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.

本研究旨在调查产前联合暴露于空气污染物对子代小鼠哮喘发展的影响，并划定敏感暴露窗口。怀孕的 ICR 小鼠分别在妊娠第 1-6、7-12、13-18 和 1-18 天（GD）暴露于空气复合污染物或清洁空气中。2-4 周龄的子代小鼠接受卵清蛋白 (OVA) 或生理盐水致敏和攻击。检查幼犬的哮喘特征，如气道高反应性 (AHR)、肺部炎症、粘液分泌、OVA 特异性免疫球蛋白 (Ig) E 水平和细胞因子水平。利用OVA成功建立子代哮喘模型。在 OVA 诱发的哮喘后代中，母体在 GD7-12 时暴露于大气复合污染物显着增加了 AHR、肺部炎症浸润、粘液分泌、OVA 特异性 IgE 水平、肿瘤坏死因子 (TNF)-α 和 T 辅助细胞水平。 Th) 2 偏斜响应，Th17 偏斜响应除外。GD1-6 母体暴露对后代哮喘影响不大，仅增加哮喘后代的粘液分泌和 TNF-α 水平。GD13-18的母亲暴露对哮喘后代的所有指标均无显着影响。此外，母体在GD1-18时的暴露仅增加了哮喘后代的OVA特异性IgE水平，对其他哮喘指标没有显着影响。重要的是，如果后代没有受到 OVA 的致敏和刺激，怀孕期间接触大气化合物污染物不会引起后代的哮喘反应。怀孕期间接触大气化合物污染物可能会加重子代小鼠 OVA 诱发的哮喘的严重程度，其中妊娠中期是敏感窗口。