Abstract
Urban populations are often simultaneously exposed to air pollution and environmental noise, which are independently associated with cardiovascular disease. Few studies have examined acute physiologic responses to both air and noise pollution using personal exposure measures. We conducted a repeated measures panel study of air pollution and noise in 46 non-smoking adults in Toronto, Canada. Data were analyzed using linear mixed-effects models and weighted cumulative exposure modeling of recent exposure. We examined acute changes in cardiovascular health effects of personal (ultrafine particles, black carbon) and regional (PM2.5, NO2, O3, Ox) measurements of air pollution and the role of personal noise exposure as a confounder of these associations. We observed adverse changes in subclinical cardiovascular outcomes in response to both air pollution and noise, including changes in endothelial function and heart rate variability (HRV). Our findings show that personal noise exposures can confound associations for air pollutants, particularly with HRV, and that impacts of air pollution and noise on HRV occur soon after exposure. Thus, both noise and air pollution have a measurable impact on cardiovascular physiology. Noise should be considered alongside air pollution in future studies to elucidate the combined impacts of these exposures in urban environments.
Highlights
Cardiovascular diseases (CVD), including ischemic heart disease and stroke, are the leading causes of death globally[1]
Means and distributions of Reactive Hyperemia Index (RHI) and heart rate variability (HRV) parameters did not reflect any aberrations in morning baseline endothelial function or HRV that would be suggestive of chronic cardiovascular illness (Supplementary Table S1)
This study examined the acute cardiovascular health effects of personal (UFPs, BC) and regional ( PM2.5, NO2, O3, Ox) measurements of air pollution exposures as well as the impact of personal noise exposures on these outcomes
Summary
Cardiovascular diseases (CVD), including ischemic heart disease and stroke, are the leading causes of death globally[1]. Little research has examined the importance of urban noise exposure as a co-occurring environmental stressor that may confound or modify the adverse health impacts of traffic-related air pollutants (TRAPs), among panel studies that assess short-term exposure in relation to acute cardiovascular outcomes. Preclinical outcomes including short-term changes in endothelial function (RHI; reactive hyperemia index, a Scientific Reports | (2020) 10:16703 All who completed both visits measure of vascular function), blood pressure and heart rate variability (HRV; a measure of autonomic heart function) are acknowledged as important physiological mechanisms through which air pollution and noise may trigger cardiovascular events[10,11,12]. Our objective was to evaluate the extent to which relationships between TRAPs and subclinical cardiovascular outcomes may be confounded by urban environmental noise using personal exposure measurements in a repeated-measures panel study design
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