Adverse Effects Of Air Pollution

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Air pollution is the result of the emission of chemicals, particulate matter, and biologic material into the atmosphere then caused adverse effect on environment and health. Major air pollutants that threatening human health are carbon monoxide, nitrogen oxide, ozone, chemical vapors, and particulate matter. Air pollution is an important risk factor for cardiovascular health, therefore In this review article, we discuss air-polluted particle and the adverse effects of them on cardiovascular disease.


With advances in technology, air pollution has also increased. Air pollution caused mortality and cardiovascular disease in population [1-3]. Studies showed that increased the daily air pollution concentrations associated with myocardial …show more content…

Studies showed that nanoparticles like TiO and C caused air pollution, inflammation, skin injury, and lung accumulation [15].

Air pollutants include gaseous pollutants (e.g, carbon mono oxide, ozone, oxides of nitrogen and sulfur dioxide) and particulate matters (PMs). In this review article, we discuss air-polluted particle (include ambient air particles, disel exhaust, ozone and carbon monoxide) and adverse effects of them on cardiovascular disease.

Ambient Particulate Matter …show more content…

Exposure of diesel exhaust particles (DEP) used as particulate air pollution models in experimental studies [46, 48]. Experimental studies showed that exposure of air pollution increased leukocyte and erythrocyte numbers, and hematocrit [49-51]. A key mechanism of air pollution relationship to the generation of inflammation and induce oxidative stress [46, 52, 53].

Recently, studies showed that exposed to air pollution induced myocardial inflammation characterized by increased of TNFα and IL1β [54]. Studies showed that emodin adminstraton following DEP decreased cardiac proinflammatory cytokine TNFα and IL1β [55]. Exposed to DEP caused a significant decreased of SOD in heart tissue. Studies showed that exposure of DEP caused shortening of the thrombotic occlusion time in venules and pial arterioles. Also, emodin has protective effect against DEP-induced thrombotic complications in pial arterioles and venules [55].

Clinical studies showed that acute DE inhalation caused systolic blood pressure increasing, vasodilation imapairs, and/or vasoconstriction improves in humans [56, 57]. DE exposure caused moderate changes in HRV and electrocardiography in rats with minimal cardiac hypertrophy

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