Occupational & Environmental Health
Ask what they do — the job is often the diagnosis.
The exposure history and occupational asthma
Ask about work. Many toxic and respiratory diagnoses are missed simply because no one asked what the patient does. Record the job title and the actual tasks, materials and chemicals handled, ventilation and protective equipment, coworkers with similar symptoms, hobbies and side jobs (stained glass, ceramics glazing, indoor shooting, home renovation), and exposures at home. The timing is often the clue: symptoms that ease on weekends or vacations and return at work point to a workplace cause.
Occupational asthma. Sensitizing agents produce asthma after a latent period of exposure. Classic culprits are isocyanates (spray painting, polyurethane foam, varnishes), flour and enzymes (bakers), latex, laboratory animal proteins, wood dusts, and cleaning products. Confirm the diagnosis with spirometry and serial peak expiratory flow recordings at work and away from work; specific inhalation challenge is the reference standard. Early and complete removal from exposure is the strongest predictor of recovery, alongside standard asthma therapy. A single high-level irritant exposure (chlorine, ammonia) can cause reactive airways dysfunction syndrome, with asthma beginning within 24 hours and no prior sensitization, and preexisting asthma can be aggravated by workplace irritants (work-exacerbated asthma).
Heavy metals
Lead. Adults absorb lead mainly by inhaling fumes and dust in battery manufacture or recycling, smelting, indoor firing ranges, renovation of pre-1978 paint, radiator repair, and stained glass or pottery work; dust carried home on clothing can poison children. Symptoms include crampy abdominal colic, constipation, fatigue, headache, irritability, and memory problems, with a motor neuropathy producing wrist or foot drop. Lead inhibits ALA dehydratase and ferrochelatase, so ALA and zinc protoporphyrin rise and heme synthesis fails, and it blocks pyrimidine 5′-nucleotidase, leaving ribosomal remnants seen as basophilic stippling in a microcytic anemia. Chronic exposure also causes interstitial nephropathy with hypertension, saturnine gout from reduced urate excretion, and gingival lead lines. The venous blood lead level confirms the diagnosis; zinc protoporphyrin reflects longer-term exposure. Removal from the source is the key intervention, and OSHA mandates medical removal of workers with elevated levels. Chelation is reserved for severe symptoms or very high levels — oral succimer, or dimercaprol followed by IV CaNa2EDTA for encephalopathy — and prophylactic chelation of workers who remain exposed is prohibited.
Mercury. Inhaled elemental mercury vapor (thermometer and instrument manufacture, artisanal gold mining, chloralkali plants, dental amalgam work) causes intention tremor, erethism (shyness, irritability, emotional lability, insomnia), gingivitis and stomatitis with hypersalivation, and proteinuria. Methylmercury from contaminated fish is a neurotoxin causing ataxia, paresthesias, visual field constriction, and fetal neurotoxicity. Urine mercury measures elemental and inorganic exposure, whereas whole-blood mercury reflects methylmercury.
Arsenic. Sources include pesticides and herbicides, wood preservatives, copper smelting, and contaminated well water. Arsenic binds sulfhydryl groups and disrupts cellular energy production. Acute poisoning brings garlic-scented breath, vomiting, rice-water diarrhea, hypotension, and QT prolongation; chronic exposure produces Mees lines (transverse white nail bands), palmar and plantar hyperkeratosis, raindrop hyperpigmentation, a painful stocking-glove neuropathy, and cancers of the skin, lung, and bladder. A 24-hour urine arsenic, speciated to exclude harmless seafood arsenic, confirms exposure.
| Feature | Lead | Mercury | Arsenic |
|---|---|---|---|
| Typical sources | Batteries, smelting, firing ranges, renovation | Instruments, gold mining, chloralkali plants; fish (methylmercury) | Pesticides, wood preservatives, smelting, well water |
| Hallmarks | Colic, wrist drop, basophilic stippling, nephropathy, saturnine gout | Tremor, erethism, gingivitis, proteinuria | Garlic breath, Mees lines, hyperkeratosis, stocking-glove neuropathy |
| Diagnosis | Venous blood lead; zinc protoporphyrin | Urine mercury; blood for methylmercury | Speciated 24-h urine arsenic |
| Treatment | Remove from exposure; succimer, or dimercaprol + CaNa2EDTA if severe | Remove from exposure; dimercaprol, succimer, or DMPS | Remove from exposure; dimercaprol, DMPS, or succimer |
Noise-induced hearing loss
Pattern. Sustained exposure above about 85 dBA damages cochlear outer hair cells, producing bilateral, symmetric sensorineural hearing loss that is deepest at 3–6 kHz — classically a 4 kHz notch — with partial recovery at 8 kHz, often with tinnitus. Presbycusis, by contrast, slopes steadily downward into the high frequencies without recovery. A single blast can also cause acoustic trauma. The loss is permanent.
Prevention. OSHA sets an action level of 85 dBA as an 8-hour time-weighted average, triggering a hearing conservation program: noise monitoring, hearing protection, worker training, and baseline and annual audiograms. The permissible exposure limit is 90 dBA, above which feasible engineering or administrative controls are required.
If you must shout to be heard by someone at arm's length, the noise is probably at least 85 dB.
Bloodborne pathogen exposure in healthcare workers
- Immediate careWash wounds with soap and water and flush mucous membranes with water; do not squeeze or apply bleach.
- Report and testReport at once; test the source (with consent) for HIV by rapid test, HBsAg, and HCV antibody with reflex RNA; draw baseline HIV, anti-HBs, and HCV tests from the worker.
- Decide on prophylaxisHIV PEP as early as possible; HBV prophylaxis based on the worker's immune status.
- Follow upRepeat HIV and HCV testing over the following months and counsel on safer sex and deferring blood donation meanwhile.
| Pathogen | Transmission risk | Post-exposure management |
|---|---|---|
| HBV | Highest — up to ~30% from an HBeAg-positive source | Documented responder (anti-HBs ≥10 mIU/mL): nothing. Unvaccinated: HBIG plus vaccine series (ideally within 24 h, no later than 7 days) if source HBsAg-positive or high-risk unknown; vaccine alone if source negative. Known nonresponder: HBIG ×2 if source HBsAg-positive or high-risk unknown; nothing if source negative |
| HCV | Intermediate | No vaccine or PEP; HCV RNA at 3–6 weeks and antibody at 4–6 months; treat infection with direct-acting antivirals (cure >95%) |
| HIV | About 0.3% | Three-drug PEP (integrase inhibitor such as bictegravir or dolutegravir plus tenofovir/emtricitabine), started as soon as possible, ideally within hours and no later than 72 h, for 28 days; stop if the source tests negative |
Workers' compensation, fitness for duty and reporting
Workers' compensation. These state-run, no-fault insurance systems pay medical costs and lost wages for work-related injury or illness; in exchange, the worker generally gives up the right to sue the employer. The physician's role is to document the diagnosis, whether it is work-related, any restrictions, and when the worker can return.
Fitness for duty. The examining physician judges whether the worker can safely perform the essential functions of the job, and employers must offer reasonable accommodations under the Americans with Disabilities Act. Without the patient's consent, the employer receives only work status and functional restrictions, never the diagnosis or medical details.
Reporting duties. Employers record work-related injuries and illnesses on the OSHA 300 log and must report a work-related death within 8 hours and an inpatient hospitalization, amputation, or loss of an eye within 24 hours. Clinicians report sentinel occupational illnesses, such as elevated blood lead levels, to public health authorities as state law requires.
A company physician owes the same confidentiality as any other physician: disclosing a worker's diagnosis to a supervisor without consent is a breach.