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Biomedical subjects

G R Howe

Publications and source records attributed to G R Howe.

At least 55 records · Page 3Linked to original sources
PubMed1995

Lung cancer in radon-exposed miners and estimation of risk from indoor exposure.

BACKGROUND: Radioactive radon is an inert gas that can migrate from soils and rocks and accumulate in enclosed areas, such as homes and underground mines. Studies of miners show that exposure to radon decay products causes lung cancer. Consequently, it is of public health interest to estimate accurately the consequences of daily, low-level exposure in homes to this known carcinogen. Epidemiologic studies of residential radon exposure are burdened by an inability to estimate exposure accurately, low total exposure, and subsequent small excess risks. As a result, the studies have been inconclusive to date. Estimates of the hazard posed by residential radon have been based on analyses of data on miners, with recent estimates based on a pooling of four occupational cohort studies of miners, including 360 lung cancer deaths. PURPOSE: To more fully describe the lung cancer risk in radon-exposed miners, we pooled original data from 11 studies of radon-exposed underground miners, conducted a comprehensive analysis, and developed models for estimating radon-associated lung cancer risk. METHODS: We pooled original data from 11 cohort studies of radon-exposed underground miners, including 65,000 men and more than 2700 lung cancer deaths, and fit various relative risk (RR) regression models. RESULTS: The RR relationship for cumulative radon progeny exposure was consistently linear in the range of miner exposures, suggesting that exposures at lower levels, such as in homes, would carry some risk. The exposure-response trend for never-smokers was threefold the trend for smokers, indicating a greater RR for exposure in never-smokers. The RR from exposure diminished with time since the exposure occurred. For equal total exposure, exposures of long duration (and low rate) were more harmful than exposures of short duration (and high rate). CONCLUSIONS: In the miners, about 40% of all lung cancer deaths may be due to radon progeny exposure, 70% of lung cancer deaths in never-smokers, and 39% of lung cancer deaths in smokers. In the United States, 10% of all lung cancer deaths might be due to indoor radon exposure, 11% of lung cancer deaths in smokers, and 30% of lung cancer deaths in never-smokers. This risk model estimates that reducing radon in all homes exceeding the U. S. Environmental Protection Agency's recommended action level may reduce lung cancer deaths about 2%-4%. These estimates should be interpreted with caution, because concomitant exposures of miners to agents such as arsenic or diesel exhaust may modify the radon effect and, when considered together with other differences between homes and mines, might reduce the generalizability of findings in miners.

Adult↗
PubMed1995

Prostate cancer in relation to diet, physical activity, and body size in blacks, whites, and Asians in the United States and Canada.

BACKGROUND: International and interethnic differences in prostate cancer incidence suggest an environmental, potentially modifiable etiology for the disease. PURPOSE: We conducted a population-based case-control study of prostate cancer among blacks (very high risk), whites (high risk), and Asian-Americans (low risk) in Los Angeles, San Francisco, Hawaii, Vancouver, and Toronto. Our aim was to evaluate the roles of diet, physical activity patterns, body size, and migration characteristics on risk in these ethnic groups and to assess how much of the interethnic differences in risk might be attributed to interethnic differences in such lifestyle characteristics. METHODS: We used a common protocol and questionnaire to administer personal interviews to 1655 black, white, Chinese-American, and Japanese-American case patients diagnosed during 1987-1991 with histologically confirmed prostate carcinoma and to 1645 population-based control subjects matched to case patients by age, ethnicity, and region of residence. Sera collected from 1127 control subjects were analyzed for levels of prostate-specific antigen (PSA) to permit comparison of case patients with control subjects lacking serological evidence of prostate disease. Odds ratios were estimated using conditional logistic regression. We estimated the proportion of prostate cancer attributable to certain risk factors and the proportion of interethnic risk differences attributable to interethnic differences in risk-factor prevalence. RESULTS: A positive statistically significant association of prostate cancer risk and total fat intake was found for all ethnic groups combined. This association was attributable to energy from saturated fats; after adjusting for saturated fat, risk was associated only weakly with monounsaturated fat and was unrelated to protein, carbohydrate, polyunsaturated fat, and total food energy. Saturated fat intake was associated with higher risks for Asian-Americans than for blacks and whites. In all ethnic groups combined, the risk tended to be higher when only case patients with advanced disease were compared with control subjects with normal PSA levels. Among foreign-born Asian-Americans, risk increased independently with years of residence in North America and with saturated fat intake. Crude estimates suggest that differences in saturated fat intake account for about 10% of black-white differences and about 15% of white-Asian-American differences in prostate cancer incidence. Risk was not consistently associated with intake of any micronutrients, body mass, or physical activity patterns. CONCLUSIONS: These data support a causal role in prostate cancer for saturated fat intake but suggest that other factors are largely responsible for interethnic differences in risk.

