Cardiovascular effects of chronic carbon monoxide and high-altitude exposure

At higher altitudes, ambient carbon monoxide levels are increasing with the number of residents and tourists and their use of motor vehicles and heating devices (such as fireplaces, furnaces, and stoves). Although chronic exposure to carbon monoxide or high altitude causes pronounced cardiovascular changes in humans as well as in animals, there is little information on the effects elicited by these stressors combined. Data from acute studies and theoretical considerations suggest that carbon monoxide inhaled at altitude may be more detrimental than carbon monoxide inhaled at sea level. It is not known, however, if the cardiovascular system adapts or deteriorates with continuous, concurrent exposure to carbon monoxide and high altitude. Male laboratory rats were exposed for six weeks in steel barometric chambers to altitudes ranging from 3,300 ft (ambient) to 18,000 ft and to concentrations ranging from 0 to 500 parts per million (ppm)2. Carbon monoxide had no effect on body weight at any altitude. There was a tendency for hematocrit to increase even at the lowest concentration of carbon monoxide (9 ppm), but the increase did not become significant until 100 ppm. At 10,000 ft, there was a tendency for total heart weight to increase in rats inhaling 100 ppm carbon monoxide. Although its effects on the heart at altitude are complex, carbon monoxide, in concentrations of 500 ppm or less, had little effect on the right ventricle; it did not exacerbate any effects due to altitude. There was a tendency for the left ventricle weight to increase with exposure to 35 ppm carbon monoxide at altitude, but the increase was not significant until 100 ppm carbon monoxide. Heart rate, blood pressure, cardiac output, and peripheral resistance were unaffected by exposure to 35 ppm carbon monoxide or 10,000-ft altitude singly or in combination. I conclude that six weeks of exposure to 35 ppm carbon monoxide does not produce measurable effects in the healthy laboratory rat, nor does it exacerbate the effects produced by exposure to 10,000-ft altitude. Basal carboxyhemoglobin (COHb) level (due to endogenous carbon monoxide production) was increased from 0.7 to 1.0 percent at 10,000 ft, and to 1.7 percent at 15,000 ft. This suggests that the high-altitude resident has a greater initial body burden of COHb and will attain the COHb level associated with the National Ambient Air Quality Standard for carbon monoxide more quickly than the sea-level resident.