In our population-based study, we found a positive association between road traffic noise exposure and incident T2DM. This association was independent of concurrent AP exposure. We observed similar point estimates with smaller CIs in an analysis with indoor noise exposure in a reduced sample. Sensitivity analyses with different noise thresholds and subgroups supported our conclusions.
Three recently published prospective cohort studies investigating the association between road traffic noise and incident T2DM showed similar or even more pronounced results in comparison to ours.5,6,43 In contrast, a study investigating the effect of aircraft noise on pre-diabetes and T2DM reported unclear associations.10 This might be a consequence of different noise patterns of aircraft noise compared to road traffic noise. Second, Eriksson et al.10,13 also included psychological distress which could have acted as a mediator and therefore attenuated risk estimates. In line with our results, two studies10,13 observed increased effect estimates for those participants who did not move during the study period.
The evidence base of overweight/obesity being a possible mediator for the association between road traffic noise and T2DM remains conflicting, with several epidemiological studies observing positive associations between noise and the obesity markers BMI and/or WC10,13 or both,11 while others found no associations for BMI10,12 or any markers of obesity.13 Our study indicates a minor mediating role of obesity assessed by WC as a marker of central adipose tissue or BMI, with hardly reduced effect estimates in the models adjusted for WC or BMI. Another factor influencing the relationship between noise and T2DM might be high depressive symptoms through annoyance, sleeping disorders, and/or several physiological stress effects: A depression-related activation of the autonomic nervous system and the HPA axis may promote inflammatory processes which could contribute to the development of T2DM.44 The evidence base for the link between noise and depression is very limited, while the evidence regarding the association between depression and T2DM is conflicting.41,42 In our study, there was no sign of high depressive symptoms mediating the association between road traffic noise and T2DM.
While the underlying pathomechanisms of noise and AP with regard to metabolic health effects overlap to some extent, they differ in several ways. Exposure to AP and noise both increase the activation of the nervous system able to induce metabolic imbalance, but noise perception partly represents a psychological stressor, whereas AP acts without major personal perception. Furthermore, originating from traffic as a common source, road traffic noise and AP are highly interrelated, due to diverging dispersion patterns. Although AP dispersion depends highly on meteorological conditions, noise is influenced strongly by noise barriers and buildings. Specifically, the building density influences correlations of noise and AP with street canyons, leading to higher correlations.43 Furthermore, traffic attributes as volume, speed, and vehicle type lead to different dispersion patterns.15,43 Two review articles point out the need to disentangle these potentially mutually confounded exposures.15,44 In our study, participants were affected by noise and AP differently with only a moderate correlation. Upon mutual adjustment, estimates remained stable, indicating independence of noise effects from AP in our study area.
Indoor noise exposure may better reflect the true personal exposure and is less correlated with ambient AP exposure. While a few studies have analyzed indoor noise exposures with cardiovascular and metabolic health outcomes, to our knowledge, there is no other study investigating indoor noise exposures with T2DM. One cross-sectional study in Spain focused on noise-related hypertension and blood pressure.14 In this study area, outdoor road traffic noise and ambient AP were highly correlated, leading to instable results in mutually adjusted regression analyses. However, when using indoor noise estimates, they found more consistent associations for indoor noise than for outdoor noise exposure. In comparison, our outdoor noise exposures are less correlated with AP exposures than in Foraster’s study (0.37 vs. 0.75), which may explain why our indoor and outdoor noise exposure-related RRs in the two-pollutant models are similar. Importantly, both Forasters’ and our study observed more precise effect estimates when using indoor noise exposure estimates. Similarly, a Swiss study by Eze et al.5 observed stronger associations between road traffic noise and T2DM in participants with bedrooms facing the street or sleeping with open windows.5 Another study investigating the association between road traffic noise and markers of obesity found positive associations for the subset of participants with bedrooms facing a road.13 Overall, our study and the other studies mentioned above suggest that derived indoor noise estimates may reduce exposure estimation error and may be a more precise marker for the actual noise exposure of individuals than outdoor noise and may help disentangle overlapping effects of ambient AP and ambient noise, specifically in situations of high correlation.
A strength of our study is the prospective design in a population-based cohort with detailed assessment of demographic and lifestyle factors. In addition, we were able to use both indoor and outdoor noise variables for this analysis. We further were able to use two-exposure models with both PM and NO2. One limitation with regard to our results is that our study had limited statistical power to find significant associations between noise and T2DM. Another limitation is that information on family history of diabetes and/or metabolic diseases was not available. Furthermore, we had no information on hearing aid use or aural deficits among our participants. In addition, we lacked information on traffic noise from railway traffic. Aircraft noise was not included in this analysis, because only a very small part of the study population (less than 1%) was estimated to be exposed to elevated noise levels from aircraft traffic. Moreover, indoor noise models have not been validated yet. We also had no information on noise exposure at work or time spent at the residence. Finally, a possible selection effect toward healthier and better-educated participants at baseline and a possible healthy survivor effect may have biased our effect estimates.
Our analyses of a population-based prospective cohort study suggest that long-term exposure to indoor and outdoor road traffic noise may increase the risk of developing T2DM, independent of AP exposure. Using estimated indoor noise exposures derived from individual apartment information improves estimation of noise effects
We thank the Heinz Nixdorf Foundation (chairman: M. Nixdorf; former chairman: Dr. jur. Schmidt) for the generous support of this study. We are indebted to the investigative group, the study personnel, and the participants of the Heinz Nixdorf Recall study. We also thank the North Rhine-Westphalia State Agency for Nature, Environment and Consumer Protection for providing emission and land use data for North Rhine-Westphalia. We specifically thank Anna Buschka for her data management work.
The authors declare that they have no conflicts of interest with regard to the content of this report.
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