Black or African American↗
PubMed1995

Vasectomy and prostate cancer: results from a multiethnic case-control study.

BACKGROUND: Vasectomy, a widely used form of contraception, has been associated in some studies with increased prostate cancer risk. PURPOSE: We assessed this association on the basis of data collected in a large multiethnic case-control study of prostate cancer that was conducted in the United States (Los Angeles, San Francisco, and Hawaii) and Canada (Toronto and Vancouver). METHODS: In home interviews conducted with newly diagnosed prostate cancer case patients and population control subjects, we obtained information on the participants' medical history, including a history of vasectomy and the age at which the procedure was performed, as well as other potential risk factors. Blood samples were collected from control subjects only and were assayed for concentration of sex hormones and sex hormone-binding globulin. RESULTS: The present analysis was based on 1642 prostate cancer patients and 1636 control subjects. A history of vasectomy was not significantly associated with prostate cancer risk among all racial/ethnic groups combined (odds ratio [OR] = 1.1; 95% confidence interval [CI] = 0.83-1.3), whites (OR = 0.94; 95% CI = 0.69-1.3), blacks (OR = 1.0; 95% CI = 0.59-1.8), or Chinese-Americans (OR = 0.96; 95% CI = 0.42-2.2). Among Japanese-Americans, the OR was 1.8 (95% CI = 0.97-3.4), but the statistically nonsignificant elevation in risk was limited to more educated men and those with localized cancers. ORs did not vary significantly by age at vasectomy or years since vasectomy. We found a lower serum concentration of sex hormone-binding globulin and a higher ratio of dihydrotestosterone to testosterone among vasectomized control subjects than among nonvasectomized control subjects. CONCLUSIONS: The findings of this study do not support previous reports of increased prostate cancer risk associated with vasectomy. However, the altered endocrine profiles of vasectomized control subjects seen in this cross-sectional comparison warrant further evaluation in longitudinal studies.

Aged↗
PubMed1995

Family history and prostate cancer risk in black, white, and Asian men in the United States and Canada.

Increased risk of prostate cancer in men with a family history of the disease has been observed consistently in epidemiologic studies. However, most studies have been confined to white men; little is known about familial aggregation of prostate cancer in populations with unusually high incidence, such as African Americans, or in populations with low incidence, such as Asian-Americans. The authors report results from a population-based case-control study of prostate cancer among blacks, whites, and Asian-Americans in the United States and Canada. Controls were matched to cases on age (5-year groups), ethnicity (black, white, Chinese-American, Japanese-American), and region of residence (Los Angeles, San Francisco, Hawaii, Vancouver, Toronto). In the combined group of participants, 5% of controls and 13% of cases reported a father, brother, or son with prostate cancer. These prevalences were somewhat lower among Asian-Americans than among blacks or whites. A positive family history was associated with a statistically significant two- to threefold increase in risk in each of the three ethnic groups. The overall odds ratio associated with such a family history, adjusted for age and ethnicity, was 2.5 (95% confidence interval 1.9-3.3). This odds ratio varied by neither ethnicity nor age of the participants. Sera from 1,087 controls were used to examine the relations between family history and serum concentrations of androgens and prostate-specific antigen. The concentrations of sex hormone-binding globulin were slightly higher in men with than without a positive family history. Prostate-specific antigen concentrations were unrelated to family history.

Aged↗
PubMed1995

Radon and cancers other than lung cancer in underground miners: a collaborative analysis of 11 studies.

