The prevalence of carboxyhemoglobinemia in New Yorkers and its effects on the coronary and systemic circulation

Ayres, Stephen M.; Evans, Robert G.; Buehler, Meta E.

doi:10.1016/0091-7435(79)90009-4

Cited by 11 publications

(2 citation statements)

References 17 publications

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“…In underdeveloped countries, fumes from heating and cooking equipment are far more important CO sources. CO levels in the open air may reach 50 to 100 ppm, or even higher on occasion, and in certain locations may result in carboxyhemoglobin (COHb) saturations of 5 to 12 % or above (1). Cigarette smoke contains 30,000 to 50,000 ppm CO and, depending upon smoking frequency and the extent of inhalation of the smoke, can produce up to 12 to 14% COHb (2).…”

Section: Introductionmentioning

confidence: 99%

Is there a connection between carbon monoxide exposure and hypertension?

Penney

Howley

1991

Environ Health Perspect

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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.

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Section: Introductionmentioning

confidence: 99%

Is there a connection between carbon monoxide exposure and hypertension?

Penney

Howley

1991

Environ Health Perspect

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“…Smoking is a major contributing factor to elevated COHb levels. In the study by Ayres and co-workers (57), policemen from congested areas who did not smoke had COHb levels of 3.14%, whereas policemen from the same areas who did smoke had COHb levels of 8.11%. The NHANES II report describes average COHb levels of 4.53% in smokers and 0.88% in nonsmokers (58).…”

Section: Relevance Of Exposure Conditionsmentioning

confidence: 92%

Effects of carbon monoxide on myocardial ischemia.

Allred

Bleecker

Chaitman

et al. 1991

Environ Health Perspect

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The purpose of this study was to determine whether low doses of carbon monoxide (CO) exacerbate myocardial ischemia during a progressive exercise test. The effect of CO exposure was evaluated using the objective measure of time to development of electrocardiographic changes indicative of ischemia and the subjective measure of time to onset of angina. Sixty-three male subjects (41-75 years) with well-documented coronary artery disease, who had exertional angina pectoris and ischemic ST-segment changes in their electrocardiograms, were studied. Results from three randomized, double-blind test visits (room air, low and high CO) were compared. The effect of CO exposure was determined from the percent difference in the end points obtained on exercise tests performed before and after a 1-hr exposure to room air or CO. The exposures resulted in postexercise carboxyhemoglobin (COHb) levels of 0.6% +/- 0.3%, 2.0% +/- 0.1%, and 3.9% +/- 0.1%. The results obtained on the 2%-COHb day and 3.9%-COHb day were compared to those on the room air day. There were 5.1% (p = 0.01) and 12.1% (p less than or equal to 0.0001) decreases in the time to development of ischemic ST-segment changes after exposures producing 2.0 and 3.9% COHb, respectively, compared to the control day. In addition, there were 4.2% (p = 0.027) and 7.1% (p = 0.002) decreases in time to the onset of angina after exposures producing 2.0 and 3.9% COHb, respectively, compared to the control day. A significant dose-response relationship was found for the individual differences in the time to ST end point and angina for the pre- versus postexposure exercise tests at the three carboxyhemoglobin levels. These findings demonstrate that low doses of CO produce significant effects on cardiac function during exercise in subjects with coronary artery disease.

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Smoking and Health

Berton¹,

Odom²

1980

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The prevalence of carboxyhemoglobinemia in New Yorkers and its effects on the coronary and systemic circulation

Cited by 11 publications

References 17 publications

Is there a connection between carbon monoxide exposure and hypertension?

Is there a connection between carbon monoxide exposure and hypertension?

Effects of carbon monoxide on myocardial ischemia.

Smoking and Health

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