PS PSP PTP PVNTMED Q QL R RCA REL RF RMP O National Cancer Institute noncommissioned officer sulphur with small amounts of silica gel nanograms ammonia National Institute for Occupational Safety and Health New Jersey Dimethylpolysulfide NIOSH Pocket Guide National Priorities List none recommended National Response Center National Technical Information Service National Toxicity Program Navy Warfare Development Command Navy Tactical Reference Publication New York capsaicin outside the continental United States Ohio isopropylamine and isopropyl alcohol office of primary responsibility Office of the Secretary of Defense Occupational Safety and Health Administration pyridostigmine bromide polychlorinated biphenyls phosphorus trichloride phencyclidine phenyldichloroarsine. Pierce’s disease permissible exposure limit potential of hydrogen Public Health Service prior informed consent pinacolyl methylphosphonic acid parts per million peste des petits ruminants (pest of small ruminants) chloropicrin (a choking agent) paralytic shellfish poisoning Porton Technical Paper preventive medicine 2-diisopropylanminoethyl riot control agent recommended exposure limit Russian Federation risk management program Glossary-5 .

embryonic death and infertility sulphur dioxide special operations forces State Research Center supertropical bleach Shiga toxin-producing E. mummification.ROA ROD ROE RP RTECS RVF S SA SCP SCT SDK SEB SGF SGF-2 SME SMEDI SO2 SOF SRC STB STEC STEL SVD SWO T t½ TIB TIC TIM TIR TLE TLV TM TO TOF TRADOC TWA U UK UN UNEP UNEPO US USA USACMLS USAF USAMRIID USCG Glossary-6 rate of action rate of detoxification route of exposure red phosphorous Registry of Toxic Effects of Chemical Substances Rift Valley Fever arsine Standards Completion Program Secretariat of Communications and Transportation (Mexico) skin decontamination kit staphylococcal enterotoxin B smoke generation fuels fog oil subject matter expert stillbirths. coli short-term exposure limit swine vesicular disease staff weather officer half-life of a reaction toxic industrial biological toxic industrial chemical toxic industrial material toxic industrial radiological toxic load exponent threshold limit value technical manual theater of operation trioctylophosphite United States Army Training and Doctrine Command time-weighted average United Kingdom United Nations United Nations Environment Program United Nations Environmental Protection Organization United States United States of America United States Army Chemical School United States Air Force United States Army Medical Research Institute of Infectious Diseases United States Coast Guard .

coli a persistent nerve agent a persistent nerve agent western equine encephalitis tungsten hexafluoride World Health Assembly World Health Organization weapons of mass destruction white phosphorous World War I World War II zinc chloride Z Symbols µg µg/kg microgram micrograms per kilogram Glossary-7 .USDA USEPA USMC USN USSR UV V VEE VHF VND vol FP VTEC VX Vx WEE WF6 WHA WHO WMD WP WWI WWII ZnCl2 W United States Department of Agriculture United States Environmental Protection Agency United States Marine Corps United States Navy Union of Soviet Socialist Republics ultraviolet Venezuelan equine encephalitis viral hemorrhagic fever velogenic Newcastle disease volume vapor pressure vertoxin-producing E.

’s. (Stedman’s Medical Dictionary) acidosis – A state characterized by actual or relative decrease of alkali in body fluids in relation to the acid content. polybasic. and smoke. (The Textbook of Military Medicine) acetylcholinesterase – An enzyme that hydrolyzes acetylcholine very rapidly (thereby stopping its activity). Bilea. 4. nonflowering organisms that includes many seaweeds. Terms of Environment) amino acids – An organic acid in which one of the CH hydrogen atoms has been replaced by NH2. and one containing more than two. sharp to the taste. (Stedman’s Medical Dictionary) analogue – A compound that resembles another in structure but is not necessarily as isomer. Acetylcholinesterase is found at the receptor sites of tissue supplied with nerves by the cholinergic nervous system. giving an a. taurocholic and glyocholic a. algae (p) – A division of eukaryotic. In popular language. dibasic.g. (Stedman’s Medical Dictionary) anthrax – An acute bacterial disease caused by Bacillus anthracis. Most cholinesteraseinhibiting compounds are either organophosphates or carbamates. e. (Review and Recommendations for Human Toxicity Estimates for FM 311.a.. (EPA. (Stedman’s Medical Dictionary) acute – Of short and sharp course. Relating to a. sodium hydroxide.’s form salts by replacing all or part of the ionizable hydrogen with an electropositive element or radical. see specific names. any chemical compound that has a sour taste (given by the hydrogen ion). (JP 1-02) alga. (Stedman’s Medical Dictionary) ambient temperature . containing one ionizable atom of hydrogen in the molecule is called monobasic. used when bilary secretion is inadequate and for biliary colic.g. Sour.PART II – TERMS AND DEFINTIONS acetylcholine – The neurotransmitter of the cholinergic portion of the nervous system. For individual acids. (The Textbook of Military Medicine) acid – 1. ECBC-TR-349) aerosol – A liquid or solid composed of finely divided particles suspended in a gaseous medium. the L forms of these are the hydrolysis products of proteins. not chronic. Examples of common aerosols are mist. An α-amino acid is an amino acid of the general formula RCHNH2COOH. (Stedman’s Medical Dictionary) acute toxicity – Toxic effects occurring within moments to a few days of toxic exposure. A compound yielding a hydrogen ion in a polar solvent (e. 3. fog. photosynthetic.’s.Temperature of the surrounding air or other medium.9. one containing two such atoms.. potassium hydroxid. (Control of Communicable Diseases Manual) Glossary-8 . in water). An a.. 2. said of a disease. reaction. (Stedman’s Medical Dictionary) alkali – A strongly basic substance yielding hydroxide ions (OH-) in solution.

b. Arachnida (spiders. so that smooth movements occur. NH3. like. The components for binary VX (VX2) are ethyl 2-didsopropyl aminoethyl methylphosphonite (QL) and dimethylpolysulfide (NM). or otherwise initiated to produce a chemical agent. (USACHPPM TG 204) antiplant (biological) – Living organisms that cause disease or damage to plants.antibiotics – a soluble substance derived from a mold or bacterium that inhibits the growth of other microorganisms. It inhibits the action of acetylcholine at the muscle junction by binding to acetylcholine receptors. the effect of which depends o its arsenic content. (AR 50-6) Glossary-9 . crayfish. CN-. (JP 1-02) binary precursors . scorpions. react when mixed or combined as a result of being fired. launched. (The Biological & Chemical Warfare Threat) antigen – a molecule capable of eliciting a specific antibody or T-cell response. held in separate containers.The component chemicals that combine to produce binary chemical agents.. (Stedman’s Medical Dictionary) ataxia – An inability to coordinate muscle activity during voluntary movement. microscopic. plant-like organisms. Diplopoda (millipedes). (Medical Management of Biological Casualties Handbook) aqueous – Watery. especially one not inflammatory in character. Insecta. Chilopoda (centipedes). (Textbook of Military Medicine) antitoxin – An antibody formed in response to and capable of neutralizing a biological poison. (Stedman’s Medical Dictionary) arthralgia – Severe pain in a joint. (Stedman’s Medical Dictionary) antibody – A protein made by vertebrates as the immune response to a foreign macromolecule or antigen. (TM 3-216/AFM 355-6) base – Any molecule or ion that combines with a hydrogen ion. an animal serum containing antitoxins. Merostomata (horseshoe crabs). shrimps. mites. (Stedman’s Medical Dictionary) arrhythmia – Loss of rhythm. OH-. lobsters).g. ticks). (Stedman’s Medical Dictionary) binary chemical munition – A munition in which chemical substances. (Stedman’s Medical Dictionary) arsenical – Drug or agent. (Textbook of Military Medicine) bacteria – Single-celled. denoting especially an irregularity of the heartbeat. and various other extinct or lesser known groups. e. of. (Medical Management of Biological Casualties Handbook) arthropods – A member of the phylum Arthropoda that includes the classes Crustacea (crabs. or containing water. (Medical Management of Biological Casualties Handbook) atropine – Is used as an antidote for nerve agent poisoning. The components for binary GB (GB2) are methylphosphonic difluoride (DF) and isopropyl alcohol with an amine added (OPA). Examples of two common binary chemical agent components are as follows: a.

