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Epidemiology
Original research
Exposure to traffic-related particle matter and effects on lung function and potential interactions in a cross-sectional analysis of a cohort study in west Sweden
  1. Hanne Krage Carlsen1,
  2. Fredrik Nyberg1,2,
  3. Kjell Torén1,
  4. David Segersson3,
  5. Anna-Carin Olin1
  1. 1Occupational and Environmental Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
  2. 2Register Epidemiology, School of Public Health and Community Medicine, Sahlgrenska Academy, Gothenburg, Sweden
  3. 3Swedish Meteorological and Hydrological Institute, Norrkoping, Sweden
  1. Correspondence to Dr Hanne Krage Carlsen; hanne.krage.carlsen{at}amm.gu.se

Abstract

Objectives To investigate the long-term effects of source-specific particle matter (PM) on lung function, effects of Surfactant Protein A (SP-A) and glutathione S-transferase (GST) genes GSTP1 and GSTT1 gene variants and effect modification by single-nucleotide polymorphism (SNP) genotype.

Design Cohort study with address-based annual PM exposure assigned from annual estimates of size (PM10, PM2.5 and PMBC) and source-specific (traffic, industry, marine traffic and wood burning) dispersion modelling.

Setting Gothenburg, Sweden.

Participants The ADult-Onset asthma and NItric oXide Study had 6685 participants recruited from the general population, of which 5216 (78%) were included in the current study with information on all variables of interest. Mean age at the time of enrolment was 51.4 years (range 24–76) and 2427 (46.5%) were men.

Primary and secondary outcome measures The primary outcome was forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1). Secondary outcome measures were effects and gene–environment interactions of SP-A and GSTT1 and GSTP1 genotypes.

Results Exposure to traffic-related PM10 and PM2.5 was associated with decreases in percent-predicted (% predicted) FEV1 by −0.48% (95% CI −0.89% to −0.07%) and −0.47% (95% CI −0.88% to −0.07%) per IQR 3.05 and 2.47 µg/m3, respectively, and with decreases in % predicted FVC by −0.46% (95% CI −0.83% to −0.08%) and −0.47% (95% CI −0.83% to −0.10%). Total and traffic-related PMBC was strongly associated with both FEV1 and FVC by −0.53 (95% CI −0.94 to −0.13%) and −0.43% (95% CI −0.77 to −0.09%) per IQR, respectively, for FVC, and similarly for FEV1. Minor allele carrier status for two GSTP1 SNPs and the GSTT1 null genotype were associated with decreases in % predicted lung function. Three SP-A SNPs showed effect modification with exposure to PM2.5 from industry and marine traffic.

Conclusions PM exposure, specifically traffic related, was associated with FVC and FEV1 reductions and not modified by genotype. Genetic effect modification was suggested for industry and marine traffic PM2.5.

  • epidemiology
  • genetics
  • particle matter
  • surfactant protein A
  • glutathione S-transferase
  • lung function
http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

https://doi.org/10.1136/bmjopen-2019-034136

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    Footnotes

    • Contributors HKC analysed the data and drafted the manuscript. FN, KT and A-CO provided the cohort and genetic data, contributed to essential parts of the Introduction and Discussion sections and the final manuscript. DS provided and documented the particle matter exposure data. All authors approved the final version of the manuscript and contributed to the discussion.

    • Funding This work was supported by the Swedish Heart and Lung Foundation, The Swedish Research Council Formas, The Swedish Society for Medical Research and the Swedish Environmental Protection Agency.

    • Competing interests None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

    • Patient consent for publication Obtained.

    • Ethics approval The Västra Götaland Region ethical review board approved the study (ref no. Ö 092-01) and participants gave informed consent.

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

    • Data availability statement Data are available upon reasonable request. Additional data from the ADult-Onset asthma and NItric oXide Study exist and are held by the authors.