Environment Pathology and

Disease

Ismet M Nur dr Sp PA (K)

MM
Environmental Disease

‫ ٭‬Diseases & lesions caused by chemical or

physical injuries

‫ ٭‬Environmental disease : common

‫ ٭‬ILO (International Labor Organization)

estimated : 1.1 million people, work-related
injuries & illnesses
Environmental Pollution

Air pollution
1. Outdoor Air Pollution
1.1. Ozone
1.2. Nitrogen dioxide
1.3. Sulfur dioxide
1.4. Carbon monoxide
1.5. Lead
1.6 Particulates
 Major Outdoor Air pollutants
Air Origin(s) Consequences
pollutants
Ozone Interactions of oxygen with Is highly reactive & oxidizes
various pollutants such as polyunsaturated lipids that
oxide of nitrogen, sulfur, & become irritants & induce
hydrocarbons release of inflammatory
mediators affecting all airways
down to bronchoalveolar
junctions
Nitrogen
dioxide Combustion of fossil fuel such
as coal, gasoline, & wood Dissolves in secretions in
airways to form nitric & nitrous
Sulfur acids, which irritate & damage
dioxide linings of airway
Combustion of fossil fuel such
as coal, gasoline, & wood Yields sulfuric acid, bisulfites,
and sulfites, which irritate &
damage linings of airways;
together with nitric acid,
contributes to acid rain
Carbon Incomplete combustion of Combines with
monoxide gasoline, oil, wood, and hemoglobin to displace
natural gas oxyhaemogloblin &
thus induce systemic
Discussed in a subsequent asphyxia
Lead
section

particulates Great variety of finely

divided (and therefore Major contributor to
airborne) pollutants smog & a major cause
ranging from relatively of respiratory disease
innocuous plaster dust to
highly dangerous asbestos
dust
May include lead, ash,
hydrocarbon residues, and
other industrial and
nuclear wastes
 Patterns Of Lung injury Related To Air Pollution

Lung response Pathogenic Mechanism(s)

Acute or chronic Direct cell injury

inflammation (e.c. Chronic
bronchitis) Enhanced proteolysis
Emphysema
Asthma Allergic or irritant effect
Hypersensitivity pneumonia Immunologic injury
Pneumoconiosis Fibrotic reactions caused by
cytokines released from
macrophages & other
Neoplasia recruited leucocytes
Mutagenic & promoting
effects
Air pollution
2. Indoor Air Pollution
2.1. Tobacco smoke
2.2. Carbon monoxide
2.3. Nitrogen dioxide
2.4. Wood Smoke
2.5. Formaldehyde
2.5. Radon
2.6. Asbestos fibers
2.7. Manufactured mineral fibers
2.8 Bioaerosol
Health Effects Of Indoor Air Pollutans
 Industrial Exposures
Organ/System Effect Toxicant
Cardiovasc Heart disease Carbon monoxide,
Syst lead,,solvent,cobalt

Respiratory Nasal cancer Isopropyl alcohol,wood dust

Syst Lung cancer Radon, asbestos, silica,nickel,
arsenic, chromium
Chronic obstructive lung Grain dust, coal dust,
disease cadmium
Hypersensitivity Beryllium, isocyanates
Irritation Ammonia,sulfur
oxides,formaldehyde
Silica,asbestos, cobalt
Fibrosis
Nervous Syst
Peripheral neuropathies
Solvents,lead, arsenic,DDT
Ataxic gait
Chlordane, toluene, mercury
CNS depression
Alcohols, ketones, solvents
Cataracts
UV radiation
Urinary Syst Toxicity Mercury, lead, solvents
Bladder cancer Naphtylamines,
benzidine

Reproductive Male infertility Lead, phthalate

Syst Female infetility plasticizers
Teratogenesis Cadmium, lead
Mercury

Hematopoietic Leukemia Benzene, radon,

Syst uranium

Skin Polychlorinated
Folliculitis & biphenyls
acneiform
dermatosis
Cancer UV radiation

