Cigarette smoking is a major risk factor for acute coronary thrombosis. In fact, both active/first-hand smoke and passive/second-hand smoke exposure are known to increase the risk of coronary thrombosis. Although recently a new risk has been identified and termed third-hand smoke (THS), which is the residual tobacco smoke contaminant that remains after a cigarette is extinguished, it remains to be determined whether it can also enhance the risk of thrombogenesis, much like first-hand smoke and second-hand smoke. Therefore, the present studies investigated the impact of THS exposure in the context of platelet biology and related disease states. It was found that THS-exposed mice exhibited an enhanced platelet aggregation and secretion responses as well as enhanced integrin GPIIb-IIIa activation. Furthermore, it was found that THS exposure shortens the tail bleeding time and the occlusion time in a model of thrombosis. Thus, our data demonstrate for the first time (at least in mice) that THS exposure increases the risk of thrombosis-based disease states, which is attributed, at least in part, to their hyperactive platelets.
*Department of Pharmaceutical Sciences, College of Pharmacy, Western University of Health Sciences, Pomona, CA; and
†Department of Cell Biology and Neuroscience, University of California, Riverside, CA.
Reprints: Fadi T. Khasawneh, PhD, Department of Pharmaceutical Sciences, College of Pharmacy, Western University of Health Sciences, 309 E. Second St, Pomona, CA 91766 (e-mail: email@example.com).
Supported by funds from the College of Pharmacy, Western University of Health Sciences, Pomona, CA (F.T.K.), and the Tobacco-Related Disease Research Program (19XT-0166; M.M.-G.).
The authors report no conflicts of interest.
Received February 01, 2015
Accepted March 18, 2015