Am J Epidemiol 2003; 158:1227-1228.
Copyright © 2003 by the Johns
Hopkins Bloomberg School of Public Health
LETTERS TO THE EDITOR |
THE FIRST AUTHOR REPLIES
Department of Biostatistics and Epidemiology, School of Public Health, University of Massachusetts, Amherst, MA 01003-9304
We are happy to address the concerns raised by Dr. Denson in his letter (1) about our study of environmental tobacco smoke exposure and malignant lymphoma in domestic cats (2). Denson suggests that the environmental tobacco smoke dose received by cats in smoking households is likely to be insufficient to contribute to the development of cancer. Although we were unable to evaluate this directly in our case-control study subjects, we have assessed the relation between environmental tobacco smoke exposure and cotinine in a cross-sectional study of cats that were presented to Foster Hospital at Tufts University School of Veterinary Medicine (3). Prior to their clinic visit, owners of 184 cats (93 percent of those eligible) completed a questionnaire measuring household smoking level in the previous 24 hours, as well as other demographic and lifestyle factors. Urine samples, which were assayed for cotinine, were collected from 70 of these cats during the same clinic visit. Urinary cotinine increased significantly with the total number of cigarettes smoked per day in the household. The mean urinary cotinine levels in cats exposed to 0, 1–19, and 20 or more cigarettes per day were 7.0 (standard deviation (SD), 4.1) ng/ml, 12.6 (SD, 10.2) ng/ml, and 40.0 (SD, 20.8) ng/ml, respectively (p < 0.001). These levels are comparable with those observed in humans; the established cutoff values for this assay to define environmental tobacco smoke exposure levels in humans are 3–10 ng/ml for no substantial environmental tobacco smoke exposure, 11–30 ng/ml for passive exposure or light smoking, and 30–>500 ng/ml for active smoking (4). Our results suggest that cats living with smokers can be exposed to a substantial dose of environmental tobacco smoke.
Denson also suggests that the observed association may be the result of confounding by feline leukemia virus vaccination status, because the likelihood of vaccination is probably inversely associated with environmental tobacco smoke exposure. We assessed the relation between environmental tobacco smoke exposure and feline leukemia virus vaccination status in cats treated at the Foster Hospital in the cross-sectional study described above. Vaccination history was available for 167 of 184 cats. Feline leukemia virus vaccination status did not vary by household smoking status, with 79.8 percent of cats in smoking households vaccinated compared with 80.8 percent of cats in nonsmoking households. This similarity existed for cats acquired more than a decade ago as well as for recently acquired cats. Although these data do not directly address the question of vaccination in our case-control study subjects, they do suggest that the large majority of cats in our source population have been vaccinated against feline leukemia virus, and that vaccination does not vary by owner’s smoking status. Furthermore, the fact that we observed a higher proportion of gastrointestinal tumors, which tend to be associated with feline leukemia virus-negative lymphoma (5), in cases exposed to environmental tobacco smoke than in unexposed cases does not support the hypothesis that case-control differences in feline leukemia virus infection may explain the positive relation between environmental tobacco smoke and lymphoma.
We clearly differ with Dr. Denson in our reading of the literature concerning exposure to passive smoking and the potential for adverse health effects. Although the jury is still out concerning the relation between active and passive smoking and non-Hodgkin’s lymphoma, the observation of positive associations between active smoking and non-Hodgkin’s lymphoma in numerous studies (6) suggests that such an association in cats is indeed plausible. Studies of companion animals like cats may actually provide an even better opportunity to study the effects of environmental tobacco smoke exposure because of reduced confounding by active smoking (7).
Our findings clearly need to be replicated before conclusions can be drawn. The magnitude of the associations observed, the presence of a significant dose-response, the biologic plausibility, and the lack of a clear alternative explanation for these results suggest that this question does warrant further study.
REFERENCES
REFERENCES
- Denson KWE. Re: "Environmental tobacco smoke and risk of malignant lymphoma in pet cats." (Letter). Am J Epidemiol 2003;158:1227.
[Free Full Text] - Bertone ER, Snyder LA, Moore AS. Environmental tobacco smoke and risk of malignant lymphoma in pet cats. Am J Epidemiol 2002;156:268–73.
[Abstract/Free Full Text] - Clancy EA, Moore AS, Bertone ER. Feline and owner characteristics and outdoor access. J Am Vet Med Assoc 2003;222:1541–5.[CrossRef][ISI][Medline]
- Chilmonczyk BA, Knight GJ, Palomaki GE, et al. Environmental tobacco smoke exposure during infancy. Am J Public Health 1990;80:1205–8.
[Abstract/Free Full Text] - Moore AS. Treatment of feline lymphoma. Feline Pract 1996;24:17–20.
- Scherr PA, Mueller NE. Non-Hodgkin’s lymphoma. In: Schottenfeld D, Fraumeni JF Jr, eds. Cancer epidemiology and prevention. 2nd ed. New York, NY: Oxford University Press, 1998:920–45.
- Kelsey JL, Moore AS, Glickman LT. Epidemiologic studies of risk factors for cancer in pet dogs. Epidemiol Rev 1998;20:204–17.
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  E. R. Bertone-Johnson THE FIRST AUTHOR REPLIES Am. J. Epidemiol., December 15, 2003; 158(12): 1227 - 1228. [Full Text] [PDF]
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