GENERAL PHYSIOLOGY AND TOXICOLOGY

C. Insect Toxicology
C.1 Insecticides
1. Primary route of entry
2. Primary division
3. Nomenclature
4. Toxicity
5. Mode of actions
6. Formulations

C.2 Movement of Insecticides in the environment

1. Contamination of natural resource
2. Residues of insecticide
3. Hazards and Effects on non-target organisms

C.3 Insecticide Research and Development and Bioassay

1. Economic and legal aspects of insecticide
use
2. Research and development process
3. Data generation and their value of safety
4.Types of bioassay and the factors to consider
5. Probit analysis

C.4 Challenges and Trends

Toxicology (Ancient Greek words, “Toxikos”=
poisonous and “logos”= study) ia a very broad
field of study involving multidisciplinary
sciences related to adverse chemical effects on
living organisms. Generally, toxicology can be
defined as “the study of adverse, deleterious,
and /or poisonous effects of chemicals on living
organisms” or “the study of symptoms,
mechanisms/modeof action, treatments, and
detection of poisoning and cause of resulting
death”- IRRI, 2011
Two main fields in Toxicology

Toxicokinetics- the field that deals on how an organism handles toxic

substances, such as (1) absorption; (2) distribution within its body ,
biotransformation or metabolism and (3) excretion or elimination

Toxicodynamics- the field that deals with the effects of toxic substances
to an organisms such as (1) irritant, (2) corrosive, (3) teratogenic
or sterilizing agent (4) asphyxiation or suffocation, (5) carcinogen
(6) mutagen , (7) anaesthetic or narcotic

Subdisciplines of Toxicology

1. Aquatic toxicology
2. Chemical toxicology
3. Ecotoxicology
4. Entomotoxicology (insect toxicology)
5. Environmental toxicology
6. Forensic toxicology
7. Medical toxicology
8. Toxicogenomics
Entomotoxicology or insect toxicology
the science that deals with the effects of chemicals that
affects normal physiological processes of insects. Specifically,
chemicals that retard insect development, growth and
metamorphosis and/ or reproduction, as well as cause death in
insects and among others.

Multidisciplinary sciences involved:

1. Entomology- anatomy, morphology, taxonomy
2. Chemistry- inorganic or organic insecticides
3. Insect biochemistry
4. Insect ecology--- chemical ecology, behavior, and
population dynamics
5. Genetics (related to insecticide resistance)
6. Insect physiology
7. Statistics
8. Techniques (related to application and bioassay)
 German: 'Alle Ding sind
Gift und nichts ohn'
Gift; allein die Dosis
macht, das ein Ding
kein Gift ist.
English: All things are
poison and nothing (is)
without poison; only
the dose makes that a
thing is no poison.
Philippus Aureolus Theophrastus Bombastus von Hohenheim .
1493-1541
Toxicity

LD50 (Lethal Dose)– a quantitative

expression used in quantal response experiments
in order to estimate the median (50 %) response
level of a population. It provides estimates of the
toxicity of an insecticide used. Other expressions
include LC50 (Lethal Concentration), LT50 (Lethal
Time), and among others. Please note that the
higher the LD50, the lower the toxicity.
 LD50 of some food and non-food
materials
1. Water : 80 g/kg
2. Sugar (sucrose) : 30 g/kg
3. Alcohol (ethanol) : 13.7 g/kg

Note:
Substances have varying degrees of toxicity.
The lesser the value of LD50 of a substance
the more toxic it becomes.
 PESTICIDES
“Pesticide” is any substance or product, or mixture
thereof, including active ingredients, adjuvants and
pesticide formulations, intended to control, prevent,
destroy, repel or mitigate directly of indirectly, any
pest. The term shall be understood to include
insecticide, fungicide, bactericide, nematocide,
herbicide, molluscicide, avicide, rodenticide, plant
regulator, defoliant, desiccant and the like.

