I was a smoker in my teens and early twenties, but when the price of a pack went above $2.00 I could not rationally pay that much to kill myself daily. So I stopped...
A few weeks ago I wrote this for my Anatomy class...
4) Explain how smoking effects the respiratory tract, and how it can deplete the body of essential nutrients.
Let’s first get some information about cigarette smoking…
“Cigarette smoke consists of more than 7300 chemical constituents distributed between the gas and tar (particulate) phases, many of which are potent carcinogens.19,20 Notwithstanding various hydrocarbons, such as isoprene, benzene and benzo[a]pyrene, other major toxic constituents of cigarette smoke include nicotine, carbon monoxide, nitric oxide, hydrogen cyanide, tobacco-specific nitrosamines, and various pro-oxidative heavy metals (arsenic, cadmium, chromium, iron, lead, mercury, nickel, vanadium).19e22 In addition, the gas and tar phases of cigarette smoke have been estimated to contain 1015/puff and 1017/gram of highly reactive, oxidising, toxic free radicals respectively.23 Those present in the gas phase are shortlived radicals generated via the interaction of nitrogen dioxide derived from nitric oxide with various hydrocarbons to form carbon-centered radicals which react with oxygen to produce oxyradicals.23 Both types of radical, in turn, interact with nitric oxide to form alkyl peroxynitrite and peroxynitrate esters.23 The major radical in the tar phase is a long-lived semiquinone which reacts with oxygen to generate the highly toxic reactive oxygen species (ROS), superoxide, hydrogen peroxide, and hydroxyl radical.24 Chronic exposure of the airways to this array of smokederived toxicants is the primary cause of the progressive pulmonary and immune dysfunction, as well as carcinogenesis, which typify the health risks of the smoking habit.20” (Feldman, Anderson 2013).
It sounds terrible to me. I did smoke as a teenager as an act of rebellion and into my early twenties, but usually only when going out. When I had to pay $2 for a pack of cigarettes that I knew would kill me, I quit. Cold Turkey.
“The composition of the nasopharyngeal flora of smokers has been reported to differ from that of non-smokers. Notable differences include: i) fewer competitive aerobic and anaerobic commensal organisms; and ii) an increased frequency of pathogens, specifically S. pneumoniae, nontypeable H. influenzae, Moraxella catarrhalis, and Streptococcus pyogenes. 82 Colonisation of the upper respiratory tract is a probable consequence of the interactive effects of cigarette smoke on host defences and microbial pathogens.”
“Both active and passive smoking pose a significant risk for upper respiratory tract infections, and in particular otitis media.154e157 The effects of environmental smoke exposure appears to be greatest in children less than 1 year of age.154 In one study of children exposed to passive smoking, it was found that parental smoking more than doubled the risk for recurrent otitis media,158 while an earlier study suggested that although environmental smoke exposure was more commonly associated with recurrent otitis media, there was no significant difference in the clinical course compared to that of non-exposed children.154 A more recent systematic review and meta-analysis documented that living with a smoker was associated with an increased risk of middle-ear disease, particularly in the case of maternal smoking, while prenatal maternal and paternal smoking was associated with a non-significant increase in risk; the strongest risk of both maternal and paternal smoking was for middle-ear disease, requiring surgery.157”
Cell death and damage! That’s what smoking does to you!
It leads to death. And it is preventable.
