The influence of the environment on human biology is unquestionable. Changes in climate, energy production, the degree of noise, type of food intake and the air we breathe have a decisive impact on human health, at the intersection of meteorology, atmospheric and oceanic sciences, toxicology and medicine. Thus, exposure to air pollutants is associated with increased morbidity and mortality worldwide. Deaths are largely due to increased cardiovascular and cerebrovascular diseases of an ischemic nature, including acute coronary events, stroke and arrhythmias. These appear to occur in the setting of a common atherothrombotic substrate. While both particulate and gaseous components have been associated with cardiovascular pathology, epidemiological studies show stronger associations with fine particulate matter (PM) with an aerodynamic diameter < 2.5 µm (PM2.5). A large body of evidence, employing hyperlipidemic animal models, supports the causal link between PM exposure and atherosclerosis. In addition, recent epidemiological and experimental studies support the causal association between PM exposure and various metabolic endpoints including insulin resistance, diabetes and fatty liver disease. However, the pathogenic mechanisms how PM induces all this cardiometabolic toxicity remain unknown. Our recent work has allowed us to identify effects induced by motor vehicle emissions on lipid metabolism and liver steatosis, and alteration in cellular respiration. This talk summarizes our efforts to dissect molecular pathways responsible for the induction of cardiometabolic effects, with especial attention to the disturbance of mitochondrial processes.