Longitudinal association of polycyclic aromatic hydrocarbons and genetic risk with lung function.

To quantify the association of polycyclic aromatic hydrocarbons (PAHs) and the polygenic risk score (PRS) with lung function decline, we developed a repeated-measures study with 4681 observations from baseline and 6-year follow-up of the Wuhan-Zhuhai cohort. Lung function and urinary monohydroxylated PAH metabolites (OH-PAHs) were measured for each observation. The PRS was derived from 246 lung function-associated genetic variants weighted by the effect size of the decreasing ratio of forced expiratory volume in 1 s by forced vital capacity (FEV1/FVC). Linear mixed models were used to estimate the longitudinal exposure-response relationships between OH-PAHs and lung function, and to evaluate the interactions between OH-PAHs and PRS on the longitudinal change of lung function. We found that each 1-unit increase in log-transformed values of 9-hydroxyfluorene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 9-hydroxyphenanthrene, 2-hydroxyphenanthrene, 1-hydroxyphenanthrene, 1-hydroxypyrene, low molecular weight OH-PAHs (ΣLMW-OH-PAHs), and total OH-PAHs (ΣOH-PAHs) was associated with an annual change in FEV1/FVC of -0.140, -0.112, -0.260, -0.300, -0.159, -0.220, -0.145, -0.156, and -0.177 %/year, respectively. Interactions on the annual decline of FEV1/FVC were detected between ΣLMW-OH-PAHs and PRS (-0.010 %/year, 95% confidence interval -0.018 to -0.001, P

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Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.