Respiratory
Pneumoconioses: silicosis, asbestosis, coal worker's, berylliosis
— Silicosis: sandblasting, mining, quarrying, stone cutting (especially engineered/artificial stone countertops — a re-emerging epidemic in young workers), foundry work, tunneling.
— Asbestosis: shipbuilding, insulation, brake lining, demolition, plumbing/pipefitting, Navy veterans pre-1980, roofers.
— Coal worker's pneumoconiosis (CWP): underground coal miners; resurgence in Appalachian miners with rapidly progressive disease.
— Berylliosis (chronic beryllium disease, CBD): aerospace, nuclear weapons, electronics, dental prosthetics, ceramics, alloy manufacturing.
— Upper-lobe predominant nodules + occupational dust → silicosis or CWP.
— Lower-lobe reticular changes + pleural plaques → asbestosis.
— Sarcoid-like granulomas + machinist/aerospace history → berylliosis.
Board pearl: A 35-year-old immigrant countertop fabricator with progressive dyspnea and upper-lobe nodules has accelerated silicosis until proven otherwise — ask about engineered quartz stone, the dominant emerging silicosis exposure in the US, and report to OSHA/NIOSH as a sentinel event.

— Chronic (classic) silicosis: >10 years exposure, upper-lobe small (<10 mm) rounded nodules; mostly asymptomatic until PMF develops.
— Accelerated silicosis: 5–10 years of heavy exposure (engineered stone, sandblasting); faster decline, higher autoimmune/TB risk.
— Acute silicoproteinosis: months–5 years of intense exposure; PAP-like alveolar filling, rapidly fatal dyspnea and hypoxemia.
— Every job since age 16, with duration and specific tasks.
— Materials: silica, asbestos, coal, beryllium, hard metals.
— Respiratory protection used (fit-tested? consistently?).
— Prior B-reader CXR surveillance results.
— Secondhand exposures (family members, neighborhood).
— Smoking, TB exposure, prior IGRA/PPD.
— Connective tissue symptoms (silica → scleroderma, RA, ANCA vasculitis, lupus).
Key distinction: Asbestosis = lower-lobe reticular disease with pleural plaques; silicosis and CWP = upper-lobe nodular disease. PMF can complicate either silicosis or CWP and presents as conglomerate upper-lobe masses that mimic malignancy on imaging.

— Bibasilar fine end-inspiratory "velcro" crackles (hallmark, present in >80% with established disease).
— Digital clubbing in up to 40% — should prompt evaluation for superimposed malignancy if new.
— Decreased breath sounds and dullness over pleural effusions (benign asbestos pleural effusion or mesothelioma).
— Often normal lung exam in simple disease.
— Diminished breath sounds, hyperresonance if emphysema coexists (especially in CWP miners).
— In PMF: bronchial breathing or dullness over conglomerate masses; cyanosis with advanced disease.
— Bibasilar crackles, occasional wheeze, palpable lymphadenopathy, skin granulomas at trauma/exposure sites; hepatosplenomegaly possible.
— Loud P2, fixed split S2, right parasternal heave, JVD with prominent a wave, hepatojugular reflux, peripheral edema, ascites.
— Resting hypoxemia or exertional desaturation on 6-minute walk test (6MWT) signals pulmonary hypertension risk.
— Sclerodermatous skin changes, Raynaud, RA joints → silica-associated autoimmunity (Erasmus/Caplan syndromes: silicosis or CWP + rheumatoid nodules).
— Erythema nodosum, uveitis → consider berylliosis vs sarcoidosis.
— Constitutional fevers + weight loss → rule out superimposed TB or nontuberculous mycobacteria, especially in silicosis.
Step 3 management: At every visit, document resting SpO2 and ambulatory SpO2 with 6MWT; a drop to ≤88% qualifies the patient for long-term supplemental O2 (Medicare criterion) and changes the entire long-term care plan, including air-travel counseling and pulmonary rehab referral.

