Respiratory Responses to Ozone Exposure. MOSES (The Multicenter Ozone Study in Older Subjects)

Arjomandi, Mehrdad; Balmes, John R.; Frampton, Mark W.; Bromberg, Philip A.; Rich, David Q.; Stark, Paul C.; Alexis, Neil E.; Costantini, Maria; Hollenbeck-Pringle, Danielle; Dagincourt, Nicholas; Hazucha, Milan J.

doi:10.1164/rccm.201708-1613oc

Cited by 56 publications

(31 citation statements)

References 38 publications

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“…Ozone enhanced plasma CC16 levels and sputum neutrophilia in a dose-dependent manner after 4 h and sputum neutrophil counts correlated with airway biopsy counts (56). Sputum neutrophilia returned to normal levels 18 h post-ozone exposure (55, 56). Worryingly, concentrations of ozone close to the National Ambient Air Quality Standard (0.06 ppm) decreased lung function and increased airway inflammation in healthy young adults (57).…”

Section: Epidemiological Impact Of Ozone In Healthy and At Risk Subjectsmentioning

confidence: 93%

“…Controlled exposure studies support these epidemiological reports. The recent Multicenter Ozone Study in Older Subjects (MOSES) examined the respiratory responses to low concentrations of ozone in 87 healthy adults aged 60 years (55). Exposure to filtered air rapidly increased mean FEV 1 and FVC values but ozone attenuated these increases in a dose-dependent manner.…”

Section: Epidemiological Impact Of Ozone In Healthy and At Risk Subjectsmentioning

confidence: 99%

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Transcriptional Effects of Ozone and Impact on Airway Inflammation

2019

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Epidemiological and challenge studies in healthy subjects and in individuals with asthma highlight the health impact of environmental ozone even at levels considered safe. Acute ozone exposure in man results in sputum neutrophilia in 30% of subjects particularly young children, females, and those with ongoing cardiopulmonary disease. This may be associated with systemic inflammation although not in all cases. Chronic exposure amplifies these effects and can result in the formation of asthma-like symptoms and immunopathology. Asthmatic patients who respond to ozone (responders) induce a greater number of genes in bronchoalveolar (BAL) macrophages than healthy responders with up-regulation of inflammatory and immune pathways under the control of cytokines and chemokines and the enhanced expression of remodeling and repair programmes including those associated with protease imbalances and cell-cell adhesion. These pathways are under the control of several key transcription regulatory factors including nuclear factor (NF)-κB, anti-oxidant factors such as nuclear factor (erythroid-derived 2)-like 2 NRF2, the p38 mitogen activated protein kinase (MAPK), and priming of the immune system by up-regulating toll-like receptor (TLR) expression. Murine and cellular models of acute and chronic ozone exposure recapitulate the inflammatory effects seen in humans and enable the elucidation of key transcriptional pathways. These studies emphasize the importance of distinct transcriptional networks in driving the detrimental effects of ozone. Studies indicate the critical role of mediators including IL-1, IL-17, and IL-33 in driving ozone effects on airway inflammation, remodeling and hyperresponsiveness. Transcription analysis and proof of mechanisms studies will enable the development of drugs to ameliorate the effects of ozone exposure in susceptible individuals.

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Section: Epidemiological Impact Of Ozone In Healthy and At Risk Subjectsmentioning

confidence: 93%

Section: Epidemiological Impact Of Ozone In Healthy and At Risk Subjectsmentioning

confidence: 99%

Transcriptional Effects of Ozone and Impact on Airway Inflammation

2019

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“…Secondary outcomes included markers of oxidative stress and endothelial function. Ozone effects on pulmonary and cardiovascular function in this study are reported elsewhere [34–36].…”

