Impacts of long-term ambient particulate matter and gaseous pollutants on circulating biomarkers of inflammation in male and female health professionals

Environ Res. 2022 Nov;214(Pt 1):113810. doi: 10.1016/j.envres.2022.113810. Epub 2022 Jul 4.

Abstract

Background: Systemic inflammation may serve as a biological mechanism linking air pollution to poor health but supporting evidence from studies of long-term pollutant exposure and inflammatory cytokines is inconsistent.

Objective: We studied associations between multiple particulate matter (PM) and gaseous air pollutants and pro- and anti-inflammatory cytokines within two nationwide cohorts of men and women.

Methods: Data were obtained from 16,151 women in the Nurses' Health Study and 7,930 men in the Health Professionals' Follow-up Study with at least one measure of circulating adiponectin, C-Reactive Protein (CRP), Interleukin-6 (IL-6) or soluble tumor necrosis-factor receptor-2 (sTNFR-2). Exposure to PM with aerodynamic diameter ≤2.5, 2.5-10, and ≤10 μm (PM2.5, PM2.5-10, PM10) and nitrogen dioxide (NO2) was estimated using spatio-temporal models and were linked to participants' addresses at the time of blood draw. Averages of the 1-, 3-, and 12-months prior to blood draw were examined. Associations between each biomarker and pollutant were estimated from linear regression models adjusted for individual and contextual covariates.

Results: In adjusted models, we observed a 2.72% (95% CI: 0.43%, 5.95%), 3.11% (-0.12%, 6.45%), and 3.67% (0.19%, 7.26%) increase in CRP associated with a 10 μg/m3 increase in 1-, 3-, and 12- month averaged NO2 in women. Among men, there was a statistically significant 5.96% (95% CI: 0.07%, 12.20%), 6.99% (95% CI: 0.29%, 14.15%), and 8.33% (95% CI: 0.35%, 16.94%) increase in CRP associated with a 10 μg/m3 increase in 1-, 3-, and 12-month averaged PM2.5-10, respectively. Increasing PM2.5-10 was associated with increasing IL-6 and sTNFR-2 among men over shorter exposure durations. There were no associations with exposures to PM2.5 or PM10, or with adiponectin. Findings were robust to sensitivity analyses restricting to disease-free controls and non-movers.

Conclusions: Across multiple long-term pollutant exposures and inflammatory markers, associations were generally weak. Focusing on specific pollutant-inflammatory mechanisms may clarify pathways.

Keywords: Air pollution; Biomarkers; Inflammation; Nitrogen dioxide; Particulate matter.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural

MeSH terms

  • Adiponectin
  • Air Pollutants* / metabolism
  • Air Pollutants* / toxicity
  • Air Pollution* / adverse effects
  • Biomarkers / blood
  • C-Reactive Protein
  • Environmental Exposure
  • Environmental Pollutants* / metabolism
  • Environmental Pollutants* / toxicity
  • Female
  • Follow-Up Studies
  • Gases
  • Health Personnel
  • Humans
  • Inflammation* / metabolism
  • Interleukin-6
  • Male
  • Nitrogen Dioxide
  • Particulate Matter* / metabolism
  • Particulate Matter* / toxicity

Substances

  • Adiponectin
  • Air Pollutants
  • Biomarkers
  • Environmental Pollutants
  • Gases
  • Interleukin-6
  • Particulate Matter
  • C-Reactive Protein
  • Nitrogen Dioxide