“Although the effects of cigarette smoking on a variety of diseases, from cancer through emphysema and cardiovascular illness are well documented, direct effects on the levels of macro- and micronutrients in the body are reported less frequently. In fact, imbalances in these nutrients may have a role in many of the pathological conditions attributed to smoking. Tobacco smoke contains numerous compounds emitted as gases and condensed tar particles, many of them being oxidants and prooxidants, capable of producing free radicals thus enhancing lipid peroxidation in biological membranes. Vitamin E, vitamin C, B-carotene and selenium are involved in the overall cellular anti-oxidant defense against deleterious effects of reactive oxygen species. Smoking has been shown to lower the level of vitamin C and B-carotene in plasma. Cadmium, naturally found in tobacco, decreases the bioavailability of selenium and acts antagonistically to zinc, a cofactor for the antioxidant enzyme, superoxide dismutase. Vitamin E, the principle lipid-soluble antioxidant, may be at suboptimal levels in tissues of smokers. In addition, tobacco constituents have been shown to reduce levels of several vitamins of the B-complex. Nutritional status in smokers may be further compromised by an inadequate diet. Data from the Second National Health and Nutrition Examination Survey indicates that smokers are less likely to consume fruits and vegetables, particularly those high in vitamin C and carotenes. Cessation of smoking is the obvious solution to ending cigarette-related problems. In the world as it is, however, the medical community should be responsible for making recommendations to lower the risk in smokers to tobacco related diseases. Nutritionists could have a role in this process. There exists a lively debate as to where levels of nutrients should be set. Additional vitamin C has already been recommended for smokers. Should other antioxidants also be increased? Arguments for the against are considered.” (Preston, 1991).
This research says something else.
“Smoking is associated with oxidative stress and increased risks of many chronic diseases that both shorten life and impair its quality. Low concentrations of several micronutrients, especially the antioxidants vitamin C and beta-carotene, are also associated with smoking, and there has been much interest in determining whether deficiencies in micronutrients are involved etiologically in smoking-related diseases. The objective of this review was to bring together reports on dietary intakes, biochemical indicators of micronutrient status, and results of some intervention studies on micronutrients where authors had compared outcomes in smokers and non-smokers. The micronutrients discussed are vitamins A, E, and C; the carotenoids; some of the B-vitamin group; and the minerals selenium, zinc, copper, and iron. The data were then examined to determine whether effects on the biochemical markers of micronutrient status were due to differences in dietary intakes between smokers and non-smokers or to the consequences of inflammatory changes caused by the oxidative stress of smoking. It was concluded that although smoking is associated with reduced dietary intake of vitamin C and carotenoid-containing foods, inflammatory changes increase turnover of these micronutrients so that blood concentrations are still lower in smokers than non-smokers even when there is control for dietary differences. In the case of vitamin E, there is some evidence for increased turnover of this nutrient in smokers, but this has little to no influence on blood concentrations, and there are no differences in dietary intake of vitamin E between smokers and non-smokers. Serum concentrations of vitamin A, folate, and vitamin B12 and B6 markers do not appear to be influenced by smoking, although there is some influence of dietary intake on concentrations of these nutrients in the body. In the case of the minerals examined, the main effects on biochemical markers of mineral status were attributed to inflammation and were therefore greater in heavy or long-term smokers. Serum concentrations of selenium and erythrocyte GPx activity were lower in smokers. Erythrocyte CuZn-SOD activity and serum ceruloplasmin concentrations were elevated, while serum zinc concentrations were depressed only in heavy smokers. Lastly, smoking appears to affect iron homeostasis mainly by changing hemoglobin concentrations, which were in general increased. Serum iron, TfR, and ferritin were mostly unaffected by smoking, except in pregnancy where there is evidence of increased erythropoiesis causing lower saturation of plasma transferrin and some evidence of lowering of iron stores.” (Northrop-Clewes, Thurnham 2007).
Overall, smoking can lead to many preventable health issues.
Feldman, C., & Anderson, R. (2013). Cigarette smoking and mechanisms of susceptibility to infections of the respiratory tract and other organ systems. Journal of Infection, 67(3), 169–184.
Preston, AM (1991). Cigarette smoking-nutritional implications. Prog Food Nutr Sci, 1991;15(4):183-217.
Northrop-Clewes CA1, Thurnham DI. (2007). Monitoring micronutrients in cigarette smokers. Clin Chim Acta. 2007 Feb;377(1-2):14-38. Epub 2006 Sep 1.
Thank you for reading!