Cancer in smokers

There has been some success with vitamin A and its derivatives for treatment of certain types of cancer (Niles, 2000). However, the use of P-carotene as a therapeutic agent suffered a setback when the results from two of three large human intervention studies indicated that high doses of P-carotene caused an increased risk of lung cancer in smokers and subjects exposed to asbestos. This increased risk is thought to be due to metabolites associated with high doses of p-carotene in the presence of smoke (Russell, 2004). 

The observations from the epidemiological studies conducted in the early 1980s resnlted in a nnmber of randomized clinical trials with pharmaceutical doses of P-carotene that showed either no effect or an increased risk of lung cancer in smokers." ... 

Polonium was discovered in 1898 by Marie and Pierre Curie in their search for the sources of radioactivity in pitchblende. Polonium has 27 isotopes and is highly toxic and very radioactive. It has been suggested that the isotope 210Po, a natural contaminant of tobacco and an a-particle producer (see Section 21.1), might be at least partly responsible for the incidence of cancer in smokers. 

Omenn GS, Goodman G, Grizzle J, et al. 1992. Recmitment for the P-carotene and retino efficacy trial (caret) to prevent lung cancer in smokers and asbestos-exposed workers. West J Med 156 540-544. 

Cancer The increased risk of cancer in vitamin deficiency is thought to be the result of depletion in beta-carotene. Beta-carotene is a very effective antioxidant and is suspected to reduce the risk of cancer is known to be initiated, by the production of free radicals. Of particular interest is the potential benefit of increased b-carotene intake to reduce the risk of lung cancer in smokers. However, caution needs to be taken when increasing the intake of any of the lipid soluble vitamins. 

An imaginary study involved smokers and lung cancer. The cases (persons with disease) consisted of 75 smokers and 20 nonsmokers. The controls (no disease) consisted of 175 smokers and 180 nonsmokers. The risk of cancer in smokers was... 

To compare the risk of cancer in smokers to the risk in nonsmokers, one can calculate the risk ratio- The risk ratio, from the above study, is 0.3/0,1 - 3,0. The risk ratio is a number that contains two different rates of risk. Risk ratio is also called relative risk-... 

The odds of finding cancer in smokers (0.429) is greater than the odds of finding cancer in nonsmokers 0.111). These two numbers are used to create a ratio. The odds ratio (Oft) is a number that is found by dividing the two sets of odds, as... 

The two trials also showed that beta-carotene supplementation increased the incidence of pulmonary cancer in smokers. Because heavy smokers are commonly heavy drinkers it was supposed that alcohol might have contributed to the increased incidence of lung cancer. Subsequent analysis showed that there was indeed a relation between the incidence of pulmonary cancer and the amount of alcohol consumed. 

Successively after the late 1950s, various classes of smoke components were proposed as either the cause of (as tumor initiators) or contributors to (as promoters, cocarcinogens, ciliastats) lung cancer in smokers ... 

The failure to explain the observed tumorigenicity of CSC in the mouse-skin bioassay by consideration of the following tobacco smoke systems led to the inclusion of ciliastasis by various water-soluble vapor-phase (VP) tobacco smoke components in an attempt to explain the causation of respiratory tract cancer in smokers ... 

These exposure estimates [for benzo[a]pyrene] and the determinations of the tumorigenic potential of [polycyclic aromatic hydrocarbons] in bioassays strongly suggest that [polycyclic aromatic hydrocarbons] play a significant role in the induction of respiratory tract cancer in smokers... 

Polynuclear aromatic hydrocarbons and NNK [4-(A-methyl-nitrosamino)-l-(3-pyridinyl)-l-butanone] are the major carcinogens involved in lung cancer induction by cigarette smoke and that NNK [4-(A-methylnitrosamino)-l-(3-pyridinyl)-l-butanone] is a likely candidate for induction of pancreatic cancer in smokers. 

The presence of P-naphthylamine in cigarette smoke has been demonstrated [Hoffmann et al. (1747)], along with other carcinogenic aromatic amines [Patrianakos et al. (2900)]. The yield was so low that [the researchers] did not believe these agents contributed significantly to the risk of bladder cancer in smokers [see p. 41 in (4009)]. 

Stram, D.O., Huberman, M., and Wu, A.H., Is residual confounding a reasonable explanation for the apparent protective effects of beta-carotene found in epidemiologic studies of lung cancer in smokers Am. J. Epidemiol, 155, 622,2002. 

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