The pathology of cardiovascular disease is multi-faceted, with links to many modifiable and non-modifiable risk factors. Epidemiological evidence now implicates exposure to persistent organic pollutants, such as polychlorinated biphenyls (PCBs), with an increased risk of developing diabetes, hypertension, and obesity; all of which are clinically relevant to the onset and progression of cardiovascular disease. PCBs exert their cardiovascular toxicity either directly or indirectly via multiple mechanisms, which are highly dependent on the type and concentration of PCBs present. However, many PCBs may modulate cellular signaling pathways leading to common detrimental outcomes including induction of chronic oxidative stress, inflammation, and endocrine disruption. With the abundance of potential toxic pollutants increasing globally, it is critical to identify sensible means of decreasing associated disease risks. Emerging evidence now implicates a protective role of lifestyle modifications such as increased exercise and/or nutritional modulation via anti-inflammatory foods, which may help to decrease the vascular toxicity of PCBs. This review will outline the current state of knowledge linking coplanar and non-coplanar PCBs to cardiovascular disease and describe the possible molecular mechanism of this association.
|Number of pages||13|
|Journal||Environmental Science and Pollution Research|
|State||Published - Feb 1 2016|
Bibliographical noteFunding Information:
Supported by grant number P42ES007380 from the National Institute of Environmental Health Sciences. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Environmental Health Sciences or the National Institute of Health.
© 2015, Springer-Verlag Berlin Heidelberg.
- Cardiovascular disease
- Cardiovascular risk factors
- Nutritional modulation
- Oxidative stress
- Persistent organic pollutants
- Polychlorinated biphenyls
ASJC Scopus subject areas
- Environmental Chemistry
- Health, Toxicology and Mutagenesis