OBJECTIVE: To assess the risk of invasive breast cancer associated with total and beverage-specific alcohol consumption and to evaluate whether dietary and nondietary factors modify the association. DATA SOURCES: We included in these analyses 6 prospective studies that had at least 200 incident breast cancer cases, assessed long-term intake of food and nutrients, and used a validated diet assessment instrument. The studies were conducted in Canada, the Netherlands, Sweden, and the United States. Alcohol intake was estimated by food frequency questionnaires in each study. The studies included a total of 322647 women evaluated for up to 11 years, including 4335 participants with a diagnosis of incident invasive breast cancer. DATA EXTRACTION: Pooled analysis of primary data using analyses consistent with each study's original design and the random-effects model for the overall pooled analyses. DATA SYNTHESIS: For alcohol intakes less than 60 g/d (reported by >99% of participants), risk increased linearly with increasing intake; the pooled multivariate relative risk for an increment of 10 g/d of alcohol (about 0.75-1 drink) was 1.09 (95% confidence interval [CI], 1.04-1.13; P for heterogeneity among studies, .71). The multivariate-adjusted relative risk for total alcohol intakes of 30 to less than 60 g/d (about 2-5 drinks) vs nondrinkers was 1.41 (95% CI, 1.18-1.69). Limited data suggested that alcohol intakes of at least 60 g/d were not associated with further increased risk. The specific type of alcoholic beverage did not strongly influence risk estimates. The association between alcohol intake and breast cancer was not modified by other factors. CONCLUSIONS: Alcohol consumption is associated with a linear increase in breast cancer incidence in women over the range of consumption reported by most women. Among women who consume alcohol regularly, reducing alcohol consumption is a potential means to reduce breast cancer risk.
Comment In: JAMA. 1998 Oct 7;280(13):1138-99777807
To identify potential associations between workplace exposures and cancer mortality risks, job titles collected from 1965 to 1971 for 58,678 men (a subset of a large representative sample of the Canadian workforce) were transformed into probable chemical exposures using a job-exposure matrix developed in Montreal. Mortality follow-up was determined through computerized record linkage with the National Mortality Database in Canada for 1965-1991. Cancer mortality risk was evaluated at two levels of exposure, any and substantial, using Poisson regression controlling for age, calendar period, and social class. Among the 58,678 men, 3,160 died of cancer. Using a liberal reporting criterion, relative risk (RR) >1.0, five or more exposed cancer deaths, p
A case-control study of cancer of the colon and rectum has been conducted in Calgary, Alberta and Toronto, Ontario, Canada. A total of 348 cases of cancer of the colon and 194 cases of cancer of the rectum were individually matched by age, sex and neighbourhood of residence to 542 population controls and frequency match to 535 hospital controls who had undergone an abdominal operation. Each subject received a personal medical history questionnaire and a quantitative diet history questionnaire. Data on a number of potential non-nutrient risk factors for bowel cancer and on the consumption of 9 nutrients in the 2-month period up to 6 months before interview were analysed. The dietary data thus refer to recent diet consumed in a period antedating the diagnosis of, and in most cases symptoms from, large-bowel cancer in the cases, and a corresponding time period in the controls. The major findings were an elevated risk for those with a history of bowel polyps, and for those with an elevated intake of calories, total fat, total protein, saturated fat, oleic acid and cholesterol. No association was seen with an elevated intake of crude fibre, Vitamin C and linoleic acid. The nutrients for which an increased risk was demonstrated were highly correlated, though multivariate analysis using logistic regression indicated highest risk for saturated fat, with evidence of a dose-response relationship. The findings in both cancer sites, both sexes and with both sets of controls were quantitatively very similar. The population-attributable risk for colon and rectal cancer combined was estimated from the neighbourhood controls to be 41% for males and 44% for females for saturated fat intake and 9.8% and 6.4% respectively for any history of polyps.
Dietary information from a case-control study of pancreatic cancer conducted in Metropolitan Toronto between 1983 and 1986 is reported. A total of 249 cases and 505 population-based controls completed quantitative diet histories from which total caloric intake and the intake of a number of nutrients were estimated. A positive association with total caloric intake was observed with a relative risk of 2.39, 95% confidence interval 1.18-4.83 (highest versus lowest quartile), due primarily to the intake of carbohydrates. Inverse associations were seen with fibre from fruit, vegetable and cereal sources, with a relative of risk of 0.42, 0.22-0.78 (highest versus lowest quartile), for total fibre intake.
The contributions of food items and food groups as risk factors in a previously reported case-control study of diet and colo-rectal cancer have been analyzed. The study included 348 patients with colon cancer, 194 with rectal cancer, 542 neighbourhood controls individually matched to the cases on the basis of age and sex and a second control series of 535 surgical hospital controls frequency matched to the cases. For colon cancer, as in the previous analysis, the major risk factor was saturated fat, individual food items or groups failing to make a significant contribution to the risk. In particular there was no protective effect of dietary fibre and, for cruciferous vegetables, only a minor protective effect in females. No individual cruciferous vegetable made an important contribution to this effect. For rectal cancer, on the other hand, a significant effect of saturated fat, independent of other food items or groups, was only found for females in the highest consumption category. For males, consumption of eggs, beef and veal significantly increased risk but not consumption of pork, while for females, there was a non-significant increase in risk with consumption of eggs, no increased risk with consumption of beef or veal and a significantly increased risk with consumption of pork. There was no protective effect of dietary fibre or of cruciferous vegetables for rectal cancer, but in females, there was a significantly increased risk for consumption of beer, though this was somewhat reduced when controlled for consumption of saturated fat. There was no indication of an effect of alcohol in either sex or of beer in males. Thus, these results confirm the previous report in showing a significant effect of saturated fat in increasing risk of colon cancer but suggest a contribution of meats to risk of rectal cancer.
