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Background: A recent meta-analysis suggested an association between exposure to paternal smoking during pregnancy and childhood brain tumor risk, but no studies have evaluated whether this association differs by polymorphisms in genes that metabolize tobacco-smoke chemicals., Methods: We assessed 9 functional polymorphisms in 6 genes that affect the metabolism of polycyclic aromatic hydrocarbons (PAH) to evaluate potential interactions with parental smoking during pregnancy in a population-based case-control study of childhood brain tumors. Cases (N = 202) were ≤10 years old, diagnosed from 1984-1991 and identified in three Surveillance, Epidemiology, and End Results (SEER) registries in the western U.S. Controls in the same regions (N = 286) were frequency matched by age, sex, and study center. DNA for genotyping was obtained from archived newborn dried blood spots., Results: We found positive interaction odds ratios (ORs) for both maternal and paternal smoking during pregnancy, EPHX1 H139R, and childhood brain tumors (P(interaction) = 0.02; 0.10), such that children with the high-risk (greater PAH activation) genotype were at a higher risk of brain tumors relative to children with the low-risk genotype when exposed to tobacco smoke during pregnancy. A dose-response pattern for paternal smoking was observed among children with the EPHX1 H139R high-risk genotype only (OR(no exposure) = 1.0; OR(≤3 hours/day) = 1.32, 95% CI: 0.52-3.34; OR(>3 hours/day )= 3.18, 95% CI: 0.92-11.0; P(trend )= 0.07)., Conclusion: Parental smoking during pregnancy may be a risk factor for childhood brain tumors among genetically susceptible children who more rapidly activate PAH in tobacco smoke.

Objective: To analyze the role of smoking, alcohol, coffee and tea in relation to thyroid cancer, we conducted a pooled analysis of 14 case-control studies conducted in the United States, Europe, and Asia., Methods: The sample consisted of 2725 thyroid cancer cases (2247 females, 478 males) and 4776 controls (3699 females, 1077 males). Conditional logistic regression with stratification on study, age at diagnosis, and gender was used to compute odds ratios and 95% confidence intervals., Results: Thyroid cancer risk was reduced in persons who had ever smoked. The relationship was more pronounced in current smokers (OR = 0.6, 95% CI = 0.6-0.7) than former smokers (OR = 0.9, 95% CI = 0.8-1.1). There were significant trends of reduced risk with greater duration and frequency of smoking. For consumption of wine and beer, there was a significant trend of decreasing thyroid cancer risk (p = 0.02) that was not maintained after adjustment for current smoking (p = 0.12). Thyroid cancer risk was not associated with consumption of coffee or tea. These findings were consistent in both gender-specific and histology-specific (papillary and follicular) analyses., Conclusions: Pooled analyses of these geographically diverse case-control data indicate a reduced thyroid cancer risk associated with current smoking. A reduced risk associated with alcohol was eliminated after adjustment for smoking, and caffeinated beverages did not alter thyroid cancer risk.

Acute myelogenous leukemia (AML) is a heterogeneous disease with distinct histologic subtypes likely to have distinct risk factors. The authors examined smoking and the risk of adult AML by French-American-British (FAB) subtype in a Los Angeles County, California, population-based case-control study of 412 cases diagnosed between 1987 and 1994 and 412 matched controls. Consistent with previous studies, smoking was not a substantial risk factor for AML overall (odds ratio (OR) = 1.2, 95% confidence interval (CI): 0.9, 1.6). However, increased risk was observed for FAB subtype M2 (OR = 2.3, 95% CI: 1.1, 4.4), particularly for subjects aged 60-75 years (OR = 3.3, 95% CI: 1.1, 10.0). For M2, significant dose-response was associated with total years smoked (p = 0.02), cigarettes per day (p = 0.007), and product filter status (filtered vs. nonfiltered; p = 0.03). The authors estimate that 42% (standard error = 13%) of M2 cases are attributable to smoking. There were no or weak associations between smoking and increased AML risk for other FAB subtypes. The finding by this study of an association between smoking and FAB subtype M2 confirms a previously published report and suggests that earlier findings of no or weak smoking-AML associations may have been due to lack of subtype-specific analysis.