— Read by an ILO-certified B-reader (NIOSH program) using the ILO classification for profusion (0–3), shape (rounded p/q/r vs irregular s/t/u), and size of opacities.
— Silicosis/CWP: small rounded upper-lobe opacities; eggshell calcification of hilar/mediastinal lymph nodes is classic for silicosis (also seen in sarcoid).
— Asbestosis: lower-lobe reticular/linear opacities + pleural plaques (often calcified along diaphragm and lateral chest wall).
— PMF: conglomerate masses >1 cm, often upper-lobe, may cavitate.
— Silicosis: centrilobular and subpleural micronodules, upper-lobe predominant.
— Asbestosis: subpleural reticulation, honeycombing, traction bronchiectasis (UIP-like) + plaques.
— Berylliosis: peribronchovascular nodules with mediastinal/hilar adenopathy (sarcoid-like).
— Restrictive pattern with ↓TLC, ↓DLCO is typical; CWP often shows mixed or obstructive pattern from coexisting emphysema.
— DLCO is the most sensitive early marker.
Board pearl: Eggshell calcification of hilar nodes is classic for silicosis (and may be seen in CWP and sarcoidosis); when accompanied by upper-lobe nodules in a sandblaster, no biopsy is needed — diagnosis is made on history + imaging alone.

— Beryllium lymphocyte proliferation test (BeLPT) on blood or BAL lymphocytes — confirms beryllium sensitization.
— Diagnosis of chronic beryllium disease (CBD) requires: (1) exposure history, (2) positive BeLPT, and (3) non-caseating granulomas on lung biopsy (transbronchial or VATS).
— This distinguishes CBD from sarcoidosis when imaging looks identical.
— Asbestosis: ferruginous (asbestos) bodies — golden-brown, beaded, iron-coated fibers; >1 per mL of BAL or per cm² of lung tissue supports diagnosis.
— Silicosis: lymphocytic alveolitis; acute silicoproteinosis shows PAS-positive proteinaceous material (mimics PAP).
— Berylliosis: CD4-predominant lymphocytic alveolitis + positive BAL BeLPT.
— Atypical imaging, rapid progression, suspicion of malignancy, or to confirm berylliosis.
— Silicosis: silicotic nodules with whorled hyalinized collagen and birefringent particles under polarized light.
— CWP: coal macules with dust-laden macrophages around respiratory bronchioles ± focal emphysema.
— Asbestosis: diffuse interstitial fibrosis + asbestos bodies (required for histologic diagnosis).
Key distinction: Sarcoidosis vs chronic berylliosis — radiographically and histologically identical (non-caseating granulomas, hilar adenopathy); only a positive BeLPT distinguishes them. Always ask aerospace/nuclear/dental lab history before labeling "sarcoid."

1. Halt further exposure (most important intervention).
2. Treat complications and comorbidities.
3. Surveillance for TB, malignancy, and progression.
4. Symptom relief and rehabilitation.
5. Compensation and legal documentation.
— Mild: asymptomatic, normal/mild PFT changes, no hypoxemia → annual CXR, PFTs, IGRA.
— Moderate: dyspnea on exertion, restrictive PFTs with DLCO 40–60%, exertional desaturation → pulmonology referral, 6-month follow-up, pulmonary rehab.
— Severe: PMF, resting hypoxemia, cor pulmonale, FVC <50% → lung transplant evaluation (especially in young patients with accelerated silicosis from engineered stone).
— Notify OSHA/NIOSH; document via state workers' compensation system.
— Workplace controls: wet methods, local exhaust ventilation, fit-tested N95/PAPR, medical surveillance program.
— Permanent reassignment from exposure for berylliosis (any sensitization) and accelerated/acute silicosis.
— Asbestos + smoking → ~50× increased lung cancer risk (multiplicative synergy).
— Use varenicline or combination NRT + behavioral support; document at every visit.
Step 3 management: For any newly diagnosed pneumoconiosis: (1) remove from exposure, (2) test for latent TB with IGRA (especially silicosis), (3) update vaccines, (4) initiate smoking cessation, (5) refer to pulmonary rehab, and (6) file workers' compensation paperwork — these are the six high-yield ambulatory orders.

