SierraScape April - May 2007
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by Ken Schechtman, PhD
Air pollution is commonly perceived as being associated with an increased risk of lung diseases such as lung cancer, asthma, and chronic bronchitis. However, there is a broad body of scientific literature demonstrating that polluted air is also correlated with increased cardiovascular risk. A report by Miller et al in the February 1, 2007 issue of the New England Journal of Medicine (NEJM) highlights this reality.
The referenced study evaluated long-term follow-up data from 72,569 postmenopausal women between the ages of 50 and 79 when they were enrolled initially in the Women's Health Initiative between 1994 and 1998. To be eligible for the present study, the women had to have been free of physician-diagnosed cardiovascular disease when they were first enrolled. All results regarding the association between pollution exposure and cardiovascular events were adjusted for risk factors that included age, race, smoking status, educational level, household income, body mass index, and the presence of diabetes, hypertension or elevated cholesterol. These adjustments mean that observed associations between cardiovascular events and air pollution could not be explained by the effects of the stated risk factors. Cardiovascular events of interest included fatal and non-fatal heart attack and stroke, the need for coronary artery bypass surgery, and other cardiovascular surgical procedures.
Data on long-term air pollution exposure were obtained from the Environmental Protection Agency's Aerometric Information retrieval System (www.epa.gov/oar/data). That system consists of a nationally distributed set of monitors that record information about pollutants that include small particulate matter, carbon monoxide, sulfur dioxide, ozone, and nitrogen dioxide. Of particular interest in the NEJM study was small particulate matter with a diameter of less than 2.5 microns (denoted PM2.5). Such particles are small enough to penetrate deep into the lungs and have been associated with a variety of disease processes. Exposure to PM2.5 was measured in micrograms per cubic meter of air.
A total of 1816 women (2.5%) had at least one cardiovascular event during follow-up. Median exposure to PM2.5 was 13.4 micrograms per cubic meter (range 3.4 to 28.3). A total of 573 air pollution monitors were used, with subjects living a median of 5.6 miles from the monitor that generated their exposure data.
Results indicated that each increase of 10 micrograms per cubic meter of exposure to PM2.5 was associated with an adjusted 24% increase in the overall risk of a cardiovascular event and with an adjusted 74% increase in the risk of a fatal event. This strong positive association between the event rate and PM2.5 exposure was maintained when specific events such as heart attack, stroke, fatal heart attack, and fatal stroke were evaluated. The investigators also performed adjusted within city comparisons of event rates using data from the multiple measuring stations that were present in all participating cities. They found that living in a neighborhood with PM2.5 levels that were 10 micrograms greater than in another area of the same city was associated with a 64% increase in the cardiovascular event rate and a 128% increase in the rate of fatal events. The implications for a city like St. Louis are that, all other factors being equal, people living in industrial or congested inner city areas have a substantially greater risk for cardiovascular events than do individuals residing in less busy suburbs.
The results of this study both confirm and extend those of prior reports that have suggested a strong causative association between air pollution and increased cardiovascular event rates. However, confidence in the quantitative precision of the results is limited somewhat by uncertainty as to the true magnitude of the PM2.5 exposure of each individual. This uncertainty reflects the average 5.6 mile distance from subject homes to the nearest air pollution monitor. Moreover, although participants did not move away from the metropolitan area that was their residence when initially enrolled in the Women's Health Initiative, information about changed residences within that area was not available. A further limitation is the absence of data regarding occupational exposure and time spent in traffic. These factors might be correlated with residential exposure and might therefore lead to an underestimate of the exposure levels of some individuals and, in turn, to an overestimate of the magnitude of the true effect of PM2.5.
The above limitations suggest a cautions interpretation of the magnitude of the reported effects. However, the inaccuracies they might cause are unlikely to be large. Moreover, in light of the consistent supportive results in other studies, the present investigation should be viewed as one more confirmation of the negative health consequences of air pollution exposure and of the urgent need for concerted societal efforts to clean our polluted air.