气候变化领域集成服务门户

Epidemiological and experimental data suggest that obesity exacerbates the health effects of air pollutants such as ozone (O-3). Maternal inactivity and calorically rich diets lead to offspring that show signs of obesity. Exacerbated O-3 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 O-3 for two consecutive days (0.8ppm, 4h/day). Glucose tolerance tests (GTT), ventilatory parameters (plethysmography), and bronchoalveolar fluid (BALF) cell counts and protein biomarkers were performed to assess response to O-3. Exercise and diet altered body weight and %fat of young offspring. GTT, ventilation and BALF cell counts were exacerbated by O-3 with responses markedly exacerbated in males. HF diet and O-3 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 O-3 exposure and exhibited exacerbated GTT responses. Ventilatory dysfunction was also exacerbated in males. Maternal exercise had minimal effects on O-3 response. The results of this exploratory study suggest a link between maternal obesity and susceptibility to O-3 in their adult offspring in a sex-specific manner.