Background: Numerous studies suggest that long-term exposure to ambient particulate matter (PM) and nitrogen oxide (NOx) air pollution may be diabetogenic, but little is known about the effects of shorter-term exposures on markers of diabetes risk. Therefore, our objective was to determine whether short- and long-term ambient PM and NOx exposures are associated with glucose, insulin, and insulin resistance measures. Methods: We studied a stratified, random minority oversample of non-diabetic Women’s Health Initiative (WHI) clinical trials participants for whom estimates of fasting glucose, fasting insulin, insulin resistance, and geocoded address-specific daily mean concentrations of PM < 10 μm (PM 10 ), PM < 2.5 μm (PM 2.5 ), and NOx were available at screening and up to three follow-up visits between 1993-2004 (total n=4,019; mean age: 62.2 yr; 24% black; 12% Hispanic; 51% white). We measured insulin resistance using the homeostatic model assessment [HOMA], triglyceride to high-density lipoprotein cholesterol ratio, and the triglyceride-glucose index. We log-transformed the glucose, insulin, and insulin resistance measures, then used multi-level, mixed, longitudinal models weighted for sampling design / attrition and adjusted for sociodemographic, clinical, and meteorological covariates to estimate their associations with 2- and 365-day mean PM 10 and NOx and 365-day mean PM 2.5 concentrations. Results: Measures of glucose homeostasis decreased with short-term exposure to ambient PM 10 . For example, we found a -0.2% (95% confidence interval: -0.4%, 0.1%), -0.9% (-1.7%, -0.1%), and -1.1% (-2.0%, -0.3%) change in glucose, insulin, and HOMA per 10 μg/m 3 increase in the 2-day mean PM 10 concentration. In contrast, we found generally null results per 10 μg/m 3 increase in 365-day mean PM 10 concentration. Measures of glucose homeostasis similarly did not appear to be associated with short- and long-term increases in mean NOx or PM 2.5 concentrations. Conclusion: The findings suggest that responses to ambient exposure to PM 10 in women may be adaptive (i.e. capable of re-establishing normal glucose homeostasis and improving insulin sensitivity) over the short-term. Endoplasmic reticulum stress-response mechanisms involving decreases in protein misfolding may help explain this observed phenomena. Contrary to previous studies, results also suggest that sustained exposure to ambient PM and NOx has nominal influence on glucose homeostasis.