Abstract
Polyfluoro- and perfluoro–alkyl substances (PFAS) are organic chemicals extensively used worldwide for industry and consumer products. Due to their chemical stability, PFAS represent a major cause of environmental pollution. PFAS accumulate in animal and human blood and tissues exerting their toxicity. We performed a review of the epidemiological studies exploring the relationship between exposure to PFAS and thromboembolic cardiovascular disease. An increase in cardiovascular disease or death related to PFAS exposure has been reported from cross-sectional and longitudinal observational studies with evidence concerning the relation with early vascular lesions and atherosclerosis. Several studies indicate an alteration in lipid and glucose metabolism disorders and increased blood pressure as a possible link with cardiovascular thromboembolic events. We also examined the recent evidence indicating that legacy and new PFAS can be incorporated in platelet cell membranes giving a solid rationale to the observed increase risk of cardiovascular events in the populations exposed to PFAS by directly promoting thrombus formation. Exposure to PFAS has been related to altered plasma membrane fluidity and associated with altered calcium signal and increased platelet response to agonists, both in vitro and ex vivo in subjects exposed to PFAS. All the functional responses are increased in platelets by incorporation of PFAS: adhesion, aggregation, microvesicles release and experimental thrombus formation. These findings offer mechanistic support the hypothesis that platelet-centred mechanisms may be implicated in the increase in cardiovascular events observed in populations chronically exposed to PFAS.
Highlights
Polyfluoro- and perfluoro–alkyl substances (PFAS) represent a large class of organic chemicals derived from the substitution of hydrogen with fluorine attached to hydrocarbon chain, that has been extensively used since the 1940s [1]
Several studies indicate that metabolic disorders, including hyperlipidaemia, diabetes mellitus, obesity and increased blood pressure may translate into increased cardiovascular events in the exposed populations, possibly through the endocrine disrupting activity of PFAS
New data from mechanistic studies suggest that platelets may be the target of PFAS, altering the characteristics of plasma membranes, apparently in a dose-independent manner
Summary
Polyfluoro- and perfluoro–alkyl substances (PFAS) represent a large class of organic chemicals derived from the substitution of hydrogen with fluorine attached to hydrocarbon chain, that has been extensively used since the 1940s [1]. PFAS and Cardiovascular Disease characteristics, PFAS are used as oil and water repellents and flame retardants, raw materials for fire-fighting equipment and mist suppression as well as coating for cookware, carpets, textiles, component of paints, lubricants and fire-fighting foams [1,2,3,4] Their presence in the environment increased steadily until early 2000 when, at least in some countries, regulatory laws led to a decrease in the industrial utilization, at least of some PFAS (legacy PFAS). Different PFAS, that are considered to accumulate in lower amounts and for shorter periods of time, have been introduced on the market and are currently in use These new formulations are widely used without proper knowledge of their environmental disposition and potential toxicity [1, 5, 6]
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