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doi: 10.1016/j.scitotenv.2021.150817

Components of tobacco smoke also induce endothelial dysfunction, increase blood thrombogenicity, enhance the inflammatory response, cause oxidative stress, and adversely affect lipid profile giving rise to the development of atherosclerosis.1 Examples of factors involved in the pathogenesis of CAD are shown in Table 1.2,3 As well as inducing physiological changes, smoking is a risk factor for hard endpoints, such as onset of angina and myocardial infarction.7,8 The INTERHEART study provided evidence of the risk of non-fatal myocardial infarction (MI) associated with smoking.9 Over 12 000 cases of first acute MI were evaluated for a number of factors including smoking status and compared to 14 000 age and sex matched controls