Occupational Medicine

Peter J. Mazzone

Debasis Sahoo

Edward P. Horvath Jr.

RAPID BOARD REVIEW—KEY POINTS TO REMEMBER:

Asphyxiants—Carbon Monoxide

Nonexposed persons have ≤1% blood carboxyhemoglobin. Smokers as high as 18%.
At levels of 10% to 30%, patients may complain of headache, nausea, weakness, and dizziness. Mentation begins to be impaired at 30% to 35%, and levels of 35% to 40% may result in coma. “Cherry red color” of the skin and mucous membranes is only seen in lethal levels of carbon monoxide poisoning. Death can occur with levels exceeding 50%.
A key diagnostic clue is the discordance between the oxygen saturation as measured by pulse oximetry (falsely normal) and that measured by an arterial blood gas (decreased).
Measurement of the carboxyhemoglobin level confirms the diagnosis.
100% oxygen reduces the half-life for carbon monoxide elimination from 5.5 hours to 1.5 hours. Oxygen at 3 atm reduces the half-life to 23 minutes.

Cholinesterase Inhibitors—Organophosphate Insecticides

Clinical effects, nicotinic (ganglionic and neuromuscular) and muscarinic (parasympathetic), through phosphorylation of the acetylcholinesterase enzyme at nerve endings:
- STUMBLED = Salivation, Tremors, Urination, Miosis, Bradycardia, Lacrimation, Emesis, and Diarrhea.
Measure:
- Plasma cholinesterase (pseudocholinesterase), synthesized by the liver, declines sooner and regenerates faster (days to a few weeks).
- Red cell cholinesterase (true acetylcholinesterase), depressed more slowly and for longer periods of time (regeneration time is 1 to 3 months).

Heavy Metals—Lead Intoxication

Organic lead can be absorbed via skin; distributed to the erythrocytes, liver, and kidneys.
Insidious gastrointestinal symptoms, including vague abdominal discomfort, anorexia, and constipation. A bluish gray line along the gingiva called “Lead line.”
Involvement of the peripheral nervous system and lead encephalopathy are rare.
Anemia, microcytic, hypochromic or normocytic, normochromic; reticulocytosis and basophilic stippling of red blood cells.
Heavy persistent exposure ≥10 years may result in lead nephropathy, tubular dysfunction, Fanconi-like syndrome with aminoaciduria, glucosuria, and hyperphosphaturia.
Hyperuricemia with saturnine gout.
Blood lead is the single most useful diagnostic test. Free erythrocyte protoporphyrin and zinc protoporphyrin levels begin to increase when the blood lead level is >40 µg/dL. They stay elevated longer than blood lead and are therefore better indicators of chronic intoxication.

Asbestos

Pleural Disease

Pleural Plaques: smooth, white, raised, irregular lesions on the parietal pleura; typically asymptomatic, recognized only on chest imaging.
Benign Asbestos Pleural Effusions: silent or pain, fever, and shortness of breath; early manifestation of asbestos exposure (within 15 years); diagnosis of exclusion.
Pleural Fibrosis: progressive shortness of breath; focal or diffuse fibrosis; remote exposure, but short-lived and heavy in intensity (more than 20 years before).
Malignant Mesothelioma: insidious onset of nonpleuritic chest wall pain, 20 to 40 years after the initial exposure, often associated with dyspnea and systemic symptoms.