BACKGROUND: Exposure to the radioactive gas radon and its progeny (222Rn and its radioactive decay products) has recently been linked to a variety of cancers other than lung cancer in geographic correlation studies of domestic radon exposure and in individual cohorts of occupationally exposed miners. PURPOSE: This study was designed to characterize further the risks for cancers other than lung cancer (i.e., non-lung cancers) from atmospheric radon. METHODS: Mortality from non-lung cancer was examined in a collaborative analysis of data from 11 cohorts of underground miners in which radon-related excesses of lung cancer had been established. The study included 64,209 men who were employed in the mines for 6.4 years on average, received average cumulative exposures of 155 working-level months (WLM), and were followed for 16.9 years on average. RESULTS: For all non-lung cancers combined, mortality was close to that expected from mortality rates in the areas surrounding the mines (ratio of observed to expected deaths [O/E] = 1.01; 95% confidence interval [CI] = 0.95-1.07, based on 1179 deaths), and mortality did not increase with increasing cumulative exposure. Among 28 individual cancer categories, statistically significant increases in mortality for cancers of the stomach (O/E = 1.33; 95% CI = 1.16-1.52) and liver (O/E = 1.73; 95% CI = 1.29-2.28) and statistically significant decreases for cancers of the tongue and mouth (O/E = 0.52; 95% CI = 0.26-0.93), pharynx (O/E = 0.35; 95% CI = 0.16-0.66), and colon (O/E = 0.77; 95% CI = 0.63-0.95) were observed. For leukemia, mortality was increased in the period less than 10 years since starting work (O/E = 1.93; 95% CI = 1.19-2.95) but not subsequently. For none of these diseases was mortality significantly related to cumulative exposure. Among the remaining individual categories of non-lung cancer, mortality was related to cumulative exposure only for cancer of the pancreas (excess relative risk per WLM = 0.07%; 95% CI = 0.01-0.12) and, in the period less than 10 years since the start of employment, for other and unspecified cancers (excess relative risk per WLM = 0.22%; 95% CI = 0.08-0.37). CONCLUSIONS: The increases in mortality from stomach and liver cancers and leukemia are unlikely to have been caused by radon, since they are unrelated to cumulative exposure. The association between cumulative exposure and pancreatic cancer seems likely to be a chance finding, while the association between cumulative exposure and other and unspecified cancers was caused by deaths certified as due to carcinomatosis (widespread disseminated cancer throughout the body) that were likely to have been due to lung cancers. This study, therefore, provides considerable evidence that high concentrations of radon in air do not cause a material risk of mortality from cancers other than lung cancer. IMPLICATIONS: Protection standards for radon should continue to be based on consideration of the lung cancer risk alone.

Adult↗
PubMed1995

Dietary factors and risk of prostate cancer: a case-control study in Ontario, Canada.

The relationship between risk of prostate cancer and dietary intake of energy, fat, vitamin A, and other nutrients was investigated in a case-control study conducted in Ontario, Canada. Cases were men with a recent, histologically confirmed diagnosis of adenocarcinoma of the prostate notified to the Ontario Cancer Registry between April 1990 and April 1992. Controls were selected randomly from assessment lists maintained by the Ontario Ministry of Revenue, and were frequency-matched to the cases on age. The study included 207 cases (51.4 percent of those eligible) and 207 controls (39.4 percent of those eligible), and information on dietary intake was collected from them by means of a quantitative diet history. There was a positive association between energy intake and risk of prostate cancer, such that men at the uppermost quartile level of energy intake had a 75 percent increase in risk. In contrast, there was no clear association between the non-energy effects of total fat and monounsaturated fat intake and prostate cancer risk. There was some evidence for an inverse association with saturated fat intake, although the dose-response pattern was irregular. There was a weak (statistically nonsignificant) positive association between polyunsaturated fat intake and risk of prostate cancer. Relatively high levels of retinol intake were associated with reduced risk, but there was essentially no association between dietary beta-carotene intake and risk. There was no alteration in risk in association with dietary fiber, cholesterol, and vitamins C and E. Although these patterns were evident both overall and within age-strata, and persisted after adjustment for a number of potential confounding factors, they could reflect (in particular) the effect of nonrespondent bias.

Adenocarcinoma↗
PubMed1995

Lung cancer mortality between 1950 and 1987 after exposure to fractionated moderate-dose-rate ionizing radiation in the Canadian fluoroscopy cohort study and a comparison with lung cancer mortality in the Atomic Bomb survivors study.