PRESIDENTIAL DECREE NO.1144

CREATING THE FERTILIZER AND PESTICIDE AUTHORITY AND ABOLISHING THE
FERTILIZER INDUSTRY AUTHORITY
Different types of pesticides:
1. Insecticides
a) Ovicides
b) Larvicides
c) Adulticides
2. Rodenticides
3. Molluscicides
4. Fungicides
5. Bactericides
6. Nematicides or nematocides
7. Herbicides or weedicides
8. Miticides and acaricides
 Type
Brand Name
“Insecticide”
“SUPRACIDE”

Hazard Level
Common Name “Danger/poison”
“methadithion” Poison Icon

Chemical Family
Antidote ‘organophosphate’
“atropine”

Manufacturer
Gowan
1. Brand name - the name of the product given by the manufacturer.
2. Ingredient statement (for active ingredient)- this part provides
ingredient or material (chemical) added to the product.
a. chemical name
b. common name
3. Registration and establishment numbers– these are numbers given by
the authority.
a. registration number (for example, EPA Reg. No. 62719-324)
b. establishment number (for example, EPA Est. No. 2217-KS-1)
4. Name and address of manufacturer - It provides the name of the
manufacturer and its address.
5. Net contents- this information is usually expressed in gallons, ml, L
,quartz and among others depending on what type the material is.
6. Type of pesticide- it provides what type of pesticide the material is.
(example: insecticide, herbicide, molluscicide etc.)
7. Type of formulation- it provides the information on how the pesticide
is formulated such as WP for wettable powder, D for dust, or EC for
emulsifiable concentrate.
8. Restricted-Use Designation it describes the reason for the restricted-
use classification. Usually another statement will describe the category of
certified applicator who can buy and use the product. Unclassified
pesticides have no designation on the product label.
9. Precautionary statements- these are words and/or symbols that give
caution or warning to the user.

a. DANGER - This word signals you that the pesticide is highly toxic. The
product is very likely to cause acute illness from oral, dermal, or
inhalation exposure, or to cause severe eye or skin irritation.
b. POISON/SKULL AND CROSSBONES - All highly toxic pesticides that are
likely to cause acute illness through oral, dermal, or inhalation exposure
also will carry the word POISON printed in red and the skull and
crossbones symbol. Products that have the signal word DANGER due to
skin and eye irritation potential will not carry the word POISON or the
skull and crossbones symbol.
c. WARNING - This word signals you that the product is moderately
likely to cause acute illness from oral, dermal, or inhalation exposure or
that the product is likely to cause moderate skin or eye irritation.
d. CAUTION - This word signals you that the product is slightly toxic or
relatively nontoxic. The product has only slight potential to cause acute
illness from oral, dermal, or inhalation exposure. The skin or eye
irritation it would cause, if any, is likely to be slight.

10. Statement of practical treatment (first aid)-- Most pesticide

products are required to include instructions on how to respond to an
emergency exposure involving that product. The instructions usually
include first aid measures and may include instructions to seek medical
help.
11. Personal protective equipment (PPE) statements– it provides the
necessary equipments to be used or worn before using the product.
12. Environmental Hazards– it tells the effects of the products to the
environment and to organisms
13. Physical or Chemical Hazards– it tells any physical hazards such as
special fire, explosion, or chemical hazards the product may pose.
14. Directions for Use –- it contains specific directions for product use.
 Categories of pesticides based on level of toxicity

Category Color Toxicity Hazard Signal Oral LD50

Band Words (mg/kg BW)

I RED Highly Extremely Danger, < 50

toxic hazardous poison

II YELLOW Moderately Highly Warning 50-500

toxic hazardous

III BLUE Slightly Moderately Caution 500-5000

toxic hazardous

IV GREEN Relatively Slightly - > 5000

non-toxic hazardous

MEABDetalla’s Weed Science Lecture…

INSECTICIDE
(IRRI, 2011)
Classification of Insecticide is based on
the following:
1. Target insect (ovicides, larvicides and
adulticides)
2. Application technique (dusting, fumigant,
spray, residual, and topical)
3. Modes of action
4. Active group in the insecticide (carbamate,
organochlorine, organophosphate)
5. Chemical nature
 Based on Chemical nature
1. Arsenical insecticides- based on inorganic
arsenite ; e.g. potassium/sodium arsenite
2. Botanical insecticides – e.g. azadirachtin,
pyrethrins
3. Antibiotic/microbial insecticides
4. Organochlorine insecticides- e.g. DDT,
pentachlorophenol
5. Organophosphorus insecticides- e.g.
malathion, diazinon
 Based on Chemical nature
6. Carbamate insecticides- e.g. carbaryl,
carbofuran
7. Flourine insecticides- e.g. sodium flouride
8. Oxadiazine insecticides- e.g. indoxacrab
9. Pyrrole insecticides- e.g. chlorfenapyr
10.Pyrazole insecticides- e.g. dimetilan, tolfenpyrad
-phenylpyrazole insecticides- e.g. fipronil
11. Pyrethroid insecticides- e.g. cypermithrin,
permethrin
 Based on Chemical Nature
12. Nicotinoid insecticides- e.g. flonicamid -
neonicotinoids e.g. acetamiprid
13. Insect growth regulators (IGR)
i. Chitin synthesis inhibitors
ii. Juvenoids/ juvenile hormone mimics
iii. Anti-JH/precocenes
iv. Molting hormone agonists
v. Prothoracicotropic hormone (PTTH) antagonists
14. Thiourea insecticides- e.g. difenthiuron
Mode of Action

