Abstract Exposure to environmental pollutants during key stages of development increases the risk of disease later in life. One such toxicant with growing evidence of this response is the air pollutant, ozone (O3). Exposure to O3 during the implantation receptivity period in rats affects the metabolic status of offspring at adolescence, which may increase their susceptibility to subsequent environmental exposures. Herein, we studied the impacts of maternal O3 exposure on postnatal systemic responses to O3 in male and female offspring. Following peri-implantation O3 exposure (0.8 ppm for 4 hours/day on gestation days 5 and 6), offspring were exposed to O3 for 1 day/week on postnatal weeks 5–7. After the final exposure, metabolic effects were analyzed by circulating hormones and clinical chemistries, as well as hepatic lipid status and transcriptomic alterations. By and large, male offspring from O3-exposed dams were more greatly impacted than those from air-exposed dams. This included increased hepatic lipid mobilization, increased circulating glucose, and a robust number of differentially expressed genes (2,348). Interestingly, many of these transcriptomic differences were attributed to maternal O3 exposure, with 1,741 of these genes sharing directional similarity with postnatally exposed air littermates. Females, on the other hand, reported minimal baseline effects of maternal O3 exposure (108). However, postnatal O3 exposure in female offspring substantially increased these differences to 947 genes. Collectively, this work supports the growing evidence that early pregnancy exposure to O3 alters the metabolic development of the offspring. Furthermore, postnatal exposure to environmental stressors reveals hepatic susceptibilities that are sexually dimorphic.
Dye et al. (Wed,) studied this question.