(Stedman’s Medical Dictionary) carcinogen – Any cancer-producing substance.boiling point – The temperature at which the vapor pressure of a liquid equals the pressure of the gas above it. including the cyanide group. (Control of Communicable Diseases Manual) brucellosis – A systemic bacterial disease characterized by irregular fever . (JP 1-02) bioregulator – Organic chemicals that regulate cell processes. Formerly called biotype. the filler of which is primarily a biological agent. (JP 1-02) botulism – Poisoning by toxin derived from the microorganism Clostridium botulinum. (General Chemistry with Qualitative Analysis. Normal boiling point is the temperature at which vapor pressure of a liquid equals one atmosphere (atm). (JP 1-02) biological environment – Conditions found in an area resulting from direct or persisting effects of biological weapons. This term is most frequently applied to a specific outbreak of acute disease in which all patients have been followed for an adequate period of time to include all attributable deaths. (JP 1-02) blood agent – A chemical compound. (JP 1-02) biological defense –The methods. (JP 1-02) biological operation – employment of biological agents to produce casualties in personnel or animals or damage to plants. (Control of Communicable Diseases Manual) Glossary-10 . or contraction of the orbicularis oculi muscle. and procedures involved in establishing and executing defensive measures against attacks using biological agents. plants. (The Biological & Chemical Warfare Threat) biovar – A group of bacterial strains distinguishable from other strains of the same species o the basis of physiological characters.) biological agent – A microorganism that caused disease in personnel. (JP 1-02) biological threat – A threat that consists of biological material planned to be deployed to produce casualties in personnel or animals or damage plants. (Stedman’s Medical Dictionary) blepharospasm – Spasmodic winking. the affects bodily functions by preventing the normal utilization of oxygen by body tissues. (JP 1-02) biological weapon – An item of materiel which projects. plans. or disseminates a biological agent including arthropod vectors. (Control of Communicable Diseases Manual) bubo – Inflammatory swelling of one or more lymph nodes in the groin. (Stedman’s Medical Dictionary) blister agent – A chemical agent which injures the eyes and lungs. Also called vesicant agent. (JP 1-02) biological ammunition – a type of ammunition. and burns or blisters the skin. (Stedman’s Medical Dictionary) case-fatality rate – Usually expressed as the percentage of persons diagnosed as having a specified disease who die as a result of that illness within a given period. disperses. or animals or causes the deterioration of materiel. 9th ed.

(JP 102) chemical warfare – All aspects of military operations involving the employment of lethal and incapacitating munitions/agents and the warning and protective measures associated with such offensive operations. that is taken or absorbed by the body. those two items will by referred to separately or under the broader term “chemical. duty status – whereabouts unknown. WHO) chemical agent – Any toxic chemical intended for use in military operations. of small ineffective doses of certain chemical agents to a point where eventual effect is similar to one large dose. (JP 1-02) chemical dose – the amount of chemical agent. (Hazardous Chemicals in Human and Environmental Health. (JP 1-02) chemical. or material. (JP 1-02) chemical environment – conditions found in an area resulting from direct or persisting effects of chemical weapons.casualty – Any person who is lost to the organization by having been declared dead. Also called CW. (JP 1-02) chemical operations – employment of chemical agents to kill. (JP 1-02) Chikungunya virus disease – A febrile viral disease characterized by arthalgia or arthritis. expressed in milligrams. (Stedman’s Medical Dictionary) central nervous system – The nervous system consisting of the brain and spinal cord. biological. (JP 1-02) chemical monitoring – the continued or periodic process of determining whether or not a chemical agent is present. and deny or hinder the use of areas. (JP 1-02) chemical ammunition – a type of ammunition. man or animals. (JP 102) chemical agent cumulative action – the building up. missing. (JP 1-02) chemical ammunition cargo – cargo such as white phosphorous munitions (shell and grenades). biological. ill. within the human body. or defense against such employment. plans and procedures involved in establishing and executing defensive measures against attack utilizing chemical agents. or injured. the filler of which is primarily a chemical agent. injure. facilities. and radiological operation – a collective term used only when referring to a combined chemical. (JP 1-02) catalyst – A substance that accelerates a chemical reaction but is not consumed or changed permanently thereby. and radiological operation (JP 102) chemical defense – the methods. (Control of Communicable Diseases Manual) Glossary-11 . or incapacitate for a significant period of time.” which will be used to include all types of chemical munitions/agents collectively. Since riot control agents and herbicides are not considered to be chemical warfare agents. (JP 1-02) chemical survey – the directed effort to determine the nature and degree of chemical hazard in an area and to delineate the perimeter of the hazard area.

temporarily or permanently . personnel. 2. Food and/or water made unfit for consumption by humans or animals because of the presence of environmental chemicals. (Medical Management of Biological Casualties Handbook) contamination – 1. or absorption of radioactive material. areas. remove. denoting the blood vessels of the heart. conjunctivae – The mucous membrane inventing the anterior surface of the eyeball and the posterior surface of the lids. that inhibits or prevents the functions of cells. (Control of Communicable Diseases Manual) cholinergic – Relating to nerve cells or fibers that employ acetylcholine as their neurotransmitter. (College Chemistry with Qualitative Analysis) Glossary-12 .cholera – An acute bacterial disease of serious consequence. nuclear. or both. (JP 102) contamination control – Procedures to avoid. (Stedman’s Medical Dictionary) cutaneous – Relating to the skin. or waste in the food or water. and chemical contamination for the purpose of maintaining or enhancing the efficient conduct of military operations. usually with reference to antibody. biological. evident when reduced hemoglobin I the blood exceeds 5 g/mL. or render harmless. bacteria or organisms. the decomposing material (to include the food substance itself). or objects. (JP 1-02) convulsion – A violent spasm or series of jerkings of the face. radioactive elements. or of biological or chemical agents on or by structures. or extremities. absorption. generally differing entirely in physical characteristics from any of its components. pl. (Medical Management of Biological Casualties) cyanosis – A dark bluish or purplish coloration of the skin and mucous membrane due to deficient oxygenation of the blood. (Stedman’s Medical Dictionary) coronary – Specifically. the byproduct of the growth of bacteria or organisms. (Stedman’s Medical Dictionary) compound – A substance formed by the covalent or electrostatic union of two or more elements. (Stedman’s Medical Dictionary) decomposition temperature – The temperature at which a chemical breaks down into two or more substances. trunk. (Stedman’s Medical Dictionary) conjunctiva. (Medical Management of Biological Casualties Handbook) coagulate – To convert a fluid or a substance in solution into a solid or gel. The deposit. reduce. (Stedman’s Medical Dictionary) corrosive – Causing gradual deterioration or consummation of a substance by another. causes destruction of cells. (Medical Management of Biological Casualties) cytotoxin – A specific substance. especially by biochemical or chemical reaction. (Stedman’s Medical Dictionary) concentration – The quantity of a substance per unit volume or weight.

