About this Research Topic
Emerging evidence indicates that exposure to environmental toxicants including air pollutants (indoor and outdoor pollutants) and various contaminants present in drinking water and food have been shown to either contribute to or be associated with the development and progression of multiple cardiopulmonary diseases (CPD). According to the world health organization (WHO) statement, around 4.2 million deaths globally are linked to ambient air pollution, primarily due to heart disease, stroke, asthma, chronic obstructive pulmonary disease (COPD), lung cancer, and acute respiratory infections. In addition, exposure to other environmental toxins such as heavy metals, aldehydes, and polyaromatic hydrocarbons has been reported to elevate cardiovascular diseases (CVD) risk by affecting atherogenesis, thrombosis, or blood pressure regulation. Maternal exposure to drugs, toxins, and infection has been linked with cardiac birth defects and premature CVD in later life. First -, second- and third-hand tobacco smoke exposure is paradigmatic of such environmental risk and is strongly associated with increased cardiopulmonary morbidity and mortality all over the world. Extensive laboratory research showed that tobacco smoke exposure induces endothelial dysfunction and prothrombotic responses and exacerbates atherogenesis and myocardial ischemic injury in various animal model. Similar mechanism may be engaged by other pollutants or food constituents. Numerous large population-based studies also stipulated that exposure to fine or ultrafine particles increases CVD and COPD-associated morbidity and mortality, and the plausibility of this association is supported by data from animal studies.
Collectively, the above-mentioned information support the notion that acute or chronic environmental stress including toxins is an important determinant of CPD risk. The possible underlying mechanisms that could cause the cardiopulmonary diseases include (1) damage to the endothelial barrier in the vascular system, (2) activation of leukocytes and platelets, (3) initiation of plaque formation, (4) alteration of the inflammatory response, (5) kidney-related hypertension, and (6) direct damage to blood vessel tissue. There is still much unknown about harmful effects of environmental toxicants and the mechanistic pathways responsible for triggering adverse cardiopulmonary health effects. The role of environmental toxicants on cardiopulmonary consequences is becoming an important public health topic, and needs to be considered in the overall paradigm of understanding susceptibility to, controlling risk and prevention for cardiopulmonary diseases.
Therefore, the main goal of this Research Topic is to seek new mechanistic insights on pathophysiological events that are associated with cardiopulmonary complications mediated by various environmental toxicants. Topic editors welcome manuscripts of the following types: Original Research articles, epidemiological or clinical study, Reviews, or Methodology papers.
Keywords: Environmental Toxins, Public Health, Cardiopulmonary Diseases, Protection/Prevention, Cell Signaling diseases
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