Is there a connection between carbon monoxide exposure and hypertension?

Exposure to carbon monoxide in our society is a frequent occurrence, from auto exhaust, industrial effluents, and cigarette smoke, and takes place over a wide range of concentrations. It has been suggested that chronic CO inhalation may alter blood pressure, even possibly provoking hypertension by acting alone or in combination with other environmental stressors. Some studies examining the response to CO exposure have reported decreases in blood pressure, whereas others have found increases or no change. Blood pressure in long-term cigarette smokers is generally decreased relative to nonsmokers, albeit a slight decrease. The strength of this finding is somewhat clouded by the effect of the lower body weight in smokers. The increases in blood pressure observed acutely with smoking are mainly due to nicotine. Chronically, the hypertensive action of nicotine is largely offset by the hypotensive action of CO. Several studies support the notion that environmental CO exposure or smoking accelerates or exacerbates hypertension in some people. It has been asserted that chronic CO exposure increases the development of atherosclerotic disease; however, convincing evidence from animal experiments is lacking. Nevertheless, CO may elevate plasma cholesterol and does appear to enhance atherosclerosis when serum cholesterol is greatly elevated by diet. Using the borderline hypertensive rat, an animal model reputed to have increased sensitivity to environmental stimuli, we found no evidence to suggest a provocatory role for CO in the development of hypertension; instead, CO exposure produced hypotension. On the whole, the human and animal literature, as well as our studies, fail to support the hypothesis that long-term CO exposure is capable of provoking an increase in blood pressure, even in borderline hypertensive or sensitive individuals.