a. Physical poisons- the action of the chemical is by

asphyxiation, that is , blocking the flow of oxygen through
the insect tracheal system. (ex. Dusts, fumigants and oils)
also abrasions and sorption.
b. Protoplasmic poisons- chemicals that are usually inorganic
that destroy cells physically.
c. Metabolic inhibitors- these type of chemicals interfere
with the metabolic pathways or inhibit certain enzymes.
d. Neuroactive agents- (nerve poisons) they affect the
transmission of nerve impulses or the neurotransmitter.
e. Insect growth regulators- (insect growth inhibitors)-
chemicals that disrupt growth and development or
malformation of cuticle.
Primary route of entry / (site of action)

1. Stomach poisons: ingestion and absorption via alimentary

canal
2. Contact poisons: through the cuticle
3. Fumigants: through spiracles/ tracheal system (suffocation)
4. Systemic poison: absorbed and translocated by plants

2 Primary Division (based on chemical structure)

1. Organic- carbon based

2. Inorganic- non-carbon based

• Ligand- any substance that binds reversibly to another
chemical group/entity to form a larger complex
compound. (examples: drug, hormone, insecticide
functional group). It may function as an agonist or
antagonist.
• Agonist- is a chemical, often mimic of a natural
compound like hormone that binds to a receptor of a
cell to produce an action.
• Antagonist- is a chemical that blocks or acts against an
action.
• synergists- substances that have properties that could
increase the level of toxicity of insecticides
• synergistic action- the increased toxicity is markedly
greater than the sum of two used separately
Formulations

I. Sprays
1. Emulsifiable concentrates (EC)
2. Water-miscible liquids (S)
3. Wettable powders (WP)
4. Flowable suspensions (F)
5. Water-soluble powders (SP)
6. Water-soluble granules (WSG)
7. Ultra-low-volume concentrates (WSG)

II. Dusts
1. Undiluted toxic agent
2. Toxic agent with active diluents (e.g. sulfur)
3. Toxic agents with inert diluents (e.g. pyrophyllite)
III. Granules

IV. Soil fumigants

V. Baits

VI. Animal systemics

VII. Fertilizer insecticide combinations (FM)

VIII. Encapsulated insecticides

 General Toxicological Process

Activated
Insecticide Target sites

Detoxified
Intoxication
Sequestered (Death)

Excreted
 ACETYLCHOLINESTERASE INHIBITORS
1. Organophosphates and carbamates inhibit
acetylcholinesterase from binding to its active
binding site. Thus, acetylcholinesterase is
unable to degrade acetylcholine- causing the
sodium channels to remain open. As a result,
there is continuous inflow of sodium ions
inside the membrane (or uncontrolled firing of
nerve impulses). Hence, it causes uncontrolled
muscle twitching to the organism then the
organism gets exhausted and eventually dies.
 Acetylcholinesterase inhibitors
1. Non-competitive inhibition: when a chemical
binds to the active site of the enzyme and
destroys the enzyme’s activity. (ex.
Organophosphates like Malathion, Diazinon,
Chlorpyrifos)

2. Competitive inhibition: when a chemical

competes with the enzyme for its binding site.
(ex. Carbamates like Carbaryl and Propoxur)
 ACETYLCHOLINE MIMIC
1. Nicotine- a natural compound that can be extracted from
tobacco. Its insecticidal action is by binding to the
acetylcholine binding site of the synaptic sodium
channels.