Gastrointestinal Liver angiosarcoma Venyl chloride

Tract
Toxic And carcinogenic Metals
Pneumoconiosis

‫ ٭‬The non-neoplastic lung reaction to

inhalation of mineral dust
‫ ٭‬Agent : coal dust, silica, asbestos, beryllium
‫ ٭‬Coal Workers’ Pneumoconiosis (CWP)
Spectrum of lung finding in coal workers
1. Asymptomatic anthracosis
2. Simple Coal workers pneumoconiosis
3. Progressive massive fibrosis (PMF)
Mineral Dust –Induced Lung Disease
Pathogenesis of Pneumoconiosis
Morphology

1. Pulmonary anthracosis
Inhaled carbon pigment is engulfed by alveolar or
interstitial macrophage, then accumulate in
connective tissue  linear streak & aggregates
pigment identify pulmonary lymphatic & mark the
pulmonary lymph node
2. Simple CWP
Characterized : coal macules & coal nodule.
coal macules consist : dust-laden macrophages.
The lesion scattered, but uppers lobes & upper
zones of the lower lobes more heavily involved
 Morphology
3. Caplan syndrome
Coexistence of rheumatoid arthritis with a
pneumoconiosis  development distinctive
nodular develop fairly rapidly
The nodular lesions  central necrosis
surrounded by palisading fibroblast, palsma
cells, macrophages containing coal dust &
collagen
The syndrome also occur in asbestosis &
silicosis
Clinical course CWP

1. CWP usually benign  produce little decrement

in lung function
2. Minority cases pulmonary dysfunction,
hypertension & cor pulmonale
3. CWP  PMF (progressive massive fibrosis) linked
variety factors : coal dust exposure level & total
dust burden
4. PMF  tendency to progress even absence
exposure
 Silicosis
‫ ٭‬Caused by inhalation crystalline silica
‫ ٭‬Occupations associated development silicosis : quarry
mining, sandblasting, drilling, tunneling, & stone
cutting
‫ ٭‬Incidence : 1500 cases each year in US
‫ ٭‬Silica :
1. Crystalline : quartz, cristobalite, tridymite ( most
toxic and fibrogenic)
2. Amorphous forms (most commonly implicated in
silicosis)
 Classification Silicosis
1. Acute silicosis : exposure very high level of
silica & develops quickly
2. Chronic ( nodular ) silicosis: exposure over
prolonged periods  Characteristic fibrotic
nodules of silicosis
3. Complicated ( conglomerate silicosis)  result
progression of chronic silicosis
4. Other pulmonary disease : silicosis associated
with TBC
Morphology

Gross : Characteristic nodule in early

stage: tiny, barely palpable, discrete,
pale-to-blackened, nodules in upper
zones
Microscopically : silicotics nodule
demonstrates concentrically arranged
hyalinized collagen fibers surrounding
an amorphous center.
Microscopically: Silicosis
Clinical course

≈ Chronic silicosis  detected routine

chest radiographs (asymptomatic)
≈ Radiographs : fine nodularity in the
upper zones  function : normal/
moderately affected
≈ Most patients do not develop shortness
of breath until late in the course
≈ The disease  slow to kill
Asbestosis
» Asbestos  family of crystalline hydrated
silicates
» Occuaptional exposure to asbestos, linked to:
1. Parenchymal interstitial fibrosis (asbestosis)
2. Bronchogenic carcinoma
3. Pleural effusions
4. Localized fibrous plaque, rarely diffuse
fibrous plaque
5. Malignant pleural & peritoneal
mesothelioma
6. Laryngeal carcinoma
Morphology

Gross: diffuse pulmonary interstitial fibrosis

Microscopically : Characteristic  asbestos
bodies : golden brown, fusiform or beaded
rods with a translucent center. They consist
of asbestos fibers coated with an iron
containing proteinaceous material.
Pleural plaque : well-circumscribes plaque of
dense collagens
Asbestos Body
Clinical course

