RESUMEN
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 (LAeq24h), 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 LAeq24h 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.
Asunto(s)
Hipertensión , Infarto del Miocardio , Accidente Cerebrovascular , Humanos , Estudios de Cohortes , Ruido , Accidente Cerebrovascular/epidemiología , Accidente Cerebrovascular/etiología , Hipertensión/epidemiología , Hipertensión/etiología , Infarto del Miocardio/epidemiología , Infarto del Miocardio/etiología , Exposición a Riesgos Ambientales/efectos adversosRESUMEN
Background: Noise has been related to several cardiovascular diseases (CVDs) such as coronary heart disease and to their risk factors such as hypertension, but associations with stroke remain under-researched, even if CVD likely share similar pathophysiologic mechanisms. Aim: The objective of the study was to examine the association between long-term residential exposure to total environmental noise and stroke incidence in Montreal, Canada. Materials and Methods: We created an open cohort of adults aged ≥45years, free of stroke before entering the cohort for the years 2000 to 2014 with health administrative data. Residential total environmental noise levels were estimated with land use regression (LUR) models. Incident stroke was based on hospital admissions. Cox hazard models with age as the time axis and time-varying exposures were used to estimate associations, which were adjusted for material deprivation, year, nitrogen dioxide, stratified for sex, and indirectly adjusted for smoking. Results: There were 9,072,492 person-years of follow-up with 47% men; 26,741 developed stroke (21,402 ischemic; 4947 hemorrhagic; 392 had both). LUR total noise level acoustic equivalent for 24 hours (LAeq24h) ranged 44 to 79 dBA. The adjusted hazard ratio (HR) for stroke (all types), for a 10-dBA increase in LAeq24h, was 1.06 [95% confidence interval (CI): 1.03-1.09]. The LAeq24h was associated with ischemic (HR per 10 dBA: 1.08; 95% CI: 1.04-1.12) but not hemorrhagic stroke (HR per 10 dBA: 0.97; 95% CI: 0.90-1.04). Conclusion: The results suggest that total environmental noise is associated with incident stroke, which is consistent with studies on transportation noise and other CVD.
Asunto(s)
Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Cardiovasculares , Ruido del Transporte , Accidente Cerebrovascular , Adulto , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Contaminación del Aire/efectos adversos , Enfermedades Cardiovasculares/epidemiología , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Femenino , Humanos , Incidencia , Masculino , Ruido del Transporte/efectos adversos , Material Particulado/efectos adversos , Accidente Cerebrovascular/epidemiología , Accidente Cerebrovascular/etiologíaRESUMEN
BACKGROUND: Cardiovascular effects of environmental noise are a growing concern. However, the evidence remains largely limited to the association between road traffic noise and hypertension and coronary heart diseases. OBJECTIVES: To investigate the association between long-term residential exposure to environmental/transportation noise and the incidence of myocardial infarction (MI) in the adult population living in Montreal. METHODS: An open cohort of adults aged 45 years old and over, living on the island of Montreal and free of MI before entering the cohort was created for the years 2000-2014 with the Quebec Integrated Chronic Disease Surveillance System; a systematic surveillance system from the Canadian province of Quebec starting in 1996. Residential noise exposure was calculated in three ways: 1) total ambient noise levels estimated by Land use regression (LUR) models; 2) road traffic noise estimated by a noise propagation model CadnaA and 3) distances to transportation sources (roads, airport, railways). Incident MI was based on diagnostic codes in hospital admission records. Cox models with time-varying exposures (age as the time axis) were used to estimate the associations with various adjustments (material deprivation indicator, calendar year, nitrogen dioxide, stratification for sex). Indirect adjustment based on ancillary data for smoking was performed. RESULTS: 1,065,414 individuals were followed (total of 9,000,443 person-years) and 40,718 (3.8%) developed MI. We found positive associations between total environmental noise, estimated by LUR models and the incidence of MI. Total noise LUR levels ranged from ~44 to ~79 dBA and varied slightly with the metric used. The adjusted hazard ratios (HRs) (also adjusted for smoking) were 1.12 (95% Confidence Intervals [CI]: 1.08-1.15), 1.11 (95%CI: 1.07-1.14) and 1.10 (95%CI: 1.06-1.14) per 10 dBA noise levels increase respectively in Level Accoustic equivalent 24 h (LAeq24 h), Level day-evening-night (Lden) and night level (Lnight). We found a borderline negative association between road noise levels estimated with CadnaA and MI (HR: 0.99 per 10 dBA; 95%CI: 0.98-1.00). Distances to major roads and highways were not associated with MI while the proximity to railways was positively associated with MI (HR for ≤100 vs > 1000 m: 1.07; 95%CI: 1.01-1.14). A negative association was found with the proximity to the airport noise exposure forecast (NEF25); HR (<1 vs >1000 m) = 0.88 (95%CI: 0.81-0.96). CONCLUSIONS: These associations suggest that exposure to total environmental noise at current urban levels may be related to the incidence of MI. Additional studies with more accurate road noise estimates are needed to explain the counterintuitive associations with road noise and specific transportation sources.