Effects of maternal high-fat diet and sedentary lifestyle on susceptibility of adult offspring to ozone exposure in rats

Epidemiological and experimental data suggest that obesity exacerbates the health effects of air pollutants such as ozone (O₃). Maternal inactivity and calorically rich diets lead to offspring that show signs of obesity. Exacerbated O₃ susceptibility of offspring could thus be manifested by maternal obesity. Thirty-day-old female Long-Evans rats were fed a control (CD) or high-fat (HF) (60% calories) diet for 6 wks and then bred. GD1 rats were then housed with a running wheel (RW) or without a wheel (SED) until parturition, creating four groups of offspring: CD-SED, CD-RW, HF-SED and HF-RW. HF diet was terminated at PND 35 and all offspring were placed on CD. Body weight and %fat of dams were greatest in order; HF-SED?>?HF-RW?>?CD-SED?>?CD-RW. Adult offspring were exposed to O₃ for two consecutive days (0.8?ppm, 4?h/day). Glucose tolerance tests (GTT), ventilatory parameters (plethysmography), and bronchoalveolar fluid (BALF) cell counts and protein biomarkers were performed to assess response to O₃. Exercise and diet altered body weight and %fat of young offspring. GTT, ventilation and BALF cell counts were exacerbated by O₃ with responses markedly exacerbated in males. HF diet and O₃ led to significant exacerbation of several BALF parameters: total cell count, neutrophils and lymphocytes were increased in male HF-SED versus CD-SED. Males were hyperglycemic after O₃ exposure and exhibited exacerbated GTT responses. Ventilatory dysfunction was also exacerbated in males. Maternal exercise had minimal effects on O₃ response. The results of this exploratory study suggest a link between maternal obesity and susceptibility to O₃ in their adult offspring in a sex-specific manner.