ENVIRONMENTAL PATHOLOGY

Diseases related to  Occupation  Drug reactions  Poisoning  Life style  Drugs of abuse

RESPONSE OF THE RESPIRATORY SYSTEM TO PHYSICAL AND CHEMICAL AGENTS Physical agents: (Aerodynamics)

  Particles bigger than

10



m

Particles of

2 to 10



m

in diameter are

trapped by

in diameter are

disposed by

the

nose

the

muco ciliary blanket



Smaller particles

that

land in air-spaces

are

removed by alveolar



macrophages

.

Very small particles (2



m) are exhaled

Chemical agents:

 Ozone, Nitrogen dioxide, Sulfur dioxide cause airway inflammation. Further, these gases potentiate the adverse effects of tobacco smoke

Occupational diseases

Pneumoconioses:



Fibrosing pulmonary disease

reaction to inhalation of an aerosol (mineral dusts, particles, vapors, or fumes) which is non-neoplastic lung Key factors:  Type of aerosol and its ability to stimulate fibrosis   Dose and duration of exposure Size of the particle    Pneumoconioses are diseases caused by

inorganic dusts.

Lesions produced depend on the

dose

,

size

nature

of the inhaled particles.

and

chemical Tobacco smoking

worsens the effects of inhaled dusts.

Coal – worker’s Pneumoconiosis

 Occupation: coal mining (smokers). Types:     Anthracosis Simple coal worker’s pneumoconiosis Complicated coal worker’s pneumoconiosis Caplan Syndrome

Anthracosis:



Carbon pigment

(anthracotic pigment) accumulates

in macrophages

pleural lymphatics, bronchial lymphatics, lung hila

along the  Asymptomatic

Simple coal worker’s pneumoconiosis:

   Also called

Black lung disease

Coal-dust macules and nodules

in the

upper lobes Little

pulmonary dysfunction

Complicated coal workers pneumoconiosis:

   Progressive

massive fibrosis

Increasing respiratory distress

Pulmonary hypertension and cor pulmonale Caplan syndrome: Pneumoconiosis plus rheumatoid arthritis

& Intrapulmonary nodules

Asbestosis

 Occupations: shipyard workers, insulation and construction industries, brake-lining.

Lung pathology



Localized or Diffuse interstitial fibrosis

which is most severe in the

lower lobes

 Asbestos bodies that may become

coated with iron

(

ferruginous bodies

)  Dyspnea  Pulmonary hypertension and cor pulmonale

Bronchogenic carcinoma 

Most common tumor

in

asbestos-exposed

individuals.



Synergistic effect

of

smoking

and asbestos exposure

Malignant Mesothelioma:  Rare

highly malignant

neoplasm   Occupation exposure to

asbestos

in 90% of cases Presents with

recurrent pleural effusions , dyspnea, chest pain

  Gross:- encases and compresses the lung EM:- long thin

microvilli

 Poor prognosis 

Increased risk of laryngeal, stomach and colon cancers is also seen in persons having asbestosis.

Silicosis

  Occupation: Sandblasters, metal grinders, miners Exposure to

Silicon dioxide

(

silica

) Pathology: 

Dense nodular fibroses of the upper lobes

  Birefringent

silica particles polarized light

can be seen with May develop

progressive massive fibrosis

Clinical course   X-ray shows fibrotic nodules in the upper zones Insidious onset of dyspnea   

Slowly progressive although exposure

is stopped Increased risk of

tuberculosis Caplan syndrome

Other important industrial toxins



Vinyl chloride

– plastic industry – causes

angiosarcoma of the liver



Naphthylamine

–

dye makers

and

rubber workers

– causes

bladder cancer



Carbon tetrachloride

( CCl 4 ) – Dry cleaners – causes

Liver

( centri- lobular necrosis and fatty acid change) and

Kidney toxicity

.

Poisoning

Carbon monoxide (CO):

Sources:   auto emissions, home heaters, byproduct of fires, cigarette smoking Should be less than 9ppm in atmosphere.

