A 2018 report published by the National Academy of Sciences, based upon data from 41 cohorts within 16 countries, implicated air pollution (i.e., ambient fine particulate matter (PM2.5)) in the deaths of 8.9 million people in 2015. This parallels the predictions published in the Lancet in 2015, which found ambient PM2.5 to be the 5th leading cause of death globally, contributing to 17.1% of ischemic heart disease and 14.2% of cerebrovascular disease, as well as over 100 million lost years of healthy life. In the U.S., every 10 μg/m3 increase in PM2.5 levels is associated with a 14-16% increase in mortality from stroke and ischemic heart disease.
It’s important to note that this increase in risk occurs at levels frequently encountered in the U.S., and it is not limited to risk due to long-term exposure. For example, a study in the Boston area found that even at PM2.5 levels considered safe under US regulations, a 34% higher risk of ischemic stroke was found among people exposed to “moderate” vs. “good” levels, with the highest risk found 12 hours after exposure.
A variety of mechanisms explain this link, including altered cardiac autonomic function (indicated by changes in heart rate variability), as well as endothelial dysfunction, oxidative damage, and ultimately accelerated atherosclerosis. Inflammation is also likely to play an important role, as suggested by a just released study which found arterial inflammation and an increase in the production of white blood cells in the bone marrow and spleen to be responsible for cardiovascular events associated with PM2.5 exposure.
Clinically Relevant Steps
Are there any actionable clinical steps to mitigate this increase in risk, given that it’s impractical to avoid breathing the air? One step is to monitor air quality levels, with a number of online tools offering the ability to check both current levels as well as historical data for a specific area. This background exposure turns out to be quite relevant to cardiovascular disease management; in the March issue of Hypertension, for example, data from over 9000 participants in SPRINT (the Systolic BP Intervention Trial) was analyzed to see if PM2.5 levels influenced the benefit from using standard vs. intensive therapy for hypertension. Although intensive therapy was found to support positive cardiovascular outcomes in groups with both low and high levels of air pollution, the effect was much greater in those with high exposure. In other words, controlling blood pressure may be especially important for individuals with high (defined as >12 ug/m3) PM2.5 exposure, with less (though still relevant) benefit for people breathing cleaner air.
A Healthy Diet
Diet is also another potent tool to mitigate the cardiovascular harm caused by air pollution and may be especially important for people with either greater cardiovascular risk or higher levels of exposure. In a very large prospective cohort study which followed nearly 600,000 participants in the U.S. over 17 years, air pollution was associated with greater risk for both cerebrovascular and ischemic heart disease. However, this risk was substantially reduced by following the Mediterranean diet. Indeed, among individuals most closely following the Mediterranean diet pattern, the increase in risk from higher levels of air pollution was completely eliminated. For clinicians, this should emphasize the importance of making dietary interventions among patients most at risk.
Another action step for clinicians is to recommend air purifiers for those patients most susceptible, or with the highest levels of exposure. In a small randomized and controlled study published in JAMA Internal Medicine, portable air filters reduced PM2.5 levels among older adults, as well as systolic blood pressure within just a few days. Although this study was only conducted over a few days, the authors speculate that if the blood pressure reduction was maintained, it could bring about a 16% reduction in cardiovascular events. In a report on a cross-over trial, HEPA filters were found to mitigate the effects of traffic related air pollution on systolic blood pressure, which increased in proportion to the magnitude of acute exposure.
Nutritional supplementation has also been reported to help minimize the effects of air pollution. Perhaps most notably, several randomized trials have shown a benefit for omega-3 fatty acid supplementation, in part by supporting the inflammatory pathways affected by pollution. In one randomized trial, 3g fish oil per day was shown to attenuate increases in lipids (very low-density lipoprotein and triglyceride concentrations) as well as unfavorable changes in HRV and other electrocardiographic measures following exposure to particulate matter. In a second randomized trial, fish oil supplemented at 2.5g per day was found to help fight against the adverse effects of PM2.5 exposure on diverse biomarkers related to the inflammatory response, coagulation, oxidative stress, and the neuroendocrine stress response. For example, fish oil blocked the increase in C-reactive protein, interleukin-6, and tumor necrosis factor-α following PM2.5 exposure relative to placebo.
A number of antioxidants, including lycopene, vitamins C and E, and broccoli sprouts have also demonstrated clinical benefit, though research has focused more on the benefits related to the respiratory system than the cardiovascular system. PM2.5 exposure has also been associated with higher homocysteine levels, a known risk factor for cardiovascular disease, but the effect was more pronounced among individuals with poorer folate and B12 status.
There is almost certainly a genetic component which mediates the adverse effects of air pollution, but as of yet only limited gene-environment associations have been reported, such as greater inflammation following PM2.5 exposure among individuals with difficulty synthesizing glutathione. This suggests that supplementation with glutathione precursors, shown to enhance detoxification of airborne pollutants, may be particularly important for some individuals.
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