Associations between environmental noise and myocardial infarction and stroke: Investigating the potential mediating effects of hypertension

BACKGROUND: We investigated whether hypertension may be a mediator in the pathway linking environmental noise exposure to incident MI and stroke. METHODS: Separately for MI and stroke, we built two population-based cohorts from linked health administrative data. Participants were residents of Montreal (Canada) between 2000 and 2014, aged 45 years and older who were free of hypertension and MI or stroke at time of entry. MI, stroke and hypertension were ascertained from validated case definitions. Residential long-term environmental noise exposure, expressed as the annual mean level acoustic equivalent 24 h (L(Aeq24h)), was estimated from a land use regression model. We performed mediation analysis based on the potential outcomes framework. We used a Cox proportional hazards model for the exposure-outcome model and a logistic regression for the exposure-mediator model. In sensitivity analysis we applied a marginal structural approach to estimate the natural direct and indirect effects. RESULTS: Each cohort included approximately 900 000 individuals, with 26 647 incident cases of MI and 16 656 incident cases of stroke. 36% of incident MI and 40% of incident stokes had previously developed hypertension. The estimated total effect per interquartile range increase (from 55.0 to 60.5 dB A) in the annual mean L(Aeq24h) was 1.073 (95% confidence interval (CI): 1.070-1.077) for both MI for stroke. We found no evidence of exposure-mediator interaction for both outcomes. The relationships between environmental noise and MI and stroke was not mediated by hypertension. CONCLUSIONS: This population-based cohort study suggests that the main route by which environmental noise exposure may cause MI or stroke is not through hypertension.