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Assessing the Particulate Matter Removal Abilities of Tree Leaves
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Air pollution, particulate matter composition and methylation-based biologic age.

Alexandra J White1, Jacob K Kresovich1, Joshua P Keller2

  • 1Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, USA.

Environment International
|August 7, 2019
PubMed
Summary

Air pollution exposure, specifically nitrogen dioxide (NO2) and fine particulate matter (PM2.5) components, can accelerate epigenetic aging. Certain PM2.5 compositions are linked to increased epigenetic age, a predictor of disease and mortality risk.

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Area of Science:

  • Environmental Epigenetics
  • Molecular Epidemiology
  • Toxicology

Background:

  • Epigenetic age, determined by DNA methylation patterns, serves as a biomarker for biological aging.
  • Emerging evidence suggests environmental exposures, including air pollution, may influence epigenetic aging.
  • Understanding these links is crucial for public health, as epigenetic age is associated with mortality and disease risk.

Purpose of the Study:

  • To investigate the association between exposure to nitrogen dioxide (NO2), particulate matter (PM10, PM2.5), and their components with epigenetic age acceleration.
  • To explore how different chemical compositions of PM2.5 modify the relationship with epigenetic age.
  • To identify specific air pollutants and PM2.5 profiles linked to accelerated biological aging.

Main Methods:

  • A cohort of 2747 non-Hispanic white women in the contiguous U.S. was analyzed.
  • Residential exposure to NO2, PM10, and PM2.5 was estimated using land-use regression and kriging models.
  • DNA methylation was measured, and epigenetic age was calculated using established clocks (Hannum, Horvath, Levine). Age acceleration was determined by regressing epigenetic age on chronological age.

Main Results:

  • Nitrogen dioxide (NO2) showed an inverse association with age acceleration (Hannum clock).
  • No significant associations were found for PM10 exposure.
  • Particulate matter 2.5 (PM2.5) demonstrated varied associations with age acceleration depending on its component profiles, with some profiles linked to significant age acceleration (Levine clock).
  • Epigenome-wide analyses identified associations between NO2 and methylation at two CpG sites.

Conclusions:

  • Air pollution exposure is associated with epigenetic age acceleration, particularly concerning specific profiles of PM2.5.
  • The findings highlight the differential impact of air pollutant components on biological aging.
  • Epigenetic age acceleration linked to air pollution may serve as a marker for increased mortality and disease risk.