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Occupational Lung Diseases — Complete Notes (Pulmonology)

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Overview

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I. PNEUMOCONIOSES

Pneumoconioses are fibrotic lung diseases caused by inhalation of inorganic mineral dusts. The term means "dusty lung."

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A. SILICOSIS

Etiology & Exposure

• Agent: Crystalline silica (SiO₂), particularly quartz
• Occupations at risk: Sandblasting, tunneling, mining, quarrying, stone cutting, ceramic/glass manufacturing, abrasive soap manufacturing

Pathogenesis

1. Silica particles (<10 µm) deposited in alveoli
2. Phagocytosed by alveolar macrophages → macrophage death → release of fibrogenic cytokines (IL-1, TNF-α)
3. Cycle of macrophage ingestion and death leads to progressive fibrosis
4. Formation of silicotic nodules (concentric whorls of collagen + silica particles)

Types & Clinical Features

• Progressive dyspnea on exertion
• Cough (may be productive if complicated by infection)
• Constitutional symptoms in accelerated/acute forms
• Late: respiratory failure, cor pulmonale

Radiological Features

• Small (<1 cm), rounded nodular opacities
• Predominant in upper lobes
• "Eggshell calcification" of hilar lymph nodes (pathognomonic)

• Nodules ≥1 cm, coalescing into large masses (>1 cm)
• Upper-lobe dominant conglomerate masses

• Diffuse miliary infiltrates or consolidation
• "Crazy paving" pattern on HRCT (similar to alveolar proteinosis)

Complications

• Progressive Massive Fibrosis (PMF) — most serious
• Silicotuberculosis — silica impairs macrophage killing of mycobacteria; TB risk ↑ 2–3x
• Lung cancer — silica is a Group 1 carcinogen (IARC)
• Scleroderma and other connective tissue diseases — Erasmus syndrome (silicosis + scleroderma)
• Caplan syndrome — silicotic nodules + seropositive rheumatoid arthritis
• Chronic renal disease (rare)

Diagnosis

• Clinical + occupational history (exposure ≥10 years for chronic form)
• CXR / HRCT (ILO classification of pneumoconioses)
• PFTs: restrictive pattern (may have mixed/obstructive in PMF)
• Exclude TB (sputum, IGRA)
• Biopsy rarely needed; histology shows birefringent silica crystals in fibrotic nodules

Management

• No curative treatment
• Remove from further exposure
• Symptom management: bronchodilators, supplemental O₂
• Treat latent/active TB aggressively
• Whole-lung lavage for acute silicosis (provides symptomatic relief, slows progression)
• Lung transplantation for end-stage disease
• Vaccinations: influenza, pneumococcal

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B. COAL WORKERS' PNEUMOCONIOSIS (CWP) — "Black Lung Disease"

Etiology & Exposure

• Agent: Coal dust (mixed organic + inorganic particles; anthracite coal has higher silica content)
• Occupations: Underground coal miners, surface miners, coal processing

Pathogenesis

• Coal dust particles → macrophage ingestion → formation of coal macules (aggregates of dust-laden macrophages) around respiratory bronchioles
• Can also cause chronic bronchitis and COPD (additive to cigarette smoking effects)
• Effects of coal dust + cigarette smoke are additive

Types & Clinical Features

Complications

• PMF — upper lobe conglomerate masses; severe restrictive + obstructive deficits
• COPD — particularly with smoking
• Caplan Syndrome — CWP nodules + seropositive rheumatoid arthritis (first described in coal miners; subsequently found in silicosis too)
• Cor pulmonale

Diagnosis

• Occupational history + CXR findings
• PFTs: mixed pattern (restrictive + obstructive)
• HRCT: upper lobe predominant small rounded opacities; PMF masses

Management

• Remove from exposure
• Supportive care (O₂, bronchodilators)
• No disease-modifying therapy
• Lung transplantation for advanced disease

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C. ASBESTOSIS

Etiology & Exposure

• Agent: Asbestos fibers (amphibole types — crocidolite, amosite — most fibrogenic; chrysotile also causes disease)
• Occupations: Construction workers (insulation, flooring, roofing), shipbuilding, asbestos mining, brake lining manufacturing, demolition workers
• Latency: Long — typically 15–40 years from first exposure

Pathogenesis

• Long, thin fibers deposited in alveoli and respiratory bronchioles
• Incomplete macrophage clearance → persistent inflammation → progressive interstitial fibrosis
• Fibrosis begins at lung bases (lower lobes) — opposite of silicosis/CWP
• "Asbestos bodies" = ferruginous bodies — asbestos fibers coated in iron-protein complex (visible on BAL or biopsy)

