Association of Long-term Ambient Ozone Exposure With Respiratory Morbidity in Smokers

Paulin, Laura M.; Gassett, Amanda; Alexis, Neil E.; Kirwa, Kipruto; Kanner, Richard E.; Peters, Stephen P.; Krishnan, Jerry A.; Paine, Robert; Dransfield, Mark T.; Woodruff, Prescott G.; Cooper, Christopher B.; Barr, R. Graham; Comellas, Alejandro P.; Pirozzi, C.S.; Han, MeiLan K.; Hoffman, Eric A.; Martínez, Fernando J.; Woo, Han; Peng, Roger D.; Fawzy, Ashraf; Putcha, Nirupama; Breysse, Patrick N.; Kaufman, Joel D.; Hansel, Nadia N.; Investigators, for the GARFIELD‐AF

doi:10.1001/jamainternmed.2019.5498

Cited by 60 publications

(46 citation statements)

References 46 publications

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“…Using percent emphysema obtained by cardiac computed tomography scan, this study found the association with greater increase in percent emphysema at baseline (0.43 for 10 ppb increase in ozone; 95% CI, 0.10–0.80) as well as during follow-up (0.60; 95% CI, 0.27–0.93) [ 3 ]. Long-term ozone was associated with lung function, emphysema severity, respiratory symptoms, and exacerbations in a heavy smoker cohort with or without COPD [ 43 ]. Findings of cardiovascular outcomes have been sparse.…”

Section: Association With Long-term Exposure To Ozone In Epidemiologimentioning

confidence: 99%

Health Effects of Ozone on Respiratory Diseases

Kim

2020

Tuberc Respir Dis

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Ozone is known to cause bronchial inflammation and airway hyper-responsiveness via oxidative injury and inflammation. While other ambient air pollutants such as particulate matter (PM) and NO 2 showed decreasing trends of mean annual concentrations, ozone concentration did not decline recently in most countries worldwide. Short-term exposure to high concentration of ozone has been associated with increased mortality and cardiovascular and respiratory morbidity in many regions of the world. However, long-term effects of ozone were less investigated than short-term exposure due to the difficulty of modeling for ozone exposure and linking between individual exposure and health outcome data. Recently developed modeling of ozone exposure enabled investigation of long-term ozone effects on health outcomes. Recent findings suggested that long-term exposure to ozone is associated with an increased risk of cardiovascular and respiratory mortality. Longitudinal studies using large cohorts also revealed that long-term exposure to ozone was associated with a greater decline in lung function and progression of emphysema. Keeping standards for ozone as well as PM is needed to protect respiratory health of the general population and subjects with chronic respiratory diseases.

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Section: Association With Long-term Exposure To Ozone In Epidemiologimentioning

confidence: 99%

Health Effects of Ozone on Respiratory Diseases

Kim

2020

Tuberc Respir Dis

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“…And we hypothesize that this exposure method is more realistic than other previous methods, such as intratracheal instillation in the form of PM2.5 suspension liquid with a stable PM2.5 concentration or ultrasonic nebulization in the form of PM2.5 aerosols [17,18,40,41]. However, it is regrettable that the levels of other gas pollutants including ozone, SO 2 , and NO 2 , which have also been demonstrated to contribute to lung injury and COPD development, were ignored to be measured in this study [42]. But according to Chu et al and Zhou et al's studies, in which the same PM2.5 exposure equipment was used, concentrations of CO, O 3 , NO 2 , and SO 2 were monitored both in filtered air and concentrated PM2.5 air chambers and no significant differences were found during the exposure [43,44].…”

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confidence: 95%

Exposure to Air Pollution Exacerbates Inflammation in Rats with Preexisting COPD

Wang

Zhao

et al. 2020

Mediators of Inflammation

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Particulate matter with an aerodynamic diameter equal or less than 2.5 micrometers (PM2.5) is associated with the development of chronic obstructive pulmonary disease (COPD). The mechanisms by which PM2.5 accelerates disease progression in COPD are poorly understood. In this study, we aimed to investigate the effect of PM2.5 on lung injury in rats with hallmark features of COPD. Cardinal features of human COPD were induced in a rat model by repeated cigarette smoke inhalation and bacterial infection for 8 weeks. Then, from week 9 to week 16, some of these rats with COPD were subjected to real-time concentrated atmospheric PM2.5. Lung function, pathology, inflammatory cytokines, oxidative stress, and mucus and collagen production were measured. As expected, the COPD rats had developed emphysema, inflammation, and deterioration in lung function. PM2.5 exposure resulted in greater lung function decline and histopathological changes, as reflected by increased Mucin (MUC) 5ac, MUC5b, Collagen I, Collagen III, and the profibrotic cytokine α-smooth muscle-actin (SMA), transforming growth factor- (TGF-) β1 in lung tissues. PM2.5 also aggravated inflammation, increasing neutrophils and eosinophils in bronchoalveolar lavage fluid (BALF) and cytokines including Interleukin- (IL-) 1β, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-4. The likely mechanism is through oxidative stress as antioxidants levels were decreased, whereas oxidants were increased, indicating a detrimental shift in the oxidant-antioxidant balance. Altogether, these results suggest that PM2.5 exposure could promote the development of COPD by impairing lung function and exacerbating pulmonary injury, and the potential mechanisms are related to inflammatory response and oxidative stress.

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“…Thus, short-term changes in ozone levels have been associated with increased mortality ( 1 , 2 ), and a positive association between ozone and hospital admissions for asthma and COPD in the elderly and between ozone levels and asthma emergency visits in children ( 3 , 4 ). Indeed, more recent studies have linked long-term exposure to ozone with reduced lung function and an increasing risk of developing emphysema irrespective of being a cigarette smoker ( 5 , 6 ).…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease

et al. 2020

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Oxidative stress plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD) caused by cigarette smoke and characterized by chronic inflammation, alveolar destruction (emphysema) and bronchiolar obstruction. Ozone is a gaseous constituent of urban air pollution resulting from photochemical interaction of air pollutants such as nitrogen oxide and organic compounds. While acute exposure to ozone induces airway hyperreactivity and neutrophilic inflammation, chronic ozone exposure in mice causes activation of oxidative pathways resulting in cell death and a chronic bronchial inflammation with emphysema, mimicking cigarette smoke-induced COPD. Therefore, the chronic exposure to ozone has become a model for studying COPD. We review recent data on mechanisms of ozone induced lung disease focusing on pathways causing chronic respiratory epithelial cell injury, cell death, alveolar destruction, and tissue remodeling associated with the development of chronic inflammation and AHR. The initial oxidant insult may result from direct effects on the integrity of membranes and organelles of exposed epithelial cells in the airways causing a stress response with the release of mitochondrial reactive oxygen species (ROS), DNA, and proteases. Mitochondrial ROS and mitochondrial DNA activate NLRP3 inflammasome and the DNA sensors cGAS and STING accelerating cell death pathways including caspases with inflammation enhancing alveolar septa destruction, remodeling, and fibrosis. Inhibitors of mitochondrial ROS, NLRP3 inflammasome, DNA sensor, cell death pathways, and IL-1 represent novel therapeutic targets for chronic airways diseases underlined by oxidative stress.

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Association of Long-term Ambient Ozone Exposure With Respiratory Morbidity in Smokers

Cited by 60 publications

References 46 publications

Health Effects of Ozone on Respiratory Diseases

Health Effects of Ozone on Respiratory Diseases

Exposure to Air Pollution Exacerbates Inflammation in Rats with Preexisting COPD

Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease

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