Current lung cancer risk estimates after exposure to low-linear energy transfer radiation such as X rays are based on studies of people exposed to such radiation at high dose rates, for example the atomic bomb survivors. Radiobiology and animal experiments suggest that risks from exposure at low to moderate dose rates, for example medical diagnostic procedures, may be over-estimated by such risk models, but data for humans to examine this issue are limited. In this paper we report on lung cancer mortality between 1950 and 1987 in a cohort of 64,172 Canadian tuberculosis patients, of whom 39% were exposed to highly fractionated multiple chest fluoroscopies leading to a mean lung radiation dose of 1.02 Sv received at moderate dose rates. These data have been used to estimate the excess relative risk per sievert of lung cancer mortality, and this is compared directly to estimates derived from 75,991 atomic bomb survivors. Based on 1,178 lung cancer deaths in the fluoroscopy study, there was no evidence of any positive association between risk and dose, with the relative risk at 1 Sv being 1.00 (95% confidence interval 0.94, 1.07), which contrasts with that based on the atomic bomb survivors, 1.60 (1.27, 1.99). The difference in effect between the two studies almost certainly did not arise by chance (P = 0.0001). This study provides strong support from data for humans for a substantial fractionation/dose-rate effect for low-linear energy transfer radiation and lung cancer risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Parity, contraception, infertility, and the risk of epithelial ovarian cancer.

A case-control study of reproductive factors and cancer of the ovary was conducted during 1989-1992 in metropolitan Toronto and nearby areas of Southern Ontario, Canada. In total, 450 women aged 35-79 years with histologically verified new primary epithelial ovarian cancers were interviewed concerning their reproductive histories. Over the same time period, 564 randomly selected population controls, frequency-matched to the cases according to three 15-year age groups, were also interviewed. Continuous unconditional logistic regression methods were used for analysis. It was found that childbearing and use of oral contraceptives were associated with significant decreasing trends in risk of ovarian cancer; the respective odds ratios were 0.78 for each full-term pregnancy (p < 10(-8)) and 0.92 for each year of use (p < 10(-6)). Hysterectomy was also associated with reduced risk, even after more than 20 years. Among parous women, infertility did not appear to affect risk; for nulliparous women, some evidence of increased risk was present, although fertility problems were reported by only a small fraction of nulliparae. It is suggested that the relatively lower parity of cases as compared with controls may be due to voluntary choices for having fewer children.

Adult↗
PubMed1994

Dietary fat intake and risk of epithelial ovarian cancer.

BACKGROUND: Evidence exists that dietary fat may be a contributory factor in the development of hormone-related cancers such as ovarian cancer. Previous studies have demonstrated significantly higher circulating-estrogen levels among nonvegetarian women than among vegetarian women; the increase correlated directly with consumption of saturated fat. However, the contribution that dietary fat plays in the development of hormone-related cancers remains unresolved. PURPOSE: Our purpose was to evaluate whether saturated fat intake increases the risk of ovarian cancer development. METHODS: Population-based sampling was used to acquire cases and controls over a 3-year period from the study area, which included the highly populated region surrounding the western end of Lake Ontario, Canada. From the Ontario Cancer Registry, all histologically confirmed, primary malignant or borderline malignant epithelial ovarian tumors first diagnosed from November 1989 through October 1992 among study-area residents aged 35-79 years were determined. In total, 631 eligible case subjects were identified, of whom 450 (71.3%) were interviewed concerning reproduction and diet; 564 randomly selected population control subjects were similarly interviewed. From the quantitative diet-history information, average daily intakes of macronutrients and micronutrients were calculated. Unconditional continuous logistic regression methods were used for analysis, with adjustment for age at interview, number of full-term pregnancies, years of oral contraceptive use, and total daily caloric intake. RESULTS: Saturated fat consumption was associated with increasing risk of ovarian cancer (odds ratio [OR] = 1.20 for each 10 g/day of intake; 95% confidence interval [CI] = 1.03-1.40; one-sided P = .0082). No relationship was seen with intake of unsaturated fats. Egg consumption also appeared related to increased risk (OR = 1.42 for each 100 mg of egg cholesterol per day; 95% CI = 1.18-1.72; two-sided P = .0002), though this association may have resulted from disease-related changes in the dietary practices of case subjects prior to diagnosis. Consumption of vegetable fiber (but not fruit or cereal fiber) was associated with decreased risk (OR = 0.63 for each 10 g/day; 95% CI = 0.49-0.80; two-sided P = .0001). All three nutrients (saturated fat, egg cholesterol, and vegetable fiber) remained statistically significant when included in the same regression model. CONCLUSION: Diet may contribute to risk of ovarian cancer development. IMPLICATION: If confirmed in further studies, this association may allow women to appreciably lower their risk of ovarian cancer through dietary modifications: reducing the intake of saturated fats and eating more vegetables.

Adult↗
PubMed1994

Dietary fat and breast cancer risks. An epidemiologic perspective.

