Early-life ozone exposure associated with asthma without sensitization in Latino children

Nishimura, Katherine K.; Iwanaga, Kensho; Oh, Sam S.; Pino-Yanes, María; Eng, Celeste; Keswani, Anjeni; Roth, Lindsey A.; Nguyen, Elizabeth A.; Thyne, Shannon; Farber, Harold J.; Serebrisky, Denise; Meade, Kelley; LeNoir, Michael A.; Rodríguez-Cintrón, William; Borrell, Luisa N.; Bibbins‐Domingo, Kirsten; Lurmann, Fred; Sen, Sáunak; Rodríguez‐Santana, José; Brigino-Buenaventura, Emerita; Avila, Pedro C.; Balmes, John R.; Kumar, Rajesh; Burchard, Esteban G.

doi:10.1016/j.jaci.2016.03.058

Cited by 19 publications

(16 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, repeated O 3 exposures may induce a nonatopic asthma phenotype characterized by innate type 2 immunity, eosinophilic inflammation, and mucous cell metaplasia. These findings provide plausible paradigms for biological mechanisms underlying the epidemiologically identified associations between airway eosinophilic inflammation and new onset of nonatopic asthma (106,107). In addition, after this Workshop was conducted in May 2018, another study evaluated the current scientific evidence of a causal link between DEP and asthma, and found consistent evidence of physiological mechanisms by which DEPs can cause new asthma (108).…”

Section: A Mechanism For Nonatopic Asthmamentioning

confidence: 87%

Outdoor Air Pollution and New-Onset Airway Disease. An Official American Thoracic Society Workshop Report

Thurston¹,

Balmes²,

Garcia³

et al. 2020

Annals ATS

Self Cite

143

View full text Add to dashboard Cite

Although it is well accepted that air pollution exposure exacerbates preexisting airway disease, it has not been firmly established that long-term pollution exposure increases the risk of new-onset asthma or chronic obstruction pulmonary disease (COPD). This Workshop brought together experts on mechanistic, epidemiological, and clinical aspects of airway disease to review current knowledge regarding whether air pollution is a causal factor in the development of asthma and/or COPD. Speakers presented recent evidence in their respective areas of expertise related to air pollution and new airway disease incidence, followed by interactive discussions. A writing committee summarized their collective findings. The Epidemiology Group found that long-term exposure to air pollution, especially metrics of traffic-related air pollution such as nitrogen dioxide and black carbon, is associated with onset of childhood asthma. However, the evidence for a causal role in adultonset asthma or COPD remains insufficient. The Mechanistic Group concluded that air pollution exposure can cause airway remodeling, which can lead to asthma or COPD, as well as asthma-like phenotypes that worsen with long-term exposure to air pollution, especially fine particulate matter and ozone. The Clinical Group concluded that air pollution is a plausible contributor to the onset of both asthma and COPD. Available evidence indicates that long-term exposure to air pollution is a cause of childhood asthma, but the evidence for a similar determination for adult asthma or COPD remains insufficient. Further research is needed to elucidate the exact biological mechanism underlying incident childhood asthma, and the specific air pollutant that causes it.

show abstract

Section: A Mechanism For Nonatopic Asthmamentioning

confidence: 87%

Outdoor Air Pollution and New-Onset Airway Disease. An Official American Thoracic Society Workshop Report

Thurston¹,

Balmes²,

Garcia³

et al. 2020

Annals ATS

Self Cite

143

View full text Add to dashboard Cite

show abstract

“…Given the connection of other AAPs such as O 3 to asthma risk, other exposures should be considered in future studies. [70,71] In addition, other prenatal exposure metrics should be considered such as exhaled FeNO, which could provide more direct indication of maternal respiratory inflammation. Future studies should also consider an interaction between prenatal AAP exposure and maternal stress.…”

Section: Discussionmentioning

confidence: 99%

Ambient Air Pollution and Asthma-Related Outcomes in Children of Color of the USA: a Scoping Review of Literature Published Between 2013 and 2017

Nardone

Neophytou

Balmes

et al. 2018

Curr Allergy Asthma Rep

View full text Add to dashboard Cite

AAP is likely a key contributor to the excess burden of asthma in children of color due to pervasive exposure before birth, at home, and in school. Recent findings suggest that psychosocial stressors may modify the relationship between AAP and asthma. The effect of AAP on asthma in children of color is likely modulated by multiple unique psychosocial stressors and gene-environment interactions. Although children of color are being included in asthma studies, more research is still needed on impacts of specific criteria pollutants throughout the life course. Additionally, future studies should consider historical factors when analyzing current exposure profiles.

show abstract

“…Although associations between human exposures to elevated levels of ambient ozone and the new onset of chronic airway diseases such as asthma have been epidemiologically identified, 66 few toxicology-based models have been proposed for the toxicologic pathobiology responsible for air pollutant-driven respiratory diseases. Figure 5 summarizes our proposed ILC2-dependent paradigm for the development of airway mucous cell metaplasia, eosinophilic inflammation, and type 2 immunity in mice repeatedly exposed to ozone—a novel model for the new onset of nonallergic rhinitis and asthma associated with exposures to high ambient concentrations of ozone in children living in areas with repeated occurrences of photochemical air pollution (smog).…”

Section: Summary Conclusion and Future Studiesmentioning

confidence: 99%

Innate Lymphoid Cell–Dependent Airway Epithelial and Inflammatory Responses to Inhaled Ozone: A New Paradigm in Pathogenesis

Harkema

Wagner

2019

Toxicol Pathol

View full text Add to dashboard Cite

Epidemiological associations have been made between the new onset of childhood rhinitis/asthma and exposures to elevated ambient levels of ozone, a commonly encountered gaseous air pollutant. Our laboratory was the first to find that mice repeatedly exposed to ozone develop nasal type 2 immunity and eosinophilic rhinitis with mucous cell metaplasia. More recently, we have found that these ozone-induced upper airway alterations are mediated by group 2 innate lymphoid cells (ILC2s) and not by T and B cells that are important in adaptive immune responses typically associated with allergic rhinitis and asthma. Furthermore, repeated exposures of mice to ozone cause ILC2-mediated type 2 immunity and airway pathology in the lungs, like those found in the nasal airways. Our recent findings in ozone-exposed mice complement and extend previous reports of nonallergic nasal airway disease in ozone-exposed rats and nonhuman primates. Overall, these experimental results in laboratory animals suggest a plausible ILC2-dependent paradigm for the toxicologic pathobiology that underlies the development of nonallergic rhinitis/asthma in children who live in environments with repeated occurrences of high ambient concentrations of ozone.

show abstract

Early-life ozone exposure associated with asthma without sensitization in Latino children

Cited by 19 publications

References 9 publications

Outdoor Air Pollution and New-Onset Airway Disease. An Official American Thoracic Society Workshop Report

Outdoor Air Pollution and New-Onset Airway Disease. An Official American Thoracic Society Workshop Report

Ambient Air Pollution and Asthma-Related Outcomes in Children of Color of the USA: a Scoping Review of Literature Published Between 2013 and 2017

Innate Lymphoid Cell–Dependent Airway Epithelial and Inflammatory Responses to Inhaled Ozone: A New Paradigm in Pathogenesis

Contact Info

Product

Resources

About