neutralizing. to lose water. (The Biological & Chemical Warfare Threat) dosage – The amount of substance administered (or received) per body weight. (Stedman’s Medical Dictionary) dilate – To perform or undergo a physiologic or artificial enlargement of a hollow structure or opening. or removing chemical or biological agents. biological or radiological contaminants. (Review and Recommendations for Human Toxicity Estimates for FM 3-11. systems. in the strictest sense. group of diseases. (USACHPPM TG 204) Glossary-13 . ECBC-TR-349). is the dimmer of nitrogen dioxide. making harmless.9. sickness. Also called RDTE dilute solution. (Stedman’s Medical Dictionary) detection – The act of locating NBC hazards by use of NBC detectors or monitoring and/or survey teams. or organs. or disorder of body functions. cessation.decontamination – The process of making any person.the genetic material of all organisms and viruses (except for a small class of RNA-containing viruses) that code for structures and materials used in normal metabolism. (JP 102) decontamination station – A building or location suitably equipped and organized where personnel and material are cleansed of chemical. or area safe by absorbing. N2O4. object. destroying. (Stedman’s Medical Dictionary) disease – Morbus. (General Chemistry with Qualitative Analysis. (JP 1-02) defoliant operation . without loss of atoms (thus nitrogen tetroxide. (JP 1-02) degree of confidence – An indication of the level of confidence in each toxicity estimate.) desiccate – Exsiccation. or by removing radioactive material clinging to or around it. to dry thoroughly. (AR 50-6) dimer – A compound or unit produced by the combination of two like molecules. dehydrate – To extract water from. (Stedman’s Medical Dictionary) dilute solution – Solutions of chemical agents in concentration and quantities reduced by admixture (dilution) to levels that present significantly reduced hazards. It is a subjective evaluation based on the quality and quantity of the underlying data and the method(s) by which the estimate was derived. an interruption. (Stedman’s Medical Dictionary) density (liquid/solid) – Is the mass per unit volume of the substance. illness. (Stedman’s Medical Dictionary) deoxyribonucleic acid . 9th ed.The employment of defoliating agents on vegetated areas in support of military operations. (JP 1-02) defoliating agent – A chemical which causes trees. shrubs. and other plants to shed their leaves prematurely. or metabolic or structural anomaly. NO2). (JP 1-02) diathesis – The constitutional or inborn state disposing to a disease. to render free from moisture.

an organ. (Stedman’s Medical Dictionary) enterotoxin – Intestinotoxin. it is formed within the cell. (Stedman’s Medical Dictionary) enzyme – Organic catalyst. or energy absorbed in a unit volume. a protein. (Medical Management of Biological Casualties Handbook) Eastern and Western Equine Encephalitis. spinal cord. and characterized clinically by pain. the amount of substance. soluble. distinguished from endemic. tenesmus. radiation. (Stedman’s Medical Dictionary) environment – The milieu. usually heat labile. since the disease is not continuously present but has been introduced from outside. a subjective difficulty or distress in breathing. (Stedman’s Medical Dictionary) epidemic – A disease whose frequency of occurrence is in excess of the expected frequency in a population during a given time interval. JE) – A group of acute inflammatory disease involving the brain. antigenic. and meninges. WHO. often with blood and mucus. (Control of Communicable Diseases Manual) edema – An accumulation of an excessive amount of watery fluid in cells. secreted by cells. (Stedman’s Medical Dictionary) dyspnea – Shortness of breath. (Stedman’s Medical Dictionary) eruption – A breaking out. in contrast to exotoxin. usually associated with disease of the heart or lungs. a cytotoxin specific for the cells of the intestinal mucosal. (Stedman’s Medical Dictionary) end point – A biological effect used as an index of the effect of a chemical on an organism. (Medical Management of Biological Casualties Handbook) endemic –Present in a community or among a group of people. Japanese Encephalitis (EEE. that acts as a catalyst to induce chemical changes in other substances. the aggregate of all the external conditions and influences affecting the life and development of an organism. said of a disease prevailing continually in a region. (Stedman’s Medical Dictionary) erythema – Inflammatory redness of the skin. specially the appearance of lesions on the skin.dose – The amount of substance or energy that is taken into or absorbed by the body. fever. tissues. and dehydration. (USACHPPM TG 204) dysentery – A disease marked by frequent watery stools. itself remaining apparently unchanged by the process. WEE. or an individual. but is released into the environment Glossary-14 . injurious substance elaborated by certain gram-positive bacteria (rarely by gramnegative species). (Stedman’s Medical Dictionary) exotoxin – Extracellular toxin. or serous cavities. 2000) endogenous – Originating or produced within the organism or one of its parts. (Hazardous Chemicals in Human and Environmental Health. (Stedman’s Medical Dictionary) endotoxin – A bacterial toxin not freely liberated into the surrounding medium. a specific.

dissolution. 13th ed. (Hawley’s Condensed Chemical Dictionary. (Medical Management of Biological Casualties) flaccid – Relaxed. (The Biological & Chemical Warfare Threat) half-life – Of a reaction-time required for half of the original concentration of the limiting reactant to be consumed Also called t1/2. (Stedman’s Medical Dictionary) hemorrhage – Bleeding. 8th ed. and GF. is cable of reproducing itself exactly at each cell division. sarin (GB). (Stedman’s Medical Dictionary) genetic engineering – The directed alteration or manipulation of genetic material. (Stedman’s Medical Dictionary) flash point – The temperature at which a liquid or volatile solid gives off sufficient vapor to form an ignitable mixture near the surface of the liquid.where it is rapidly active in extremely small amounts.g. (Stedman’s Medical Dictionary) Far Eastern Tickborne Encephalitis – A tick-born viral diseases often associated with focal epilepsy and flaccid paralysis. or destruction of red blood cells in such a manner that hemoglobin is liberated into the medium in which the cells that are suspended. an escape of blood through ruptured or unruptured vessel walls. 9th ed. (Control of Communicable Diseases Manual) G-series nerve agents – Chemical agents of moderate to high toxicity developed in the 1930s that act by inhibiting a key nervous system enzyme. (JP 1-02) hemolysis – Alteration. (General Chemistry with Qualitative Analysis. or mission degradation. damage to or loss of equipment or property. flabby. and is capable of directing the formation of an enzyme or other protein.) gene – A functional unit of heredity which occupies a specific place or locus on a chromosome. (Stedman’s Medical Dictionary) freezing point/melting point – The temperature at which the solid and liquid phases of a given substance are in equilibrium and is generally equivalent to the melting point. various chemical agents.) hazard – A condition with the potential to cause injury. (Stedman’s Medical Dictionary) hepatitis – Inflammation of the liver. (Stedman’s Medical Dictionary) Glossary-15 . but sometimes from toxic agents. (The Biological & Chemical Warfare Threat) glanders – Communicable disease of horses. illness. alteration of temperature. toxins. usually from a viral infection. or without tone. tonicity. or death of personnel. soman (GD). e. mules. (College Chemistry with Qualitative Analysis. and donkeys. (Control of Communicable Diseases Manual) febrile – Denoting or relating to a fever.. by specific complement-fixing antibodies.) foliar – Pertaining to or resembling a leaf or leaflet. Examples are Tabun (GA).

