Air pollution and traffic noise associated with increase in CVD risk factors
Long-term exposure to road traffic noise, ambient air pollution, and cardiovascular risk factors in the HUNT and lifelines cohorts
Long-term exposure to road traffic noise and ambient air pollution have been linked to cardiovascular disease (CVD) morbidity and mortality. This is attributed by several mechanisms, including oxidative stress or overproduction of cortisol, which leads to increased glucose and lipid levels . However, there are limited epidemiological data on the association of noise and air pollution with CVD risk.
In this analysis, the cross-sectional associations between long-term road traffic noise, ambient air pollution and high-sensitive c-reactive protein (hsCRP), blood lipids and glucose levels were evaluated in two large European cohorts. These include the population-based HUNT3 survey, with data from 50 805 individuals in Norway from 2006-2008  and the Lifelines, a prospective, multi-generational, population-based cohort study, with data from 93 277 individuals in the Netherlands from 2006-2013 . Non-fasting blood samples from HUNT3 and fasting blood samples from Lifelines were analysed in a central laboratory, where hsCRP, total cholesterol, triglycerides and HDL-C levels were measured in samples from both cohorts, whereas fasting blood glucose and HbA1c concentrations were additionally measured in the Lifelines samples. A simplified version of the CNOSSOS-EU noise modelling framework was used to assess the sound pressure levels at the recruitment address of the participants, whereas a ‘European harmonized Land Use Regression model’ was used to assign annual air pollution (pollutants PM10 and NO2) estimates at each participant’s recruitment address [4,5].
- An interquartile range (IQR) increase in daytime noise (5.1 dB(A)), PM10 (2.0 µg/m3) and NO2 (7.4 µg/m3) was significantly associated with higher levels of hsCRP in the fully adjusted model. After further adjustment for noise (mutually adjusted model), only the association with NO2 remained significant (1.7%; 95% CI: 0.2–3.2%).
- An IQR increase in daytime noise, PM10 and NO2 was significantly associated with higher levels of triglycerides (noise: 0.7%; 95% CI: 0.3–1.1%; PM10: 1.9%; 95% CI: 1.5–2.4%; NO2: 2.2%; 95% CI: 1.6–2.7%). In the mutually adjusted model for both noise and air pollution, the associations remained significant for both air pollutants, but not for noise.
- There were significant positive associations between noise or NO2, and HDL-C. The association between NO2 and HDL-C lost significance after adjustment for BMI. There were no associations between any of the exposures and total cholesterol.
- In Lifelines, an IQR increase in daytime noise (4.2 dB(A)), PM10 (2.4 µg/m3) and NO2 (8.8 µg/m3) was significantly associated with higher fasting glucose levels (noise: 0.2%; 95% CI: 0.1–0.3%; PM10: 0.6%; 95% CI: 0.4–0.7%; NO2: 0.6%; 95% CI: 0.4–0.8%). These associations remained significant in the mutually adjusted models. Corresponding associations were not seen for HbA1c.
- For hsCRP, triglycerides and fasting glucose, significant associations were only observed among those with a daytime noise level ≥60 vs. <50 dB(A).
In two large European cohorts, long-term exposures to road traffic noise and ambient air pollution were significantly associated with increased systemic inflammation (hsCRP), blood glucose levels and risk for potential elevation of lipid levels. These data suggest a possible link between noise or air pollution with CVD and highlight the importance to consider environmental causes in the prevention of CVD as well as the need of collective efforts to mitigate noise and air pollution.
In their editorial article , Münzel et al highlight the global health burden of environmental stressors and comment on the study published by Cai et al as follows: ‘As commented by the authors, the observed effects of road traffic noise and air pollution on CVD risk factors were small. However, given the high proportion of the population exposed to high levels of these pollutants, the effect of this observation could be that the entire distribution of these risk factors may be shifted towards a less favourable profile at population level, i.e. ‘at-risk’ populations may be increased.’
They also discuss open questions resulting from studies examining the associations between air pollution and traffic noise, like for example the finding that the link between road traffic noise and CVD disappeared after adjustment for air pollution, and the other way around, and they conclude:
‘For the future, the development of technologies that provide measures of personal environmental exposure in conjunction with measures of health may provide an unprecedented opportunity for research and may allow an extraordinary understanding of the interactions between environment and health. To conclude, with this new study by Cai et al., the evidence that environmental stressors can cause cardiovascular and metabolic disease is growing, although mechanistic insights into how traffic noise and air pollution interplay are still warranted.’