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While cigarette smoking is the single most preventable risk factor for cardiovascular disease, a significant percentage of disabilities and deaths are attributable to it. In fact, cardiovascular disease such as the thrombosis-based disorders heart attacks and strokes are considered the main cause of death due to smoking. In this connection, thrombosis is defined as the formation of a blood clot inside a blood vessel, thereby obstructing blood flow to a particular organ or area of the body. To this end, smoking accelerates the hardening and narrowing process in blood vessels, which substantially contributes to the pathogenesis of certain cardiovascular disease such heart attacks. Importantly, it has been established that activation of blood cells known as platelets is an important risk factor in atherosclerosis caused by smoking.
In this connection, while the toxicity of first-hand smoke and second-hand smoke is well recognized, much less is known regarding that of third-hand smoke (THS). THS is formed from toxicants produced by second-hand smoke that end up depositing on surfaces such as upholstery, curtains, car seats, carpet, etc., which over time can undergo chemical reactions and changes that may make them more toxic. Those can then be reabsorbed upon direct exposure by a child or an adult. There has been a growing interest in understanding the toxicity of this form of smoke exposure, and whether it has any detrimental effects on human health. To this end, while we have very recently shown that THS does modulate platelet activity, and increase the risk of thrombosis, the mechanism by which THS does so, and whether the effects are dependent on the amount and duration of exposure remains to be determined. Our goal is to investigate these issues by employing a THS exposure model that mimics that of humans. Thus, we should not only learn about the negative effects of THS, but also better understand mechanistically how those effects are exerted on the cardiovascular system. The outcome of these studies may also result in new or better ways for managing smoking induced platelet-dependent diseases.
In summary, our study aims to better understand the health consequences of exposure to THS in the context of platelet activation and thrombotic diseases. It is expected that those studies will inform the public of the seriousness of THS exposure, and perhaps guide policy for effective control & prevention measures, and may lay down the foundation for better therapeutic approaches for managing THS-dependent thrombosis, such as that seen in heart attacks. |