Pathogens with high infectivity cause disease with relatively few organisms. (General Chemistry with Qualitative Analysis. (Stedman’s Medical Dictionary) intoxication – Poisoning. (Stedman’s Medical Dictionary) ileus – Mechanical. absence of passage of stool. or academia. When an inversion exists.) hygiene – Cleanliness that promotes health and well being. (FM 8-9) inflammation – aA fundamental pathologic process consisting of a dynamic complex of cytologic and histologic reactions that occur in the affected blood vessels and adjacent tissues in response to an injury or abnormal stimulation caused by a physical. 9th ed. may be accompanied by severe colicky pain. especially of a personal nature. Also called III. or areas dangerous for human use. dynamic. natural to the country where found. (Stedman’s Medical Dictionary) intravenous – Within a vein or veins. (Stedman’s Medical Dictionary) insecticide – An agent that kills insects. vomiting. or (b) seriously ill or injured and the illness or injury makes the person physically or mentally unable to communicate with the next of kin. The atmosphere is stable and normally is considered the most favorable state for ground release of chemical agents. which will render individuals incapable of concerted effort in the performance of their assigned duties. (Stedman’s Medical Dictionary) inversion – An increase of air temperature with increase in altitude (the ground being colder than the surrounding air). (Stedman’s Medical Dictionary) incapacitating agent – An agent that produces temporary physiological or mental effects. (JP 1-02) hydrolysis – The reaction of a compound with water whereby decomposition of the substance occurs. or biologic agent. abdominal distention. (Control of Communicable Diseases Manual) indigenous – Native. or adynamic obstruction of the bowel.herbicide – A chemical compound that will kill or damage plants. (FM 3-6) Glossary-16 . there are no convection currents and wind speeds are below 5 knots. government. and chloropicrin are industrial chemicals that also can be military chemical agents. (Stedman’s Medical Dictionary) industrial chemicals – Chemicals developed or manufactured for use in industrial operations or research by industry. Hydrogen cyanide. or both. facilities. (JP 1-02) incubation period – The interval (in hours. These chemicals are not primarily manufactured for the specific purpose of producing human casualties or rendering equipment. or weeks) between the initial. days. phosgene. (JP 1-02) infectivity – The infectivity of an agent reflects the relative ease with which microorganisms establish themselves in a host species. cyanogen chloride. (JP 1-02) incapacitating illness or injury – The casualty status of a person (a) whose illness or injury requires hospitalization but medical authority does not classify as very seriously ill or injured. effective exposure to an infectious organism and the first appearance of symptoms of the infections. chemical. and often fever and dehydration.

(Stedman’s Medical Dictionary) jaundice – A yellowish staining of the integument. lesion – One of the individual points or patches of a multifocal disease. serving as a covering or envelope of a part. (Stedman’s Medical Dictionary) lachrymator (lacrimator) – An agent (such as tear gas) that irritates the eyes and produces tears. hurricane. which are increased in the plasma. and deeper tissues and the excretions with bile pigments. 13th ed. sclerae. often the first indication of an infection or other disease. (Stedman’s Medical Dictionary) mass casualty – Any large number of casualties produced in a relatively short period of time. (Stedman’s Medical Dictionary) malaise – A feeling of general discomfort or uneasiness. or armed attack that exceeds local logistical support capabilities. (Stedman’s Medical Dictionary) meningitis – Inflammation of the membranes of the brain or spinal cord. (JP 1-02) mean lethal dose – The dose of chemical agent that would kill 50 percent of exposed. flood. (JP 1-02) median incapacitating dose – The amount or quantity of chemical agent which when introduced into the body will incapacitate 50 percent of exposed. unprotected personnel. (Control of Communicable Diseases Manual) macular – Relating to or marked by a small spot. an out-of-sorts feeling. For chemical operations. (Control of Communicable Diseases Manual) membrane – A thin sheet or layer of pliable tissue. perceptibly different in color from the surrounding tissue. (FM 3-6) latent heat of vaporization – The quantity of energy absorbed or given off as a substance undergoes a change in state with no change in temperature. earthquake.ion – An atom or group of atoms carrying an electric charge by virtue of having gained or lost one or more valence electrons. This condition usually occurs when skies are clear and between 1100 and 1600 hours. (Stedman’s Medical Dictionary) Lymphocytic Choriomeningitis – A viral infection of animals. (JP 1-02) Melioidosis – An uncommon bacterial infection with manifestations ranging from benign to fatal septicemia. Strong convection currents exist during lapse conditions. transmissible to humans. (Hawley’s Condensed Chemical Dictionary. (Stedman’s Medical Dictionary) Glossary-17 .) Also called Enthalpy of vaporization (∆Hv). (Stedman’s Medical Dictionary) lapse – A marked decrease in air temperature with increasing altitude because the ground is warmer than the surrounding air. unprotected and untreated personnel. usually as the result of a single incident such as a military aircraft accident. local time. the state is defined as unstable. This condition is normally considered the most unfavorable for the release of chemical agents. as a partition or septum or to connect two structures. the lining of a cavity.

(USACHPPM TG 204) nerve agent – A potentially lethal chemical agent which interferes with the transmission of nerve impulses. headaches. or of a portion of tissue or organ. This amount represents mild activity. (Stedman’s Medical Dictionary) Glossary-18 . navigating on foot. full-strength (as manufactured) chemical agent. (Control of Communicable Diseases Manual) morbidity – The ratio of sick to well individuals in a community. (USACHPPM TG 204) miscible – Capable of being mixed and remaining so after the mixing process ceases. (JP 1-02) neural – Relating to any structure composed of nerve cells or their processes.) molecule – The smallest possible quantity of a di-. or that o further development will evolve into nerve cells. or inhalation. to identify. (USACHPPM TG 204) myalgia – Muscular pain. They exhibit great stability and heat resistance. (Stedman’s Medical Dictionary) minute volume – The amount of air expelled from the lungs in a minute that is assumed to be 15 L. (USACHPPM TG 204) mydirasis – Dilation of the pupil. resulting from irreversible damage. Mycotoxins are difficult to detect. They can cause illness or death upon ingestion skin contact. The pupil is unable to dilate and remains contracted. or polyatomic substance that retains the chemical properties of the substance. (Steadman’s Medical Dictionary) myiasis – Any infection due to invasion of tissues or cavities of the body by larvae of dipterous insects. (Medical Management of Biological Casualties Handbook) mycotoxin – A fungal toxin. sick rate. (AR 50-6) necrosis – Pathologic death of one or more cells. identifying or engaging targets. performance of tasks. unless otherwise stated. 9th ed. or driving vehicles is practically impossible. (Stedman’s Medical Dictionary) Monkeypox – A sporadic zoonosic infection resembling smallpox. and to decontaminate. (USACHPPM TG 204) miosis – The excessive smallness or contraction of the pupil of the eye.microbes – Any very minute organism. consisting of cardiac muscle. tri-. (Steadman’s Medical Dictionary) neat chemical agent – A nondiluted. thus. A chemical agent manufactured by the binary synthesis route will also be considered a neat agent regardless of purity. and pinpointing of the pupils. (General Chemistry with Qualitative Analysis. (Stedman’s Medical Dictionary) molecular weight – The value represented by the sum of the atomic weights of all the atoms in a molecule. (Stedman’s Medical Dictionary) myocardia – The middle layer of the heart. Miosis is often accompanied by pain.

