Key result
This review highlights the chemical constituents of environmental tobacco smoke and outlines its effects on atherogenesis and thrombosis in animal and human models.
Why the study?
Although the relationship between active smoking and atherosclerosis is well-described, the specific mechanisms by which environmental tobacco smoke influences atherosclerosis remain incompletely understood.
Does environmental tobacco smoke influence atherogenesis and thrombosis?
Does environmental tobacco smoke influence atherogenesis and thrombosis?
This review highlights the mechanisms by which environmental tobacco smoke influences atherosclerosis and thrombosis, emphasizing its significant public health implications.
Answers are grounded in this paper and cite their sources.
Supports avoidance of environmental tobacco smoke; extends mechanistic evidence on atherothrombosis but leaves open prospective clinical validation.
Environmental tobacco smoke (ETS) and its sequelae are among the largest economic and healthcare burdens in the United States and worldwide. The relationship between active smoking and atherosclerosis is well-described in the literature. However, the specific mechanisms by which ETS influences atherosclerosis are incompletely understood. In this paper, we highlight the definition and chemical constituents of ETS, review the existing literature outlining the effects of ETS on atherogenesis and thrombosis in both animal and human models, and briefly outline the public health implications of ETS based on these data.
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DiGiacomo et al. (2018) conducted a review in Cardiovascular Disease. Environmental tobacco smoke (ETS) was evaluated. This review highlights the chemical constituents of environmental tobacco smoke and outlines its effects on atherogenesis and thrombosis in animal and human models.
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