ORAL HEALTH EVIDENCE-BASED PRACTICE PROGRAM
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Title Exposure to Secondhand Tobacco Smoke Increases The Risk Of Developing Oral Cancer
Clinical Question In an otherwise healthy patient, does exposure to secondhand tobacco smoke pose an increased risk of developing oral cancer as compared to patients without exposure to secondhand smoke?
Clinical Bottom Line There is an enzyme in the saliva called oral peroxidase (OPO) that helps attack the free radicals in cigarette smoke relating to oral cancer. Exposure to tobacco smoke caused a sharp drop in OPO activity. In addition, p53 is the most frequently mutated gene in human oral cancer, and it is over expressed in oral squamous cell carcinoma tumors linked to tobacco smoke. Tumors exposed to environmental tobacco smoke were more likely to over express p53.
Best Evidence (you may view more info by clicking on the PubMed ID link)
PubMed ID Author / Year Patient Group Study type
(level of evidence)
#1) 12543253Reznick/200317 smokers, 16 nonsmokers (in vivo); 7 smokers, 11 nonsmokers (in vitro) Case Control Study
Key resultsBoth smokers and nonsmokers experienced decreased amounts of oral peroxidase after exposure to tobacco smoke, but nonsmokers experienced a greater decrease. The authors stated the results as follows - “After smoking a single cigarette, a sharp drop of OPO activity was observed in both groups: 42.5% in smokers and 58.5% in nonsmokers (p <.05).”
#2) 15133168Snyder/200428 cats were placed in the study; 23 biopsy samples were examined for the resultsAnimal Research
Key resultsFor felines that had oral squamous cell carcinoma, those that were exposed to secondhand tobacco smoke experienced a higher level of the mutated p53 gene than felines that had not been exposed. Longer exposures to the secondhand smoke resulted in a higher level of over expression of p53. The authors stated the results as follows - “Tumor biopsy samples from cats exposed to any ETS [environmental tobacco smoke] were 4.5 times more likely to over express p53 than were tumors from unexposed cats (P = 0.19). Among cats with any ETS exposure, those with 5 years or longer of exposure were 7.0 times more likely to over express p53 (P = 0.38)."
Evidence Search "Mouth Neoplasms"[Mesh] AND "Tobacco Smoke Pollution"[Mesh]
Comments on
The Evidence
For both studies, the evidence was conclusive to their own particular questions. However, in order to further evaluate the validity of the results in relation to the question presented in this CAT, it might be wise to use a larger study group to ensure that the results are representative of the population and that no individual variables are affecting the conclusions. For example, the first study mentioned had <20 subjects per study group. It is difficult to apply a conclusion to the general public that has only been verified on such a small group of subjects. In addition, the study did not directly address oral cancer, but instead studied oral peroxidase activity in the oral cavity. Though those conclusions relate to oral cancer, one cannot draw a direct correlation between secondhand smoke and oral cancer when the study itself does not directly address the correlation. The second study mentioned contains evidence that is more directly related to the presented question; however, the study was performed in animals, thus weakening the validity of the evidence for human subjects. Unfortunately, there are currently no other human subject studies available, so more direct studies should be conducted in the future to further evaluate the effect secondhand tobacco smoke has an effect on lung and heart related conditions.
Applicability Subject selection for this study was based upon examination of their way of life. This evidence is useful for dentists regarding tobacco counseling. While the correlation between tobacco smoke and oral cancer is well—founded, the connection between secondhand tobacco smoke and oral cancer is not at the same extent. This evidence is of practical use for patient populations that are in close contact with smokers.
Specialty/Discipline (Public Health) (General Dentistry) (Periodontics)
Keywords Oral cancer, secondhand smoke, environmental tobacco smoke, p53, oral peroxidase, squamous cell carcinoma
ID# 2374
Date of submission: 03/11/2013spacer
E-mail Macaden@livemail.uthscsa.edu
Author Mabel Macaden
Co-author(s)
Co-author(s) e-mail
Faculty mentor/Co-author Moshtagh R. Farokhi, DDS, MPH
Faculty mentor/Co-author e-mail farokhi@uthscsa.edu
Basic Science Rationale
(Mechanisms that may account for and/or explain the clinical question, i.e. is the answer to the clinical question consistent with basic biological, physical and/or behavioral science principles, laws and research?)
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Comments on the CAT
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