conducts or transmits nerve impulses. and chemical capable nation – A nation that has the capability to produce and employ one or more types of nuclear. WHO) neutralization – The act of altering chemical. (Hazardous Chemicals in Human and Environmental Health.neuro. or intramedullary injection. (JP 1-02) nuclear. (AR 50-6). and toxicological properties to render the chemical agent ineffective for use as intended. WHO) neurotoxin – Any substance that is capable of destroying or adversely affecting nerve tissue. WHO) neurotransmitter – Chemical responsible for the transfer of information along the nervous system. referring particularly to the introduction of substances into an organism by intravenous. (Stedman’s Medical Dictionary) operational decontamination – Decontamination carried out by an individual and/or a unit. subcutaneous. (Stedman’s Medical Dictionary) oxidize – To combine or cause an element or radical to combine with oxygen or lose electrons. many pesticides and virtually all nerve agents are organophosphorus combpounds. as well as decontamination of mission-essential spares and limited terrain decontamination. (General Chemistry with Qualitative Analysis) organophosphorus compound – A compound. NH2OH. (JP 1-02) organic solvent – An organic chemical compound that dissolves another to form a solution. biological. (Stedman’s Medical Dictionary) parenteral – By some other means that through the GI tract. and chemical weapons across the full range of military operations and at any level of war in order to achieve political and military objectives. (JP 1-02) pathogenic – Causing disease or abnormality. nonpersistent agent – A chemical agent that when released dissipates and/or loses its ability to cause casualties after 10 to 15 minutes.Combining form denoting a nerve or relating to the nervous system. physical. material and/or working areas. (Stedman’s Medical Dictionary) oxime – A compound resulting from the action of hydroxylamine. intramuscular. (JP 1-02) odor – Emanation from any substance that stimulates the olfactory cells in the organ of smell. (Hazardous Chemicals in Human and Environmental Health. This may include decontamination of the individual beyond the scope of immediate decontamination. restricted to specific parts of operationally essential equipment. on a ketone or an aldehyde to yield the group ═N-OH attached to the former carbonyl carbon atom. in order to minimize contact and transfer hazards and to sustain operations. (Steadman’s Medical Dictionary) Glossary-19 . whose physiological effects include inhibition of cholinesterase. (Stedman’s Medical Dictionary) pathogen – A disease-producing microorganism. containing phosphorus and carbon. (Hazardous Chemicals in Human and Environmental Health. (Stedman’s Medical Dictionary) neuron – The functional unit of the nervous system. biological..

(General Chemistry with Qualitative Analysis. or treated to protect personnel against hazards cause by extreme changes in physical environment. which transfer the bacterial infection to various animals and to people. 9th ed. (Stedman’s Medical Dictionary) prostration – A marked loss of strength. (JP 1-02) pesticide – General term for an agent that destroys fungi. rodents. Strictly speaking. (General Chemistry with Qualitative Analysis. dangerous working conditions. (JP 1-02) Glossary-20 . insects. when released. refers to route of entry into the body. or enemy action. (JP 1-02) persistent agent – A chemical agent that. (Stedman’s Medical Dictionary) polypeptide – A petide formed by the union of an indefinite (usually large) number of amino acids by peptide likes (-NH-CO-). A value of seven is neutral. when applied to chemical agents. pH is the negative logarithm of the hydrogen-ion concentration.Chemical agents may exist as solids. large numbers are alkaline. (Stedman’s Medical Dictionary) potable – Water that is free from disease-producing organisms.peptide – Molecules formed from two or more amino acids linked by peptide bonds. poisonous substances.) plague – A zoonosis involving rodents and their fleas. as distinguished from the serum obtain after coagulation. (Stedman’s Medical Dictionary) polymerize – To bring about a reaction in which a high molecular-weight product is produced by successive addition to or condensations of a simpler compound. or gases. (The Biological & Chemical Warfare Threat) persistency – In biological or chemical warfare. as in exhaustion.) percutaneous – Through the skin. remains able to cause casualties for more than 24 hours to several days or weeks. and chemical or biological agents and radioactive contaminants that make it unfit for human consumption and many other uses. (Stedman’s Medical Dictionary) protective clothing – Clothing especially designed. low numbers are acid. (Stedman’s Medical Dictionary) pH – A measure of the acidity or alkalinity of a solution. (Stedman’s Medical Dictionary) postmortem – Pertaining to or occurring during the period after death. (FM 10-52) physical state . (FM 10-52) prophylaxis – Prevention of disease or of a process which can lead to disease. or any other pest. 9th ed. liquids. (Medical Management of Biological Casualties Handbook) proteins – Macromolecules consisting of long sequences of α-amino acids in peptide (amide) linkage. (Control of Communicable Diseases Manual) plasma – The fluid (noncellular) portion of the circulating blood. the characteristics of an agent which pertains to the duration of its effectiveness under determined conditions after its dispersal. fabricated.

by chemical or biological means. generalized chlamydial disease caused by Chlamydia psittaci. formations and equipment in the control of violent disorders. (Stedman’s Medical Dictionary) pyridostigmine bromide – An antidote enhancer that blocks acetylcholinesterase. including radies virus and vesicular stomatitis virus (of cattle). antigen. PB increases survival provided that atropine and oxime (Mark I NAAK) and other measures are taken. Also called PB. (Textbook of Military Medicine) Q fever – An acute febrile rickettsial disease caused by Coxiella burnetii. protecting it from nerve agents. which can produce rapidly in humans sensory irritate or disabling physical effects which disappear within a short time following termination of exposure. (Stedman’s Medical Dictionary) reagent – Any substance added to a solution of another substance to participate in a chemical reaction. of a sequence (a whole or partial chain of DNA) not originally present in that chain. new ones being formed in their place. Also called ROA. or neurotransmitter. Also called RCA. whereby these substances are caused to disappear. a family of rod. such as hormone. (JP 1-02) reaction – In chemistry. the intermolecular action of two or more substances upon each other. (Stedman’s Medical Dictionary) rhabdovirus – Any virus of the family Rhabdoviridae. When taken in advance of nerve agent exposure. (Stedman’s Medical Dictionary) rickettsiae – Intracellular parasitic organisms in size between bacteria and viruses. (JP 1-02) Rocky Mountain Spotted Fever – A disease of the spotted fever group rickettsiae caused by Rickettsia rickettsii.or bulletshaped viruses of vertebrates. (TM 3-216/AFM 355-6) riot control agent – Any chemical that is not listed in the Chemical Weapons Convention. (Stedman’s Medical Dictionary) recombinant DNA – DNA resulting from the insertion into the chain. (Stedman’s Medical Dictionary) rate of action – The rate at which the body reacts to or is affected by agent.Psittacosis – An acute. (JP 1-02) riot control operations – The employment of riot control agents and/or special tactics. and plants. insects. (Control of Communicable Disease Manual) Glossary-21 . (Stedman’s Medical Dictionary) receptor – A structural protein molecule on the cell surface or within the cytoplasm that binds to a specific factor. (Control of Communicable Disease Manual) quarantine – The isolation of a person with a known or possible contagious disease. (DA PAM 385-61) rate of detoxification – The rate at which the body is able to counteract the effects of poisonous substance (DA PAM 385-61) ratification – The declaration by which a nation formally accepts with or without reservation the content of a standardization agreement. (Control of Communicable Disease Manual) pulmonary – Relating to the lungs.

