Air pollution is the largest environmental risk factor for disease and premature death. Among the different components that are present in polluted air, fine particulate matter below 2.5 μm in diameter (PM_2.5) has been identified as the main hazardous constituent. PM_2.5 mainly arises from fossil fuel combustion during power generation, industrial processes, and transportation. Exposure to PM_2.5 correlates with enhanced mortality risk from cardiovascular diseases (CVD), such as myocardial infarction and stroke. Over the last decade, it has been increasingly suggested that PM_2.5 affects CVD already at the stage of risk factor development.

Among the multiple biological mechanisms that have been described, the interplay between oxidative stress and inflammation has been consistently highlighted as one of the main drivers of pulmonary, systemic, and cardiovascular effects of PM_2.5 exposure. In this context, PM_2.5 uptake by tissue-resident immune cells in the lung promotes oxidative and inflammatory mediators release that alter tissue homeostasis at remote locations. This pathway is central for PM_2.5 pathogenesis and might account for the accelerated development of risk factors for CVD, including obesity and diabetes. However, transmission and end-organ mechanisms that explain PM_2.5-induced impaired function in metabolic active organs are not completely understood.

In this review, the main features of PM_2.5 physicochemical characteristics related to PM_2.5 ability to induce oxidative stress and inflammation will be presented. Hallmark and recent epidemiological and interventional studies will be summarized and discussed in the context of current air quality guidelines and legislation, knowledge gaps, and inequities. Lastly, mechanistic studies at the intersection between redox metabolism, inflammation, and function will be discussed, with focus on heart and adipose tissue alterations.

By offering an integrated analysis of PM_2.5-induced effects on cardiometabolic derangements, this review aims to contribute to a better understanding of the pathogenesis and potential interventions of air pollution-related CVD.