BACKGROUND: Breast cancer is one of the most important public health problems facing women in the United States and similar populations today. No readily modifiable risk factors for the disease have been conclusively identified, hence establishment of a positive association between fat intake and risk is of major public health importance. METHODS: An evaluation of the strengths and limitations of epidemiologic studies addressing the postulated association between fat intake and breast cancer risk is presented. In light of this assessment, an evaluation of the results of ecologic and case-control studies has been conducted. RESULTS: Of the three types of epidemiologic studies considered, ecologic studies provide the weakest evidence. Although case-control studies are more prone to bias than cohort studies, there is conflicting evidence as to the existence and magnitude of bias in previously conducted case-control studies. Ecologic studies and case-control studies support the existence of a positive association, particularly for saturated fat intake in postmenopausal women. However, given the methodologic limitations of these types of study and the more equivocal nature of evidence from cohort studies, it would be imprudent to interpret these associations as representing causality. CONCLUSIONS: The totality of the epidemiologic evidence does not support the existence of a strong association between fat intake and breast cancer risk; however, the possibility of a weak association cannot be excluded. Even a weak association could be important in terms of public health. The most fruitful area for future research is likely to be the establishment of new cohort studies and the continued follow-up of existing cohorts, particularly if these could address diet at different times in life, for example, during adolescence.

Adult↗
PubMed1994

Menopausal hormone usage and breast cancer in Saskatchewan: a record-linkage cohort study.

The association between the occurrence of carcinoma of the breast and previous usage of menopausal estrogens, progestins, and oral contraceptives is examined in a record-linkage study using the Saskatchewan Health Prescription-Drug-Plan Database. Saskatchewan Health is a governmental agency that funds publicly insured health care for essentially all residents of the province. For this study, all women aged 43-49 years in 1976 resident in Saskatchewan were identified from the Saskatchewan Health master registration file. These women were linked by registration beneficiary number to the Drug-Plan Database for the period from January 1976 to June 1987 and to the Provincial Cancer Registry Database for the period from March 1960 to December 1990. The fact and date of death or emigration from the province were obtained through the annual updates of the health plan. Of the 33,003 women initially in the cohort, 213 had a breast cancer diagnosed before 1976 and were omitted from this analysis. Between 1976 and 1990, 742 new primary breast cancer cases occurred. Women taking estrogens unopposed by progestins had an elevated risk of breast cancer, the risk increasing by 7% (relative risk = 1.072, 95% confidence interval 1.02-1.13; p = 0.008) for each 252 tablets used (approximately 1 year of use). Usage of estrogens opposed by progestins showed no association with risk (p = 0.48). Women taking oral contraceptives during this follow-up period also had a higher risk, increasing by 14% (relative risk = 1.144, 95% confidence interval 1.05-1.24; p = 0.002) for every 252 tablets used. These 1-year risk elevations are small but become appreciable at longer durations. For example, at 5 years of unopposed estrogen use, the relative risk is 1.42; for 5 years of oral contraceptive use, it is 1.96.

Adult↗
PubMed1994

Dietary lactose intake, lactose intolerance, and the risk of epithelial ovarian cancer in southern Ontario (Canada).

A case-control study of dietary factors and cancer of the ovary was conducted during 1989-92 in metropolitan Toronto and surrounding areas of southern Ontario, Canada. Four hundred and fifty women aged 35-79 years, with newly diagnosed, histologically verified, primary epithelial ovarian-cancer were interviewed concerning reproduction and diet. Over the same period, 564 randomly-selected population controls, frequency-matched to the cases within three 15-year age groups, also were interviewed. From information obtained by quantitative diet history, average daily macro- and micronutrient intake values were calculated through use of the United States Department of Agriculture Food Composition Databank, which was extended and modified for Canadian items and recipes. Analysis was performed with continuous, unconditional logistic-regression methods, adjusting for age at interview, number of full-term pregnancies, total duration of oral contraceptive use, and total daily caloric intake. Neither reported history of lactose intolerance, nor average daily consumption of lactose or free galactose, were found to be associated with risk of ovarian cancer. Lactose intake or intolerance did not appear to modify the protective effects of parity and oral contraceptive use. Nevertheless, other studies suggest that ovarian galactose metabolism still may have a relationship with risk of ovarian cancer, though more evidence is needed.

Adult↗
PubMed1994

Utility of a surveillance system to detect associations between work and cancer among women in Canada, 1965-1991.