(Stedman’s Medical Dictionary) synergistic – Acting together to enhance the effect of another force or agent. (General Chemistry with Quyalitative Analysis.) specific heat – The quantity of heat required to raise the temperature of 1 gram of a substance one degree C. or antelope.g. such as a gas. supply routes. cow. an effector (muscle. affecting all body systems and organs. or a sensory receptor cell. the sheep. (Stedman’s Medical Dictionary) systemic – Spread throughout the body. gland) cell. logistic facilities.rodenticide – An agent legal to rodents. recovery operations. 9th ed. (Stedman’s Medical Dictionary) Smallpox – A systemic viral disease caused by the Variola virus. obstacle breaching.. (USACHPPM TG 204) Glossary-22 . (USACHPPM TG 204) synthesize – The formation of compounds by the union of simpler compounds or elements. (Control of Communicable Disease Manual) septicemia – Systemic disease caused by the spread of microorganisms and their toxins via the circulating blood. (USACHPPM TG 204) synapse – The functional membrane-to-membrane contact of the nerve cell with another nerve cell. (Control of Communicable Disease Manual) slurry – A thin semifluid suspension of a solid in a liquid. (USACHPPM TG 204) sternutator – A substance. and amphibious assault operations as well as key assembly areas. 9th ed. (JP 1-02) solubility – The quantity of solute that will dissolve in a given amount of solvent to produce a saturated solution. dormant cell of some bacteria. e. (Stedman’s Medical Dictionary) ruminant – An animal that chews the cud.) spore – Resistant. (General Chemistry with Qualitative Analysis. material regurgitated from the rumen for rechewing. primitive reproductive bodies of fungi. deer. (Stedman’s Medical Dictionary) Shigellosis – An acute bacterial disease involving the large and distal small intestine. that induces sneezing. (Stedman’s Medical Dictionary) Salmongellosis – A bacterial disease manifested by acute enterocolitis. (Stedman’s Medical Dictionary) stupor – A state of impaired consciousness in which the individual shows a marked diminution in his reactivity to environmental stimuli. Signs or observations are made about an individual or an animal that may indicate illness or injury. (Control of Communicable Disease Manual) smoke screen – A cloud of smoke used to conceal ground maneuver. (Stedman’s Medical Dictionary) symptoms – Information related by an individual about himself/herself that may indicate illness or injury. not localized in one spot or area.

(Control of Communicable Disease Manual) Glossary-23 . or ideological. Volume V. (JP 1-02) toxoid – A toxin biologically inactivated by chemical or physical means. Chronic toxicity is the ability of a substance or mixture of substances to cause harmful effects over an extended period. (JP 1-02) tetrodotoxin – A highly poisonous fugu toxin. and the passage of but little fecal matter or urine. usually for vaccine production purposes. animals. as distinguished from inorganic poisons. Acute toxicity involves harmful effects in an organism through a single or short-term exposure. or ideological objectives. (Stedman’s Medical Dictionary) terrorism – The calculated use of unlawful violence or threat of unlawful violence to inculcate fear. Because a prerequisite for toxoid generation is toxin production. usually upon repeated or continuous exposure sometimes lasting for the entire life of the exposed organism. (JP 1-02) toxicity – The degree to which a substance or mixture of substances can harm humans or animals. or crops. (Joint CB Technical Data Source Book. intended to coerce or to intimidate governments or societies in the pursuit of goals that are generally political. Terms of Environment) toxins – Poisonous substances produced by living organisms. religious. Such poisons can also be manufactured by a synthetic process. terror. Subchronic toxicity is the ability of the substance to cause effects for more than one year but less than the lifetime of the exposed organism.tenesmus – A painful spasm of the anal sphincter with an urgent desire to evacuate the bowel or bladder. (JP 1-02) terrorist – An individual who uses violence. using injurious agents of chemical. (EPA. (USACHPPM TG 204) toxic chemical. (USACHPPM TG 204) toxic – Harmful to living organisms. and intimidation to achieve a result. (JP 1-02) terrorist groups – Any element regardless of size or espoused cause. oisonous. or radiological attack – An attack directed at personnel. involuntary straining. biological. (The Biological & Chemical Warfare Threat) toxin agent – A poison formed as a specific secretion product in the metabolism of a vegetable or animal organism. that commits acts of violence or threatens violence in pursuit of its political. religious. the technology involved has applicability to BW. (Textbook of Military Medicine) thickened agent – An agent to which a polymer or plastic has been added to minimize vaporization prior to its deposition on the target. (The Biological & Chemical Warfare Threat) Trench fever – A nonfatal bacterial disease. biological. Part One: Agent H) toxemia – A condition caused by the circulation of toxins in the blood. or radiological origin.

13th ed. VM. spiders. Different microorganisms and different strains of the same microorganism may cause diseases of different severity. although not a true vesicant.trichothecene mycotoxin – A very large family of chemically related toxins produced by various species of mold to include Fusarium. (Stedman’s Medical Dictionary) urticant – The third group listed under blister agent. (General Chemistry with Qualitative Analysis. of a virus in the bloodstream.) vector – An animal. 9th ed. (FM 8-9) Glossary-24 . VS. scorpions. (The Biological & Chemical Warfare Book) vaccine – A substance administered to induce immunity in the recipient. (Stedman’s Medical Dictionary) viremic – The presence. (Stedman’s Medical Dictionary) viable – Capable of living. etc. (Control of Communicable Disease Manual) ultraviolet – Denoting electromagnetic rays beyond the violet end of the visible spectrum. mosquitoes and man. The are generally persistent and have a moderate to high toxicity. insect. and VX. (Textbook of Military Medicine) Tularemia – A zoonotic bacterial disease. and urticaria. (The Biological & Chemical Warfare Threat) vapor density – The ratio of the weight of a given volume of a gaseous substance and that of the same volume of another gas measured under the same conditions of pressure and temperature. (The Biological & Chemical Warfare Threat) The virulence of an agent reflects the relative severity of disease produced by that agent. Examples are VE. (Stedman’s Medical Dictionary) vesicle – A small circumscribed elevation of the skin containing fluid. (USACHPPM TG 204) Venezuelan Equine Encephalomyelitis Virus Disease – A viral infection involving a cycle with horses. (Textbook of Military Medicine) V-series nerve agents – A class of chemical agents developed in the 1950s that act by inhibiting a key nervous system enzyme. wheals. Causes erythema. (Control of Communicable Disease Manual) venom – A poisonous fluid secreted by snakes. or other organism that carries and transmits a virus or other microorganism. VG. as in smallpox. (Hawley’s Condensed Chemical Dictionary. (Stedman’s Medical Dictionary) virulence – The capacity of a microorganism to produce disease. (Control of Communicable Disease Manual) Typhus fever – A rickettsial disease transmitted by body lice.) vapor pressure – The pressure exerted by a vapor when a state of equilibrium exists between the vapor and its liquid (or solid) state.

the resistance to flow or alteration of shape. animals. (Stedman’s Medical Dictionary) volatile – Capable of vaporizing or evaporating readily. Weapons of mass destruction can be high explosives or nuclear. hollow and multilayered walled organs. WHO) volatility – The tendency of a solid or liquid material to pass into the vapor state at a given temperature. (Stedman’s Medical Dictionary) viscosity – In general. Also called WMD. and radiological weapons. urogenital. a disease of humans acquired from an animal source. (USACHPPM TG 204) Glossary-25 . and means of delivery and deployment (if applicable) required for self-sufficiency.virus – Any of a large group of submicroscopic agents infecting plants. respiratory. chemical. 13th ed. personnel. services. (JP 1-02) weapon(s) system – A combination of one or more weapons with all related equipment. and endocrine systems as well as the spleen. (JP 1-02) zoonosis – An infection or infestation shared in nature by humans and other animals that are the normal or usual host. the heart. (Hazardous Chemicals in Human and Environmental Health. by any substance as a result of molecular cohesion.) weapons of mass destruction – Weapons that are capable of a high order of destruction and/or of being used in such a manner as to destroy large numbers of people. (USACHPPM TG 204) visceral – Relating to an organ of the digestive. materials. (Hawley’s Condensed Chemical Dictionary. biological. most frequently applied to liquids as the resistance of a fluid to flow because of a shearing force. and bacteria and unable to reproduce outside the tissues of the host. and great vessels. but exclude the means of transporting or propelling the weapon where such means is a separable and divisible part of the weapon.