A large case-control study of children was used to test mothers' reporting of information on fathers' background, lifestyle and occupational factors. For a subset (104) of 1341 enrolled families, both parents were interviewed about fathers' characteristics. Reliability of reporting was determined for fathers' race, education, smoking status, non-recent job history and use of occupational agents. The ability of mothers to report fathers' race, education and smoking status was high (kappa > 0.70). Mothers were generally able to report jobs held by the fathers in the 5 years preceding the birth of the child, but reliability was higher for jobs held for longer (kappa typically above 0.70), rather than shorter periods (kappa above 0.40). The finding that mothers' reporting on fathers' background, lifestyle and non-recent job history was reliable is encouraging, because many studies on childhood health rely exclusively on information from interviews with mothers. However, mothers were not reliably able to describe exposure to specific occupational agents.

Data from a large, population-based case-control study were analyzed to investigate the relationship between prenatal exposure to tobacco smoke and childhood brain tumors (CBTs). A total of 540 CBT patients, diagnosed between 1984 and 1991, were identified from population-based tumor registries in 19 West Coast counties that included Seattle, WA (13 counties), San Francisco, CA (5 counties), and Los Angeles, CA (1 county). Random digit dial was used to select 801 control subjects from the three geographical regions to obtain a case:control ratio of 1:2 in San Francisco and Seattle and 1:1 in Los Angeles. The data first were analyzed separately by geographical site and then were combined with adjustments made for gender, age at the time of diagnosis (or reference date of control subjects), birth year of the index child, and maternal race. No association was found between the risk of CBTs and maternal or paternal smoking before pregnancy and there was no association between CBTs and maternal smoking during pregnancy [odds ratio (OR) = 0.98; 95% confidence interval (CI) = 0.72-1.3]. A slightly increased OR for CBTs was found for paternal smoking during pregnancy in the absence of maternal smoking (OR = 1.2; 95% CI = 0.90-1.5) and for maternal exposure to passive smoke from any source (OR = 1.2; 95% CI = 0.95-1.6). The results of this analysis are consistent with results from several prior epidemiological studies that showed no significant association between CBTs and maternal smoking before or during pregnancy or maternal exposure to passive smoke during pregnancy.

Brain tumors are the second most common cancer in children after leukemia, yet the etiology of childhood brain tumors remains unknown. Tobacco smoke contains several dozen compounds that are known to be carcinogens. Among these are N-nitroso compound precursors, principally tobacco-specific nitrosamines. Although smoking has not been identified as a significant risk factor for the development of brain tumors in adults, fetuses and infants have incompletely formed blood-brain barriers that may allow the passage of carcinogenic tobacco metabolites into the central nervous system and initiate the formation of neural tumors. In this review, we present data from case-control and cohort studies published between 1971 and 1995 that examined the relationship between parental smoking during pregnancy and childhood brain tumors (CBTs). The majority of these studies found little association between CBTs and maternal smoking before or during pregnancy or between CBTs and maternal exposure to passive smoke during pregnancy.

The IARC collaborative study on exposure to environmental tobacco smoke (ETS) involved collecting interview data and biochemical indicators of exposure from 1369 nonsmoking women in 13 centers in 10 countries. Information on childhood and adulthood exposure to other people's smoke and duration of this exposure from both parents and spouse was gathered at the interview. Of the 900 women whose husbands smoked (current or exsmokers), 71.3% had one or both parents who smoked (predominantly the father), whereas among the 277 women married to never-smokers, only 60.3% had at least one parent who smoked. The odds ratio for the daughter of a smoker to marry a smoker was, therefore, 1.64 (95% confidence interval = 1.24-2.17; P > 0.001), and there was an exposure-response relation between the number of years of childhood exposure to ETS from the parents and the likelihood of being married to a smoker. These results show that nonsmoking women married to smokers are more likely to have been exposed to tobacco pollution during their whole life. Because the duration of exposure is known to be important in the genesis of lung cancer, some of the excess risk of lung cancer in nonsmoking women married to smokers may be due exposure to ETS from parents during childhood.

