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Rapid Responses to:
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James L. Repace, Visiting Assistant Clinical Professor, Tufts University School of Medicine Repace Associates, Inc. 101 Felicia Lane, Bowie, MD 20720 U.S.A.
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While I agree with most of what Chen et al. say, the statement, "Banishing the traditional clouds of tobacco smoke forever may be dear to the hearts of many of us for social as well as medical reasons, but were any exposure to smoke from combustion of vegetable matter, however caused, to be labelled dangerous this might have severe long term occupational and economic consequences." is incorrect. Biomass combustion of any sort, whether from tobacco, wood, or dung fires, releases the same sort of toxins because it combusts at low temperatures, and in doing so, manufactures a variety of carcinogenic or toxic organic chemicals. Insofar as their main point, I agree that cotinine values vary from person to person for the same exposure, and if cotinine measurements at different times post exposure are uncorrected, this will introduce additional variability, as cotinine is excreted with a 19-hour half-life. Nevertheless, this does not vitiate cotinine as a valid measure of exposure, dose, and risk (Repace et al., 1998). Epidemiologists investigating the risks of passive smoking using questionnaires only have not been mindful of the fact that many people are exposed to secondhand smoke (SHS) unknowingly, a point I have made explicitly in an earlier communication (Repace, 2003). In this communication, I give an illustrative colour figure adapted from the U.S. CDC national probability sample of serum cotinine (NHANES III): in this figure I illustrate the finite distribution of serum cotinine in persons who report on a questionnaire they have no exposure to SHS at work or at home in contrast to the distribution of serum cotinine in persons who report they do have exposure to SHS at work or at home. These two distributions have a significant overlap. Epidemiologists using questionnaires often incorrectly assume that subjects reporting no SHS exposure are unexposed. The NHANES III study shows that some of those who report being unexposed in fact have exposures as large or larger than people who report SHS exposure. This has the effect of reducing the magnitude of the epidemiologically estimated risk of passive smoking as well as its statistical significance, and inter alia, pointedly illustrates the fatal flaw in exposure assessment for the Enstrom and Kabat study, which uses only spousal smoking status as a surrogate for total SHS exposure. James Repace References: Repace JL. 2003. Passive Smoking Risks: From Pollution, Not Bias. (2 December 2003) BMJ Online, Rapid Responses; <http://bmj.bmjjournals.com/cgi/eletters/327/7413/503-a#37052>. Repace JL, Jinot J, Bayard S, Emmons K, and Hammond SK. Air nicotine and saliva cotinine as indicators of passive smoking exposure and risk. Risk Analysis 18: 71-83 (1998) Competing interests: The author is a secondhand smoke consultant. This work is supported by the Flight Attendant Medical Research Institute. |
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