Clinical Features

• Slowly progressive exertional dyspnea
• Dry cough
• Bibasilar fine crackles (Velcro crackles)
• Clubbing (in advanced disease)
• Signs of cor pulmonale (late)
• Pleural disease is common: pleural plaques (pathognomonic of exposure), benign pleural effusions, diffuse pleural thickening, rounded atelectasis

Radiological Features

• CXR: bilateral lower-lobe reticulation, honeycombing; pleural plaques (often calcified, "holly leaf" appearance)
• HRCT (high-resolution CT): Subpleural reticulation, traction bronchiectasis, honeycombing, pleural plaques — lower-lobe predominant; paraseptal fibrosis

PFTs

• Restrictive pattern: ↓ FVC, ↓ TLC, ↓ DLCO
• FEV₁/FVC ratio preserved or increased

Asbestos-Related Malignancies

Diagnosis

• Occupational/exposure history + clinical + imaging
• HRCT findings consistent with UIP pattern + lower-lobe fibrosis
• BAL or biopsy: asbestos bodies (ferruginous bodies)
• Exclude other causes of ILD

Management

• No specific therapy — supportive care same as for any diffuse interstitial fibrosis (Harrison's, p. 7978)
• Remove from exposure
• Smoking cessation (critical — multiplicative effect on lung cancer risk)
• Surveillance for malignancy (annual low-dose CT chest)
• O₂ therapy, pulmonary rehabilitation
• Mesothelioma: chemotherapy (cisplatin + pemetrexed), immunotherapy (nivolumab + ipilimumab in unresectable disease)

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D. BERYLLIOSIS (Chronic Beryllium Disease — CBD)

Etiology & Exposure

• Agent: Beryllium (metallic element)
• Occupations: Aerospace, nuclear weapons/power, electronics, ceramic manufacturing, dental alloy production
• Even brief or low-level exposure can cause disease in sensitized individuals (~2–6% of exposed workers)

Pathogenesis

• Beryllium is a hapten → acts as antigen → Type IV hypersensitivity (delayed-type, T-cell mediated)
• Genetically predisposed individuals: HLA-DPB1 Glu69 allele confers susceptibility
• Leads to non-caseating granulomas (identical to sarcoidosis histologically)

Clinical Features

• Mimics sarcoidosis clinically and histologically
• Dyspnea, cough, fatigue, chest pain
• Bilateral hilar lymphadenopathy
• May have extrapulmonary involvement (skin, liver, lymph nodes)
• Skin patch testing (beryllium lymphocyte proliferation test, BeLPT) differentiates from sarcoidosis

Diagnosis

• Beryllium Lymphocyte Proliferation Test (BeLPT) — specific for beryllium sensitization (blood or BAL)
• HRCT: bilateral micronodules, lymphadenopathy, fibrosis (upper lobe predominant)
• BAL + transbronchial biopsy: non-caseating granulomas + positive BeLPT

Management

• Remove from beryllium exposure
• Corticosteroids (prednisolone) for symptomatic disease — same as sarcoidosis treatment
• Long-term follow-up (can progress to fibrosis despite treatment)

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E. OTHER PNEUMOCONIOSES (Brief)

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II. OCCUPATIONAL ASTHMA

Definition

Agents & Occupations

Clinical Features

• Work-related pattern — symptoms worse at work, improve on weekends/holidays
• Wheezing, chest tightness, dyspnea, rhinitis
• RADS: acute onset after a single massive irritant exposure; persists >3 months

Diagnosis

• Serial peak flow monitoring (at work vs away from work)
• Specific bronchial provocation challenge (gold standard)
• Skin prick test / specific IgE (for HMW allergens)
• Methacholine challenge: demonstrates non-specific bronchial hyperresponsiveness

Management

• Remove from exposure (early removal = better outcome)
• Inhaled corticosteroids + bronchodilators (same as non-occupational asthma)
• Avoidance measures if full removal not possible
• Compensation/medicolegal assessment

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III. HYPERSENSITIVITY PNEUMONITIS (Extrinsic Allergic Alveolitis)

Definition

Common Forms & Antigens

Pathogenesis

• Type III (immune complex) + Type IV (T-cell mediated) hypersensitivity
• Sensitization → re-exposure → alveolar inflammation → non-caseating granulomas → fibrosis (chronic)