2. Neonicotinoids- synthetic chemical that mimics nicotine.

It binds to the acetylcholine binding site of the synaptic
sodium channels. Since it is not degraded by enzymes, the
continuous binding keeps the sodium channels to open
and allows the entry of sodium ions. Hence, the constant
inflow causes constant depolarization. The constant
depolarization causes over stimulation of the nervous
system. In effect to the insect, there is uncontrolled
muscle shaking. It gets exhausted, it collapses and dies.
(ex. Imidacloprid)
AXON SODIUM CHANNELS INHIBITORS
1. Pyrethrins are natural insecticides that can be
extracted from Chrysanthemum spp.
2. Pyrethroids are synthetic chemicals that mimic
pyrethrins. They interact with the axonal sodium
channels and hold them in their open confirmation.
This causes the uncontrolled difussion of sodium ions
inside the axon membrane (excessive action potential
and hyper depolarization). When the number of
diffusable ions is in equillibrium, the charge of the
axon membrane is lost. The hyper depolarization
causes the insect uncontrolled muscle twitching and
the lost charge of the axonal membrane causes the
insect paralysis.
 CHLORINATED HYDROCARBONS
INSECTICIDES
Are nerve poisons with slow acting effect and
negative temperature correlation.

1. DDT interferes with the surface recalcification

which is needed to restore a normal resting
potential after a single depolarization of the
axonic membrane. As result, insect do
hyperextension of its legs, there is
uncoordinated body movement and
tremulousness. DDT also interacts with the
sodium gates by slowing down their closing that
causes repetitive action potential.
 CHLORINATED HYDROCARBONS
INSECTICIDES
Are nerve poisons with slow acting effect and
negative temperature correlation.

1. DDT interferes with the surface recalcification which is

needed to restore a normal resting potential after a
single depolarization of the axonic membrane.
2. It reduces the permeability of potassium ions across
the nerve membrane
3. It inhibits nerve ATPases.
4. It hinders permeability of ions by entering fitting itself
into the intermolecular spaces within the cylindrical
lipoprotein lattice.
 CHITIN SYNTHESIS INHIBITORS
The effects of this compounds on this insects
can be grouped into two broad categories: a.
inhibition of chitin synthesis and b. interference
with the organization of exoskeletons.

1. Buprofezin keeps the levels of ecdysone from

decreasing during the first stage of molting.
Hence, the old cuticle does not get digested and
cuticle does not form properly if ecdysone is
maintained at high level.
 CHITIN SYNTHESIS INHIBITORS
2. Cyromazine. Insects exposed to this chemical
have cuticle that is abnormally hard.
3. Benzoyphenyl ureas (ex. Diflubenzuron and
teflubenzuron) inhibits the membrane transport
step involving UDP-N-acetylglucosamine
production by chitin synthase, hence, blocking
the polymerization. It causes thin and brittle
cuticle that is unable to support the insect or
withstand molting process.
 PROTHORACICOTROPHIC HORMONE
INHIBITOR (PTTH Inhibitor)
1. Azadirachtin insecticide inhibits the synthesis
and production of prothoracicotrophic
hormone. PTTH is important in stimulating the
brain to secrete the molting hormone. Hence,
growth and development of insects is affected
since development and metamorphosis are
dependent in the interactions of hormones.
The chemical is derived from neem tree
(Azadirachta indica). It is also a potent anti-
feedant (feeding deterrent)
 SYNERGISM
Insecticide synergist is a chemical that does not
possess inherent insecticide activity on its own.
Examples:
1. piperonyl butoxide (PBO)
2. S,S,S-tributyl phosphorotrithiolate (DEF)
3. diethyl maleate (DEM)
4. 2-phenyl-4H-1,3,2-benzodioxaphosphorothiolate (K1)
 SYNERGISM
Combinations of insecticide also has
synergistic effects:

1. N-methyl-and N-phenyl-carbamates mixture

(Nephotettix cincticeps)
2. Pyrethroid with carbamate or organophosphate
(Nephotettix cincticeps)
3. Permethrin and propoxur mixture (Periplaneta
americana)
4. Neonicotinoids with pyrazole or pyrrole
insecticide (Nilaparvata lugens)
 ANTAGONISM
Antagonism occurs when the effect of two
pesticides is less effective than applied
separately.