In studies of the health effects of exposure to environmental tobacco smoke (ETS), misclassification of active smokers has the potential to bias the estimates of disease risk. Biochemical validation of exposure to ETS can provide objective evidence of current smoking status in epidemiological studies. Intrinsic to this effort is the establishment of appropriate cut-off points for the measurements of tobacco biomarkers. Within a collaborative study on ETS co-ordinated by the International Agency for Research on Cancer, questionnaire data and urine samples were collected from 1,369 women at 13 centres in 10 countries. Forty seven of these women had urine cotinine levels above 50 ng.mg-1 creatinine, a level used to discriminate smokers from nonsmokers in previous studies. The distributions of the subjects across cotinine values and self-reported exposure to ETS was consistent with the association, at one extreme, of moderate cotinine levels (50-150 ng.mg-1) with very high exposure to ETS, and, at the other extreme, of very high cotinine levels indicating actual use of nicotine-containing products in women with low ETS exposure. Using the cut-off point of 150 ng.mg-1, only 1.5% of the alleged nonsmokers were reclassified as current light smokers. Potential bias due to smoker misclassification is very unlikely to be responsible for the increased health risks observed in epidemiological studies on ETS.

Background: The exceptionally high rate of second primary cancers among patients with oral and pharyngeal cancers is well recognized, yet there has been limited epidemiologic study of risk factors for second tumors., Purpose: To evaluate the relation of smoking and alcohol consumption to the development of second cancers among this high-risk patient group, we conducted a nested case-control study., Methods: A total of 1090 patients enrolled in a 1984-1985 population-based, case-control study of oral cancer in four areas of the United States were followed through June 1989 for the occurrence of second primary cancers. Information on tobacco and alcohol consumption was obtained from the original interviews and was updated by follow-up interviews obtained for 80 case patients with second cancers and 189 sex-, study area-, and survival-matched cancer patients free of second cancers (control subjects)., Results: Tobacco smoking and alcohol drinking each contributed to risk of second cancers, with the effects of smoking more pronounced than those of alcohol. The odds ratios (ORs) for smoking (adjusted for alcohol) rose with duration and intensity of smoking and were strongest for tumors of the aerodigestive tract (oral cavity, pharynx, esophagus, larynx, and lungs), with ORs reaching 4.7 (95% confidence interval [CI] = 1.4-16) among smokers of 40 or more cigarettes per day for 20 or more years. Current smokers as of the baseline survey experienced a fourfold increased risk of a second aerodigestive tract cancer relative to nonsmokers and former smokers. No reduction in risk was associated with cessation of smoking or drinking at or after the index diagnosis, although the short median interval (27 months) between tumor diagnoses limited observation of the effects due to recent cessation. Risk was significantly reduced, however, 5 years after smoking cessation. Among drinkers, second cancer risk was greatest for beer intake, with an OR for a second aerodigestive tract cancer of 3.8 (95% CI = 1.2-12) for 15 or more beers per week., Conclusions: Oral and pharyngeal cancer patients with the highest intakes of tobacco and alcohol are the ones most prone to develop second primary cancers., Implications: Avoidance of tobacco smoking and alcohol drinking is the most desirable way not only to prevent primary oral cancers, but also to reduce risk of second cancers of the aerodigestive system.

Background: In the United States, Blacks have increasingly higher rates of oral and pharyngeal cancer (oral cancer) than Whites, but determinants of the racial disparity have not been clear., Purpose: The purpose of this study was to explore reasons for the higher incidence of oral cancer among Blacks than Whites., Methods: We used data from a large, population-based case-control study of oral cancer risk factors conducted in four areas of the United States. On the basis of interviews that ascertained characteristics of 1065 oral cancer patients (871 Whites and 194 Blacks) and 1182 controls (979 Whites and 203 Blacks), we examined racial differences in exposure prevalences and relative risks for a number of known etiologic factors, including tobacco and alcohol consumption, diet, and socioeconomic and other variables. To evaluate the extent to which the major risk factors explained the excess risk of oral cancer among Blacks, population-attributable risks were calculated., Results: Differences with respect to alcohol consumption, especially among current smokers, emerged as the most important explanatory variables. After adjusting for smoking, heavy drinking (> or = 30 drinks/week) resulted in a 17-fold increased risk among Blacks and a ninefold increase among Whites. Among drinkers, Blacks tended to drink more than Whites. Also, a higher (P = .01) percentage of Blacks (37%) than Whites (28%) were current smokers, although there were little or no racial differences in relative risks or patterns of use for other smoking variables, including number of cigarettes smoked per day, years of smoking, and age started smoking. From population-attributable risk calculations, we estimated that differences in alcohol and tobacco use account for the bulk of the higher incidence of oral cancer among Blacks in the United States and that, in the absence of alcohol and tobacco, the rates of this cancer according to race (Black, White) and gender would be nearly equal. With regard to other potential etiologic factors, protective effects provided by higher dietary intake of fruits and vitamin C were more pronounced for Whites, while Blacks more often tended to be in sociodemographic and medical or dental health categories associated with increased risk., Conclusions: These analyses provide evidence that various environmental or lifestyle determinants of oral cancer may contribute to the higher oral cancer rates in Blacks than in Whites in the United States, but that patterns and risks associated with alcohol consumption, particularly among current smokers, are the most important contributors to the excess risk in Blacks., Implications: These findings suggest that the key to prevention of oral and pharyngeal cancers among both Blacks and Whites is reduced intake of alcoholic beverages and, because of strong interactive effects, the cessation of smoking.

