Long-term exposures to low concentrations of source-specific air pollution, road-traffic noise, and systemic inflammation and cardiovascular disease biomarkers

Environ Res. 2024 Dec 1;262(Pt 1):119846. doi: 10.1016/j.envres.2024.119846. Epub 2024 Aug 24.

Abstract

Objectives: Air pollution and traffic noise are detrimental to cardiovascular health. However, the effects of different sources of these exposures on cardiovascular biomarkers remain unclear. We explored the associations of long-term exposure to source-specific air pollution (vehicular exhausts and residential woodsmoke) at low concentrations and road-traffic noise with systemic inflammation and cardiovascular disease biomarkers.

Material and methods: Modeled outdoor exposure to fine particulate matter (aerodynamic diameter ≤2.5 μm; PM2.5) from vehicular exhausts and residential woodsmoke, nitrogen dioxide (NO2) from road traffic, and road-traffic noise were linked to the home addresses of the participants (Finnish residents aged 25-74) in the FINRISK study 1997-2012. The participants were located in the cities of Helsinki, Vantaa, and the region of Turku, Finland. The outcomes were high-sensitivity C-reactive protein (CRP), a biomarker for systemic inflammation, and cardiovascular disease biomarkers N-terminal pro-B-type natriuretic peptide (NT-proBNP) and troponin I. We performed cross-sectional analyses with linear and additive models and adjusted for potential confounders.

Results: We found no association between PM2.5 from vehicular exhausts (% CRP difference for 1 μg/m3 increase in PM2.5: -0.9, 95% confidence interval, CI: -7.2, 5.8), or from residential woodsmoke (% difference: -8.1, 95% CI: -21.7, 7.9) and CRP (N = 4147). Road-traffic noise >70 dB tended to be positively associated with CRP (% CRP difference versus noise reference category of ≤45 dB: 18.3, 95% CI: -0.5, 40.6), but the association lacked significance and robustness (N = 7142). Otherwise, we found no association between road-traffic noise and CRP, nor between NO2 from road traffic and NT-proBNP (N = 1907) or troponin I (N = 1951).

Conclusion: Long-term exposures to source-specific, fairly low-level air pollution from vehicular exhausts and residential woodsmoke, or road-traffic noise were not associated with systemic inflammation and cardiovascular disease biomarkers in this urban area.

Keywords: CRP; NT-proBNP; Noise; PM(2.5); Source-specific exposure; Troponin I.

MeSH terms

  • Adult
  • Aged
  • Air Pollutants* / analysis
  • Air Pollution / adverse effects
  • Air Pollution / analysis
  • Biomarkers* / blood
  • C-Reactive Protein / analysis
  • Cardiovascular Diseases* / etiology
  • Cross-Sectional Studies
  • Environmental Exposure* / adverse effects
  • Environmental Exposure* / analysis
  • Female
  • Finland
  • Humans
  • Inflammation* / blood
  • Inflammation* / chemically induced
  • Male
  • Middle Aged
  • Natriuretic Peptide, Brain / analysis
  • Natriuretic Peptide, Brain / blood
  • Nitrogen Dioxide / analysis
  • Noise, Transportation / adverse effects
  • Particulate Matter* / analysis
  • Peptide Fragments / analysis
  • Peptide Fragments / blood
  • Troponin I / analysis
  • Troponin I / blood
  • Vehicle Emissions / analysis

Substances

  • Biomarkers
  • Particulate Matter
  • Air Pollutants
  • C-Reactive Protein
  • Vehicle Emissions
  • Nitrogen Dioxide
  • Troponin I
  • Peptide Fragments
  • Natriuretic Peptide, Brain
  • pro-brain natriuretic peptide (1-76)