Clinical Forms

Diagnosis

• Exposure history + temporal relationship of symptoms
• HRCT: Bilateral ground-glass opacities, poorly defined centrilobular nodules, mosaic attenuation (air trapping); fibrosis in chronic form
• BAL: Lymphocytosis (CD4:CD8 ratio <1 in HP vs >3.5 in sarcoidosis) — key differentiator
• Precipitating antibodies (IgG precipitins) against causative antigens — indicate exposure, not disease
• Biopsy (if needed): non-caseating granulomas, lymphocytic alveolitis, bronchiolocentric distribution
• Inhalation challenge (gold standard but rarely needed)

Management

• Antigen avoidance — cornerstone of management
• Corticosteroids — accelerate resolution in acute/subacute forms (prednisone 40–60 mg/day, taper over months)
• Chronic fibrotic HP: antifibrotic therapy (nintedanib) — similar to IPF management
• Supplemental O₂, pulmonary rehab for advanced disease
• Lung transplantation for end-stage fibrotic disease

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IV. BYSSINOSIS ("Monday Fever" / "Brown Lung")

Etiology & Exposure

• Agent: Cotton dust (also flax and hemp dust)
• Occupations: Cotton textile workers (card room workers most affected)
• Active agent: endotoxin from gram-negative bacteria in cotton + bracts (outer cotton plant parts)

Pathogenesis

• Non-immunological mechanism — endotoxin-mediated airway inflammation
• Leads to bronchoconstriction and chronic airway disease

Clinical Features

• Classic "Monday fever" — chest tightness, cough, dyspnea on return to work after weekend (worst on first workday)
• Symptoms improve as week progresses (tachyphylaxis)
• Chronic byssinosis: persistent symptoms, progressive COPD-like picture

Grading (Schilling Classification)

Diagnosis

• Occupational history + Monday symptom pattern
• Serial PFTs (FEV₁ change across a Monday work shift — ≥10% fall diagnostic)
• CXR usually normal until late stages

Management

• Reduce cotton dust exposure (engineering controls, respirators)
• Bronchodilators
• Smoking cessation
• Corticosteroids for symptomatic relief
• Advanced disease: COPD management principles

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V. TOXIC INHALATION INJURIES

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VI. GENERAL APPROACH TO OCCUPATIONAL LUNG DISEASE

History Taking (Key Elements)

1. Occupational history — all jobs held chronologically, durations
2. Exposure history — specific agents, use of PPE
3. Temporal relationship — onset relative to work schedule
4. Latency period — time from first exposure to symptom onset
5. Co-exposures — smoking (multiplicative effect with many occupational agents)
6. Hobbies/home exposures — birds, humidifiers, molds

Diagnostic Approach

Step 1: Occupational/exposure history
Step 2: CXR → HRCT chest
Step 3: Pulmonary function tests (PFTs)
Step 4: BAL (lavage differential)
Step 5: Specific serology (precipitins, BeLPT)
Step 6: Lung biopsy (if diagnosis unclear)

PFT Patterns Summary

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VII. COMPARISON TABLE — KEY PNEUMOCONIOSES

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VIII. ILO CLASSIFICATION OF PNEUMOCONIOSES

• Profusion (density of opacities): categories 0, 1, 2, 3
• Shape/Size:
  • Small opacities: p (rounded, <1.5mm), q (1.5–3mm), r (3–10mm); s, t, u (irregular)
  • Large opacities: A (<5cm), B (>5cm but <1/3 right lung), C (>B)
• Pleural changes: pleural plaques, diffuse thickening, costophrenic blunting
• PMF = Large opacities B or C in context of pneumoconiosis

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Key Mnemonics

• "COAL gives CAPLAN" — Caplan syndrome first described in coal workers
• "Silica = Upper, Asbestos = Lower" — distribution of fibrosis
• "No smoke no meso" — Mesothelioma NOT associated with smoking (unlike lung cancer)
• "Crazy paving = Acute silicosis" — HRCT crazy paving in acute silicosis / alveolar proteinosis
• "Monday chest = Byssinosis" — cotton dust, worst on Mondays
• "BeLPT separates Berylliosis from Sarcoid" — beryllium lymphocyte proliferation test

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Classification Corrections Before Notes

Etiological Classification — Corrections

Disease-Based Classification — Corrections

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CORRECTED CLASSIFICATIONS

✅ Etiological Classification

1. Inorganic Dusts
   - Asbestosis, Silicosis, Coal Workers' Pneumoconiosis, Berylliosis

2. Organic Dusts
   - Cotton dust (byssinosis), Grain dust, Other agricultural dusts (hay, mushroom compost, sugarcane bagasse)

