Project at a Glance

Title: Cardiac response to carbon monoxide in the natural environment

Principal Investigator / Author(s): Colome, Steven D

Contractor: UC Irvine

Contract Number: A3-138-33


Topic Areas: Health Effects of Air Pollution


Abstract:

Carbon monoxide (CO) is a toxic air pollutant normally encountered in low concentrations by people living in urban areas. This gas is a by-product of the combustion of carbon-based fuels such as gasoline and natural gas. CO disperses in air, but activities such as commuting, living near traffic, cooking, heating, working near internal combustion engines, and smoking create high exposure situations that may last minutes to hours. These exposures are usually far below those that cause acute poisoning; however, the exposures are still high enough to adversely affect the blood, heart, and nervous system. CO is toxic because it binds strongly to blood, decreasing its oxygen carrying capacity. People with ischemic heart disease (IHD) are believed to be especially susceptible to CO. The narrowing of their coronary arteries restricts blood flow to the heart tissue and prevents compensation for the low blood oxygen due to CO. Low oxygen conditions disturb the normal beating of the heart and could potentially lead to a heart attack. Thirty-six subjects with MD were selected from approximately 2800 medical records of cardiac patients and were continuously monitored as they went about their normal day-to-day activities. Each subject wore a personal CO monitor recording one- minute average exposures in an electronic memory and a portable heart monitor for twenty-four hour periods. All subjects maintained a written diary of activities, locations, symptoms, and psychologic tension during sampling periods. Each subject provided end-expired samples at intervals throughout the monitoring day to assess levels of CO in the blood. Blood CO levels as measured by breath samples were compared with levels predicted from the CO exposure profiles. The association between exposures to CO and predicted blood CO levels and cardiac changes indicative of insufficient oxygen supply were tested. The sample of subjects in this study indicates that the daily activities of ischemic heart disease subjects lead them to experience variable and sometimes elevated exposures to CO. Over half of these subjects were estimated to spend approximately 2% of their time in exposure conditions leading to blood CO levels shown in laboratory studies to affect II-ID subjects. Highest personal exposures were experienced in activities associated with gasoline engines, including passenger automobiles and small gasoline appliances. To examine whether myocardial ischemia associated with exposure to CO, ST- segment depression on the ECG was used as a marker of ischemia, and an episode was defined as depression of at least l-mm and lasting for at least one minute. ST-segment analysis was performed on the recordings of 20 men (40 person-days) whose ECG was not confounded by digitalis medication or conduction defects. A total of 340 episodes of ST- segment depression occurred in 8 subjects, with a mean duration of 5.7 minutes. Using multivariate logistic regression, the probability of an episode of ST-segment depression within a 15-minute follow-up interval was significantly associated with level of metabolic activity (uniform odds ratio = 3.22, p < 0.001) and COHb estimated from the subject's personal exposure profile (uniform odds ratio = 1.34, p < 0.001). The multiple logistic repression model predicted 15 percent of the incident ST-segment episodes as attributable to ambient CO exposures. Methodological considerations precluded the use of psychological tension as an independent variable in the multivariate model. These results are consistent with the results of controlled clinical studies and suggest that urban CO exposures contribute to the total burden of myocardial ischemia experienced by men with IHD.


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