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ASCVD Mortality Linked to Specific Air Pollution Sources

— Pollution-mortality relationship evidenced at the level of PM2.5 source type

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Polluted air environment at city, vehicle traffic and toxic pollution.

Key Takeaways

  • Different components of small particular matter linked to modest cardiovascular effects.
  • Relationship persisted even in neighborhoods meeting the current National Ambient Air Quality Standard for small particular matter.
  • The source-specific pollution exposure patterns and associations with cardiovascular mortality varied regionally within the U.S.

The relationship between air pollution and cardiovascular harm was supported by another study, this time down to the level of specific types of pollution that appeared to have varying effects according to geographical region.

Analysis of individual components of fine particular matter (PM2.5) suggested that greater estimated exposure to certain pollution sources was consistently accompanied by more atherosclerotic cardiovascular disease (ASCVD) deaths on the population level:

  • Oil combustion: RR 1.051 per interquartile range increase in PM2.5 mass (95% CI 1.049-1.052)
  • Industrial pollution: RR 1.054 (95% CI 1.052-1.056)
  • Coal and biomass burning: RR 1.065 (95% CI 1.062-1.067)
  • Motor vehicle pollution: RR 1.044 (95% CI 1.042-1.045)
  • Soil and dust: No association

The exposure patterns and associations varied regionally, however -- there being no significant link between ASCVD and motor vehicle source pollution in the Southeast U.S., for example, and soil and dust pollution only showing harm in the eastern regions and the Midwest, reported Maayan Yitshak-Sade, MPH, PhD, epidemiologist of Icahn School of Medicine at Mount Sinai in New York City, and colleagues in .

"These regional differences require further investigation, as these differences can be attributed to a combination of diverse factors. For example, each U.S. region has a distinct climate. Atmospheric temperature, as well as other climate variables, were found to modify PM2.5-associated health effects," the study authors wrote.

"Furthermore, components of the built environment such as greenness levels and the socioeconomic, racial, and ethnic composition of the population can also contribute to regional differences," they added.

It is hard to see how the regional differences would be biologically plausible, according to an by economist C. Arden Pope III, PhD, of Brigham Young University in Provo, Utah, and Joshua Apte, PhD, air quality engineer and researcher of University of California Berkeley.

"Such discordant differences in responses to PM2.5 from different sources are not likely the result of regional population differences in human physiology. One must wonder how these results are affected by regional differences in exposures or if they result from artifacts of the source apportionment procedures," Pope and Apte wrote.

Otherwise, the "overall results are consistent with other studies that suggest that fine particles from combustion and industrial sources are associated with an increased rate of cardiovascular mortality -- even at levels below current air quality standards," the duo wrote.

Indeed, Yitshak-Sade's group reported that even in areas meeting the current National Ambient Air Quality Standard (NAAQS; PM2.5 <9 µg/m3), ASCVD mortality tracked with increasing PM2.5 mass (RR 1.028, 95% CI 1.026-1.029). "These results highlight the need to close the gap between the NAAQS and the World Health Organization recommendation -- currently set at <5 µg/m3," they suggested.

"These results emphasize the role of geographical context and the need to consider local population characteristics and exposure patterns when assessing health risks associated with air pollution," Yitshak-Sade and colleagues concluded.

For their study, the researchers had on hand ASCVD mortality rates compiled from Medicare records spanning the years 2000 to 2016. They also relied on machine learning models providing PM2.5 exposures -- down to a 50-m or 1-km spatial resolution -- and adjusting for individual-level demographic data, zip code-level socioeconomic characteristics, meteorological variables, and other covariates.

The study population ultimately included over 65 million Medicare beneficiaries who entered the dataset at 71 years of age on average (56% women, 85% white).

The 14 PM2.5 components of interest included sulfate, nitrate, organic and elemental carbon, silicon, lead, silicon, and copper. Different combinations of these components helped the investigators characterize the type of particulate matter likely being exposed to residents in each area.

During the study period, an estimated 7.2% of people died of ASCVD. The incidence was highest in the Northeast (9.80 per 1,000 person-years) and lowest in the West (7.71 per 1,000 person-years), the researchers found.

Important study limitations, they cautioned, include potential exposure misclassification and lack of accounting for each person's residential history prior to Medicare enrollment. Moreover, the study did not cover ASCVD other than ischemic heart disease and stroke.

And then there are the possible impacts of those "artifacts of the source apportionment procedures" on different regional results, as stressed by Pope and Apte.

"As finely resolved source-specific exposure estimates become more widely available across the United States, there may be increasing opportunities to leverage the full statistical power of large cohorts (such as Medicare data) to investigate these questions," the editorialists commented.

  • author['full_name']

    Nicole Lou is a reporter for Ƶ, where she covers cardiology news and other developments in medicine.

Disclosures

The study was supported by the HERCULES Center, the Mount Sinai Center on Health and Environment Across the LifeSpan, the National Institute on Aging, the National Institute of Environmental Health Sciences, and the United States Environmental Protection Agency (EPA).

Yitshak-Sade and co-authors had no relevant disclosures.

Pope reported institutional grants from the NIH and EPA.

Apte reported institutional research contracts with the Environmental Defense Fund and California Office of Environment Health Hazard Assessment; and personal travel costs paid for speaking at the Health Effects Institute annual meeting.

Primary Source

NEJM Evidence

Ma T, et al "Source-specific PM2.5 and atherosclerotic cardiovascular disease mortality" NEJM Evid 2024; DOI: 10.1056/EVIDoa2400182.

Secondary Source

NEJM Evidence

Pope CA, Apte JS "Atherosclerotic cardiovascular disease mortality and PM2.5 air pollution -- role of pollution sources?" NEJM Evid 2024; DOI: 10.1056/EVIDe2400371.