II-60. L-5. II-1. II35. IV-8. L-6 biological agent I-1. IV29. II-10. II-47. E-6. E-4. II-33. I-3. F-1. J-2. IV-1. G-2. I-2. G-9. I-6. I-8. I-4. II38. L-6 barley yellow dwarf IV-28. H-16 Aerosol I-3. III-10. III-11. III-13. II-58. III-14. IV-11. I-10. J-1. II-31. G-14. II-6. G-2. H-17 blood agent I-4. K-7 atomic weight II-1. I3. I-10. II-67. II-4. II-25. G-15. G-5. G-2. IV-27. IV-30. V-1. III-13. K-1. G- 5. E-5. IV-7. IV-27. I-13. K-3. II-1. G-7. II-28. G-9. IV-5. II-13. I-1. G-14. II-9. IV17. IV-12. E3. III-18. H-1 chemical agent I-1. II-42. IV-6 BZ II-1. F-1. III-16. IV-20. I-5. I-6. II-6. III-14 arsine See SA Asiatic Newcastle Disease K-4. III14. I-5. II-15. IV-27 brucella melitensis IV-3. II-35. II-78. IV-30. III-23 chemical compound I-4. IV-3. II-39. IV-3. II49. J-2 Argentine Disease IV-16 arsenicals II-38. II-77. L-1. IV-20. III-8. IV-27 brucella suis IV-3. G-15 chikungunya virus IV-12. IV-6. I-5. III-15. II-10. II-65. G-5. II-4. I-2. I-10. G-10 choking agent I-4. C-3 B bacillary dysentery IV-6 bacteria I-7. G-14. G4. G-8. I-7. I1. I-9. III-12.INDEX A AC I-4. II-62 II64. III-1. IV-21. I-5. V-2. F-1. G-8. F-1. G-2. I-10. II-4. I-2. G-7. G-1. I-5. L-5. II-55. III3. I-5. IV-27. G-15 C CG II-1. IV-27. H-1 Index-1 . K-5 aerosol stability I-2 African Swine Fever IV-28. L-2. IV-7. IV-29. IV-19. III-6. IV-23. I-4. K-4. G-3. III-13. II34. K-7 Bolivian Disease IV-16 botulinum toxin IV-20. G-3. G-6. G-5. I-4. IV-29 chlorine II-34. IV-1. IV-15. J-3 biological weapons I-2. II-51. II-16. C-2. G-4. II-78. IV-22. II-1. II-11. II-5. IV-18. IV-9. I-7. I-9. H-16 bluetongue IV-28. II-4. IV-2. G-4. II-22. II-5. IV-3. II-52. E-2. IV-3. II-67. K-2. IV-9. G-6. IV-13. IV-10. IV-27. I-11. G-3. II-4. L-6 banana bunchy top IV-28. K-7 anthrax I-9. J-2 bubonic plague IV-5. I-6. II-13. IV-25. E-4. IV-2. III-17. III-19. III-16. G-3. F-1. I9. F-1. IV-27 brucellosis IV-2. II-45. IV-16. II-32. F-1. IV-30. IV-4. I-3. I-8. II-9. IV-27 chlamydia psittaci IV-6. II-69. III-17. II-1. II-2. III-1. II-12. G-4. II4. G14. I-15 blister agent I-5. IV-4. IV-2. I-2. IV-14. II19. IV-28. D-2. III-7. III-9. II-9. IV-24. G-14. G-15. J3 brucella abortus IV-3. II-37. III-23. IV-26. III-14. G-14. IV-11. II-33. I-3. IV-27. II-32. F-1. I7. III-5. II-11. II-1. IV-23. IV-8.

E-3.cholera I-9. II-14. I-4. IV-29 Index-2 . H-8. E-5 cyanogen chloride See CK cyclosarin See GF cytotoxin IV-22. IV1. III-12. H-10. II-22. G-3. G-6. II-61. E-4. II-63. G-5. II-60. II-32. G-2. G-14. G-9. E-5. II-74. IV-27 clostridium perfringens toxin IV-21. II-7. G-14. II-26. G15 clostridium botulinum IV-20. II-50. G-14. II-70. G-14. J-2 CX II-1. II-23. II-18. II-55. II-56. G-5. K-8 crimean-congo hemorrhagic fever IV12. F-1. II-58. II-58. H-18. IV-14. IV-29. G-15 ethyldichloroarsine See ED exotoxin IV-24 F far eastern tick-borne encephalitis IV14. II-17. II-24. F-1. II-37. E-4. II-13. H32 cyanide I-4. G-2. II-34. K7 fowl plague IV-28. E-4. E-5. G-6. II-39. II-33. E-1. E-1. IV-2. E-1. J-3 contagious bovine pleuropneumonia IV-28. II-13. E-2. II-1. IV-4. H-1. E-4. I-4 E eastern equine encephalitis (EEE) IV13. II-69. E-5. H12. F-1. K-7 1. E-3. G- 7. G-4. K-2. II-59. K-1. E-5. G15. II-49. E-5. II-16. F-1. II-38. II-46. G-3. G-8. L-2 colletorichum coffeanum IV-28. G-7. IV-27 G GA II-1. II-48. K-8 contagious equine metritis IV-28. F- ED II-1. II-16. G-3. II-15. II-64. II-40. H-3. G-15. G-4. E-2. H-7 GD I-7. G-4. II-15. E-2. H-6. IV-27. II-53. IV-27. J-2 Ebola Viral Hemorrhagic Fever IV-14. H-2. IV-27. II-35. II-19. G-15. II-26. IV-15. H-10 GF II-1. II-14. H-13 glanders IV-4. G-9. J-2 CK I-4. K-3. G-6. II-12. G-8. L-2 conotoxin IV-22. G15. II-23. J-2 foot-and-mouth disease IV-28. E-1. E-3. H-17. F-1. G-7. II-20. II-11. II-79. K-6. E-4. G-14. G- 3. II-14. II-62. G-15. II-54. II-25. H-9. J-2 diphosgene See DP distilled mustard See HD DP II-1. E5. G-5. II-26. G-3. II-17. G-14. IV-27. III-16. II-23. G-14. F-1. H-1 dysentery IV-6. I-4. II-22. E-3. G-4. G-2. E-1. J3 cochiliobolus miyabeans IV-28. II-31. II-34. G-15. G-2. II-25. H-11. H-7. G-3. F-1. G-15. IV-27. E-2. II-35. II-21. G-4. E-2. H-5. II-19. G-8. G-5. K-6. G-5. II-20. G-2. G-5. III-20. J-2 goat pox IV-28. IV-23 D dengue fever IV-13. II-33. G-2. G-9. II-43. II-40. II-3. G-14. IV-27. H-19 hog cholera IV-28. IV-7. K-7 francisella tularensis IV-7. H-4 GB II-1. II-29. K-7 H hantavirus IV-15 HD II-1. G-14. K-2. G-4. F-1. H-4. IV-28.

