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Associations of long- and short-term air pollution exposure with markers of inflammation and coagulation in a population sample
  1. S Panasevich1,
  2. K Leander1,
  3. M Rosenlund1,
  4. P Ljungman1,2,
  5. T Bellander1,
  6. U de Faire1,3,
  7. G Pershagen1,4,
  8. F Nyberg1,5
  1. 1
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
  2. 2
    Department of Cardiology, South Hospital, Stockholm, Sweden
  3. 3
    Department of Cardiology, Karolinska Hospital, Stockholm, Sweden
  4. 4
    Department of Community Medicine, Karolinska Hospital, Stockholm, Sweden
  5. 5
    AstraZeneca R&D Mölndal, Mölndal, Sweden
  1. Correspondence to Sviatlana Panasevich, Unit of Environmental Epidemiology, Institute of Environmental Medicine, Nobels väg 13, Box 210 Karolinska Institutet, SE-171 77 Stockholm, Sweden; Sviatlana.Panasevich{at}ki.se

Abstract

Background: Exposure to elevated levels of ambient air pollutants can lead to adverse cardiovascular effects. Potential mechanisms include systemic inflammation and perturbation of the coagulation balance.

Objectives: To investigate long- and short-term effects of air pollution exposure on serum levels of inflammatory (IL-6, TNF-α and CRP) and coagulation (fibrinogen and PAI-1) markers relevant for cardiovascular pathology.

Methods: The study group consisted of a population sample of 1028 men and 508 women aged 45–70 years from Stockholm. Long-term air pollution exposure was assessed using spatial modelling of traffic-related NO2 and heating-related SO2 emissions at each subject’s residential addresses over retrospective periods of 1, 5 and 30 years. Short-term exposure was assessed as averages of rooftop measurements over 12–120 h before blood sampling.

Results: Long-term exposures to both traffic-NO2 and heating-SO2 emissions showed consistent associations with IL-6 levels. 30-year average traffic-NO2 exposure was associated with a 64.5% (95% CI 6.7% to 153.8%) increase in serum IL-6 per 28.8 μg/m3 (corresponding to the difference between the 5th and 95th percentile exposure value), and 30-year exposure to heating-SO2 with a 67.6% (95% CI 7.1% to 162.2%) increase per 39.4 μg/m3 (5th–95th percentile value difference). The association appeared stronger in non-smokers, physically active people and hypertensive subjects. We observed positive non-significant associations of inflammatory markers with NO2 and PM10 during 24 h before blood sampling. Short-term exposure to O3 was associated with increased, and SO2 with decreased, fibrinogen levels.

Conclusions: Our results suggest that exposure to moderate levels of air pollution may influence serum levels of inflammatory markers.

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Footnotes

  • Additional tables are published online only at http://oem.bmj.com/content/vol66/issue11

  • Funding The research was supported by the Swedish Medical Research Council (09533), the Swedish Lung and Heart Foundation, and King Gustaf the V and Queen Victoria’s Foundation.

  • Competing interests FN is employed by AstraZeneca and AstraZeneca also supports his academic part-time adjunct position as Lecturer in Molecular Epidemiology at Karolinska Institutet. FN also holds some AstraZeneca shares. MR is currently employed by GlaxoSmithKline Biologicals.

  • Ethics approval The study was approved by the Ethics Committee at Karolinska Institutet.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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