**4.3 Cardiovascular effects**

In recent studies, multiple cardiovascular effects have been documented due to the exposure of air pollutants. According to Global Burden of Disease report, 2018 air pollution was responsible for 19% of cardiovascular deaths in 2015. It was also the cause of about 21% of deaths due to stroke and 24% of deaths from coronary heart disease.

Carbon monoxide has high affinity for haemoglobin and thus it displaces the oxygen and binds with haemoglobin to form carboxyhaemoglobin. It is a stable compound which cannot bind and deliver oxygen to tissues leading to tissue hypoxia (decrease oxygen carrying capacity). Increased risks of ischemic heart disease and myocardial infarction have been demonstrated among occupational groups exposed to gaseous emissions whereas short term exposure studies have reported changes in vasomotor function among healthy individuals as well as increase in prothrombogenic effects. Increased hospital admissions due to myocardial infarctions, increased congestive heart failure among the elderly population as a result of elevated PM concentration were also reported. Long term exposure to traffic emissions have been linked to coronary arteriosclerosis while, short term exposure is related to hypertension, stroke, myocardial infarctions and heart abnormalities [44, 45]. In vitro studies in experimental animals exposed to PM results in systematic inflammation and oxidative stress in the cardiovascular system and may enhance the progression of atherosclerosis in animals predisposed to this disease. In addition to this, chronic exposure to nitrogen oxide may result in ventricle hypertrophy [45].
