» Articles » PMID: 39394095

Effects of Single and Combined Urinary Polycyclic Aromatic Hydrocarbon Effects on Lung Function in the U.S. Adult Population

Overview
Publisher Biomed Central
Specialty Public Health
Date 2024 Oct 11
PMID 39394095
Authors
Affiliations
Soon will be listed here.
Abstract

Background: The impact of polycyclic aromatic hydrocarbons (PAHs) on lung function has garnered attention, but studies mostly focus on individual effect. This study investigates urinary PAH metabolites as biomarkers of exposure and assesses the relationships between single and combined exposures to nine urinary PAH metabolites and lung function in adults.

Methods: Data from 4040 adults in the 2007-2012 National Health and Nutrition Examination Survey (NHANES) were analyzed. Weighted generalized linear models estimated the effects of individual PAH metabolites on lung function. Additionally, weighted quantile sum (WQS) regression, quantile g-computation (qgcomp), and Bayesian kernel machine regression (BKMR) were employed to evaluate the combined impacts of multiple PAH metabolites.

Results: Analyses of individual PAH metabolites revealed negative associations with lung function, excluding forced vital capacity (FVC). The WQS, qgcomp, and BKMR models consistently showed that exposure to multiple PAH metabolites was associated with lung function decrease. WQS indicated that 2-hydroxynaphthalene (2-NAP) was the largest contributor to the reductions in forced expiratory volume in 1 s (FEV1), FVC, peak expiratory flow (PEF), and forced expiratory flow from 25 to 75% of FVC (PEF25-75%). Additionally, 1-hydroxypyrene (1-PYR) was the primary PAH metabolite contributing to the decreases in FEV1/FVC and fractional exhaled nitric oxide (FeNO). The combined effect of urinary PAH metabolites did not affect FVC in the current smokers or FeNO in nonsmokers, but decreased FEV1/FVC in current smokers.

Conclusion: This study strengthens the negative relationships between multiple PAH metabolites exposure and lung function in adults. Given the limitations of this study, including the lack of knowledge of other exposure pathways and the uncertainty of urinary metabolites, further research is necessary to explore the mechanisms underlying these associations and to address the limitations in exposure assessment.

References
1.
Merianos A, Jandarov R, Cataletto M, Mahabee-Gittens E . Tobacco smoke exposure and fractional exhaled nitric oxide levels among U.S. adolescents. Nitric Oxide. 2021; 117:53-59. PMC: 8582299. DOI: 10.1016/j.niox.2021.10.004. View

2.
Ramalho S, Shah A . Lung function and cardiovascular disease: A link. Trends Cardiovasc Med. 2020; 31(2):93-98. PMC: 7332411. DOI: 10.1016/j.tcm.2019.12.009. View

3.
Wallin C, Sholts S, Osterlund N, Luo J, Jarvet J, Roos P . Alzheimer's disease and cigarette smoke components: effects of nicotine, PAHs, and Cd(II), Cr(III), Pb(II), Pb(IV) ions on amyloid-β peptide aggregation. Sci Rep. 2017; 7(1):14423. PMC: 5663743. DOI: 10.1038/s41598-017-13759-5. View

4.
Caron K, Zhu W, Bernert J, Wang L, Blount B, Dortch K . Geometric Mean Serum Cotinine Concentrations Confirm a Continued Decline in Secondhand Smoke Exposure among U.S. Nonsmokers-NHANES 2003 to 2018. Int J Environ Res Public Health. 2022; 19(10). PMC: 9140715. DOI: 10.3390/ijerph19105862. View

5.
Park H, Ha N, Kim D, Kim J, Lee C, Kim K . Relationship between residence characteristics and polycyclic aromatic hydrocarbon exposure in housewives: second Korean National Environmental Health Survey (2012-2014). Ann Occup Environ Med. 2018; 30:23. PMC: 5907289. DOI: 10.1186/s40557-018-0236-x. View