1. OP and pyrethroid against Bemisia tabaci

 SUBLETHAL EFFECT OF INSECTICIDES
Antifeeding, Knockdown, and Repellency
1. Knockdown - a state of partial paralysis or
moribund that may precede death.
2. Antifeeding- when insects does not feed due to
insecticide application (ex. Sublethal dosage of
cypermethrin and permethrin against Pieris
brassicae)
3. Repellency- insects tend to avoid its host.
(ex. Bifenthrin treated tomato plants against
Bemisia argentifolii)
4. Effects on the behavior (learning performance
and neurophysiology)- ex. Sublethal effects of
neonicotinoids show to disrupt Apis millefera
learning, behavior, and cognitive functions.
 INSECTICIDE RESISTANCE
It is the ability of an insect population to
withstand or tolerate adverse effects of an
insecticide applied to a level (dose) that would have
killed most normal/susceptible individuals. This can
be a result of adaptation, mutation and/or natural
selection.

ex. Resistance of Musca domestica in the effects of

OPs and Carbamates (after 14 and 7 years
respectively after introduction)
 Factors affecting the speed of
development
1. Intensity of selection pressure- frequency of
applications of an insecticide in the area
2. The frequency of resistance genes present
(very low initially)
3. Characteristics of resistance genes-
(dominant or recessive; multiple or single)
4. Reproductive dynamics and potentials- ex.
Number of generations per year
 PESTICIDE TREADMILL
It is the exponential increase of pest
populations resulting to pest outbreaks due to
the further intensive applications with much
higher dosages as desperate and extreme
measures of agricultural producers/farmers to
control pest populations that has already
developed resistance.
 MECHANISMS OF RESISTANCE TO
INSECTICIDES
1. Physical resistance- reduce penetration of
insecticide through the cuticle
2. Behavioral resistance- through avoidance
3. Metabolic resistance- through detoxification
by increased activity of specific enymes.
4. Genetic resistance- through mutation of a
gene in receptors or active sites of enzymes
 MOVEMENT OF INSECTICIDES IN THE
ENVIRONMENT
things to consider:
1. Effects to man and domestic animals which
may take up pesticides mostly through
contaminated food;
2. Effects to wildlife where certain species can
be severely affected by absorption or
accumulation of pesticides through the food
web- directly and indirectly affecting the
balance of the ecosystem
 MOVEMENT OF INSECTICIDES IN THE
ENVIRONMENT
Important terms (Gunther and Blinn, 1956)

1. Residue- refers to the chemicals found

regardless of the place found with the
implication by time lapse or alteration of
both;
2. Deposit- limited to the insecticidal chemical
as initially laid down.
Some Factors affecting chemical insecticide
residue decomposition and disappearance
1. Biotic factor: Enzymatic degradation, etc.
2. Abiotic factor: evaporation, weathering etc.

2 Steps of disappearance

1. Dissipation- initial phase of fast disappearance

2. Persistence- subsequent phase of slow decrease
in the amount of residue
 Movement in Terrestrial Plants
Other factors

1. Method of application
2. Frequency of application
3. Processing
4. Sizes
1. Chemical nature
2. Polar and non polar characteristics of
chemical and the type of cuticle of plants
Methods in removing pesticide residue
When in the surface
1. Washing
2. Brushing
3. Scraping
4. Peeling

When inside plant tissues

1. Degradation
2. Metabolism
3. Conjugation

Base on pesticide half-life

1. Reaction
2. Dissipation of residue
 Movement in the soil
1. Absorption by the soil particles as well as
organic matter in the soil
2. Leaching and washing off by water
3. Evaporation into the air (including mechanical
transport by water vapor)
4. Degradation/ activation by soil microorganisms
5. Physiological decomposition or activation
catalyzed by soil conditions or soil constituents
6. Photodecomposition
7. Translocation through biological systems
 Movement in the soil
Other factors:
1. Soil type
2. Soil moisture
3. Temperature
4. Mode of cultivation
5. Cover crop practices
6. Application of insecticides
7. Formulation of insecticides
 Movement in the soil
1. Presence of organic matter content can absorb
residues
2. Soil type and soil moisture could determine the depth
of penetration of insecticide residue; soil with high silt
and clay composition has less or sometimes no
migration compared to sand
3. Insecticide persist in acidic soil than alkaline
4. Mineral content influences the fate of insecticide
(catalyzing decomposition or influencing sorption
behaviors)
5. High disappearance in high temperature
6. Shading (ex. cover crops) increase persistence of
insecticide by lowering the evaporation rate in the soil
 Movement in the soil
7. Cultivation may hide or expose insecticide
8. Movement of air also affects the
disappearance from the soil (cultivation
aeration)
9. Formulations- granules persist longer than
emulsions; emulsions persist longer than
miscible liquids and wettable powder
 Movement of residue in the
environment
1. Water mediated transport: run-off,
percolation, precipitation, eluted because of
the solubility of compounds

