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Air Pollution - Pathology Exam Notes

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1. Definition & Classification

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2. Major Outdoor Air Pollutants & Pathological Effects

A. Ozone (O3)

• Source: Sunlight-driven reactions of nitrogen oxides (mainly automobile exhaust) - a photochemical pollutant
• Mechanism of injury: O3 participates in chemical reactions that generate free radicals → injure lining cells of the respiratory tract and alveoli
• Pathological effects:
  • Decreased lung function
  • Increased airway reactivity and inflammation
  • Bronchoconstriction
  • Particularly harmful in asthma, emphysema, or combined with particulate pollution
  • Children are especially susceptible

B. Particulate Matter (PM)

• Source: Coal/oil-fired power plants, industrial combustion, vehicle exhaust
• Key size threshold: Particles < 10 μm diameter are most harmful
  • Carried by airstream to alveoli
  • Phagocytosed by macrophages and neutrophils
  • Activate inflammasomes → release of inflammatory mediators → inflammatory reaction
  • Larger particles removed in nose or trapped by mucociliary barrier
• PM 2.5 (fine particles, < 2.5 μm): regional transport, greatest contributor to systemic disease and mortality
• Pathological effects:
  • Increased respiratory infections (children)
  • Decreased lung function in chronic lung/heart disease
  • Increased mortality
  • Increased asthma attacks

C. Sulfur Dioxide (SO2)

• Source: Coal/oil-fired power plants, smelters, oil refineries, kerosene heaters
• Pathological effects: Exacerbation of asthma and COPD; increased respiratory symptoms; exacerbation of pre-existing chronic lung disease

D. Nitrogen Dioxide (NO2)

• Source: Automobile exhaust, gas stoves, wood-burning stoves
• Pathological effects: Increased airway reactivity, decreased lung function, increased respiratory infections, bronchiolitis obliterans

E. Carbon Monoxide (CO) - (High-yield pathology topic)

• Source: Incomplete combustion of carbonaceous materials; auto engines, fossil fuels, cigarette smoke; accidental/suicidal exposure
• Mechanism: Hemoglobin has 200x greater affinity for CO than O2 → carboxyhemoglobin formed → cannot carry O2 → tissue hypoxia
  • 20-30% saturation: systemic hypoxia
  • 60-70% saturation: unconsciousness and death
• Morphology - Acute poisoning:
  • Mucous membranes appear cherry-red/erythematous (due to carboxyhemoglobin)
  • Rapid death: no morphological changes
  • Longer survival: brain slightly edematous, punctate hemorrhages, hypoxia-induced neuronal changes
  • Basal ganglia and lenticular nuclei particularly affected
• Morphology - Chronic poisoning:
  • Carboxyhemoglobin accumulates with low-level persistent exposure
  • Widespread ischemic changes in brain, especially basal ganglia and lenticular nuclei
  • Permanent neurological damage possible

F. Acid Aerosols

• Source: Combustion of coal and oil
• Effects: Increased mortality in COPD; increased hospitalizations; decreased lung function; altered mucociliary clearance

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3. Pneumoconioses (Dust-Induced Lung Diseases) - Exam Favourite

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A. Coal Workers' Pneumoconiosis (CWP) / Anthracosis

• Pulmonary anthracosis: Inhaled carbon pigment engulfed by alveolar/interstitial macrophages → accumulate along pulmonary/pleural lymphatics and draining lymph nodes. Most innocuous form; also seen in urban dwellers and smokers.
• Simple CWP:
  • Coal macules = dust-laden macrophages + small amounts of delicate collagen network
  • Coal nodules = larger lesions
  • Upper lobes and upper zones of lower lobes most involved
  • Centrilobular emphysema may develop
• Progressive Massive Fibrosis (PMF) / Complicated CWP:
  • Coalescence of coal nodules over years
  • Multiple dark black scars > 2 cm (up to 10 cm)
  • Dense collagen + pigment
  • < 10% of simple CWP progresses to PMF