Data on the occupation and industry in which 242,196 females worked in Canada between 1965 and 1971 are available from a national survey of employers by Statistics Canada. As an example of the future utility of this cohort, computerized record linkage was conducted with the Canadian National Mortality Data Base through 1979. This article presents selected results. Associations are measured by standardized relative risks. Those meeting specific criteria (two or more observed deaths, relative risk > 2.0, and 95% confidence interval excluding 1.00) include (a) buccal cavity and pharyngeal cancer among mechanics and repairers, tobacco preparers and product makers, and telephone systems industry workers; (b) lung cancer among service station attendants, motor vehicle mechanics, and petroleum refinery workers; and (c) breast cancer among workers manufacturing electrical industrial equipment and printing and publishing industry workers. The mortality experience of the cohort through 1991 is currently being determined by another record linkage, thus providing up to 25 years of follow-up and over 8,500 cancer deaths anticipated among females.

Adult↗
PubMed1994

Pancreatic cancer.

A detailed analysis of incidence and mortality rates for cancer of the pancreas for Ontario, Canada, over three to four decades shows that rates for men increased substantially to a peak in 1970-1974 and have fallen steadily since then. By contrast, rates for women, which also increased until the 1970s, have not subsequently fallen. These observations are consistent with a major role for cigarette smoking in accounting for the time trends, with smoking habits being particularly germane to risk in the subsequent decade in accord with results from a recent series of case-control studies. Rates from several European countries and Japan show patterns similar to those seen in the Ontario data, but the peak in rates for men has yet to be reached in some of these countries. These latter results are again generally consistent with an important role for cigarette smoking. There is no substantial evidence from comparisons of incidence and mortality rates for a recent improvement in survival, a finding in accord with current clinical observation.

Adult↗
PubMed1993

Are female smokers at higher risk for lung cancer than male smokers? A case-control analysis by histologic type.

A case-control study of male-female differences in cigarette smoking and lung cancer was conducted during 1981-1985 in Toronto, St. Catharine's, and Niagara Falls, Ontario, Canada. In total, 442 female and 403 male histologically verified cancer cases were individually matched by age and area of residence to each other and to 410 female and 362 male randomly selected population controls. Subjects were interviewed concerning their exposures to various life-style factors, and in particular, they received detailed questioning regarding their lifelong histories of usage of tobacco products. It was found that, for both sexes, a greatly elevated risk of developing lung cancer was associated with cigarette consumption, increasing with pack-years of cigarettes smoked and declining with duration of time since quitting smoking. Furthermore, the association was significantly (p = 0.010) and appreciably stronger for females than for males. At a history of 40 pack-years relative to lifelong nonsmoking, the odds ratio for women was 27.9 (95% confidence interval (CI) 14.9-52.0) and that for men was 9.60 (95% CI 5.64-16.3). Higher odds ratios for females were also seen within each of the major histologic groupings. Thus, the higher elevated risk of lung cancer currently observed in other studies for female ever smokers compared with male ever smokers, while possibly attributable in part to greater smoking cessation among males, may be due to higher susceptibility among females.

Adenocarcinoma↗
PubMed1993

A cohort study of alcohol consumption and risk of breast cancer.

The association between alcohol consumption and breast cancer risk was examined in 519 newly incident, histologically confirmed cases of breast cancer diagnosed between 1982 and 1987 within a cohort of 56,837 women enrolled in the Canadian National Breast Screening Study. These women had completed a self-administered food frequency questionnaire including alcohol consumption at enrollment into the study prior to their breast cancer diagnosis. For the total cohort, only a weak association between total alcohol consumption and breast cancer risk is observed, the adjusted relative risk for those drinking 30 or more g/day being 1.22 (95% confidence interval (CI) 0.78-1.90) compared with nondrinkers. There is some evidence for a positive association in women who were premenopausal at the time of enrollment for whom there was a monotonic increase in risk with increasing alcohol intake. Compared with nondrinkers, the adjusted relative risk for alcohol consumption of between 0 and < 10 g of alcohol daily was 1.11 (95% CI 0.71-1.71), between 10 and < 20 g was 1.37 (95% CI 0.79-2.36), between 20 and < 30 g was 1.51 (95% CI 0.80-2.86), and > or = 30 g was 1.86 (95% CI 0.96-3.66; p (trend) = 0.07). These findings contrasted with the results for postmenopausal women where there appeared to be no evidence of any relation. The association in premenopausal women is generally reasonably consistent with that of other studies that have found positive associations with alcohol intake.

Adult↗