IV-2. G-7. I-13. F-1. II-54. G-8. IV-13. G-6. J-3 lethal dose I-9. E-5. IV-8. III-7. E-5. II12. I-7. I-1. II-69. II-15. II-34. G-5. III7. II-56. IV-3. II-38. II-4. II6. II-39. E-4. III-18. F-1. III-17. II-61. G-6. III-12. II-54. K-4. I-2. II-51. I-9. IV-8. H-2. II-15. G-8. II-48. IV-17. III-21. F-1. II-53. I-11. IV-6. II-31. E-4. H-1 Newcastle Disease IV-28. IV-9. II42. H-7. II-68. II-65. IV-17. III-13. F-1. III-5. H-10. J-2 prophylaxis IV-2. G-9. I-9. II-3. II-46. II-65. J-3 N nerve agent I-4. F-1. I-3 molecular weight II-1. IV-25. IV-29. L-1 persistent I-1. G-15. H-30. IV-15. H-24. II-30. IV-28. H-32 lewisite See L lyssa virus IV-28. II-20. IV-10. I-14. II-10. IV-21. IV-27 Marburg IV-14. III-9. II-25. IV-4. IV-16. II-39. II22. III-20. G7. II-72. III-18. II-33. H-20. IV-5. II-14. IV-19. II-41. IV-12. J-3 mustard-lewisite See HL mustard-T mixture See HT mycotoxin I-9. I-2. H-29 lassa fever IV-16. V-2. II-50. F-1. III-4. G-2 I incapacitating agent I-4. IV-15. IV-7. IV-9. II-32. H-4. H-28. II-46. K-7 nitrogen mustard II-27. II-28. II-24. G-14. II-48. II-65. H-16. H-26. H-14. I-8. II-47. E-4 Index-3 . H-27 hydrogen cyanide I-4. I-12. II30. II-62. III-4. E-2. E-4 phosgene See CG phosgene oxime See CX plague IV-5. II73. II-47. E-2. II-70. H-1. II-36. IV-26. IV-1. II-68. II-63. I1. II-57. I-5. II-52. II59. G-7 microorganism I-3. D-1. II-39. G14. G-2. II-75. G-6. K-1. H-8. II-21. II77. K-5 infective dose I-9. H-22. IV-26. H-26. III-2. I-4. II-59. IV-25. G-9. IV-1. II-32. II-37. II-33. III-10. G-4. IV-29. II-78. IV30. G-6. II-37. III-15. G-9. IV-14. IV-24. G-14 incubation period I-9. IV-18. II-1. II-61. II44. II-48.HT II-1. I-4. IV-23. IV-2. IV-20. II-43. IV-27. I-5. IV-28. II-67. II-50. G8. IV-15 junin IV-16. H-5. II-24. II-49. IV-29. II-76. E-6. IV-5. II-19. II-79. II-42. I-3. IV14. II-40. IV-27 melting point I-5. II-64. V-1. IV-26. II-13. IV-30. II-51. III-19. G-15. IV-27. IV16. H-28. G-6 O organophosphate I-12 oxidase II-31 P pathogens I-2. IV-18. H-17. IV-12. E-3. I-2 J japanese encephalitis (JE) IV-13. IV-27 L L II-1. G-3. G-15 pesticide I-10. G-14. H-13. IV-22. I-7. II-1. IV-11. IV-6. G-7. G-2. III12. II-41. K-3 M Machupo IV-16. II-18. III-13. II-64. III-11. IV-23. G-10 monkeypox IV-17. I-9. II-27.

II-21. II-76. II-27. II-72. II-36. II-65. E-4. II-28. II-38. II-54. II-75. II-63. II-46. I-5. I-6. II-76. II-74. II-3. II13. K-2 shiga toxin IV-22. III-17. III-19. II-18. K-1. F-1. III-18. II-62. II-34. II-41. K-4. J-2 typhus fever IV-11. IV-27. IV-27 psittacosis IV-6. G-10 vapor pressure I-5. II-2. II-12. E-4. II-3. J3 soman See GD sternutator II-58 swine fever IV-28. II-76. G-6. II-28. II74. I-4. II-77. IV-23. II-57. III-13. K-7 rate of detoxification I-6. III-4. IV-19. II-26. II-54. H-15. J-3 rickettsiae I-7. II-12. III13. K-6 rickettsia quintana IV-27 rickettsia rickettsii IV-10 rift valley fever IV-18. G-6. I-4. G-4. II-57. J-2 R rabies K-3. II-16. IV-18. II-37. D-1. II-74. IV-29. II-54. II44. II-30. III-12. I-8. K-6 volatility I-5. K-3. III-2. E-5. III-12. III-6. II-10. IV-1. IV-27. II-38. G-3. II-74. G-5. IV-27. I-4. K8 T tabun See GA TIC I-1. H-14. II-41. J-3 sheep pox IV-28. III-19. IV-28. II-18. J-2 smallpox IV-17. II-63. III-10. III-4. II-49. III-6. IV-29. II-39. III-13. II-61. H-16 Index-4 . II-33. III8. II46. IV-27. III-18. IV-14. III-21. II-15. II-44. I-4. II-11. II-5 rate of evaporation I-3 ricin I-10. J-3 viruses I-7. IV-9. II-75. III-10. II-59. II-34. V2. II-65. G-14. II-70. II-27. III-8. II-29. II-19. II-65. G-2. K-2. II-36. H-16 sarin See GB saxitoxin IV-24. IV-27. II-72. II-49. II-51. I-6. II-18. II30. J-2 V vapor density I-5. II-31. IV-27 shigellosis IV-6. G-10 Venezuelan Equine Encephalitis (VEE) I-10. II-72. III-21. II-24. III-20. II-41. II-70. II-75. II-78. G-4. III-10. III-2. III20. II32. II-64. IV-30. III-12. K-4. G-2. IV-1. G-10 VX II-1. V-1. IV-10. G-2. II-32. J-3 rinderpest IV-28. J-2 S SA I-4. IV-9. E-6. D-1. II-36. K-5. II-34. II-24. III-13. II-27. II-73. K-7 swine vesicular disease IV-28. IV-12. II-36. II-22. II-76. II-30. G-3. II15. II-77. II-78. III-17.pseudomonas mallei IV-4. II-15. II-51. II-2. II-21. I-10. III-20. H13. IV-27. D-1. G-15. II-72. I-8. II75. E-3. II-22. III-21. V-3 toxic industrial chemical See TIC tularemia IV-7. III-17. IV-27. IV-27. G-2. II-59. II61. II-44. I-3. III-4. K1. K-5 Rocky Mountain Spotted Fever IV-10. IV-24. II-49. I-12. II-25. II-51. II-70. II-63. IV-27. III-6. II-35. III-9. IV-13. II-46. G-5. II-38. IV-30. I-11. G-2. II-10. III-15. IV-11. G15. II-61. III-15. II59. II-10. IV-15. F1. III-2. II-1. II-12. II-32. I-10. E-2. II-57. II-24. G-6. III-18. III-19. II-1. III8. II-27. IV-19. II-39. III-15. G-14. II-21.

J-3 yersinia pestis IV-5. IV-27 Index-5 . I-4. II-29. G-2. F-1. G-5. II-31. G-14. IV-27. G-15 Y yellow fever IV-20. G3.Vx II-1. II-30. G-4.

SCHOOMAKER General.32 AFTTP(I) 3-2. By Order of the Secretary of the Air Force: BENTLEY B. and US Army Reserve: To be distributed in accordance with initial distribution number 110738. Army National Guard. requirements for FM 3-11. RILEY Administrative Assistant to the Secretary of the Army 0434903 DISTRIBUTION: Active Army. United States Army Chief of Staff Official: SANDRA R.1B NTRP 3-11. RAYBURN Major General.9.FM 3-11. USAF Commander Headquarters Air Force Doctrine Center Air Force Distribution: F Marine Corps distribution: PCN 144 000154 00 .55 10 JANUARY 2005 By Order of the Secretary of the Army: PETER J.9 MCRP 3-37.

PIN: 082113-000 .