Introduction Accumulating evidence indicates that gene and air pollution are associated with pulmonary function measurements. However, gene-air pollution interaction effect on pulmonary function decline remains largely unknown.
Methods A total of 1243 coke oven workers, followed up from October 2010 to October 2014, were included in the present study. Eighty-three pulmonary function strongly associated SNPs were included in the analysis. Total polycyclic aromatic hydrocarbons (ΣOH-PAHs) were determined in baseline urinary sample. Pulmonary function, forced expiratory volume in one second/forced vital capacity (FEV1/FVC) and forced expiratory flow between 25% and 75% of vital capacity (FEF25–75), was measured in 2010 and 2014 by spirometry. The decline meant that the values of pulmonary function parameters in 2010 minus the corresponding values in 2014. Multivariate linear regression model was used to evaluate gene-ΣOH-PAHs interaction effect on pulmonary function decline.
Result For RARB rs1529672, each A allele increase was associated with 0.87 (95% CI: 0.02, 1.73; p=0.045)% increased decline in FEV1/FVC. When considering interaction of RARB rs1529672 with ΣOH-PAHs on pulmonary function decline, ΣOH-PAHs was not significantly associated with FEV1/FVC decline in CC carrier [β (95% CI)=−0.55 (-3.80, 2.70)], but each 10-fold increase in ΣOH-PAHs was related to 3.85 (95% CI: 1.01, 6.69), and 9.44 (95% CI: 4.01, 14.87)% increased decline in FEV1/FVC in AC, and AA carrier, respectively (P for interaction=0.0006). Similar results appeared for RARB rs1529672 and gene-ΣOH-PAHs interaction effect on FEF25–75 decline.
Conclusion Our findings show that minor allele carrier of RARB rs1529672 is more susceptible to ΣOH-PAHs caused pulmonary function decline than major allele homozygote, and provide evidence for gene-ΣOH-PAHs interaction effect on pulmonary function decline.
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