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

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, PM_2.5 and PM_BC) 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 PM_2.5 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 PM_BC 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 PM_2.5 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 PM_2.5.

Keywords: epidemiology; genetics; glutathione S-transferase; lung function; particle matter; surfactant protein A.

Figure 1

Change in FEV₁ and FVC (% predicted) associated with exposure to medium (50th–90th) and high (above 90th percentile) concentration of source-specific PM. FEV₁, forced expiratory volume in 1 s; FVC, forced vital capacity; PM, particle matter.

Figure 2

Unadjusted gene–environment interactions between selected single nucleotide polymorphisms and % predicted values of FEV₁ and FVC in exposure categories of selected PM2.5 sources. A) Interaction between PM2.5 from industry and rs1136451 on %predicted FEV1. B) Interaction between PM2.5 from industry and rs1136451 on %predicted FVC. C) Interaction between PM2.5 from marine traffic and rs4253527 on FEV1. D) Interaction between PM2.5 from marine traffic and rs4253527 on predicted FVC.E) Interaction between PM2.5 from marine traffic and rs1059057 on %predicted FVC. Blue lines represent effects on minor allele carriers.FEV₁, forced expiratory volume in 1 s; FVC, forced vital capacity; PM, particle matter.