3. Chemical Agents & Fumes
   - Isocyanates (TDI/MDI), Toxic gases (chlorine, phosgene, NOx), Hydrocarbons

4. Other Environmental Agents
   - Uranium, Radon, Environmental tobacco smoke (second-hand smoke), Polycyclic aromatic hydrocarbons, Biomass smoke, Diesel exhaust

✅ Disease-Based Classification

1. Pneumoconioses
   - Asbestosis, Silicosis, Coal Workers' Pneumoconiosis, Berylliosis

2. Occupational Airway Diseases
   - Occupational Asthma, Byssinosis, Chronic Bronchitis, COPD

3. Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis)
   - Farmer's Lung, Bird Fancier's Lung, Bagassosis, Mushroom Worker's Lung

4. Occupational Lung Infections
   - Tuberculosis, Anthrax, Histoplasmosis, Aspergillosis

5. Lung Malignancies
   - Mesothelioma, Bronchogenic Carcinoma (Lung Cancer)

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OCCUPATIONAL LUNG DISEASES — COMPLETE NOTES

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ETIOLOGICAL CLASSIFICATION & NOTES

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1. INORGANIC DUSTS

General Pathogenesis (All Pneumoconioses)

1. Dust particles <10 µm reach alveoli
2. Phagocytosed by alveolar macrophages
3. Macrophage activation → release of cytokines (IL-1β, TNF-α, TGF-β)
4. Progressive fibrosis, impaired mucociliary clearance
5. Fibrosis severity depends on: particle size, solubility, inherent fibrogenicity, dose, and duration

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A. SILICOSIS

• Silicotic nodule — concentric whorls of hyalinized collagen with birefringent silica crystals at center
• Nodules coalesce → Progressive Massive Fibrosis (PMF)

• Dyspnea on exertion (progressive)
• Dry cough
• Late: respiratory failure, cor pulmonale
• Acute form: fever, weight loss, rapid deterioration

• Simple: small rounded opacities, upper lobe predominant
• Complicated/PMF: masses ≥1 cm, upper lobe conglomerate nodules
• Eggshell calcification of hilar lymph nodes — pathognomonic
• Acute: miliary infiltrates, "crazy paving" pattern on HRCT

• Silicotuberculosis — silica impairs macrophage mycobacterial killing; TB risk ↑ 2–3×
• PMF — severe restrictive deficits, premature death
• Lung cancer — IARC Group 1 carcinogen (Harrison's p. 7989)
• Caplan syndrome — silicotic nodules + seropositive rheumatoid arthritis
• Erasmus syndrome — silicosis + scleroderma
• Chronic renal disease (rare)

• Occupational history + CXR/HRCT
• PFTs: restrictive (mixed in PMF)
• IGRA/Mantoux — screen for TB
• Biopsy rarely needed

• Remove from exposure
• Whole-lung lavage (acute form)
• Treat TB promptly and aggressively
• Supportive: O₂, bronchodilators, vaccinations
• Lung transplantation (end-stage)

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B. COAL WORKERS' PNEUMOCONIOSIS (CWP) — "Black Lung"

• Coal macule — focal accumulation of dust-laden macrophages around respiratory bronchioles (earliest lesion)
• Coal nodule — collagen deposition around coal macule
• PMF — masses >1 cm in upper lobes

• PMF — progressive respiratory failure
• Caplan Syndrome — first described in coal miners; CWP nodules + seropositive RA (Harrison's p. 7983)
• COPD — coal dust causes chronic bronchitis and airflow obstruction independently
• Cor pulmonale

• CXR: upper-lobe rounded opacities; ILO classification
• HRCT: confirms nodules, PMF masses
• PFTs: mixed obstructive + restrictive pattern

• Remove from exposure
• Supportive: bronchodilators, O₂
• No disease-modifying therapy available
• Lung transplantation (end-stage)

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C. ASBESTOSIS

• Long fibers deposited in alveoli → incomplete macrophage clearance → persistent inflammation → interstitial fibrosis
• Asbestos bodies (ferruginous bodies) — asbestos fibers coated with iron-protein complex; found in BAL/biopsy
• Fibrosis is lower lobe, subpleural predominant

• Progressive exertional dyspnea
• Dry cough
• Bibasilar fine Velcro crackles (hallmark)
• Digital clubbing (advanced)
• Cor pulmonale (late)
• Pleural disease: plaques, benign effusion, diffuse thickening, rounded atelectasis