— Oral corticosteroids (prednisone 0.5–1 mg/kg/day, tapered over months) for symptomatic CBD with declining PFTs or hypoxemia.
— Steroid-sparing agents: methotrexate, azathioprine, infliximab in refractory cases.
— Asymptomatic beryllium sensitization without granulomatous disease → surveillance only, no treatment.
— Bronchodilators (LABA/LAMA inhalers) if coexisting airflow obstruction, especially CWP miners with mixed obstruction.
— Inhaled corticosteroids only if asthma/COPD overlap with frequent exacerbations.
— Supplemental O2 for resting SpO2 ≤88% or PaO2 ≤55 mm Hg (or ≤89%/56–59 with cor pulmonale or polycythemia) — Medicare criteria.
— Opioids (low-dose morphine) for refractory dyspnea in end-stage disease.
— Isoniazid 300 mg/day × 9 months with pyridoxine, or
— Rifampin 600 mg/day × 4 months, or
— 3HP (INH + rifapentine weekly × 12 weeks) under DOT.
— Active TB in silicosis (silicotuberculosis): RIPE × 2 months, then INH + RIF for at least 7 months (extended continuation phase).
Board pearl: Corticosteroids do not alter outcomes in silicosis, asbestosis, or CWP and may worsen TB risk in silicosis — only berylliosis responds to steroids. Reflexively prescribing prednisone for "ILD" in a sandblaster is a wrong-answer trap.

— Indicated when FEV1 or FVC <40–50% predicted, severe hypoxemia, pulmonary hypertension, or rapidly progressive disease despite exposure removal.
— Particularly relevant in young patients with accelerated/acute silicosis from engineered stone — median age at transplant has been falling into the 30s–40s.
— Refer early to a transplant center; evaluation takes months and requires smoking cessation ≥6 months, BMI optimization, and psychosocial clearance.
— Whole lung lavage for acute silicoproteinosis — saline lavage of one lung at a time under general anesthesia to remove alveolar proteinaceous material.
— Pleurodesis or indwelling pleural catheter (IPC) for recurrent malignant or benign asbestos-related pleural effusions.
— Bronchoscopy with biopsy for suspicious nodules (rule out lung cancer, mesothelioma, TB).
— VATS pleurectomy/decortication or extrapleural pneumonectomy for selected mesothelioma (multimodal therapy).
— Asbestos exposure: increased risk of bronchogenic carcinoma (all histologies, especially with smoking) and mesothelioma (no smoking synergy).
— Silica: silica is a Group 1 IARC carcinogen for lung cancer — heightened vigilance for new nodules.
— Low-dose chest CT (LDCT) lung cancer screening still follows USPSTF criteria (age 50–80, ≥20 pack-years, current smoker or quit within 15 years) — occupational exposure alone does not currently qualify, but combined with smoking it should lower the threshold for diagnostic workup of any new symptom.
Step 3 management: A 38-year-old engineered stone fabricator with FVC 38% and resting hypoxemia → refer immediately to a lung transplant center while continuing O2, rehab, and exposure removal — do not wait for "maximum medical therapy" since none exists.

— COPD, ischemic heart disease, heart failure with preserved EF, and lung cancer often coexist and confound the dyspnea workup.
— Distinguish ILD restriction from age-related decline using PFTs with DLCO and 6MWT rather than spirometry alone.
— Frailty and sarcopenia limit transplant candidacy; focus shifts to symptom control, advance care planning, and palliative care.
— Long-term prednisone for CBD in older adults: monitor for osteoporosis (DEXA + bisphosphonate or denosumab), hyperglycemia/steroid-induced diabetes, cataracts, hypertension, and PCP prophylaxis if dose ≥20 mg/day for ≥4 weeks.
— Avoid sedating opioids and benzodiazepines as first-line dyspnea relief; use cautiously and start low.
— Dose-adjust isoniazid metabolites (generally safe but monitor neuropathy), rifampin (no renal adjustment), ethambutol (reduce dose with CrCl <50), pyrazinamide (reduce with CrCl <30).
— Silica-associated nephropathy and ANCA-associated vasculitis can cause CKD/AKI; monitor UA, creatinine, and ANCA periodically in silicosis.
— INH, rifampin, pyrazinamide are hepatotoxic — obtain baseline LFTs and monitor monthly in older adults, alcohol users, or HCV/HBV coinfected; hold if ALT >3× ULN with symptoms or >5× ULN asymptomatic.
— Methotrexate (for refractory CBD) is contraindicated in significant hepatic disease.
CCS pearl: In an 80-year-old retired pipefitter with asbestosis and new dyspnea, order CBC, BNP, troponin, ECG, CT chest with contrast before assuming progression — superimposed CHF, MI, and pulmonary embolism are more common acute causes than ILD progression itself.

