Transportation noise linked to cardiovascular disease independent from air pollution

This editorial refers to ‘A systematic analysis of mutual effects of transportation noise and air pollution exposure on myocardial infarction mortality: a nationwide cohort study in Switzerland’†, by H. Héritier et al., on page 598. Air pollution and traffic noise are the two major environmental pollutants affecting health according to the World Health Organization (WHO).1 For air pollution, the American Heart Association concluded already in 2010 that ‘the overall evidence is consistent with a causal relationship between particulate matter (PM2.5) exposure and cardiovascular morbidity and mortality’.2 However, at the time of the review there were only few studies that included both air pollution and transportation noise in their analyses, and the authors added that there was room for improvement in assessment of traffic exposures, including accounting for transportation noise.2 In a systematic review produced as a basis for the new WHO Guidelines on environmental noise, it was concluded that there is high-quality evidence linking exposure to road traffic noise with an increased risk of ischaemic heart disease.3 Epidemiological evidence also existed for hypertension and stroke, but this was considered less conclusive. The evidence on ischaemic heart disease was not used in the final establishment of a guideline value for road traffic noise (Lden: 53.3 dB(A)) because ‘unacceptable’ increases in the proportion of people reporting to be 'highly annoyed' occurred at lower noise levels than corresponding increases in the relative risk of ischaemic heart disease.4 A few recent studies have investigated the effects of mutual adjustment of transportation noise and air pollution in relation to cardiovascular disease.5–7 The results are not clear, with some studies reporting independent effects of the two exposures on risk for cardiovascular disease, whereas others report that the effects of air pollution disappears after adjustment for road traffic noise, or vice versa. The major challenge in such studies is that transportation noise and air pollution correlate, reflecting that traffic is the main source of both exposures. This collinearity makes disentangling the effects of the two exposures difficult. One explanation for the inconsistent results is that to disentangle the two exposures, high-quality assessment of both exposures is necessary to avoid one exposure being estimated more precisely than the other, which would eventually result in more robust associations for the most precise exposure. In this issue of the European Journal Heart Journal, in the study by Héritier et al., excellent state-of-the-art exposure assessment models are used for estimation of both air pollution and transportation noise.8 This study conducted in a nationwide Swiss cohort of 4.4 million adults found that residential exposure to traffic noise significantly increased the risk of mortality from myocardial infarction (MI) independent from adjustment for air pollution estimated as PM2.5 or nitrogen dioxide (NO2). In contrast, the significant associations between exposure to PM2.5 as well as NO2 and MI mortality were attenuated and became insignificant after adjustment for noise, indicating that proper adjustment for transportation noise in studies of air pollution and cardiovascular disease is important. Another aspect of concomitant exposure to air pollution and noise from road traffic is the potential for effect modification. Several mechanisms have been studied in relation to the effects of these exposures on the cardiovascular system.9 For particulate air pollution, induction of systemic inflammation is thought to be a major aetiological pathway, whereas transportation noise is believed to result in adverse cardiovascular effects through induction of chronic stress reactions and sleep disturbances. Studies have indicated that some causal mechanisms may be similar for air pollution and noise, such as endothelial dysfunction, inflammation, and oxidative stress (Figure 1).10 , 11 The few previous studies that have investigated combined effects of transportation noise and air pollution in relation to risk for cardiovascular disease showed diverging results.5 , 6 , 12 , 13 The present study by Héritier et al. found no evidence of either synergistic or antagonistic effects between road traffic noise and PM2.5 or NO2, and it is important that future epidemiological studies address this. Also, there is a need for experimental studies examining the effects of simultaneous exposure to traffic noise and air pollution in a controlled setting, to address how these exposures interact at a mechanistic level. Potential common pathophysiological pathways for induction of cardiovascular disease by air pollution and transportation noise. In the top of the figure, the relative contributions from noise (green arrows) compared with air pollution (grey arrows) at the residence for road, rail, and aircraft are shown; the size of the arrows illustrates how closely the two exposures correlate at the residence for each of the three transportation sources. A strong feature of the study by Héritier et al. is that they have estimated exposure to three sources of noise separately: road traffic noise, aircraft noise, and railway noise.8 They found significant associations with MI mortality of similar size for all three modes of transport, with hazard ratios of 1.03 for road traffic, 1.03 for aircraft, and 1.02 for railway noise per 10 dB increase (both before and after adjustment for air pollution). These findings are very important, because residential exposure to noise from aircraft and trains is less correlated with residential air pollution than noise from road traffic (Figure 1).8 This is especially true with regard to railway noise, as in many countries, including Switzerland, the majority of the operating trains are electric. Therefore, the consistent finding of an association between noise and MI mortality across the three modes of transport strongly supports an effect of transportation noise that is independent from air pollution. Although the study by Héritier et al. has many important strengths, some weaknesses also need mentioning. First, the authors had no information on lifestyle habits, such as smoking and alcohol consumption, and adjustment therefore relied entirely on socio-economic and demographic variables. The study is therefore likely to suffer from residual confounding, and the results need reproduction in large cohort studies with more detailed information on potential confounders. Secondly, it focused on mortality in spite of the fact that the vast majority of the MI cases do not die from their disease. It is not certain that the influence of air pollution and noise, respectively, is the same for incident and fatal MI. Lastly, although the exposure assessment of the study is excellent, air pollution is a highly complex mixture, and components other than PM2.5 or NO2 could be important when disentangling noise and air pollution, such as ultrafine particles, as also mentioned by the authors. In conclusion, the finding of Héritier et al. that three sources of transportation noise are associated with MI mortality independent of air pollution adds to the evidence that transportation noise is an important risk factor for cardiovascular disease. Furthermore, the study highlights the importance of proper mutual adjustment of transportation noise and air pollution using high-quality exposure assessments. Conflict of interest: none declared.