Section: Introductionmentioning

confidence: 90%

Ozone effects on blood biomarkers of systemic inflammation, oxidative stress, endothelial function, and thrombosis: The Multicenter Ozone Study in oldEr Subjects (MOSES)

et al. 2019

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The evidence that exposure to ozone air pollution causes acute cardiovascular effects is mixed. We postulated that exposure to ambient levels of ozone would increase blood markers of systemic inflammation, prothrombotic state, oxidative stress, and vascular dysfunction in healthy older subjects, and that absence of the glutathione S-transferase Mu 1 (GSTM1) gene would confer increased susceptibility. This double-blind, randomized, crossover study of 87 healthy volunteers 55–70 years of age was conducted at three sites using a common protocol. Subjects were exposed for 3 h in random order to 0 parts per billion (ppb) (filtered air), 70 ppb, and 120 ppb ozone, alternating 15 min of moderate exercise and rest. Blood was obtained the day before, approximately 4 h after, and approximately 22 h after each exposure. Linear mixed effect and logistic regression models evaluated the impact of exposure to ozone on pre-specified primary and secondary outcomes. The definition of statistical significance was p<0.01. There were no effects of ozone on the three primary markers of systemic inflammation and a prothrombotic state: C-reactive protein, monocyte-platelet conjugates, and microparticle-associated tissue factor activity. However, among the secondary endpoints, endothelin-1, a potent vasoconstrictor, increased from pre- to post-exposure with ozone concentration (120 vs 0 ppb: 0.07 pg/mL, 95% confidence interval [CI] 0.01, 0.14; 70 vs 0 ppb: -0.03 pg/mL, CI -0.09, 0.04; p = 0.008). Nitrotyrosine, a marker of oxidative and nitrosative stress, decreased with increasing ozone concentrations, with marginal significance (120 vs 0 ppb: -41.5, CI -70.1, -12.8; 70 vs 0 ppb: -14.2, CI -42.7, 14.2; p = 0.017). GSTM1 status did not modify the effect of ozone exposure on any of the outcomes. These findings from healthy older adults fail to identify any mechanistic basis for the epidemiologically described cardiovascular effects of exposure to ozone. The findings, however, may not be applicable to adults with cardiovascular disease.

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“…Many previous studies also claimed that air pollutants like carbon monoxide, NO 2 , particulate matter (PM) in dissimilar fractions such as PM 0.1 μm, PM 2.5 μm and PM 10 μm, polycyclic aromatic hydrocarbons, volatile organic compounds, and O 3 pollution, etc. Adversely affect the immune and cardio-respiratory systems of the host by altering their resistance to various bacterial and viral infections ( Arjomandi et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Asymmetric link between environmental pollution and COVID-19 in the top ten affected states of US: A novel estimations from quantile-on-quantile approach

Razzaq

Sharif

Aziz

et al. 2020

Environmental Research

128

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This study draws the link between COVID-19 and air pollution (ground ozone O 3 ) from February 29, 2020 to July 10, 2020 in the top 10 affected States of the US. Utilizing quantile-on-quantile (QQ) estimation technique, we examine in what manner the quantiles of COVID-19 affect the quantiles of air pollution and vice versa. The primary findings confirm overall dependence between COVID-19 and air pollution. Empirical results exhibit a strong negative effect of COVID-19 on air pollution in New York, Texas, Illinois, Massachusetts, and Pennsylvania; especially at medium to higher quantiles, while New Jersey, Illinois, Arizona, and Georgia show strong negative effect mainly at lower quantiles. Contrarily, COVID-19 positively affects air pollution in Pennsylvania at extreme lower quantiles. On the other side, air pollution predominantly caused to increase in the intensity of COVID-19 cases across all states except lower quantiles of Massachusetts, and extreme higher quantiles of Arizona and New Jersey, where this effect becomes less pronounced or negative. Concludingly, a rare positive fallout of COVID-19 is reducing environmental pressure, while higher environmental pollution causes to increase the vulnerability of COVID-19 cases. These findings imply that air pollution is at the heart of chronic diseases, therefore the state government should consider these asymmetric channels and introduce appropriate policy measures to reset and control atmospheric emissions.

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Respiratory Responses to Ozone Exposure. MOSES (The Multicenter Ozone Study in Older Subjects)

Abstract: Exposure to ozone at near ambient levels induced lung function effects, airway injury, and airway inflammation in older healthy adults. Clinical trial registered with www.clinicaltrials.gov (NCT01487005).

Cited by 56 publications

References 38 publications

Transcriptional Effects of Ozone and Impact on Airway Inflammation

Transcriptional Effects of Ozone and Impact on Airway Inflammation

Ozone effects on blood biomarkers of systemic inflammation, oxidative stress, endothelial function, and thrombosis: The Multicenter Ozone Study in oldEr Subjects (MOSES)

Asymmetric link between environmental pollution and COVID-19 in the top ten affected states of US: A novel estimations from quantile-on-quantile approach

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