Abstract
Approximately 1 billion people smoke worldwide, and the burden placed on society by primary and secondhand smokers is expected to increase. Smoking is the leading risk factor for myriad health complications stemming from diverse pathogenic programs. First- and second-hand cigarette smoke contains thousands of constituents, including several carcinogens and cytotoxic chemicals that orchestrate chronic inflammatory responses and destructive remodeling events. In the current review, we outline details related to compromised pulmonary and systemic conditions related to smoke exposure. Specifically, data are discussed relative to impaired lung physiology, cancer mechanisms, maternal-fetal complications, cardiometabolic, and joint disorders in the context of smoke exposure exacerbations. As a general unifying mechanism, the receptor for advanced glycation end-products (RAGE) and its signaling axis is increasingly considered central to smoke-related pathogenesis. RAGE is a multi-ligand cell surface receptor whose expression increases following cigarette smoke exposure. RAGE signaling participates in the underpinning of inflammatory mechanisms mediated by requisite cytokines, chemokines, and remodeling enzymes. Understanding the biological contributions of RAGE during cigarette smoke-induced inflammation may provide critically important insight into the pathology of lung disease and systemic complications that combine during the demise of those exposed.
Highlights
receptor for advanced glycation end-products (RAGE) is predominantly expressed in the lung, it is detectable in a variety of tissues including the heart, brain, placenta, liver, kidney, pancreas, small intestine, and colon [4,5]
As nitrosamines are readily absorbed through the alveoli and rapidly distributed through the blood, it is unsurprising that they are found to play a major role in the induction of many cancers [93,94]
Studies demonstrating the adverse effects of tobacco smoke on neurodevelopment have provided compelling evidence that nicotine increases cellular damage, reduces overall cell number, impairs synaptic activity, and influences processes such as cell replication to differentiation and apoptosis [126,127,128]
Summary
It is estimated that there are nearly 1 billion smokers worldwide (WHO Fact Sheet No 339). While the current worldwide population of smokers is estimated at 1 billion, current projections predict that this number will rise to 1.6 billion in the twenty-five years [1] With such an inordinate number of smokers world-wide, roughly 6 million people are expected to die each year because of tobacco exposure (WHO Fact Sheet No 339). Over 600,000 people will die prematurely as a result of exposure to secondhand smoke (SHS) While these numbers themselves are galling, rampant tobacco use throughout the world has had societal ramifications as exposure is believed to contribute to over $500 billion in damages annually [2]. The biochemical assessments performed to date have linked many tobacco-related substances with negative health consequences [6]; much remains to be discovered
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