Short-term ozone exposure and asthma severity: Weight-of-evidence analysis

Goodman, Julie E.; Zu, Ke; Loftus, Christine T.; Lynch, Heather N.; Prueitt, Robyn L.; Mohar, Isaac; Shubin, Sara Pacheco; Sax, Sonja N.

doi:10.1016/j.envres.2017.10.018

Cited by 33 publications

(24 citation statements)

References 37 publications

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“…After days during which ambient ozone concentrations are high, emergency room visits and hospitalizations for asthma increase (Fauroux, Sampil, Quénel, & Lemoullec, ). In human studies, ozone exposure causes asthma symptoms (Goodman et al, ), decreases in pulmonary function (Yang et al, ), and also causes airway hyperresponsiveness (AHR), a characteristic feature of asthma (Foster, Brown, Macri, & Mitchell, ). Ozone recruits neutrophils to the airways and increases the production of acute phase cytokines and chemokines (Balmes et al, ).…”

Section: Introductionmentioning

confidence: 99%

Early life microbiome perturbation alters pulmonary responses to ozone in male mice

Brown¹,

Tashiro²,

Kasahara³

et al. 2020

Physiol Rep

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Early life changes in the microbiome contribute to the development of allergic asthma, but little is known about the importance of the microbiome for other forms of asthma. Ozone is a nonatopic asthma trigger that causes airway hyperresponsiveness and neutrophil recruitment to the lungs. The purpose of this study was to test the hypothesis that early life perturbations in the gut microbiome influence subsequent responses to ozone. To that end, we placed weanling mouse pups from The Jackson Laboratories or from Taconic Farms in sex‐specific cages either with other mice from the same vendor (same‐housed) or with mice from the opposite vendor (cohoused). Mice were maintained with these cagemates until use. The gut microbial community differs in mice from Jackson Labs and Taconic Farms, and cohousing mice transfers fecal microbiota from one mouse to another. Indeed, 16S rRNA sequencing of fecal DNA indicated that differences in the gut microbiomes of Jackson and Taconic same‐housed mice were largely abolished when the mice were cohoused. At 10–12 weeks of age, mice were exposed to room air or ozone (2 ppm for 3 hr). Compared to same‐housed mice, cohoused male but not female mice had reduced ozone‐induced airway hyperresponsiveness and reduced ozone‐induced increases in bronchoalveolar lavage neutrophils. Ozone‐induced airway hyperresponsiveness was greater in male than in female mice and the sex difference was largely abolished in cohoused mice. The data indicate a role for early life microbial perturbations in pulmonary responses to a nonallergic asthma trigger.

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Section: Introductionmentioning

confidence: 99%

Early life microbiome perturbation alters pulmonary responses to ozone in male mice

Brown¹,

Tashiro²,

Kasahara³

et al. 2020

Physiol Rep

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“…Upon inhalation, O3 causes pulmonary inflammation (ARIS 1993;DEVLIN 1996), decreased lung function (SCHELEGLE et al 2009;KIM et al 2011), and impaired epithelial barrier integrity (KEHRL et al 1987;DEVLIN 1997). Together, these effects contribute to the incidence and exacerbation of chronic respiratory diseases including asthma and chronic obstructive pulmonary disease (COPD) (MCCONNELL 2002;KELLY AND FUSSELL 2011;GOODMAN et al 2018;ZU et al 2018).…”

Section: Introductionmentioning

confidence: 99%

Transcriptional profiling of the murine airway response to acute ozone exposure

Tovar

Smith

Thomas

et al. 2019

Preprint

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Exposure to ambient ozone (O3) pollution causes airway inflammation, epithelial injury, and decreased lung function. Long-term exposure is associated with increased mortality and exacerbations of respiratory conditions. While the adverse health effects of O3 exposure have been thoroughly described, less is known about the molecular processes that drive these outcomes. The aim of this study was to describe the cellular and molecular alterations observed in murine airways after exposure to either 1 or 2 ppm O3. After exposing adult, female C57BL/6J mice to filtered air, 1 or 2 ppm O3 for 3 hours, we assessed hallmark responses including airway inflammatory cell counts, epithelial permeability, cytokine secretion, and morphological alterations of the large airways. Further, we performed RNA-seq to profile gene expression in two critical tissues involved in O3 responses: conducting airways (CA) and airway macrophages (AM). We observed a concentration-dependent increase in airway inflammation and injury, and a large number of genes were differentially expressed in both target tissues at both concentrations of O3. Genes that were differentially expressed in CA were generally associated with barrier function, detoxification processes, and cellular proliferation. The differentially expressed genes in AM were associated with innate immune signaling, cytokine production, and extracellular matrix remodeling. Overall, our study has described transcriptional responses to acute O3 exposure, revealing both shared and unique gene expression patterns across multiple concentrations of O3 and in two important O3-responsive tissues. These profiles provide broad mechanistic insight into pulmonary O3 toxicity, and reveal a variety of targets for refined followup studies.

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“…The average ozone concentration in Nanjing has increased by over 25% in the last five years [1]. Numerous studies have suggested that too much exposure to ozone may cause respiratory morbidity, impaired lung function, local or systemic inflammation, cardiovascular disease, and cancer in human beings [2,3,4,5,6,7].…”

Section: Introductionmentioning

confidence: 99%

Contributions of Indoor and Outdoor Sources to Ozone in Residential Buildings in Nanjing

Huang

Yang

Gao

2019

IJERPH

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Ozone has become one of the most serious air pollutants in China in recent years. Since people spend most of their time indoors, the ozone in the indoor environment could be a major factor affecting the occupants’ health. The indoor ozone in residential buildings mainly comes from two sources: outdoor atmosphere and indoor ozone produced by electrical devices. In this study, a typical residence in Nanjing was taken as an example to calculate and compare the contributions of indoor and outdoor sources to ozone in the building. A questionnaire survey about the type, the placement, and the frequency of use of the ozone emission devices was performed to provide the basis for the settings of indoor ozone sources. The multi-zone software CONTAM was used hourly to simulate the ozone concentration in summer and in winter with inner doors either closed or open, and it was noted whether there were ozone emission devices indoors or not. Source contribution was quantified and compared by three methods in this paper: (1) the average indoor/outdoor (I/O) ratio, (2) the I/O ratio frequency, and (3) the ratio of indoor ozone concentration without ozone sources to that with ozone sources. The results showed that the contribution of outdoor sources was much greater than that of indoor sources in summer, but in winter, the frequency of I/O > 1 could reach 55.8% of the total seasonal time, and the ratio of indoor ozone concentration without sources to that with sources could reach as high as 74.3%. This meant that the indoor concentration had the potential to exceed the outdoor. Furthermore, human respiratory exposure in different ages and genders was calculated. It was found that teenagers aged 10–18 years old and female adults had a higher respiratory exposure level.

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Short-term ozone exposure and asthma severity: Weight-of-evidence analysis

Cited by 33 publications

References 37 publications

Early life microbiome perturbation alters pulmonary responses to ozone in male mice

Early life microbiome perturbation alters pulmonary responses to ozone in male mice

Transcriptional profiling of the murine airway response to acute ozone exposure

Contributions of Indoor and Outdoor Sources to Ozone in Residential Buildings in Nanjing

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