IMPORTANCE Environmental risk factors for childhood type 2 diabetes, an increasing global problem, are understudied. Air pollution exposure has been reported to be a risk factor for this condition. OBJECTIVE To examine the association between prenatal and perinatal exposures to fine particulate matter with a diameter less than 2.5 μm (PM 2.5) and changes in hemoglobin A 1c (HbA 1c), a measure of glycated hemoglobin and marker of glucose dysregulation, in children aged 4 to 7 years. DESIGN, SETTING, AND PARTICIPANTS The Programming Research in Obesity, Growth, Environment, and Social Stressors (PROGRESS) study, a birth cohort study conducted in Mexico City, Mexico, recruited pregnant women from July 3, 2007, to February 21, 2011, through public health maternity clinics. The present analysis includes 365 mother-child pairs followed up until the child was approximately 7 years of age. This study included data from only study visits at approximately 4 to 5 years (visit 1) and 6 to 7 years (visit 2) post partum because HbA 1c levels were not measured in earlier visits. The data were analyzed from March 11, 2018, to May 3, 2019. EXPOSURES Daily PM 2.5 exposure estimates at participants' home addresses from 4 weeks prior to mothers' date of last menstrual period (LMP), a marker of the beginning of pregnancy, to 12 weeks after the due date. Exposure was estimated from satellite measurements and calibrated against ground PM 2.5 measurements, land use, and meteorological variables. MAIN OUTCOMES AND MEASURES Outcomes included HbA 1c levels at 4 to 5 years and 6 to 7 years of age, and the change in the level from the former age group to the latter. RESULTS The sample included 365 children, of whom 184 (50.4%) were girls. The mean (range) age of the children was 4.8 (4.0-6.4) years at visit 1, and 6.7 (6.0-9.7) years at visit 2. At the time of delivery, the mean (range) age of the mothers was 27.7 (18.3-44.4) years, with a mean (range) prepregnancy body mass index of 26.4 (18.5-43.5). The mean (SD) prenatal PM 2.5 exposure (22.4 μg/m 3 [2.7 μg/m 3 ]) was associated with an annual increase in HbA 1c levels of 0.25% (95% CI,