≈ Indistinguishable from other diffuse

interstitial lung disease
≈ Typically, progressively worsening dyspnea
appears 10-20 years after exposure
≈ The disease may static or progress to
congestive heart failure, cor pulmonale and
death.
Tobacco smoke
Adverse effects of
smoking
Injury By Chemical Agents

Mechanisms of chemical injury:

1. Dose
2. Requirement for metabolic conversion
3. Sites of absorption, accumulation, or
excretion
4. Individual variation
5. The capacity of the chemical to induce an
immune response
6. Unintentional transmission of infections
Injury by
Therapeutic
Agents (adverse
Drug Reactions)
Exogenous Estrogens And Oral
Contraceptives
1. Exogenous Estrogens ( alone & usually
natural estrogen)
Adverse effects of estrogen therapy :
» Endometrial carcinoma
» Breast carcinoma
» Thromboembolism
» Cardiovascular disease
2. Oral contraseptives

Adverse effects of oral contraseptives

( contain synthetic estrogens & always with
progestin)
1.Breast carcinoma 6.Hypertension
. 2.Endometrial cancer 7. Hepatic
adenoma
3.Cervical cancer 8. Gallbladder disease
4.Ovarian cancer 9. Cadiovascular
5.Thromboembolism disease
 Acetaminophen
≈ When taken very large doses  hepatic
necrosis
≈ The window therapeutic dose : 0,5 gr
≈ Toxic dose : 15-25 gr
≈ Toxicity begins : nausea, vomiting, diarrhea,
sometimes shock and jaundice
≈ Serious overdose : liver failure, renal and
myocardial damage
Aspirin (Acetylsalicylic Acid)

≈ Overdose ( 2-4 gr) : accidental ingestion of

large number table  young children
≈ Suicidal ( 10-30 gr)  adult
≈ Effects : at first : respiratory alkalosis 
metabolic acidosis death
≈ Chronic : take > 3 gr daily  headache,
dizziness, tinnitus, difficulty hearing, mental
confusion, nausea, vomiting and diarrhea
Injury by Non
therapeutic Toxic Agents

1. Lead poisoning
2. Carbon monoxide
3. Alcohol and drug
abuse
Clinical And Pathologic
Features Of Lead Poisoning
Lead causes injury by its multiple
metabolic effects:
1. High affinity for sulfhydryl groups &
interferes with enzymes
2. Competes with calcium
3. Interferes with membrane-associated
enzymes
4. Interferes with nerve transmission and
brain
5. Membrane effects damage the kidneys
Morphology

Major target of Lead toxicity : blood, CNS, GIT

and kidneys
1. Blood changes  characteristic  result
lead accumulation occur fairly early.
2. Brain damage is prone to occur in children
3. GIT : colic, extremely severe
4. Kidney : proximal tubular damage with
intranuclear lead inclusions.
Carbon Monoxide

‫ ٭‬Non irritating, colorless, tasteless, odorless 

imperfect oxidation of carboneceous materials 
continues to be cause accidental & suicidal death
‫ ٭‬CO kills by inducing CNS depression
‫ ٭‬CO act as a systemic asphyxiant 
carboxyhemoglobin incapable carrying oxygen
‫ ٭‬Acute Poisoning: generalized cherry-red color skin
& mucous membrane
‫ ٭‬chronic poisoning : evoke widespread ischemic
changes in the CNS
Alcohol And Drugs Of Abuse
1. Ethanol

2. Cocaine

3. Heroin

4. Marijuana

5. Other Illicit drugs

 Classification Of Drugs Of Abuse
Class Examples

Sedatives & hypnotics Alcohol, barbiturates

CNS symphatomimetics or
stimulants Cocaine, amphetamines
Opioids Ritalin, weight loss products
Cannabinoids
Heroin, morphine, methadone
Hallucinogens or psychedelics Marijuana, hashish
Inhalants Lysergic acid diethylamide
(LSD),mescaline

