Ozone exposure and cardiovascular disease: A narrative review of epidemiology evidence and underlying mechanisms

Abstract

Ozone (O₃) poses a significant global public health concern as it exerts adverse effects on human cardiovascular health. Nevertheless, there remains a lack of comprehensive understanding regarding the relationships between O₃ exposure and the risk of cardiovascular diseases (CVD), as well as the underlying biological mechanisms. To address this knowledge gap, this narrative review meticulously summarizes the existing epidemiological evidence, susceptibility, and potential underlying biological mechanisms linking O₃ exposure with CVD. An increasing body of epidemiological studies has demonstrated that O₃ exposure heightens the incidence and mortality of CVD, including specific subtypes such as ischemic heart disease, hypertension, and heart failure. Certain populations display heightened vulnerability to these effects, particularly children, the elderly, obese individuals, and those with pre-existing conditions. Proposed biological mechanisms suggest that O₃ exposure engenders respiratory and systemic inflammation, oxidative stress, disruption of autonomic nervous and neuroendocrine systems, as well as impairment of coagulation function, glucose, and lipid metabolism. Ultimately, these processes contribute to vascular dysfunction and the development of CVD. However, some studies have reported the absence of associations between O₃ and CVD, or even potentially protective effects of O₃. Inconsistencies among the literature may be attributed to inaccurate assessment of personal O₃ exposure levels in epidemiologic studies, as well as confounding effects stemming from co-pollutants and temperature. Consequently, our findings underscore the imperative for further research, including the development of reliable methodologies for assessing personal O₃ exposure, exploration of O₃ exposure's impact on cardiovascular health, and elucidation of its biological mechanisms. These endeavors will consolidate the causal relationship between O₃ and cardiovascular diseases, subsequently aiding efforts to mitigate the risks associated with O₃ exposure.