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

Abstract

ObjectivesTo 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.DesignCohort 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.SettingGothenburg, Sweden.ParticipantsThe 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 measuresThe 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.ResultsExposure 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.ConclusionsPM 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.