Author(s): Le ND, Sun L, Zidek JV
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Abstract Toxic air pollutants are continuously released into the air supply. Various pollutants come from chemical facilities and small businesses, such as automobile service stations and dry cleaning establishments. Others, such as nitrogen oxides, carbon monoxide and other volatile organic chemicals, arise primarily from the incomplete combustion of fossil fuels (coal and petroleum) and are emitted from sources that include car exhausts, home heating and industrial power plants. Pollutants in the atmosphere also result from photochemical transformations; for example, ozone is formed when molecular oxygen or nitrogen interacts with ultraviolet radiation. An association between air pollution exposure and lung cancer has been observed in several studies. The evidence for other cancers is far less conclusive. Estimates of the population attributable risk of cancer has varied substantially over the last 40 years, reflecting the limitations of studies; these include insufficient information on confounders, difficulties in characterizing associations due to a likely lengthy latency interval, and exposure misclassification. Although earlier estimates were less than one percent, recent cohort studies that have taken into account some confounding factors, such as smoking and education amongst others, suggest that approximately 3.6\% of lung cancer in the European Union could be due to air pollution exposure, particularly to sulphate and fine particulates. A separate cohort study estimated 5-7\% of lung cancers in European never smokers and ex-smokers could be due to air pollution exposure. Therefore, while cigarette smoking remains the predominant risk factor, the proportion of lung cancers attributable to air pollution may be higher than previously thought. Overall, major weaknesses in all air-pollution-and-cancer studies to date have been inadequate characterization of long-term air pollution exposure and imprecise or no measurements of covariates. It has only been in the last decade that measurements to PM2.5 become more widely available. A key weakness of many studies is using fixed-site monitoring data and assuming everyone in a region had the same exposure. This ignores spatial variability, and does not take into account how individuals' exposures differ with pollution sources inside, outside, both at work, home and elsewhere. More recent efforts to model indicators of vehicular traffic, and residential distances to major roads and highway can allow for some of this spatial variability to be better controlled for. However, this still does not take into account differences in activity patterns. If the effect is small, these biases will compromise the ability to detect an association. In most situations, the resulting estimates tend to be biased toward the null (i.e., no effect). For misclassification of exposure the inability to adequately control for confounding variables may cause bias in either direction. Recent improvements in statistical methodology use measurements at fixed sites combined with residential histories to estimate individuals' cumulative exposures. They also recognize measurement errors associated with covariates in the analysis to improve estimates of effects. Other challenges include the fact that measurements of exposure and confounders can change over time and long term data are needed due to the anticipated latency interval between harmful exposures and development of cancer.
This article was published in Chronic Dis Can
and referenced in Journal of Addiction Research & Therapy