Invited Perspective: Diabetes and Road Traffic Noise at the Most and Least Exposed Façade

Environmental factors can act as facilitators of chronic non-communicable diseases. Ambient noise and air pollution collectively outrank all other environmental risk factors in importance, contributing to over 75% of the disease and disability burden associated with known environmental risk factors. In the first part of this review, we discussed the global burden and epidemiologic evidence supporting the importance of these novel risk factors as facilitators of cardiometabolic disease. In this part, we will discuss pathophysiological mechanisms responsible for noise and air pollution-mediated effects. Akin to traditional cardiovascular risk factors, a considerable body of evidence suggests that these environmental agents induce low-grade inflammation, oxidative stress, vascular dysfunction, and autonomic nervous system imbalance, thereby facilitating the development of diseases such as hypertension and diabetes. Through their impact on traditional risk factors and via additional novel mechanisms, environmental risk factors may have much larger impact on cardiovascular events than currently appreciated. In the second part of this review, we discuss deficiencies and gaps in knowledge and opportunities for new research.

Different elements of the environment have been posited to influence type 2 diabetes mellitus (T2DM). This systematic review summarizes evidence on the environmental determinants of T2DM identified in four databases. It proposes a theoretical framework illustrating the link between environment and T2DM, and briefly discusses some methodological challenges and potential solutions, and opportunities for future research. Walkability, air pollution, food and physical activity environment and roadways proximity were the most common environmental characteristics studied. Of the more than 200 reported and extracted relationships assessed in 60 studies, 82 showed significant association in the expected direction. In general, higher levels of walkability and green space were associated with lower T2DM risk, while increased levels of noise and air pollution were associated with greater risk. Current evidence is limited in terms of volume and study quality prohibiting causal inferences. However, the evidence suggests that environmental characteristics may influence T2DM prevention, and also provides a reasonable basis for further investigation with better quality data and longitudinal studies with policy-relevant environmental measures. This pursuit of better evidence is critical to support health-orientated urban design and city planning.

Background: Traffic noise has been associated with prevalence of hypertension, but reports are inconsistent for blood pressure (BP). To ascertain noise effects and to disentangle them from those suspected to be from traffic-related air pollution, it may be essential to estimate people’s noise exposure indoors in bedrooms. Objectives: We analyzed associations between long-term exposure to indoor traffic noise in bedrooms and prevalent hypertension and systolic (SBP) and diastolic (DBP) BP, considering long-term exposure to outdoor nitrogen dioxide (NO2). Methods: We evaluated 1,926 cohort participants at baseline (years 2003–2006; Girona, Spain). Outdoor annual average levels of nighttime traffic noise (L night) and NO2 were estimated at postal addresses with a detailed traffic noise model and a land-use regression model, respectively. Individual indoor traffic L night levels were derived from outdoor L night with application of insulations provided by reported noise-reducing factors. We assessed associations for hypertension and BP with multi-exposure logistic and linear regression models, respectively. Results: Median levels were 27.1 dB(A) (indoor L night), 56.7 dB(A) (outdoor L night), and 26.8 μg/m3 (NO2). Spearman correlations between outdoor and indoor L night with NO2 were 0.75 and 0.23, respectively. Indoor L night was associated both with hypertension (OR = 1.06; 95% CI: 0.99, 1.13) and SBP (β = 0.72; 95% CI: 0.29, 1.15) per 5 dB(A); and NO2 was associated with hypertension (OR = 1.16; 95% CI: 0.99, 1.36), SBP (β = 1.23; 95% CI: 0.21, 2.25), and DBP (β⊇= 0.56; 95% CI: –0.03, 1.14) per 10 μg/m3. In the outdoor noise model, L night was associated only with hypertension and NO2 with BP only. The indoor noise–SBP association was stronger and statistically significant with a threshold at 30 dB(A). Conclusion: Long-term exposure to indoor traffic noise was associated with prevalent hypertension and SBP, independently of NO2. Associations were less consistent for outdoor traffic L night and likely affected by collinearity. Citation: Foraster M, Künzli N, Aguilera I, Rivera M, Agis D, Vila J, Bouso L, Deltell A, Marrugat J, Ramos R, Sunyer J, Elosua R, Basagaña X. 2014. High blood pressure and long-term exposure to indoor noise and air pollution from road traffic. Environ Health Perspect 122:1193–1200; http://dx.doi.org/10.1289/ehp.1307156