Compelling evidence indicates that exposure to environmental stressors during the early life or even the preconceptional period may lead to the pathogenesis ofvarious non-communicable diseases, known as the developmental origins (or programming) of health and disease [2]. We previously showed that maternal exposureto CAP throughout the 7-week pre-conceptional periodand the whole gestation and lactation period programsthe male offspring’s development and adulthood adiposity, raising a new health concern over PM2.5 pollution.In the present study, we extended our finding, demonstrating that: (1) maternal pre-conceptional exposure toCAP was sufficient to program the male offspring’s development and adulthood adiposity; and (2) this programming of the male offspring’s development andadulthood adiposity was maternally transmitted crossthree generations (from F0 to F2). These new data notonly identify the vulnerable window for the adverse programming of male offspring’s development and adulthood adiposity by maternal exposure to PM2.5, but alsoprovide a mechanistic insight into this adverse health effect due to exposure to PM2.5.The composition of PM2.5 spatiotemporally varies andmay modulate the health effect due to exposure toPM2.5. We previously demonstrated that the offspring’sdevelopment and adulthood adiposity is persistentlyeffected by maternal exposure to CAP that has a relatively high ratio of Na/Al, which reflects the geographic