Carbon monoxide exposures in Australian workplaces could precipitate myocardial ischaemia in smoking workers with coronary artery disease.

Abstract

Quite low levels of carbon monoxide (CO) exposure have been shown experimentally to induce myocardial ischaemia in subjects with coronary artery disease. This study examines the actual exposure levels in Australian workplaces under normal operating conditions, to assess whether the resulting carboxyhaemoglobin (COHb) levels are high enough to present a risk of myocardial ischaemia in any workers who may have recognised or unrecognised coronary artery disease. A total of 84 workers took part in the study, 60 of whom were working in an environment where a combustion process was taking place indoors and were therefore classified as exposed to CO. Ambient CO levels and end-expiratory CO levels (the latter as a predictor of COHb) were measured two-hourly and the number of cigarettes smoked over an eight-hour shift recorded. Mean workplace CO levels throughout the shift ranged between three and 12 ppm. Mean COHb ranged between 0.7% and 2.1% in non-smokers and 2.1%-7.6% in smokers, except for a single reading of 12.5% in forklift operations (one smoker). Exposed workers had significantly higher COHb levels than the non-exposed, both for smokers and non-smokers. Smoking also had an important independent effect on COHb. Under workplace conditions prevailing in industries where combustion processes are occurring indoors, CO exposures are unlikely to be high enough to cause myocardial ischaemia in non-smokers. However in a worker whose COHb is already raised from smoking, an increment from such occupational environments could be sufficient to induce myocardial ischaemia in workers with coronary artery disease.