| Title: | Effect of traffic-related air pollution on cough in adults with polymorphisms in several cough-related genes |
| Author(s): | Yoon M; Ryu MH; Huff RD; Belvisi MG; Smith J; Carlsten C; |
| Address: | "Air Pollution Exposure Laboratory, Division of Respiratory Medicine, Department Medicine, Vancouver Coastal Health Research Institute, The University of British Columbia, Vancouver, BC, Canada. Research and Early Development, Respiratory Pharmacology Group, Respiratory & Immunology, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden. Airway Disease, National Heart and Lung Institute, Imperial College London, London, UK. Division of Infection, Immunity, and Respiratory Medicine, University of Manchester, 16 Manchester Academic Health Sciences Centre, and Manchester University NHS Foundation 17 Trust, Manchester, UK. Air Pollution Exposure Laboratory, Division of Respiratory Medicine, Department Medicine, Vancouver Coastal Health Research Institute, The University of British Columbia, Vancouver, BC, Canada. carlsten@mail.ubc.ca. The Lung Center, Vancouver General Hospital-Gordon and Leslie Diamond Health Care Centre, 2775 Laurel St. 7th Floor, Vancouver, BC, V5Z 1M9, Canada. carlsten@mail.ubc.ca" |
| DOI: | 10.1186/s12931-022-02031-8 |
| ISSN/ISBN: | 1465-993X (Electronic) 1465-9921 (Print) 1465-9921 (Linking) |
| Abstract: | "With prevalent global air pollution, individuals with certain genetic predispositions and sensitivities are at of higher risk of developing respiratory symptoms including chronic cough. Studies to date have relied on patient-filled questionnaires in epidemiological studies to evaluate the gene-by-environment interactions. In a controlled human exposure study, we evaluated whether genetic risk score (GRS) based on cough-related single-nucleotide polymorphisms (SNPs) are associated with a cough count over 24 h post-exposure to diesel exhaust (DE), a model for traffic-related air pollution. DE is a mixture of several known air pollutants including PM(2.5), CO, NO, NO(2), and volatile organic compounds. Under closely observed circumstances, we determined that GRS constructed from 7 SNPs related to TRPA1, TRPV1, and NK-2R were correlated with cough count. Selection of channels were based on prior knowledge that SNPs in these channels lead to acute airway inflammation as a result of their increased sensitivity to particulate matter. We performed a linear regression analysis and found a significant, positive correlation between GRS and cough count following DE exposure (p = 0.002, R(2) = 0.61) and filtered air (FA) exposure (p = 0.028, R(2) = 0.37). Although that correlation was stronger for DE than for FA, we found no significant exposure-by-GRS interaction. In summary, cough-relevant GRS was associated with a higher 24 h cough count in a controlled setting, suggesting that individuals with a high GRS may be more susceptible to developing cough regardless of their exposure. The trend towards this susceptibility being more prominent in the context of traffic-related air pollution remains to be confirmed.Trial registration: ClinicalTrial.gov NCT02236039; NCT0223603. Registered on August 11, 2014, https://clinicaltrials.gov/ct2/show/NCT02236039" |
| Keywords: | Adult *Air Pollutants/analysis/toxicity *Air Pollution/statistics & numerical data Cough/chemically induced/diagnosis/epidemiology Humans Particulate Matter/adverse effects/analysis Vehicle Emissions/toxicity *Volatile Organic Compounds Air pollution Coug; |
| Notes: | "MedlineYoon, Michael Ryu, Min Hyung Huff, Ryan D Belvisi, Maria G Smith, Jaclyn Carlsten, Chris eng Letter England 2022/05/06 Respir Res. 2022 May 4; 23(1):113. doi: 10.1186/s12931-022-02031-8" |
