Seattle, WA: IHME, University of Washington, 2015). The response function represents a meta-regressed Bayesian, regularized, trimmed (MR-BRT) curve derived by relaxing the log-linear assumption using cubic splines (extracted from the Institute for Health Metrics and Evaluation (IHME). B Exposure-response relationship for stroke and ischemic heart disease modeled for a 50-year-old adult. The Institute of Health Metrics and Evaluation, Seattle WA, 2020. Data from Global Burden of Disease Study 2019. The world map represents a heat map of deaths per 100,000 attributable to PM 2.5 air pollution in 2019. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.Ī Particulate matter air pollution and National Ambient Air Quality Standards (NAAQS). Nevertheless, due to the billions of people continually exposed to PM 2.5, the long-term pro-atherosclerotic effects of this ubiquitous air pollutant are likely to be of enormous and growing global public health importance. Even so, future research is needed to fully understand the contribution of different constituents in ambient air pollution-mediated atherosclerosis as well as how other systems may modulate the impact of exposure including adaptive immunity and the gut microbiome. Evidence from epidemiological studies including surrogates of atherosclerosis, human translational studies, and mechanistic investigations utilizing animal studies have improved our understanding of how ambient air pollution may potentiate atherosclerosis and precipitate cardiovascular events. Multiple animal exposure experiments over two decades have provided strong corroborative evidence that chronic exposure in fact does enhance the progression and perhaps vulnerability characteristics of atherosclerotic lesions.
Recent epidemiological studies have demonstrated an association between ambient PM 2.5 exposure and the presence and progression of atherosclerosis in humans. The purpose of this review is to examine the available evidence for how ambient air pollution exposure may precipitate events at various time frames. Not only can short-term PM 2.5 exposure trigger acute CV events in susceptible individuals, but longer-term exposure over years augments CV risk to a greater extent in comparison with short-term exposure.
This increased exposure has come at the cost of heightened risk for cardiovascular (CV) morbidity and mortality. During the past century, exposure to particulate matter (PM) air pollution < 2.5 μm in diameter (PM 2.5) has emerged as an all-pervading element of modern-day society.
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