• Usually benign with little decline in lung function (simple CWP)
• PMF → pulmonary dysfunction, pulmonary hypertension, cor pulmonale
• No increased lung cancer risk (unlike silica and asbestos - important distinguishing feature)

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B. Silicosis

1. Silica particles inhaled → phagocytosed by alveolar macrophages
2. Lysosomal damage
3. Activation of the inflammasome
4. Release of IL-1, TNF, oxygen-derived free radicals, fibrogenic cytokines → fibrosis

• Silicotic nodules (early): tiny, discrete, pale-to-black nodules in upper zones of lungs
• Microscopy (key features):
  • Concentrically arranged hyalinized collagen fibers surrounding an amorphous center
  • Whorled (onion-skin) appearance of collagen - characteristic
  • Polarized microscopy: weakly birefringent silica particles in center of nodules
• Progressive coalescence → hard collagenous scars → PMF
• Compressed or overexpanded intervening lung → honeycomb pattern
• Fibrotic lesions also in hilar lymph nodes and pleura

• Usually asymptomatic; detected on chest X-ray (fine nodularity, upper zones)
• Dyspnea only with PMF (late)
• PMF → pulmonary hypertension + cor pulmonale
• Increased susceptibility to tuberculosis (crystalline silica inhibits macrophage killing of mycobacteria) → Silicotuberculosis (nodules with central caseation)
• Modestly increased risk of lung cancer

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C. Asbestos-Related Diseases

1. Asbestosis - parenchymal interstitial fibrosis
2. Pleural plaques - localized fibrous pleural plaques (most common manifestation)
3. Pleural effusions
4. Lung carcinoma (~5x increased risk)
5. Malignant mesothelioma (pleural and peritoneal)
6. Laryngeal carcinoma

• Asbestos fibers phagocytosed by macrophages → activate inflammasome → damage phagolysosomal membranes → proinflammatory + fibrogenic mediators
• Free radicals induced by asbestos → mesothelial injury (mesothelioma)
• Toxic chemicals adsorbed onto fibers (e.g., tobacco carcinogens) → synergy between smoking and lung carcinoma in asbestos workers

• Diffuse pulmonary interstitial fibrosis + asbestos bodies
• Asbestos bodies: golden-brown, fusiform or beaded rods with translucent center - asbestos fibers coated with iron-containing proteinaceous material (ferritin); formed as macrophages attempt phagocytosis
• Location: Starts in lower lobes, subpleurally (opposite of silicosis/CWP which affect upper lobes)
• Spreads to middle and upper lobes as disease progresses
• Enlarged air spaces within thick fibrous walls → honeycombing
• Visceral pleural fibrosis → adhesions with chest wall
• Narrowing of pulmonary arteries → pulmonary hypertension + cor pulmonale

• Most common manifestation of asbestos exposure
• Well-circumscribed plaques of dense collagen, often calcified
• Anterior and posterolateral parietal pleura, diaphragmatic domes
• Usually asymptomatic; seen on radiology as circumscribed calcific densities

• Dyspnea: appears 10-20 years after exposure (long latency)
• Cough + sputum production
• Progressive → congestive heart failure, cor pulmonale, death
• Lung carcinoma risk: ~5x increased in asbestos workers alone; ~55x with combined smoking (synergistic effect)
• Mesothelioma risk: markedly increased

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4. Indoor Air Pollution

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5. Comparison Table - Pneumoconioses (High-Yield for Exams)

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6. Pathogenesis Summary - Common Mechanism

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Quick-Recall Mnemonics

• "Silicosis = Swirly + upper + TB risk" - Whorled (swirly) collagen, upper lobe, associated with TB
• "Asbestos = All Cancers + lower lobe + 20 years" - mesothelioma, lung cancer, laryngeal cancer; lower lobe; 20-year latency
• "CO = Cherry red mucosa + Basal ganglia" - key exam findings for CO poisoning
• "PMF = Progressive Massive Fibrosis" - end-stage of CWP, silicosis, or asbestosis; > 2 cm scars; cor pulmonale

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