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Why The End Of Smoking Is Complicated
- Thread starter 5150sick
- Start date
It's OK, but I find it too accepting of the notion that it's necessary to save the children from a lifetime of nicotine "addiction".
Why exactly do we have to do that? Nicotine itself, in the absence of smoke (tar and carbon monoxide) and TNSAs (also a problem in some but not all smokeless tobacco products) is likely no more harmful than caffeine.
Why exactly do we have to do that? Nicotine itself, in the absence of smoke (tar and carbon monoxide) and TNSAs (also a problem in some but not all smokeless tobacco products) is likely no more harmful than caffeine.
E-cigarette vapor disables key immune cells in the lung and boosts inflammation
https://www.sciencedaily.com/releases/2018/08/180813190148.htm
After 24 hours of exposure the total number of viable cells exposed to the vaped condensate was significantly reduced compared to the untreated cells, and condensate containing nicotine exaggerated this effect.
Exposure to the condensate increased cell death and boosted production of oxygen free radicals by a factor of 50, and it significantly increased the production of inflammatory chemicals -- more so when the condensate contained nicotine.
Cardiovascular Toxicity of Nicotine: Implications for Nicotine Replacement Therapy
https://www.sciencedirect.com/science/article/pii/S073510979700079X
Nicotine may contribute to cardiovascular disease, presumably by hemodynamic consequences of sympathetic neural stimulation and systemic catecholamine release.
The role of nicotine in the pathogenesis of atherosclerosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3755365/
nicotine also accelerates vascular disease. By inducing the release of catecholamines, nicotine increases heart rate and blood pressure. These adverse hemodynamic effects are associated with progression of atherosclerosis. Furthermore, nicotine-induced catecholamine release increases platelet aggregability 3. Platelets contribute to the growth of plaque through the accretion of thrombus, as well as through the release of growth factors (such as platelet derived relaxing factor) that induce vascular smooth muscle cell proliferation. In addition to these actions mediated by activation of the sympathetic nervous system, nicotine has direct actions on the cellular elements participating in plaque formation.