A case-control study of oral and pharyngeal cancer conducted in four areas of the United States provided information on the tobacco and alcohol use of 1114 patients and 1268 population-based controls. Because of the large study size, it could be shown that the risks of these cancers among nondrinkers increased with amount smoked, and conversely that the risks among nonsmokers increased with the level of alcohol intake. Among consumers of both products, risks of oropharyngeal cancer tended to combine more in a multiplicative than additive fashion and were increased more than 35-fold among those who consumed two or more packs of cigarettes and more than four alcoholic drinks/day. Cigarette, cigar, and pipe smoking were separately implicated, although it was shown for the first time that risk was not as high among male lifelong filter cigarette smokers. Cessation of smoking was associated with a sharply reduced risk of this cancer, with no excess detected among those having quit for 10 or more years, suggesting that smoking affects primarily a late stage in the process of oropharyngeal carcinogenesis. The risks varied by type of alcoholic beverage, being higher among those consuming hard liquor or beer than wine. The relative risk patterns were generally similar among whites and blacks, and among males and females, and showed little difference when oral and pharyngeal cancers were analyzed separately. From calculations of attributable risk, we estimate that tobacco smoking and alcohol drinking combine to account for approximately three-fourths of all oral and pharyngeal cancers in the United States.

Background: In the United States, Blacks have increasingly higher rates of oral and pharyngeal cancer (oral cancer) than Whites, but determinants of the racial disparity have not been clear.Purpose: The purpose of this study was to explore reasons for the higher incidence of oral cancer among Blacks than Whites.Methods: We used data from a large, population-based case-control study of oral cancer risk factors conducted in four areas of the United States. On the basis of interviews that ascertained characteristics of 1065 oral cancer patients (871 Whites and 194 Blacks) and 1182 controls (979 Whites and 203 Blacks), we examined racial differences in exposure prevalences and relative risks for a number of known etiologic factors, including tobacco and alcohol consumption, diet, and socioeconomic and other variables. To evaluate the extent to which the major risk factors explained the excess risk of oral cancer among Blacks, population-attributable risks were calculated.Results: Differences with respect to alcohol consumption, especially among current smokers, emerged as the most important explanatory variables. After adjusting for smoking, heavy drinking (> or = 30 drinks/week) resulted in a 17-fold increased risk among Blacks and a ninefold increase among Whites. Among drinkers, Blacks tended to drink more than Whites. Also, a higher (P = .01) percentage of Blacks (37%) than Whites (28%) were current smokers, although there were little or no racial differences in relative risks or patterns of use for other smoking variables, including number of cigarettes smoked per day, years of smoking, and age started smoking. From population-attributable risk calculations, we estimated that differences in alcohol and tobacco use account for the bulk of the higher incidence of oral cancer among Blacks in the United States and that, in the absence of alcohol and tobacco, the rates of this cancer according to race (Black, White) and gender would be nearly equal. With regard to other potential etiologic factors, protective effects provided by higher dietary intake of fruits and vitamin C were more pronounced for Whites, while Blacks more often tended to be in sociodemographic and medical or dental health categories associated with increased risk.Conclusions: These analyses provide evidence that various environmental or lifestyle determinants of oral cancer may contribute to the higher oral cancer rates in Blacks than in Whites in the United States, but that patterns and risks associated with alcohol consumption, particularly among current smokers, are the most important contributors to the excess risk in Blacks.Implications: These findings suggest that the key to prevention of oral and pharyngeal cancers among both Blacks and Whites is reduced intake of alcoholic beverages and, because of strong interactive effects, the cessation of smoking. [ABSTRACT FROM AUTHOR]