Effects of combined exposure to air pollutants during pregnancy on OVA-induced asthma in offspring and its sensitive window

Abstract

This study aimed to investigate the impact of prenatal combined exposure to air pollutants on asthma development in offspring mice and to delineate the sensitive exposure windows. Pregnant ICR mice were exposed to air compound pollutants or clean air at gestational day (GD) 1–6, 7–12, 13–18, and 1–18, respectively. Offspring mice aged 2–4 weeks received sensitization and challenge with ovalbumin (OVA) or normal saline. Pups were examined for features of asthma such as airway hyperresponsiveness (AHR), pulmonary inflammation, mucus secretion, OVA-specific immunoglobulin (Ig) E levels, and cytokines levels. Asthma model in offspring was successfully established with OVA. In OVA-induced asthmatic offspring, maternal exposure to atmospheric compound pollutants at GD7-12 significantly increased AHR, pulmonary inflammatory infiltration, mucus secretion, OVA-specific IgE levels, the level of tumor necrosis factor (TNF)-α, and T helper (Th) 2-skewed response, except for Th17-skewed response. Maternal exposure at GD1-6 had little effect on asthma in offspring, only increasing mucus secretion and TNF-α level in asthmatic offspring. Maternal exposure at GD13-18 had no significant effect on all indicators of asthmatic offspring. In addition, maternal exposure at GD1-18 only increased OVA-specific IgE levels in asthmatic offspring, with no significant effect on other asthma indicators. Importantly, if offspring were not sensitized and stimulated with OVA, exposure to atmospheric compound pollutants during pregnancy did not cause asthma responses in offspring. Exposure to atmospheric compound pollutants during pregnancy could aggravate the severity of OVA-induced asthma in offspring mice, with the second trimester being the sensitive window.