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.

Associations between PM10 from Traffic, Resuspension, Sand Storms and Volcanic Sources and Asthma Drugs Dispensing

“…PM 2.5 was available for only some parts of the study period, so we refrained from adjusting for this in our models. Finding mainly effects of PM 10 from tra c has been reported in other studies of speci c PM sources, where long-term exposure to particles from marine tra c or residential heating were not associated with respiratory health (33). However, when studying health effects of long-term exposure to air pollution, it is not unproblematic to disentangle resuspension and direct tra c exposure in dispersion models as these are highly correlated, giving extra importance to short-term studies with thorough source assignment.…”

Respiratory symptoms, lung function, and fraction of exhaled nitric oxide before and after assignment in a desert environment—a cohort study

“…Other studies have reported increased emergency visits due to asthma and COPD [36] and increased asthma and COPD mortality [37,38] after acute exposure to airway pollution. The pathophysiological changes due to particulate matters are not clarified, but genetic modification has been suggested [39].…”

Genetic susceptibility to airway inflammation and exposure to short-term outdoor air pollution

“…Four SFTPA1 SNPs were genotyped and used, and three SFTPA2 SNPs were genotyped successfully and used (one assay failed). These SNPs are the same as are previously reported from the same cohort [ 30 ]. For NOS2 and NOS3 we did broader tagging SNP genotyping (including also obviously known candidate SNPs) across the genes to capture LD and haplotype variation.…”