— Pneumoconioses are rare in reproductive-age women historically, but engineered stone silicosis is changing this — increasing diagnoses in young female fabricators and partners of male workers (take-home exposure).
— Reduced lung volumes and increased oxygen demand in pregnancy may unmask previously subclinical restriction; obtain baseline PFTs and 6MWT in the 2nd trimester.
— Latent TB treatment in pregnancy with silicosis: INH + pyridoxine is preferred; defer rifapentine-based regimens; treat active TB with standard RIPE (pyrazinamide use in pregnancy is accepted by WHO/CDC despite limited safety data).
— Avoid methotrexate (teratogenic); prednisone is acceptable for CBD with risk-benefit discussion.
— Take-home exposure counseling: pregnant partners of workers should not handle work clothes; employer should provide on-site laundering.
— True occupational pneumoconiosis is uncommon in children but consider:
— Child labor exposures (international vignettes: small-scale mining, gem cutting).
— Secondary/bystander exposure to dusts brought home on parents' clothing — household asbestos and beryllium cases are well documented.
— Counsel families about decontamination at work, separate work shoes/clothes, and on-site showers.
— Heavy asbestos exposure in US Navy personnel (pre-1980 ship insulation), shipyard workers, and Gulf War-era burn pit exposures.
— File VA service-connected disability claims and document exposure thoroughly; PACT Act expands coverage for respiratory conditions in post-9/11 veterans.
Board pearl: A 28-year-old pregnant Latina woman with progressive dyspnea whose husband cuts quartz countertops should prompt household silica exposure evaluation — both partners need assessment, and workplace laundering practices must change.

— Progressive massive fibrosis (PMF): conglomerate upper-lobe masses >1 cm in silicosis or CWP; causes severe restriction and cor pulmonale.
— Respiratory failure and chronic pulmonary hypertension/cor pulmonale.
— Spontaneous pneumothorax from ruptured subpleural blebs (especially CWP with emphysema).
— Bronchiectasis distal to fibrotic distortion.
— Mycobacterial disease: silicosis confers ~3× increased risk of active TB and elevated risk of NTM (M. kansasii, MAC). Screen with IGRA at diagnosis and annually; treat LTBI aggressively.
— Recurrent bacterial pneumonia in advanced disease.
— Fungal superinfection (aspergilloma in old PMF cavities).
— Asbestos: bronchogenic carcinoma (all cell types; synergistic with smoking — ~50× risk), mesothelioma (latency 20–40 years; no smoking synergy), laryngeal and ovarian cancers.
— Silica (IARC Group 1 carcinogen): lung cancer risk independently elevated.
— Beryllium: lung cancer risk also elevated.
— Caplan syndrome: RA + rheumatoid nodules in lung in CWP or silicosis.
— Scleroderma (Erasmus syndrome), SLE, ANCA-associated vasculitis, anti-GBM (Goodpasture-like) disease, silica nephropathy.
— Benign pleural plaques (often calcified, lower-lateral chest wall and diaphragm).
— Benign asbestos pleural effusion (earliest manifestation, often within 10 years; diagnosis of exclusion).
— Diffuse pleural thickening with restriction.
— Rounded atelectasis ("comet tail sign" on CT — folded lung adjacent to thickened pleura) — benign but mimics malignancy.
Key distinction: Pleural plaques = marker of asbestos exposure, not disease, and do not cause symptoms or restriction; diffuse pleural thickening causes restriction and dyspnea. Mesothelioma is not caused by smoking and not prevented by smoking cessation.