Nonprescription drugs Aerosol sprays,glues,toluene

Ingredients :Atrophine,
scopolamin, antihistamine,
weak analgesics
Metabolism of Ethanol
Ethanol

Adverse effects of ethanol:

1. Acute alcoholism  effects mainly
CNS  induced hepatic & gastric
changes

2. Chronic alcoholism  morphologic

alterations  liver & stomach
Cocaine
Manifestations of acute cocaine toxicity
1. Sympathetic nervous system stimulation 
dilatated pupils, vasoconstriction
2. Lethal arrhythmias & myocardial infarction
3. Cerebral infarction & intracranial hemorrhage
4. Rhabdomyolysis
5. In pregnant women  spontaneous abortion
Manifestations of chronic toxicity
1. Perforation nasal septum
2. Decreased lung diffusing capacity
3. Dilated cardiomyopathy
Effect of cocaine on neurotransmitters

Sympathetic Neuron-target Cell

CNS Synapse Interfere
Heroin
≈ Effects : euphoria, hallucinations, somnolence &
sedations
≈ Heroin  adversed physical effects, related to
1. Pharmacologic action of the agent
2. Reactions to the cutting agents/contaminations
3. Hypersensitivity reactions
4. Diseases contracted incident  use needle :
‫ ٭‬Sudden death
‫ ٭‬Pulmonary complication
‫ ٭‬Infectious complications
‫ ٭‬Cutaneous lesions
‫ ٭‬Kidney disease
Marijuana

• Effects:
1. Distorts sensory perception & impairs
motor coordination
2. Lung  laryngitis, bronchitis, cough,
hoarseness  increased risk for cancer
3. Increased heart rate and blood pressure 
angina
4. Induce chromosomal damage
Other Illicit Drugs

• The variety of drug try by those

seeking  new experiences
• Range : various stimulants
(amphetamines) to depressants
(benzodiazepines) to hallucinogens
(ectasy)
• Dangerous combination : alcohol &
driving
Injury By physical Agents

• Mechanical Trauma
1. Abrasion
2. Contusion
3. Laceration
4. Incised wound
5. Puncture wound
◊ Thermal Injury
• Thermal burns
• Hyperthermia
• Hypothermia
njury By physical Agents

Abrasion : A wound
produced by scraping or
rubbing
Contusion : A wound
produced by a blunt
object  damage
blood vessels &
extravasation
Injury By physical Agents

Laceration : A tear or disruptive stretching of

tissue  force by blunt object
 Injury By physical Agents

Puncture wound : caused by a long narrow instrument 

Penetrating when the instruments pieces the tissue &
Perforating  when it traverses a tissue to also create an
exit wound
Thermal injury
• Gross:
Full-thickness burn are white or charred,
dry and anesthetic, depending on the
depht, partial-thickness burns are mottled
with blisters & painful

◊ Microscopically:
Devitalized tissue  coagulative necrosis,
adjacent to vital tissue  accumulates
inflammatory cells & exudation
Hyperthermia

• Heat cramps  loss of electrolytes via

sweating
•Heat exhaustion  onset sudden, most
common hyperthermic syndrome  failure
Cardiovascular system to compensate for
hypovolemia
• Heat stroke  high ambient temperatures &
high humidity  thermoregulatory
mechanism fail
Hypothermia

• Local reaction. Chilling or freezing of

cells & tissues causes injury in two
ways
1. Direct effects  mediated by physical
dislocations within cells, high salt
consentration
2. Indirect effects  exerted by
circulatory changed
Electrical Injury

• Electrical injuries  death  arise

from low-voltage or high-power lines
or lighting
• Two types of injuries
1. Burns
2. Ventricular fibrillation or cardiac &
respiratory center standstill
Injury Produced
By Ionizing
Radiation

Effects of ionizing radiation on DNA

 Injury Produced By
Ionizing Radiation

Overview of the major

morphologic consequences
of radiation injury