It has been suggested that usage of menopausal estrogens may be associated with risk of colorectal cancer. This association was examined in a record linkage cohort study using the Saskatchewan Health Plan Databases. All women ages 43-49 who were residents in Saskatchewan in 1976 were identified from the Saskatchewan Health master registration file. These 33,003 women were linked by registration beneficiary number to the Prescription Drug Plan Database for the period January 1976 through June 1987, and to the Provincial Cancer Registry Database for the period March 1960 through December 1990. Thirty women in the cohort had colon or rectal cancer diagnosed before 1976 and were omitted from the analysis; exposures within 3.5 years of diagnosis or end of follow-up were also omitted. Between 1976 and 1990, 230 first primary colorectal cancer cases occurred. Women who took estrogens had nonsignificantly elevated risk of colon cancer in general (age-adjusted relative risk = 1.29; 95% confidence interval, 0.86-1.93) and of cancer of the distal colon (relative risk = 1.51; 95% confidence interval, 0.90-2.54). Women who took p.o. contraceptives during this follow-up period seemed to be at higher risk of cancer of the proximal colon (relative risk = 2.12; 95% confidence interval, 1.00-4.53), though this apparent association could very well have occurred by chance. No associations were seen between hormone use and risk of rectal cancer. This study provides little evidence that usage of menopausal hormones may be related to risk of colorectal cancer (either positively or negatively), though further follow-up of the cohort appears warranted.
During 1979-82, a case-control study of occupational factors and urinary bladder cancer was conducted in Edmonton, Calgary, Toronto, and Kingston, Canada. A total of 826 histologically verified cases of cancer were individually matched by sex, age, and area of residence to 792 randomly selected population controls. Subjects were specifically asked about employment in several industries thought relevant to risk of bladder cancer. Information was also obtained on lifelong occupational history, with special attention given regarding exposures to fumes, dusts, smoke, and chemicals. In addition, subjects provided data on past medical and residential history, on intake of certain dietary items, and on exposure to tobacco and other lifestyle factors. Conditional logistic regression methods were used for the analysis. Under adjustment for cumulative lifetime cigarette consumption, it appeared that for both men and women, most of the occupational factors examined were not associated with significant alteration in risk of bladder cancer. For exposures during the period eight to 28 years before diagnosis, however, raised risk was suggested for men employed at least six months in the chemicals industry (odds ratio = 2.37, p = 0.004), in dye manufacturing or the dyeing of cloth (OR = 3.62 and 4.63, p = 0.041 and 0.035, respectively), as tailors (OR = 3.85, p = 0.015), or in jobs in which contact with diesel or traffic fumes occurred (OR = 1.69, p = 0.0008). Increased risk was also seen for men occupationally exposed to tars or asphalt (OR = 3.11, p = 0.019). This study then, at least for men, supports perhaps a few of the suspect industries as related to risk of bladder cancer.
Cites: Cancer. 1972 May;29(5):1250-605021618
Cites: Am J Epidemiol. 1986 Oct;124(4):578-893752052
Cites: J Natl Cancer Inst. 1980 Apr;64(4):701-136928984
Cites: J Occup Med. 1980 Nov;22(11):722-67441390
Cites: Br J Ind Med. 1981 Aug;38(3):225-347272234
Cites: Int J Cancer. 1985 May 15;35(5):599-6063997281
Cites: J Occup Med. 1985 Apr;27(4):283-923998881
Cites: J Occup Med. 1985 Jun;27(6):420-64020500
Cites: J Natl Cancer Inst. 1986 Jan;76(1):1-83455732
Cites: Cancer. 1986 Jan 15;57(2):362-73942969
Cites: Int J Epidemiol. 1985 Dec;14(4):549-544086141
Cites: Br J Ind Med. 1986 Feb;43(2):96-1003947575
Cites: Am J Epidemiol. 1986 Jun;123(6):1033-423706274
Cites: Br J Ind Med. 1986 Jun;43(6):363-733718880
Cites: Br J Ind Med. 1986 Jun;43(6):381-63718882
Cites: Br J Ind Med. 1986 Jul;43(7):494-63718898
Cites: J Natl Cancer Inst. 1978 Oct;61(4):1025-30279708
Infertility is a common complication of pelvic inflammatory disease (PID) and may result in decreased parity. Low parity and possibly infertility are risk factors for ovarian cancer. We therefore examined the association between ovarian cancer and history of PID in a case-control study conducted during 1989-1992 in metropolitan Toronto and nearby areas of Southern Ontario, Canada. In total, 450 histologically verified new primary epithelial ovarian cancer cases ages 35-79 years were interviewed concerning their reproduction history. Over the same period, 564 randomly selected population controls, frequently matched to the cases according to three 15-year age groups, were interviewed similarly. Continuous unconditional logistic regression methods were used for analysis. It was found that cases were more likely than controls to report having had one or more episodes of PID; adjusted for age, parity, duration of oral contraceptive use, and other factors the odds ratio (OR) was 1.53 [95% confidence interval (CI), 1.10-2.13; P = 0.012]. Higher risk was present for women with recurrent PID (OR, 1.88; 95% CI, 1.13-3.12; P = 0.014). The elevated risk associated with PID was seen particularly among women