• CXR: bilateral lower-lobe reticulation, honeycombing; calcified pleural plaques ("holly leaf" pattern)
• HRCT: subpleural reticulation, traction bronchiectasis, honeycombing; lower-lobe predominant

• No specific therapy — supportive care same as any diffuse interstitial fibrosis (Harrison's p. 7978)
• Smoking cessation (critical)
• Annual low-dose CT surveillance for lung cancer
• O₂ therapy, pulmonary rehabilitation
• Mesothelioma: cisplatin + pemetrexed; nivolumab + ipilimumab (unresectable)

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D. BERYLLIOSIS (Chronic Beryllium Disease — CBD)

• Mimics sarcoidosis clinically and radiologically
• Dyspnea, cough, fatigue, chest pain
• Bilateral hilar lymphadenopathy
• Skin, liver, lymph node involvement possible

• Beryllium Lymphocyte Proliferation Test (BeLPT) — blood or BAL
• Positive BeLPT = beryllium sensitization → differentiates from sarcoidosis

• Remove from beryllium exposure
• Corticosteroids (same as sarcoidosis approach)
• Long-term follow-up (risk of progression to fibrosis)

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2. ORGANIC DUSTS

Key Organic Dust Sources:

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3. CHEMICAL AGENTS & FUMES

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4. OTHER ENVIRONMENTAL AGENTS

A. Uranium & Radon

• Uranium — direct radiation-induced carcinogen; lung cancer risk in miners and processing workers
• Radon (radon daughters) — emitted from rock formations in underground mines; alpha particle emission → DNA damage → lung cancer; risk not limited to uranium mines — any underground mining where radon is present (Harrison's p. 7989)
• Combined radon + smoking: synergistic lung cancer risk

B. Environmental Tobacco Smoke (Secondhand Smoke)

• Classified as an occupational/environmental carcinogen (Harrison's p. 7989)
• Causes lung cancer (adenocarcinoma most common in non-smokers)
• Also causes COPD, asthma exacerbations in exposed workers (hospitality, service industry workers historically)

C. Polycyclic Aromatic Hydrocarbons (PAHs)

• Sources: coke oven emissions, diesel exhaust, coal tar, asphalt
• PAHs → DNA adducts → lung cancer (squamous cell carcinoma predominant)
• Also: bladder cancer, skin cancer

D. Biomass Smoke

• Exposure in agricultural workers, developing-world indoor cooking
• Causes: COPD, chronic bronchitis, pulmonary hypertension, lung cancer (long-term exposure)
• WHO estimates biomass smoke causes ~4 million deaths/year globally

E. Diesel Exhaust

• IARC Group 1 carcinogen (since 2012)
• Contains NOₓ, PAHs, fine particulate matter
• Lung cancer risk (especially adenocarcinoma) in truck drivers, miners, dock workers
• Also contributes to COPD and asthma

F. Other Proven/Suspected Respiratory Carcinogens (Harrison's p. 7989)

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DISEASE-BASED CLASSIFICATION & NOTES

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1. PNEUMOCONIOSES

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2. OCCUPATIONAL AIRWAY DISEASES

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A. OCCUPATIONAL ASTHMA (OA)

• Work-related pattern — symptoms worse at work, improve on weekends and holidays (key history clue)
• Wheeze, chest tightness, dyspnea, rhinitis/conjunctivitis
• RADS: acute onset after single massive exposure; symptoms persist >3 months

1. Detailed occupational history
2. Serial peak expiratory flow (PEF) monitoring — at work vs away from work (standard diagnostic tool)
3. Methacholine challenge — documents non-specific bronchial hyperresponsiveness
4. Specific inhalation challenge (SIC) — gold standard (performed in specialist centers)
5. Skin prick test / specific IgE for HMW allergens

• Early removal from exposure — prognosis directly related to duration of continued exposure after diagnosis
• Inhaled corticosteroids + bronchodilators
• If removal not possible: strict exposure reduction + PPE
• Compensation and medicolegal assessment

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B. BYSSINOSIS ("Monday Fever" / "Brown Lung")

• Chest tightness, cough, dyspnea on return to work after weekend
• Symptoms improve as the working week progresses (tachyphylaxis)
• Chronic byssinosis: persistent symptoms, COPD-like picture

• Occupational history + Monday symptom pattern
• ≥10% fall in FEV₁ across a Monday work shift — diagnostic criterion
• CXR normal until late stages