— Acute hypoxemic respiratory failure (PaO2/FiO2 <300) — consider superimposed pneumonia, PE, pneumothorax, CHF, or acute exacerbation of ILD.
— Massive hemoptysis (rule out TB, aspergilloma, lung cancer, mesothelioma).
— Tension pneumothorax (especially CWP with PMF and bullous disease).
— Acute silicoproteinosis with rapidly worsening hypoxemia — urgent pulmonology + consideration of whole lung lavage.
— Hypoxemic patients requiring titration of supplemental O2.
— Suspected silicotuberculosis or active TB → negative-pressure airborne isolation, sputum AFB ×3, NAAT, empiric RIPE while results pending; notify public health.
— New pleural effusion in asbestos-exposed patient: thoracentesis with cytology, ADA, cell count, protein, LDH, glucose, pH — rule out mesothelioma vs benign effusion.
— Pulmonology: all new diagnoses, ILD management, transplant referral.
— Occupational medicine: exposure documentation, workplace assessment, return-to-work decisions.
— Rheumatology: silica-associated autoimmune disease.
— Infectious disease: silicotuberculosis, NTM.
— Thoracic surgery / interventional pulmonology: biopsy, pleural disease, suspected mesothelioma.
— Palliative care: introduce early for symptom management; not synonymous with hospice.
— Cardiology: cor pulmonale, PH evaluation.
— Transplant pulmonology: any patient with FVC <50% or rapid decline.
— Report sentinel occupational disease to state health department, OSHA, and NIOSH.
— Active TB is reportable in all states.
CCS pearl: In a hypoxic engineered stone worker admitted with bilateral infiltrates, order: ABG, CXR, CT chest, sputum AFB ×3 with NAAT, IGRA, ECHO, BNP, HIV, and infectious workup — silicosis patients deteriorating acutely need TB ruled out before steroids are even contemplated.

— Caused by organic antigens (bird droppings, moldy hay = Farmer's lung, hot tub lung); not an inorganic dust pneumoconiosis.
— Mid-upper lung centrilobular nodules, mosaic attenuation, air trapping on expiratory HRCT.
— BAL with marked lymphocytosis (CD4:CD8 reversed, <1) vs CBD which is CD4 predominant.
— Radiographically and histologically identical (non-caseating granulomas, bilateral hilar adenopathy).
— Only BeLPT distinguishes them — always ask exposure history before diagnosing sarcoid in machinists, dentists, aerospace workers.
— Both UIP pattern (basal subpleural reticulation, honeycombing).
— Asbestosis features pleural plaques and exposure history; IPF lacks both.
— IPF responds to antifibrotics (pirfenidone, nintedanib); asbestosis does not (though nintedanib is approved for PPF phenotype).
— Both upper-lobe nodular; coal macules vs silicotic nodules on histology; CWP nodules less fibrotic.
— CWP often coexists with silica exposure in mixed-dust pneumoconiosis.
— Both show alveolar PAS-positive material; silicoproteinosis requires recent intense silica exposure; PAP is autoimmune anti-GM-CSF antibody-mediated and is the textbook association.
Key distinction: When sarcoid imaging meets an aerospace, nuclear, or dental lab worker → order BeLPT before initiating steroids; this single test changes the diagnosis from sarcoidosis to chronic beryllium disease, with workers' compensation, disability, and surveillance implications.

— Heart failure with preserved or reduced EF: Kerley B lines, cephalization, pleural effusions, elevated BNP, echo with LV dysfunction.
— Pulmonary embolism: acute pleuritic chest pain, hypoxemia, normal CXR or wedge infarct; CT-PA.
— Pulmonary hypertension (Group 1–5): dilated PA on CT, RV dilation on echo, RHC for confirmation.
— Tuberculosis: upper-lobe cavitary disease, mandatory rule-out in silicosis.
— NTM (MAC, M. kansasii): cavitary or nodular bronchiectatic disease, especially in older patients.
— Endemic fungi: histoplasmosis, coccidioidomycosis, blastomycosis — can cause nodules + adenopathy.
— Lymphangitic carcinomatosis: irregular interlobular septal thickening; primary breast, lung, GI, pancreas.
— Bronchogenic carcinoma and mesothelioma (especially asbestos).
— RA-ILD, scleroderma-ILD (NSIP > UIP), MDA5/anti-synthetase syndrome, GPA, EGPA, MPA — order ANA, RF, anti-CCP, ANCA, myositis panel when extrapulmonary features present.
— Amiodarone, methotrexate, nitrofurantoin, bleomycin, immune checkpoint inhibitors, radiation pneumonitis.
— Respiratory bronchiolitis-ILD (RB-ILD), desquamative interstitial pneumonia (DIP), Langerhans cell histiocytosis (upper-lobe cysts and nodules in smokers).
Board pearl: Always confirm a vignette's "interstitial pattern" with HRCT-defined distribution: upper-lobe nodular narrows to silicosis/CWP/sarcoid/berylliosis/HP/LCH; lower-lobe reticular with honeycombing narrows to IPF/asbestosis/CTD-ILD; mismatch should prompt rethinking the diagnosis.

