© The Author 2007. Published by Oxford University Press.
CORRESPONDENCE |
Response: Re: A Prospective Study of Periodontal Disease and Pancreatic Cancer in US Male Health Professionals
Correspondence to: Dominique S. Michaud, ScD, Department of Epidemiology, Harvard School of Public Health, 677 Huntington Ave, Kresge 920, Boston, MA 02115 (e-mail: dmichaud{at}hsph.harvard.edu).
Taguchi raises the possibility that confounding by passive smoking may have explained our recent finding on periodontal disease and risk of pancreatic cancer. This is an important question, and we appreciate the opportunity to address this issue. Cigarette smoking is one of the few established risk factors for pancreatic cancer; however, the magnitude of this association is not very strong (compared with that between smoking and lung cancer, for example), given that the relative risks (RRs) associated with current smoking typically range between 1.5 and 3.0 (1). In a recent case–control study with 583 pancreatic cancer patients (2), never smokers who were exposed to environmental tobacco smoke (ETS) both as a child and as an adult had a relative risk for pancreatic cancer of 1.21 (95% confidence interval [CI] = 0.60 to 2.44) compared with those who did not have ETS exposure. In another recent study [(3), described by Taguchi], the relationship between passive smoking and pancreatic cancer was even weaker (RR = 1.1, 95% CI = 0.4 to 2.8 in one cohort, and RR = 0.9, 95% CI = 0.4 to 2.3 in another).
We do not have data on ETS exposure in the Health Professionals Follow-up Study and thus could not adjust for this potential risk factor. Controlling for passive smoking in our analysis may have attenuated the association with periodontal disease, but it could not have eliminated it. The reason for this is that among never smokers, we observed a twofold increase in risk of pancreatic cancer among those with a history of periodontal disease, which is substantially greater than the magnitude of the association between passive smoking and pancreatic cancer (2,3) and furthermore is of similar magnitude as the association between current smoking and pancreatic cancer (1). In a worst-case scenario, if the true relative risk associated with passive smoking is closer to 2.0, the correlation between passive smoking and periodontal disease would have to be close to perfect (i.e., r > .95) for it to account for our observation. Consequently, it is highly unlikely that our findings were confounded by passive smoking.
As noted by Taguchi, it is true that the duration and severity of periodontal disease may result in different associations with pancreatic cancer risk. In our study, only self-reported periodontal disease with bone loss was reported, so the association with moderate periodontal disease could not be examined. Similarly, data on duration of periodontal disease were not available, and consequently, that issue could not be examined, either. More extensive data on periodontal disease would likely lead to stronger estimates of the relationship between periodontal disease and pancreatic cancer. Future studies to address these important questions are currently being planned.
REFERENCES
(1) Michaud DS. Epidemiology of pancreatic cancer. Minerva Chir (2004) 59:99–111.[Medline]
(2) Villeneuve PJ, Johnson KC, Mao Y, Hanley AJ. Environmental tobacco smoke and the risk of pancreatic cancer: findings from a Canadian population-based case-control study. Can J Public Health (2004) 95:32–7.[Web of Science][Medline]
(3) Gallicchio L, Kouzis A, Genkinger JM, Burke AE, Hoffman SC, Diener-West M, et al. Active cigarette smoking, household passive smoke exposure, and the risk of developing pancreatic cancer. Prev Med (2006) 42:200–5.[CrossRef][Web of Science][Medline]
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J Natl Cancer Inst 2007 99: 738-739.
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