Pathogenesis:  Odorless, colorless gas   High affinity for hemoglobin Forms carboxyhemoglobin, which shifts the oxygen dissociation curve  Causes

systemic hypoxia

Symptoms depend on the

concentration

:  10% → asymptomatic  30% → headache and shortness of breath on exertion  50% → loss of consciousness, convulsions and coma  60% → death 

Bright

“

Cherry-red

"

color of the skin

,

mucosal membranes and the blood

.

 Treatment : high concentration Oxygen

Cyanide poisoning • Clinical finding: “

Bitter Almond

” scented

breath

• M/A:

blocks cellular respiration

by binding to

mitochondrial cytochrome oxidase

• Systemic asphyxiant

Treatment

• supportive care with administration of oxygen

• • •

Antidotes or Drugs

poisoning

Sodium Sodium

nitrite thiosulfate used for cyanide

Hydroxocobalamin

/ B12 • • Dicobalt EDTA

Sodium

bicarbonate • Epinephrine

Carcinogenic metals • Arsenic.

• Nickel.

• Cadmium.

• Chromium.

Arsenic poisoning

used extensively in

paints (Paris green), wall papers, pesticides

, and even medicinal.

Can be

detected in hair

and

nails long after exposure

Acute poisoning : * Hemorrhagic gastroenteritis

* CNS toxicity



coma and seizures

* "

Garlic - scented " breath

Chronic Arsenic poisoning

* Malaise and abdominal pain * Peripheral neuropathy and muscular weakness * Skin changes (hyper pigmentation and dermatitis)

* Mees lines :

transverse bands on the fingernails

Complication : Squamous cell carcinoma

of the

skin and lung

CHROMIUM

• • Chromium (III) is an essential nutrient that can be toxic in large doses. • The toxicity of chromium compounds depends on the oxidation state of the metal. • Occupational exposure to

chromium (VI)

has been associated with increased incidence of

lung cancer

.

•

CADMIUM

Part 1. Sources of cadmium exposure

– Occupational exposures – Non-occupational exposures • Affects – Kidney – liver

• Significant exposures to cadmium dusts appear to be generated at all stages in the manufacture of both industrial and household nickel-cadmium batteries, including plate-making, impregnation, plate preparation and assembly. Cadmium health effects may be confounded by associated exposures to nickel in this environment •

Overexposure

to

cadmium

fume (usually from welding or cutting materials containing cadmium)

can cause tracheo-bronchitis, pneumonitis

(inflammation of the lungs) and

pulmonary edema

•

LEAD Poisoning (Plumbism)

• Effects Immunity – – – – – – – T lymphocytes B lymphocyte Cytokine production Neutrophil Immunogenicity of normal cellular proteins Macrophages Natural killer cells Reproductive systems

Epidemiology Sources : lead paint, lead plumbing and leaded gasoline * Most common type of chronic metal poisoning in the US * Primarily affects children in poor urban areas CNS toxicity * Lethargy * Cognitive impairment and behavioral problems.

• The Mental retardation • Cerebral edema – encephalopathy

inhibition of heme synthesis

leads to anemia and the characteristic

Basophillic stippling

seen on a peripheral smear.

Diagnosis

– Blood lead levels –

Increased free erythrocyte protoporphyrin Treatment

: Chelating drugs (dimercaprol, pencillamine)

• • • • • • Wrist and foot drop occur in adults due to peripheral motor nerve demyelination Abdominal pain (lead colic) Renal tubular acidosis and renal failure

Microcytic anemia

with

basophilic stippling

– caused by precipitated ribosomes in reticulocytes Deposition of lead at the

gingivodental line

(“

Lead line

”) X-ray long bones have lead lines 

increased bone density at the epiphyseal growth plates

Lead Lines

Basophilic Stippling

MERCURY

• Although all mercury compounds are toxic, the

small-chain alkyl compounds

vary in toxicity are the

most hazardous

. Mercury compounds •

Health Effects

According to Agency for Toxic Substances and Disease Registry (ATSDR), mercury is not classifiable as a human carcinogen, although

mercury chloride and methyl mercury are possible human carcinogens

.

Mercury poisoning: Neurotoxicity

– Intention tremors – Dementia and delirium

Nephrotoxicity

(acute tubular necrosis)