Environmental tobacco smoking, mutagen sensitivity, and head and neck squamous cell carcinoma

Zf. Zhang et al., Environmental tobacco smoking, mutagen sensitivity, and head and neck squamous cell carcinoma, CANC EPID B, 9(10), 2000, pp. 1043-1049
Citations number
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
ISSN journal
1055-9965 → ACNP
Year of publication
1043 - 1049
SICI code
Although active tobacco smoking has been considered a major risk factor for head and neck cancer, few studies have evaluated environmental tobacco smo ke (ETS) and its interaction with mutagen sensitivity on the risk of head a nd neck cancer. We investigated the relationship between ETS and head and n eck cancer in a case-control study of 173 previously untreated cases with p athologically confirmed diagnoses of squamous cell carcinoma of the head an d neck and 176 cancer-free controls at Memorial Sloan-Kettering Cancer Cent er between 1992 and 1994, A structured questionnaire was used to collect ET S exposure and other covariates including a history of active tobacco smoki ng and alcohol use. ETS measures include a history of ETS exposure at home and at workplace. The associations between passive smoking and head and nec k cancer were analyzed by Mantel-Haenszel methods and logistic regression m odels. Additive and multiplicative models were used to evaluate effect modi fications between ETS and mutagen sensitivity. The crude odds ratio (OR) fo r ETS exposure was 2.8 [95% confidence intervals (CI), 1.3-6.0], Controllin g for age, sex, race, education, alcohol consumption, pack-years of cigaret te smoking, and marijuana use, the risk of squamous cell carcinoma of the h ead and neck was increased with ETS (adjusted OR, 2.4; 95% CI, 0.9-6.8). Do se-response relationships were observed for the degree of ETS exposure; the adjusted ORs were 2.1 (95% CI, 0.7-6.1) for those with moderate exposure a nd 3.6 (95% CI, 1.1-11.5) for individuals with heavy exposure (P for trend = 0.025), in comparison with those who never had ETS exposures. These assoc iations and the dose-response relationships were still present when the ana lysis was restricted to nonactive smoking cases and controls (crude OR, 2.2 ; 95% CI, 0.6-8.4), Crude odds ratios were 1.8 for those with moderate ETS exposure and 4.3 for individuals with heavy ETS exposure among nonsmoking c ases and controls (P for trend = 0.008). More than multiplicative interacti on was suggested between passive smoking and mutagen sensitivity. This stud y suggests that ETS exposure may increase the risk of head and neck cancer with a dose-response pattern. Our analysis indicated that passive smoking m ay interact with mutagen sensitivity and other risk factors to increase the risk of head and neck cancer. Our results need to be interpreted with caut ion because of potential residual confounding effects of active tobacco smo king and other methodological limitations. Future large-scale studies are w arranted to confirm our findings.