— Silica PEL: OSHA permissible exposure limit is 50 µg/m³ (8-hour TWA); engineered stone fabrication often exceeds this.
— Asbestos PEL: 0.1 fiber/cc (8-hour TWA).
— Beryllium PEL: 0.2 µg/m³ (8-hour TWA), action level 0.1 µg/m³.
— Engineering controls (wet methods, local exhaust ventilation) > administrative controls > PPE (last line).
— Fit-tested respirators (N95, half-face, PAPR depending on exposure level).
— Inhalers if obstructive overlap (LABA/LAMA ± ICS).
— Supplemental O2 if criteria met; portable system for ambulation.
— Smoking cessation pharmacotherapy (varenicline + behavioral counseling).
— Vaccinations: influenza, PCV20, COVID, RSV, Tdap, zoster (age ≥50).
— LTBI treatment if IGRA positive (silicosis).
— Steroid + bone protection (calcium/vitamin D, bisphosphonate, PCP prophylaxis if applicable) in CBD.
— Document exposure history, imaging, PFTs; file workers' comp claim promptly (state-specific statutes of limitation).
— Black Lung Benefits Program for coal miners (federal).
— VA service connection for veterans with asbestos exposure.
— Encourage legal consultation for asbestos/mesothelioma trust funds.
— Counsel on take-home exposure; provide handouts in primary language.
— Screen exposed family members with CXR if take-home exposure suspected.
Step 3 management: At discharge from a new pneumoconiosis diagnosis, ensure six items are documented: (1) exposure removal letter, (2) workers' comp filing, (3) vaccines updated, (4) IGRA result and LTBI plan, (5) smoking cessation plan, (6) pulmonary rehab referral.

— Stable simple pneumoconiosis: annual visit with CXR, spirometry with DLCO, 6MWT, symptom review, IGRA (silicosis) periodically.
— Moderate disease or recent change: every 3–6 months with PFTs, 6MWT, SpO2.
— Severe/transplant candidate: monthly–quarterly with pulmonology and transplant team coordination.
— PFTs: FVC, FEV1, TLC, DLCO — decline of FVC ≥10% or DLCO ≥15% over 1 year defines progressive pulmonary fibrosis (PPF) and may trigger antifibrotic consideration.
— 6MWT: distance and nadir SpO2; drop ≥4% or to ≤88% indicates exertional hypoxemia.
— Echo every 1–2 years to screen for PH if DLCO <50% or symptoms suggest it.
— Low-dose chest CT at clinician discretion for surveillance of suspicious nodules or progression; standard USPSTF LDCT lung cancer screening for eligible smokers.
— Annual IGRA in silicosis; mesothelioma surveillance not standardized but symptom-driven.
— Multidisciplinary program: exercise training, education, breathing techniques, nutritional support, psychosocial counseling.
— Improves dyspnea, exercise tolerance, and quality of life; covered by Medicare for symptomatic ILD.
— Smoking cessation (revisit every visit; multiplicative cancer risk with asbestos).
— Avoid further exposure: cannot return to dusty work even with respirator.
— Mental health: anxiety/depression common with chronic dyspnea; screen with PHQ-9, GAD-7.
— Advance care planning: introduce early, especially with progressive disease.
— Air travel: counsel on supplemental O2 needs if SpO2 ≤92% at rest.
Board pearl: A ≥10% FVC decline or ≥15% DLCO decline over 12 months in a patient with pneumoconiosis meets criteria for progressive pulmonary fibrosis (PPF) and is the threshold to consider nintedanib and accelerate transplant evaluation — even though baseline antifibrotics are not indicated.