2. Air mediated transport: volatilization,

evaporated with water vapor, transport with
water particles and dusts
 ENVIRONMENTAL ALTERATION OF
INSECTICIDE RESIDUE
Environmental toxicologist asks…

Is the disappearance of the insecticides means

actual degradation of the hazardous chemical
or wether it is actually a signal that the
insecticide has been translocated for, say,
bioconcentration into some ecosystem or
converted into dangerous chemicals?
 Factors affecting the speed of
degradation
1. Chemical nature
2. Physical factors (pH, temperature, humidity
etc.)
3. Biological factors (presence or absence of
potential microorganisms)
 Microbial Metabolism
1. Actinomycetes
2. Fungi
3. Bacteria
 Examples of microorganisms
1. Trichoderma virgatum
2. Talaromyces wartmanni
3. Fusarium oxysporum
4. Escherichia coli
5. Mucor alterans
EFFECTS OF INSECTICIDES TO WILDLIFE
1. Acute toxicity- the short term, direct effect of
chemicals to animals based on the LD50 of
chemicals.

2. Chronic toxicity- the long term toxicity of

chemicals due to the buildup of pesticides by
environmental concentrations.
EFFECTS OF INSECTICIDES TO WILDLIFE
1. Bioaccumulation- accumulation of persistent
insecticides in various biological systems at
levels much higher than their surroundings.

2. Biomagnification- increase of the

concentration of chemical residues in the
body of animals as it moves to the top of the
food chain.
EFFECTS OF INSECTICIDES TO WILDLIFE

Schematic diagram of biological transfer of pesticide residues (adapted from

Matsumura, 1975)
 Effects of pesticides on Benguet
Farmers
Farmers tend to have itchy skin, dry lips,
watery and red eyes that lasts for days. They
also experience abdominal pain, chest pain,
muscle cramps, body malaise, inappetens,
dizziness, epistaxis, irregular and discolored
nails. (Cheng and Bersamira, 1994)
Ecological Hazards of Pesticide Use
1. Soil degradation
2. Water pollution
3. Air pollution
4. Depletion of the ozone layer
5. Pest resistance to pesticides
6. Loss of natural enemies of pests
7. Diminution of livestock and wildlife
8. Health risks to man
 Insecticide Research
and Development and Bioassay

1. Collection of test organisms from the field

2. Mass rearing of the test organisms
3. Preparation of test media for bioassay:
dilution of chemicals
4. Computation (statistical tools like probit
analysis or PoloPlus software)
 Trends and Challenges
1. Use of Integrated Pest Management as
alternative farm practice.
2. From conventional agriculture to Sustainable
Agriculture (ex. organic agriculture)
3. Effective use of insecticides
 REFERENCES
• BALLENTES M. G. 2014. Lecture notes in General Physiology and
Toxicology. Central Mindanao University. Musuan, Bukidnon.
• Cheng C. and Bersamira K. 1994. Pesticides: Its Hazardous Effects on the
Benguet Farmers and the Environment. Allied Printing Press, Baguio City.
• Matsumura F. 1975. Toxicology of Insecticides. Plenum Press, London.
ISBN 0-306-30787-1
• D. A. Lowe and A. R. Stiles. 1973. Pesticides: nomenclature, specification,
analysis, use, and residues in foods. Bulletin of the World Health
Organization. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2481117/ .
Retrieved October 29, 2015
• Helen Murphy . Name That Pesticide: How to Identify the Products Your
Patients Are Exposed To. University of Washington, Seattle WA
• Pesticide Labeling. Montana Sate University.
http://www.pesticides.montana.edu/reference/labels.htm
• Insecticide formulations
http://www.uky.edu/Classes/ENT/574/topics/Insecticides/Formulations.p
pt.
 Larry L. Keeley
Professor Emeritus of Insect Physiology
Department of Entomology
Texas A&M University