2018
DOI: 10.1016/j.cophys.2017.11.005
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Cardiac pathophysiology in response to environmental stress: a current review

Abstract: People with existing risk factors and those with established cardiovascular disease have increased susceptibility to environmental stressors. The literature reviewed in this article thus support public health policies aimed at reducing pollutant exposure to benefit public health.

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Cited by 16 publications
(3 citation statements)
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References 50 publications
(51 reference statements)
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“…Exposure to air pollution increments morbidity and mortality of cardiovascular disease (CVD) 1 , especially exposure to emissions from traffic and industrial sources 2 . Even lower concentrations of exposure to particulate matter (PM) caused by combustion, as a significant component of urban pollution, are involved in the pathogenesis of CVD 3 . Some researchers have shown a relationship between intense or persistent exposure to PM and the rate of cardiopulmonary occasions 4 .…”
Section: Introductionmentioning
confidence: 99%
“…Exposure to air pollution increments morbidity and mortality of cardiovascular disease (CVD) 1 , especially exposure to emissions from traffic and industrial sources 2 . Even lower concentrations of exposure to particulate matter (PM) caused by combustion, as a significant component of urban pollution, are involved in the pathogenesis of CVD 3 . Some researchers have shown a relationship between intense or persistent exposure to PM and the rate of cardiopulmonary occasions 4 .…”
Section: Introductionmentioning
confidence: 99%
“…In order to explain this observation, we speculate that this increased ratio corresponds to an attempt of the lungs to compensate the locally hypoxic state induced by oxidative stress. Indeed, PM 2.5 inhalation as well as UFP exposure is associated with a reduced oxygen saturation [ 58 60 ] and can induce endothelial dysfunction, particularly by inhibiting the endothelial NO synthase [ 61 ]. Such modifications might promote development of pulmonary and systemic inflammation.…”
Section: Discussionmentioning
confidence: 99%
“…PM0.1 and PM2.5 can pass through the alveolar-endothelial interface into the systemic circulation, directly affecting the heart, vasculature, and other organs. The thrombogenic effects of PM are believed to arise from the promotion of clot formation after entering the systemic circulation and from pulmonary inflammation caused by prolonged exposure [ 48 ]. Specifically, the mechanisms by which PM directly induces cardiovascular effects are through oxidative stress and direct calcium ion channel interference of the autonomic nervous system (ANS), and pulmonary inflammation results in PM-induced indirect cardiovascular effects [ 49 , 50 ].…”
Section: Reviewmentioning
confidence: 99%