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A recently proposed stricter regulation of fine particulate matter (PM2.5) by EPA is a step toward significant reductions in morbidity and mortality, supported by many recently published articles that point to a broad range of adverse health consequences linked to air pollution. An analysis previously published in JAMA Network Open indicates that PM2.5 levels are associated with at least 9 major causes of death, including increased mortality rates from cardiovascular disease, cerebrovascular disease, COPD, type 2 diabetes, lung cancer, pneumonia, chronic kidney disease, hypertension, and dementia. The population attributable fraction (PAF) of non-accidental deaths due to PM2.5 was also estimated to be 7.76%, suggesting that nearly 8% of all non-accidental deaths have this form of air pollution as the primary driver. This review concluded that “nearly all deaths attributable to air pollution in the contiguous United States are associated with ambient air pollution concentrations below the current EPA standards.” This standard was 12 μg/m3 until February 7th 2024, with the new regulations set at 9 ug/m3. A string of recent studies suggests aging itself may be accelerated by air pollution, and similar to pollutants such as lead, no threshold is clearly without risk.
BMJ, for example, recently published the results of a population-based cohort study which included an analysis of nearly 60 million Medicare beneficiaries aged 65 and older, followed for an average of 8 years. The three-year average exposure to PM2.5 of study participants was predicted using zip code data and examined any relationship to hospital admission for 7 distinct types of cardiovascular disease (CVD), rather than only combining various types of CVD into one composite (a limitation of previous studies). Many covariates were adjusted for, including multiple parameters related to socioeconomic status, smoking, BMI, etc.
The authors concluded that the 3-year average PM2.5 level of exposure was associated with an increased risk for hospital admission for ischemic heart disease, cerebrovascular disease, heart failure, cardiomyopathy, arrhythmia, and thoracic and abdominal aortic aneurysms. A composite of CVD risk suggested there was no safe threshold of exposure; for example, a PM2.5 level of between 5-6 ug/m3 was associated with greater CVD risk than levels < 5 ug/m3, while levels between 9-10 ug/m3 carried a 29% greater risk of CVD, notable because this is within the range of the current national average ambient exposure of 9.7 ug/m3. Some subtypes of CVD seemingly were more affected than others; for example, there was an over 2-fold increase in risk for admission due to heart failure at PM2.5 levels between 12-13 ug/m3, as well as a 33% increase at levels as low as 6-7 ug/m3. This study also found evidence for both acute and lagged effects, i.e., exposure in the last year as well as exposure from several years prior were both linked to an increase in risk, suggesting both short and long-term adverse impacts. While this study did not determine mechanisms of action, PM2.5-induced lipid peroxidation, vascular inflammation, and endothelial cell injury have all been documented.
In addition to cardiovascular disease, PM2.5 exposure has also recently been associated with neurodegenerative disease. Published in Neurology, cross-sectional data using traffic-associated PM2.5 levels in the Atlanta area was associated with evidence of neuropathology among the brains of tissue donors (using the Consortium to Establish a Registry for AD (CERAD) score). This was true when looking at both 1-year and 3-year windows of exposure, and a greater effect was observed among people without the APOE ε4 allele. This is consistent with previous analyses that suggest air pollution is causally related to both cognitive decline and dementia, though the many confounding variables make this difficult to determine. It’s important to note that PM2.5 is not the only type of air pollution, though it may have the strongest correlation with cognitive decline.
The last in this string of recent analyses was published in Environment International, which reported an association between air pollution and changes in DNA methylation in a cohort of over 4,100 women living in the U.S. (a subset of the Sister Study Cohort, created to find links between the environment and breast cancer). They utilized multiple markers of epigenetic changes though to indicate more rapid aging (including PhenoAgeAccel, GrimAgeAccel, and DunedinPACE), and examined ties not only to PM2.5 exposure, but also exposure to NO2 and PM10.
Although no significant associations were found between air pollution and these epigenetic markers among non-Hispanic White (NHW) women, positive associations among Black women (who were exposed to higher ambient levels of air pollution) were observed between PM10 and NO2 levels and two of the epigenetic indices (GrimAgeAccel and DunedinPACE). Additionally, 19 individual CpG sites (specific DNA locations that are variably methylated) were associated with air pollution among Black women, and 1 site among NHW women. This is not the first study to suggest greater vulnerability to the effects of air pollution among Black Americans, in terms of alterations in DNA methylation patterns, with both differences in exposure and susceptibility potentially influencing disparities observed in multiple health outcomes. Given that the acceleration of aging itself increases the risk for nearly every chronic disease, the above studies emphasize the importance of reducing ambient air pollution as much as possible.
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