Air pollution and traffic noise: do they cause atherosclerosis?

The great majority of the world’s population is continuously exposed to some level of air pollution from transportation, household sources, agriculture, and industry, and many are also exposed to ambient noise from the same sources. It has been estimated that globally 3 million premature deaths are attributable to outdoor air pollution each year, but it is the ubiquity of air pollution and ambient noise, as much as the likely magnitudes of associated risks, which makes them important as potential causes of cardiovascular diseases. Because they share common sources, air pollution and ambient noise are correlated, and this means that any association of cardiovascular disease with either exposure may be masked or confounded by the other. Despite this, most studies have considered traffic noise or air pollution separately, and the study by Kälsch and colleagues is one of a limited number that have attempted to disentangle their effects on cardiovascular outcomes. Although their results are suggestive of independent effects of long-term particulate air pollution and night-time traffic noise on thoracic aortic calcification (TAC), they should be interpreted cautiously. Air pollution includes a variety of gaseous species, such as carbon monoxide and nitrogen oxides, as well as suspended particulate matter of various sizes. Many of these have been shown in isolation to have adverse effects on cardiovascular health at higher doses, such as those experienced by active smokers of tobacco. Observational studies also provide substantial evidence of effects on cardiovascular health at lower levels of exposure due to ambient air pollution, particularly for the risk of acute events such as myocardial infarction or heart failure in response to short-term increases in pollution over days or hours. Although most people do not experience high levels of ambient noise, it has been hypothesized that even moderate noise could activate stress responses, with detrimental cardiovascular effects, both during daytime activity and during sleep. Kälsch and colleagues examined the associations of 1-year average particulate air pollution and traffic noise with the TAC score in 4238 participants in the Heinz–Nixdorf Recall Study, who were also well characterized in terms of both lifestyle and clinical cardiovascular risk factors. They found that higher concentrations of particulate air pollution ,10 mm in diameter (PM10) and ,2.5 mm in diameter (PM2.5), and greater traffic noise at night (between 2200 and 0600 h), were each associated with a higher TAC score. Overall average traffic noise over 24 h and distance to a highly trafficked road werenot associated with TAC. There are a number of reasons to take care when interpreting these findings. First, the statistical evidence is not particularly strong for the associations with traffic noise. The change in TAC score per 5 dB increase in night-time traffic noisewas 3.9% [95% confidence interval (CI) 0.0–8.0%] in the model that was adjusted for PM2.5 concentration (table 3 in Kälsch et al.). Because the lower bound of the 95% CI is at 0.0% (no change in TAC), the P-value for this estimate is 0.05. Although 24-h traffic noisewasnot associated with TAC at the P 1⁄4 0.05 level of statistical significance, the CIs for these estimates are too wide to conclude that night-time noise is more important than noise at other times of day. Secondly, in contrast to the present study of TAC, a previous analysis of coronary artery calcification (CAC) in the same cohort found that greater distance from a major road was associated with increased CAC, while greater concentration of PM2.5 was not associated with a change in CAC (traffic noise was not examined directly). The statistical power of these studies is too low to conclude that the estimates for TAC and CAC (both of which are predictors of coronary artery disease) are inconsistent, but the differences between the headline results suggest that they should be interpreted with caution until they can be replicated. An important advantage of the study of Kälsch et al. is that in analyses of particulates and traffic noise, each exposure has been adjusted for the other, as well as for other variables which might confound their associations with TAC. Confounding is one of the most important sources of bias in observational studies; an association between an exposure and an outcome is confounded by a third variable when the latter is associated with the exposure and, independently, with the outcome of interest. For example, traffic noise and