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Dr. Lillington is Clinical Professor of Medicine, and Dr. Sachs is Clinical Associate Professor of Medicine, Stanford University Medical Center.
Correspondence to: Glen A. Lillington, MD, 1020 Siskiyou Dr, Menlo Park, CA 94025-7014; glenlill@ad.com
The demonstration of statistical associations between states or events naturally suggests that the congruity may be more than coincidental. Possibilities include that the two (or more) states have an underlying common cause, or that one event or state is affecting or causing the other. Nonskeptical acceptance of the latter post hoc, ergo propter hoc theorem may result in erroneous conclusions.
A notable example occurred early in the last century with the statistical demonstration that individuals who contracted tuberculosis appeared to have a lower subsequent incidence of bronchogenic carcinoma. A well-known statistician of that era suggested that the tuberculous infection somehow conferred some protection from neoplastic change. An equally logical explanation, which initially eluded the thinkers of that era, was that the tuberculous disease, for which there was little effective therapy, carried with it a high mortality that prevented many younger consumptives from reaching the age levels in which pulmonary neoplasms have a significant incidence.
After the statistical association between smoking and bronchogenic carcinoma was clearly demonstrated in the 1950s and 1960s, the howls of denial from the tobacco industry were echoed faintly by disinterested, honest statisticians exploring the possibilities that the association might not be cause and effect. One such postulate, the Fisher hypothesis, suggested a genetic predisposition toward smoking that might also entail a predisposition toward developing bronchogenic carcinoma.
Critics pointed out that these studies were showing associations of smoking not only with lung cancer and emphysema, but also with cancers in other organs (such as the urinary bladder), and even with the incidence of industrial accidents. It was postulated that the results were almost "too good," suggesting the presence of some type of systematic statistical error, which might even call into question the validity of the most robust association, that of smoking and primary lung cancer.
We now realize that many inhaled carcinogens can be absorbed readily through bronchial and alveolar walls and, thus, easily gain access to extrapulmonary organs through the systemic circulation. Although the rationale for increased industrial accidents in smokers is not so clear-cut, it is not too difficult to postulate a few possible explanations for the association.
The study by Murin and Inciardi in this issue of CHEST (see page 1635) indicates an association between tobacco smoking and an increased incidence of pulmonary metastases from primary breast carcinoma. Although the association appears to be real, it needs to be confirmed by further studies. A possible association of tobacco smoking with the development of pulmonary metastases from other organs, such as the kidney, also should be investigated.
It seems logical that the association may represent a cause-and-effect relationship between inhaled tobacco smoke and the development of pulmonary metastases. The mechanism, though, is not clearly definable. One may postulate that inhaled carcinogens from tobacco smoke are absorbed into the pulmonary circulation and then carried to the site of the primary breast tumor to stimulate the release of tumor material into the systemic veins or lymphatics. Conversely, the effect of the circulating carcinogens from tobacco smoke may stimulate the growth of occult metastases in the lungs. A third possibility is that the inhaled carcinogens somehow affect or alter the pulmonary tissues to make them more receptive to tumor embolization or lymphangitic spread.
This study, if confirmed by others, points to the desirability of providing effective treatment for tobacco dependence for those women who are still smoking at the time of breast carcinoma diagnosis. Proven agents, such as bupropion sustained release (Zyban; Glaxo Wellcome; Research Triangle Park, NC) and the nicotine patch are often successful.1 2 In some instances, higher doses of nicotine may be required, using multiple nicotine patches and/or nicotine nasal sprays or inhalers.2 3 4 Such regimens, with individualized doses and accurate monitoring, are safe and effective.2 5 6
Additionally, women who have stopped tobacco smoke exposure only within the previous 12 months should be closely monitored for tobacco use, since relapse back to tobacco use is greatest within the first 12 months after stopping smoking. Vigorous treatment for achieving smoking cessation will probably become part of standard therapy in smokers with breast carcinomas.
References
This article has been cited by other articles:
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  P. Reynolds, S. Hurley, D. E. Goldberg, H. Anton-Culver, L. Bernstein, D. Deapen, P. L. Horn-Ross, D. Peel, R. Pinder, R. K. Ross, et al. Active Smoking, Household Passive Smoking, and Breast Cancer: Evidence From the California Teachers Study J Natl Cancer Inst, January 7, 2004; 96(1): 29 - 37. [Abstract] [Full Text] [PDF]
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 H. W. Daniell and S. Murin Breast Cancer in Smokers Chest, May 1, 2003; 123(5): 1771 - 1772. [Full Text] [PDF]
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