Exposure to O3 during pregnancy and offspring asthma induced by OVA: Sensitive window identification

Xinai Liu; Lingling Fu; Xiwei Yang; Zhiping Wang

doi:10.1016/j.envpol.2020.116297

Exposure to O₃ during pregnancy and offspring asthma induced by OVA: Sensitive window identification

Environ Pollut. 2021 Feb 1:270:116297. doi: 10.1016/j.envpol.2020.116297. Epub 2020 Dec 13.

Authors

Xinai Liu¹, Lingling Fu¹, Xiwei Yang¹, Zhiping Wang²

Affiliations

¹ Department of Occupational and Environmental Health, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China.
² Department of Occupational and Environmental Health, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China. Electronic address: zhipingw@sdu.edu.cn.

PMID: 33348144
DOI: 10.1016/j.envpol.2020.116297

Abstract

Background: Evidence proved that gestational ozone (O₃) exposure can increase the risk of neonatal adverse respiratory outcomes, but offspring asthma is unclear.

Objective: This study aimed to investigate whether gestational O₃ exposure could exacerbate offspring asthma, and to research the differences in effects of O₃ exposure at different gestational periods on offspring asthma.

Methods: The pregnant ICR mice were randomly grouped and were administered O₃ (air as control) at gestational day (GD) 1-6, 7-12, and 13-18, respectively. The pups aged 2-4 weeks were treated with ovalbumin (OVA) to establish a model of early life asthma. Asthma characteristics such as pulmonary inflammation, goblet cell proliferation, airway remodeling, OVA-specific immunoglobulin (Ig) E secretion and cytokines were examined.

Results: OVA sensitization and challenge successfully induced asthma in offspring. Compared with the air control, pulmonary inflammation infiltration, mucous secretion, the concentration of OVA-specific IgE, the level of tumor necrosis factor (TNF)-α, and T helper (Th) 2-skewed response were significantly exacerbated when O₃ exposure at GD13-18 following inhaling OVA, while pulmonary inflammatory infiltration, mucus secretion, and Th2-skewed response were not significantly changed when O₃ exposure at both GD1-6 and GD7-12. What's more, the above indicators in asthmatic offspring due to O₃ exposure at GD13-18 were more severe than at GD1-6 and GD7-12. Interestingly, the signs of asthma only appeared in the offspring after OVA inhalation. When offspring were not treated with OVA, the prenatal O₃ exposure alone did not lead to asthmatic reactions in offspring. In addition, O₃ exposure at GD13-18 markedly increased the number of neutrophils and macrophages in Bronchoalveolar Lavage Fluid (BALF) of asthmatic offspring, and significantly exacerbated Th2 immune imbalance in asthmatic offspring, but had no effect on Th17 immune imbalance.

Conclusion: Exposure to O₃ during pregnancy aggravated asthma in offspring, in which the third trimester is the most sensitive window.

Keywords: Asthma; Ozone; Prenatal exposure; Sensitive window.

MeSH terms

Animals
Asthma* / chemically induced
Bronchoalveolar Lavage Fluid
Disease Models, Animal
Female
Lung
Mice
Mice, Inbred BALB C
Mice, Inbred ICR
Ovalbumin
Pregnancy

Substances

Ovalbumin