Research Topic

Environmental Toxicants and Cardiopulmonary Consequences: Cellular and Molecular Mechanisms

  • Submission closed.

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


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

About Frontiers Research Topics

With their unique mixes of varied contributions from Original Research to Review Articles, Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author.

Topic Editors

Loading..

Submission Deadlines

Submission closed.

Participating Journals

Loading..

Topic Editors

Loading..

Submission Deadlines

Submission closed.

Participating Journals

Loading..
Loading..

total views article views article downloads topic views

}
 
Top countries
Top referring sites
Loading..