Cardiovascular Mortality Among Tunnel and Bridge Workers Exposed To Carbon Monoxide

BACKGROUND:

A retrospective study by NIOSH found a significantly higher death rate from atherosclerotic heart disease for New York City tunnel officers compared with the expected rate for the New York City population. A Cox proportional hazards model which examined the risk of atherosclerotic heart disease for tunnel officers compared to bridge officers found a similar pattern. The Cox model also showed a significant decline in the risk of atherosclerotic heart disease among tunnel officers, when compared to the less-exposed bridge officers, after cessation of exposure with most of the risk dissipating within as little as five years.

Carbon monoxide may contribute to cardiovascular disease through several accepted and potential mechanisms including binding to hemoglobin, and reducing oxygen dissociation at the tissue level by shifting the oxygen-hemoglobin dissociation curve. Carbon monoxide in experimental animals also increases platelet stickiness which may contribute to atherogenesis, and accelerates atherosclerosis either through altered lipid metabolism or increasing vessel permeability to cholesterol. Carbon monoxide in experimental studies contributes to sudden death by reducing the cardiac threshold for ventricular fibrillation. Some of these mechanisms, such as those that would lead to transient hypoxia of the myocardium, would lead to increased risk of myocardial ischemia only when exposure is current, while other mechanisms, such as acceleration of atherogenesis, may lead to long standing elevation of risk for cardiovascular disease.

The Occupational Safety and Health Administration standard for carbon monoxide in 1987 allowed exposure of 50 parts per million (ppm) time-weighted average over an 8-hour day with no ceiling level limit. The margin of safety of this standard for workers with cardiovascular disease was questioned by a series of controversial studies of exposures averaging 50 ppm which demonstrated a decrease in exercise necessary to induce angina in experimental subjects with underlying cardiovascular disease. NIOSH recommended a standard for carbon monoxide exposure of 35 ppm as an 8-hour time-weighted average with a ceiling limit of 200 ppm.

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