— Active TB (including silicotuberculosis) is reportable to public health in all 50 states.
— Many states have sentinel occupational disease reporting for silicosis, asbestosis, CBD, and PMF; report to state health department and NIOSH.
— OSHA investigations may follow reports of workplace exposure exceeding PELs.
— Patients have the right to know their occupational diagnosis and its implications for work, life expectancy, and family.
— Disclose mesothelioma and lung cancer risk to asbestos-exposed patients, including those with only pleural plaques.
— Patients diagnosed with pneumoconiosis must be informed that return to dusty work is contraindicated even with PPE.
— Document exposure history meticulously; this directly affects benefits eligibility.
— Statutes of limitation vary by state — file promptly after diagnosis.
— Federal Black Lung Benefits Act for coal miners; Energy Employees Occupational Illness Compensation Program (EEOICPA) for beryllium-exposed nuclear workers.
— Avoid conflicts of interest if serving as both treating physician and independent medical examiner.
— At hospital discharge, ensure clear documentation of LTBI status and exposure history in transfer summaries; missed silicotuberculosis diagnosis is a sentinel event.
— Reconcile home oxygen prescriptions and verify safe storage (no smoking near O2; fire risk).
— Physician cannot disclose diagnosis to employer without patient consent; however, fit-for-duty evaluations and OSHA medical surveillance reports have specific protocols.
— Pneumoconioses disproportionately affect immigrant, undocumented, and non-English-speaking workers; provide interpreter services and connect to community legal aid for compensation claims regardless of immigration status.
Step 3 management: A monolingual Spanish-speaking engineered stone worker newly diagnosed with silicosis requires: interpreter-mediated diagnosis disclosure, workers' comp filing (which protects workers regardless of immigration status in most states), workplace OSHA report, family screening for take-home exposure, and written restriction from further silica work — all coordinated at the index visit.

— Eggshell calcification → silicosis (or CWP, sarcoid).
— Pleural plaques → asbestos exposure.
— PMF/conglomerate upper-lobe mass → silicosis or CWP.
— Honeycombing + plaques → asbestosis.
— Comet tail sign → rounded atelectasis (asbestos).
Board pearl: "Young countertop fabricator + upper-lobe nodules + rapidly progressive dyspnea" = engineered stone-associated accelerated silicosis — currently the most heavily tested emerging occupational lung disease on Step 3.

Key distinction: When a stem features a young patient with rapidly progressive ILD and a stone-cutting occupation, the answer is almost always engineered stone silicosis with transplant referral, not idiopathic pulmonary fibrosis.

— Silicosis: upper-lobe nodules + eggshell calcification; engineered stone is the modern epidemic; screen and treat latent TB; IARC Group 1 lung carcinogen; can cause autoimmune disease (Erasmus, Caplan, ANCA, SLE).
— Asbestosis: lower-lobe reticular fibrosis + pleural plaques; multiplicative lung cancer risk with smoking (~50×); mesothelioma unrelated to smoking with 20–40-year latency.
— CWP: simple (small upper-lobe nodules) → complicated (PMF with melanoptysis); Caplan syndrome; federal Black Lung benefits.
— Berylliosis: sarcoid mimic confirmed by BeLPT + non-caseating granulomas; responds to corticosteroids; aerospace/nuclear/dental lab exposure; EEOICPA compensation.
— Universal pneumoconiosis bundle: exposure removal, workers' compensation filing, OSHA/NIOSH reporting, IGRA, smoking cessation, vaccines (influenza/PCV20/COVID/RSV), pulmonary rehab, O2 if SpO2 ≤88%, early transplant referral for advanced disease, and antifibrotics (nintedanib) only when progressive pulmonary fibrosis criteria are met.
Step 3 management: Every new pneumoconiosis diagnosis triggers a six-item ambulatory order set — remove exposure, test for TB, vaccinate, counsel smoking cessation, refer to pulmonary rehab, and file workers' compensation — and every progression visit triggers reassessment of PFTs, 6MWT, echo, and transplant candidacy.

