Key result
Ambient PM2.5 air pollution causes 4.2 million deaths annually (~57% cardiovascular), and indoor air purification reduces short-term PM2.5 exposure by 50% and mitigates stress-axis activation.
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This editorial highlights the global cardiovascular burden of PM2.5 air pollution, discusses new metabolomic evidence linking PM2.5 to central nervous system stress-axis activation, and calls for definitive clinical outcome trials of personal-protection strategies like indoor air filtration and N95 respirators.
The modern era has borne witness to a dramatic shift in the global burden of disease toward noncommunicable illnesses associated with economic affluence (eg, diabetes mellitus, heart diseases). 1Although primeval problems menacing humanity since the dawn of time such as undernutrition/famine, unsafe drinking water, and infectious diseases persist (and may worsen in the future as a result of climate change), their relative importance has been considerably reduced during the past half-century. 1,2In contrast, anthropogenic ambient air pollution (mainly particulate matter <2.5 μm [PM 2.5 ]) remains a recalcitrant and growing threat to global health and well-being.As of 2015, exposure to ambient PM 2.5 ranked fifth-closely following hypertension, smoking, high glucose, and elevated cholesterol, respectively-as a leading global risk factor for morbidity and mortality. 2PM 2.5 promotes many illnesses, including cancer and lung disease.However, the greatest portion of death and disability is from cardiovascular events (myocardial infarction, stroke, heart failure), and, as such, air pollution has been formally recognized by both the American Heart Association and European Society of Cardiology as an independent risk factor. 3,4ost recent estimates are that 4.2 million deaths (7.6% of total global mortality and 700 000 more deaths in 2015 compared with 1990) 2 are attributable to ambient PM 2.5 .Cardiovascular diseases account for ≈57% of these deaths, with South and East Asia contributing ≈60% of total PM 2.5 -related mortality.Despite substantial improvements in air quality throughout much of North America, the population-weighted PM 2.5 exposure has increased worldwide from 1990 (39.7 μg/m 3 ) to 2015 (44.2 μg/m 3 ). 2 This increase was largely because of a worsening of air quality and population growth across Asia, Africa, and the Middle East.These facts paint a stark picture highlighting the clear and present danger posed by air pollution.First, forecasted demographic and epidemiological transitions in India and China, along with other rapidly developing economies, imply that a businessas-usual strategy is not tenable.Aiming to simply continue the status quo, already resulting in unacceptably high mortality rates from PM 2.5 , would require a 20% to 30% decline in levels over the next 15 years just to offset the negative influence attributable to the anticipated growth of the susceptible (aging) population.Second, the supralinear nature of the integrated exposure-response function of PM 2.5 (steeper at lower compared with higher concentrations) dictates that for a given decrease in air pollution, reductions in per-capita mortality will likely be paradoxically greater in economies with preexisting good compared with poorer air quality.Considerable positive impact on global mortality can be accomplished through aggressive national policies to improve air quality in India and China (populationweighted mean PM 2.5 exposure levels of 74.3 and 58.4 μg/m 3 , respectively), which together account for >50% of global PM 2.5 mortality. 2However, substantial public "Stressed" About Air Pollution
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Brook et al. (2017) conducted an editorial in Cardiovascular and cardiometabolic risk attributable to ambient PM2.5 air pollution. Ambient fine particulate matter (<2.5 μm [PM2.5]) exposure and personal-protection strategies (indoor air purification, N95 masks) was evaluated. Ambient PM2.5 air pollution causes 4.2 million deaths annually (~57% cardiovascular), and indoor air purification reduces short-term PM2.5 exposure by 50% and mitigates stress-axis activation.
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