{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T18:33:09Z","timestamp":1783017189402,"version":"3.54.6"},"reference-count":37,"publisher":"BMJ","issue":"1","funder":[{"name":"State Scholarship Fund of China Scholarship Council","award":["202006015008"],"award-info":[{"award-number":["202006015008"]}]},{"name":"Academy of Medical Sciences\/the Wellcome Trust\/ the Government Department of Business, Energy and Industrial Strategy\/the British Heart Foundation\/Diabetes UK Springboard Award","award":["Ref: SBF008\\1155"],"award-info":[{"award-number":["Ref: SBF008\\1155"]}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["Thorax"],"accepted":{"date-parts":[[2025,6,19]]},"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>In the UK, an estimated 15% of asthma patients have concurrent chronic obstructive pulmonary disease (COPD), yet the underlying causes and mechanisms remain largely unexplored. This study aimed to investigate the roles of both ambient air pollution and genetic susceptibility in the progression from asthma to COPD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      46\u2009832 participants with asthma were recruited from the UK Biobank during the baseline period (2006\u20132010). Particulate matter with a diameter of 2.5 \u03bcm (PM\n                      <jats:sub>2.5<\/jats:sub>\n                      ) and nitrogen dioxide (NO\n                      <jats:sub>2<\/jats:sub>\n                      ) were estimated at baseline address using land-use regression models. Air pollution score reflected joint exposure to air pollution. Polygenic risk score was calculated using novel genetic signals identified for coexistence of asthma+COPD. Cox proportional hazards regression analysis was employed to quantify the risks of both ambient air pollution and genetic scores on incident COPD among asthmatics, adjusting for covariates.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Over a median follow-up of 10.84 years, 3759 participants with asthma at baseline developed COPD. For an IQR increase in PM\n                      <jats:sub>2.5<\/jats:sub>\n                      and NO\n                      <jats:sub>2<\/jats:sub>\n                      , the HR for developing COPD was 1.07 (95% CI: 1.02 to 1.11) and 1.10 (95% CI: 1.04 to 1.15), respectively. Adverse effects could be observed at concentrations as low as 8\u2009\u00b5g\/m\n                      <jats:sup>3<\/jats:sup>\n                      for PM\n                      <jats:sub>2.5<\/jats:sub>\n                      and 12\u2009\u00b5g\/m\n                      <jats:sup>3<\/jats:sup>\n                      for NO\n                      <jats:sub>2<\/jats:sub>\n                      . A significant multiplicative interaction was identified between ambient air pollution and genetic susceptibility. Individuals with the highest genetic risk score exhibited the greatest risk, with an HR of 1.13 (95% CI: 1.05 to 1.22) per IQR increase in air pollution score (P\n                      <jats:sub>interaction<\/jats:sub>\n                      &lt;0.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Ambient air pollution is strongly associated with progression from asthma to comorbidity COPD, particularly among individuals with high genetic risk.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/thorax-2024-222871","type":"journal-article","created":{"date-parts":[[2025,7,21]],"date-time":"2025-07-21T17:20:20Z","timestamp":1753118420000},"page":"51-60","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":4,"title":["Air pollution, genetic susceptibility and risk of progression from asthma to COPD"],"prefix":"10.1136","volume":"81","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9237-0751","authenticated-orcid":false,"given":"Guoxing","family":"Li","sequence":"first","affiliation":[{"name":"Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China"},{"name":"Environmental Research Group, School of Public Health, Imperial College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-2670-0802","authenticated-orcid":false,"given":"Ke","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3255-3430","authenticated-orcid":false,"given":"Teng","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-5430-922X","authenticated-orcid":false,"given":"Jianbo","family":"Jin","sequence":"additional","affiliation":[{"name":"Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5589-9514","authenticated-orcid":false,"given":"Xinbiao","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1601-2199","authenticated-orcid":false,"given":"Yutong Samuel","family":"Cai","sequence":"additional","affiliation":[{"name":"Centre for Environmental Health and Sustainability, Department of Population Health Sciences, University of Leicester, Leicester, UK"},{"name":"National Institute for Health and Care Research, Health Protection Research Unit in Environmental Exposures and Health, University of Leicester, Leicester, UK"},{"name":"National Institute for Health and Care Research Health, Leicester Biomedical Research Centre, Leicester General Hospital, Leicester, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9697-6224","authenticated-orcid":false,"given":"Jing","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China"},{"name":"Institute for Global Health and Development, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2025,7,21]]},"reference":[{"key":"2025121510051002000_81.1.51.1","unstructured":"Momtazmanesh S , Moghaddam SS , Ghamari S , et al . Global burden of chronic respiratory diseases and risk factors, 1990\u20132019: an update from the Global Burden of Disease Study 2019. 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