Environmental exposure to cooking oil fumes and cervical intraepithelial neoplasm.

The fumes from cooking oil, similar to cigarette smoke, contain numerous carcinogens such as polycyclic aromatic hydrocarbons, aromatic amines, nitro-polycyclic aromatic hydrocarbons, etc. In this study, we examined the association between exposure to cooking oil fumes and the risk of cervical intraepithelial neoplasm. The study population in this nested case-control study consisted of women above the age of 19 years living in Chia-Yi County, located in the southwestern Taiwan, who had received pap smear screening between October, 1999, and December, 2000 (n=32,466). The potential cases were women having lesions greater than cervical intraepithelium neoplasm II (> or =CIN2) reconfirmed by cervical biopsy (n=116). The potential controls (case: control=1:2) were age-matched (+/-2 years) and residence-matched women who had normal pap smears within 6 months of the cases. In total, 100 cases and 197 controls were completely interviewed by public health nurses about cooking methods, ventilation, and other potential risk factors. Women who cooked at home in a kitchen (n=269) without the presence of a fume extractor at least once a week between the ages of 20 and 40 had a 2.29 times higher risk [95% confidence interval (CI)=1.08-4.87] of developing cervical intraepithelial neoplasm than those who did not cook once a week in such a kitchen during the same age span, after adjusting for other potential confounders. This finding was further strengthened by the finding that women who did not use the fume extractors had a 2.47 times higher risk (95% CI=1.15-5.32) of developing cervical intraepithelial neoplasm than women who cooked in kitchens with fume extractors that were always switched on while cooking. We also found a joint protective effect of fume extractor use among women older than 40 years (n=202) if they used the extractors during both age spans of their lives, ages 20-40 and >40 years. Comparing our findings on women more than 40 years old who used fume extractors during both periods, we found a 2.05-fold greater risk (95% CI=0.86-4.86) for those who used exhaust fans during only one of the two age spans and a 3.46-fold greater risk in those who had not used an exhaust fan for either period (95% CI=1.08-11.10) (trend test, P=0.02). While exposure to cooking oil fumes may cause cervical intraepithelial neoplasm, women can be protected from this risk by always cooking in kitchens equipped with fume extractors and by keeping them on while cooking.

Lifetime exposure to environmental tobacco smoke and cervical intraepithelial neoplasms among nonsmoking Taiwanese women.

Cigarette smoke is one of the most important environmental risk factors for the development of cervical intraepithelial neoplasms (CINs). Given that the prevalence of cigarette smoking in Taiwanese women is very low, compared with Caucasian women (3-4% vs. approximately 28%, respectively), direct smoking is likely a minimal risk factor in the Taiwanese group. However, the evaluation of the association between indirect tobacco exposure, or exposure to environmental tobacco smoke (ETS), and CIN risk in Taiwanese women may be enlightening. The authors designed a community-based nested case-control study to examine the association between ETS exposure and CIN risk among Taiwanese women who were nonsmokers. The study was conducted in Chia-Yi, a city in southwestern Taiwan. The test population comprised adult females (n = 32,466) who had undergone Pap smear screening during the 14-mo period that preceded this study. Potential cases were chosen from individuals who demonstrated positive Pap smear results, which were indicative of at least a level II cervical intraepithelial neoplasm (i.e., > or = CIN2), as confirmed by cervical biopsy (n = 116). The authors chose 2 matched controls for each case; criteria used were (a) the 2 controls for each case had to be approximately the same age (+/- 2 yr) as the case; (b) each case and respective control lived in the same residential area; and (c) each control had a negative Pap smear, determined during the same time frame (+/- 6 mo) that the matched study subject was tested. A total of 100 study subjects and 197 control females (3 cases had only 1 control) underwent interviews by public health nurses, who obtained information about the participants' active and passive smoking histories and other potential risk factors. The incidence of cigarette smoking was low (5.0% [n = 5]) in study subjects and lower in controls (3.1% [n = 6]). The authors' final analysis was restricted to 89 nonsmoking pairs (89 subjects and 175 controls). Of the affected subjects, 85.4% reported exposure to passive smoke at home during their adulthood, vs. 61.1% of controls. The authors found that, after adjusting for other covariates, there was a 2.73-fold increased risk of contracting CIN (95% confidence interval [CI] = 1.31, 5.67) among ETS-exposed individuals. The authors assessed cumulative dose in terms of pack-years (i.e., average daily exposure [number of packs smoked] multiplied by the number of years the same exposure continued). Compared with nonsmokers, women exposed to 1-20 pack-yr and more than 20 pack-yr had 1.90-fold (95% CI = 0.72, 5.03) and 2.99-fold (95% CI = 1.10, 8.09) increased risks, respectively, of developing CIN. The authors concluded that lifetime ETS exposure is a major determinant for contracting cervical neoplasms among nonsmoking women in Taiwan.

No association between polymorphisms of the DNA repair geneXRCC1 and cervical neoplasm risk.

OBJECTIVES: To investigate the association between genetic polymorphisms ofX-ray repair crosscomplementing group 1 (XRCC1) codons 194, 280, and 399 and cervical neoplasm susceptibility. METHODS: A community-based nested case-control study was conducted. The study population consisted of women living in Chiayi City, located in southwestern Taiwan, who had received pap smear screening between October, 1999, and December, 2000 (n=32,466). The potential cases were women having lesions greater than cervical intraepithelium neoplasm II (C1N2) reconfirmed by cervical biopsy. The potential controls (case: control=1∶2) were age matched (±2 yrs) and residency matched women who had had normal pap smears. In total, 100 cases (39 C1N2, 12 C1N3, 46 carcinoma in situ (CIS), and 3 invasive cancer) and 196 controls had the information on both questionnaire and data ofXRCC1 polymorphisms. RESULTS: The frequency ofArg/Arg, Arg/Gln, andGln/Gln in codon 399 among cases and controls was 54% (54/100), 38% (38/100), and 8% (8/100) and 58% (114/196), 37% (73/196), and 5% (9/196), respectively, which were not significantly different. No associations were also observed betweenXRCC1 codon 194 and 280 genotypes and cervical neoplasm. While dichotomized by age (<40 vs. ≥40 yrs), smoking status (active and passive smokers vs. non-smokers), and disease status (C1N2 and C1N3 vs. CIS and invasive cancer), the results remained insignificant. CONCLUSIONS: The present findings suggest thatXRRC1 codon 194, 280 and 399 genotypes may not influence cervical neoplasm risk in the Taiwanese population.