• Dust control measures (engineering controls)
• Bronchodilators
• Smoking cessation
• Advanced disease: COPD management principles

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C. OCCUPATIONAL CHRONIC BRONCHITIS

• Chronic productive cough for >3 months/year for ≥2 consecutive years, attributable to occupational dust/fume exposure
• Agents: coal dust, silica, grain dust, cadmium fumes, wood dust
• Distinguishable from smoking-related bronchitis only by careful exposure history
• Management: same as non-occupational chronic bronchitis (inhaled therapies, smoking cessation, exposure reduction)

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D. OCCUPATIONAL COPD

• Occupational exposures account for 10–20% of COPD cases (ATS statement); up to 31% in never-smokers (GOLD 2025, p. 22)
• Agents: coal dust, silica, cadmium, grain dust, isocyanates, vapors/gases/dusts/fumes (VGDF)
• Risk is higher in less regulated work environments globally
• COPD attributable to occupational exposure is underdiagnosed as the clinical picture is identical to smoking-induced COPD
• Pesticide inhalation → increased COPD incidence, even in non-smokers (GOLD 2025, p. 22)
• Management: standard COPD guidelines (GOLD strategy) + mandatory removal from exposure

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3. HYPERSENSITIVITY PNEUMONITIS (HP) / Extrinsic Allergic Alveolitis (EAA)

• Type III (immune complex deposition) — acute phase
• Type IV (T-lymphocyte-mediated, delayed) — chronic granulomatous inflammation
• Result: lymphocytic alveolitis → non-caseating granulomas → fibrosis (if chronic/untreated)

Key Diseases:

Clinical Forms:

• Fever, chills, myalgia — "flu-like" 4–8 hours after antigen exposure
• Cough, dyspnea, crackles on auscultation
• Resolves spontaneously on antigen removal

1. Detailed antigen exposure history + temporal relationship
2. HRCT: Ground-glass opacities, centrilobular nodules, mosaic attenuation (air trapping); fibrosis in chronic form
3. BAL: Lymphocytosis; CD4:CD8 ratio <1 (vs. sarcoidosis where ratio >3.5) — key differentiator
4. Precipitating IgG antibodies (precipitins) against causative antigen — confirms exposure, not disease activity
5. Lung biopsy: non-caseating granulomas, lymphocytic alveolitis, bronchiolocentric distribution
6. Inhalation challenge — gold standard (rarely performed)

• Antigen avoidance — cornerstone; most important intervention
• Acute/subacute: Corticosteroids (prednisolone 40–60 mg/day, tapered over months) — accelerate resolution
• Chronic fibrotic HP: Nintedanib (antifibrotic) — approved for progressive fibrotic ILD including HP
• Supplemental O₂, pulmonary rehabilitation
• Lung transplantation for end-stage disease

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4. OCCUPATIONAL LUNG INFECTIONS

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A. TUBERCULOSIS (TB)

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B. ANTHRAX (Pulmonary / Inhalation Anthrax)

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C. HISTOPLASMOSIS

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D. ASPERGILLOSIS

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5. LUNG MALIGNANCIES

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A. BRONCHOGENIC CARCINOMA (Lung Cancer)

• Asbestos + Smoking → multiplicative (not merely additive) lung cancer risk; up to 50–90× baseline risk in asbestos workers who smoke (Harrison's p. 7978)
• Radon + Smoking → synergistic elevated lung cancer risk

• Asbestos, silica, PAHs: all types (squamous, adenocarcinoma, SCLC)
• Bis(chloromethyl) ether: specifically small cell lung cancer
• Secondhand smoke in non-smokers: predominantly adenocarcinoma

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B. MESOTHELIOMA

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GENERAL PRINCIPLES IN OCCUPATIONAL LUNG DISEASE

Exposure History — Must Cover:

1. All jobs held (chronological list with durations)
2. Specific agents encountered and intensity of exposure
3. Temporal relationship of symptoms to work schedule
4. Use of personal protective equipment (PPE)
5. Co-exposures — especially cigarette smoking (major effect modifier)
6. Latency period — time from first exposure to first symptom
7. Hobbies and home exposures (birds, humidifiers, molds)

PFT Pattern Summary:

Prevention Framework:

Hierarchy of Controls (most → least effective):
1. Elimination — remove the hazardous agent entirely
2. Substitution — replace with a less hazardous material
3. Engineering controls — local exhaust ventilation, wet drilling, enclosure
4. Administrative controls — job rotation, reduced shift duration
5. Personal Protective Equipment (PPE) — respirators, masks (last resort)

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