Linchen He*, Charles J. Weschler, Glenn Morrison, Feng Li, Yinping Zhang, Michael H. Bergin, Marilyn Black and Junfeng Jim Zhang*,
{"title":"Synergistic Effects of Ozone Reaction Products and Fine Particulate Matter on Respiratory Pathophysiology in Children with Asthma","authors":"Linchen He*, Charles J. Weschler, Glenn Morrison, Feng Li, Yinping Zhang, Michael H. Bergin, Marilyn Black and Junfeng Jim Zhang*, ","doi":"10.1021/acsestair.4c0008010.1021/acsestair.4c00080","DOIUrl":null,"url":null,"abstract":"<p >After being transported from outdoor to indoor environments, a large portion of ozone (O<sub>3</sub>) reacts with indoor chemicals to generate O<sub>3</sub> reaction products. A fraction of these products can partition to fine particulate matter (PM<sub>2.5</sub>). Hence, we hypothesize that PM<sub>2.5</sub> serves as a carrier to deliver O<sub>3</sub> reaction products to the deep lung, leading to synergistic adverse pulmonary effects. In a panel study involving 43 children with asthma, each was assessed 4 times (2-week interval) for biomarkers of respiratory pathophysiology and personal exposures to PM<sub>2.5</sub> and O<sub>3</sub>. We also assessed O<sub>3</sub> loss exposures, calculated by taking the difference between the outdoor and indoor O<sub>3</sub> concentrations, which was proportional to the net exposure to O<sub>3</sub> reaction products. We found the adverse effects of O<sub>3</sub> loss exposure on biomarkers of pulmonary inflammation, airway (especially lower airway) mechanics, and spirometry lung function were greater at higher PM<sub>2.5</sub> exposure levels. We also found that the adverse effects of PM<sub>2.5</sub> exposure were greater at higher O<sub>3</sub> loss exposure levels. This suggests an additional mechanism for the synergistic pulmonary effects: PM<sub>2.5</sub> predisposes the lung to be more susceptible to O<sub>3</sub> reaction products and vice versa. However, our data is limited in differentiating the two potential mechanisms.</p><p >Little is known regarding the health impacts of O<sub>3</sub> reaction products. This study presents mechanistic explanations for the synergistic effects of O<sub>3</sub> reaction products and PM<sub>2.5</sub> on respiratory pathophysiology.</p>","PeriodicalId":100014,"journal":{"name":"ACS ES&T Air","volume":"1 8","pages":"918–926 918–926"},"PeriodicalIF":0.0000,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/acsestair.4c00080","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS ES&T Air","FirstCategoryId":"1085","ListUrlMain":"https://pubs.acs.org/doi/10.1021/acsestair.4c00080","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
After being transported from outdoor to indoor environments, a large portion of ozone (O3) reacts with indoor chemicals to generate O3 reaction products. A fraction of these products can partition to fine particulate matter (PM2.5). Hence, we hypothesize that PM2.5 serves as a carrier to deliver O3 reaction products to the deep lung, leading to synergistic adverse pulmonary effects. In a panel study involving 43 children with asthma, each was assessed 4 times (2-week interval) for biomarkers of respiratory pathophysiology and personal exposures to PM2.5 and O3. We also assessed O3 loss exposures, calculated by taking the difference between the outdoor and indoor O3 concentrations, which was proportional to the net exposure to O3 reaction products. We found the adverse effects of O3 loss exposure on biomarkers of pulmonary inflammation, airway (especially lower airway) mechanics, and spirometry lung function were greater at higher PM2.5 exposure levels. We also found that the adverse effects of PM2.5 exposure were greater at higher O3 loss exposure levels. This suggests an additional mechanism for the synergistic pulmonary effects: PM2.5 predisposes the lung to be more susceptible to O3 reaction products and vice versa. However, our data is limited in differentiating the two potential mechanisms.
Little is known regarding the health impacts of O3 reaction products. This study presents mechanistic explanations for the synergistic effects of O3 reaction products and PM2.5 on respiratory pathophysiology.