Background: Accumulating evidence suggests that individuals with glucose metabolism disorders are susceptible to mortality associated with fine particles. However, the mechanisms remain largely unknown.
Objectives: We examined whether particle-associated respiratory inflammation differed between individuals with prediabetes and healthy control participants.
Methods: Based on a panel study [A prospective Study COmparing the cardiometabolic and respiratory effects of air Pollution Exposure on healthy and prediabetic individuals (SCOPE)] conducted in Beijing between August 2013 and February 2015, fractional exhaled nitric oxide (FeNO) was measured from 112 participants at two to seven visits to indicate respiratory inflammation. Particulate pollutants-including particulate matter with an aerodynamic diameter of (), black carbon (BC), ultrafine particles (UFPs), and accumulated-mode particles-were monitored continuously at a single central monitoring site. Linear mixed-effects models were used to estimate associations between ln-FeNO with pollutant concentrations at individual 1-h lags (up to 24 h) and with average concentrations at 8 and 24 h before the clinical visit. We evaluated glucose metabolism disorders as a potential modifier by comparing associations between participants with high vs. low average fasting blood glucose (FBG) and homeostasis model assessment insulin resistance (HOMA-IR) levels.
Results: FeNO was positively associated with all pollutants, with the strongest associations for an interquartile range increase in 1-h lagged exposures (ranging from 21.3% for to 74.7% for BC). Associations differed significantly according to average HOMA-IR values when lagged 6-18 h for , 15-19 h for BC, and 6-15 h for UFPs, with positive associations among those with while associations were closer to the null or inverse among those with . Associations between and FeNO were consistently higher among individuals with average vs. low FBG, with significant differences for multiple hourly lags.
Discussion: Glucose metabolism disorders may aggravate respiratory inflammation following exposure to ambient particulate matter. https://doi.org/10.1289/EHP4906.