Parental ages at birth in relation to a daughter's risk of breast cancer among female participants in the Framingham study (United States)

Data from the Framingham Heart Study, collected in Framingham, MA (United States) during 1948–86, were used to evaluate the relation of parental age at birth to the risk of breast cancer among daughters. After 38 years of follow-up, 149 breast cancer cases occurred among 2,662 women. All but two cases were confirmed by histologic report. The rate of breast cancer increased among daughters with increasing maternal age at birth up to the mid-30s, where the rate levelled off. A similar pattern was observed with paternal age. After adjustment for other confouding factors and paternal age, the rate ratios for breast cancer in daughters whose mothers were aged 26 to 31 years and 32 or more years at their birth, relative to women whose mothers were aged 25 years or younger, were 1.5 (95 percent confidence interval [CI]=1.0–2.4) and 1.3 (CI=0.8–2.2), respectively. However, there was no longer an association between paternal age at birth and risk of breast cancer after controlling for maternal age and other risk factors.Drs Zhang, Cupples, and Coulton are with the Department of Epidemiology and Biostatistics, School of Public Health, Boston University, Boston, MA, USA, Dr Rosenberg is with the Slone Epidemiology Unit, Boston University School of Medicine, Brookline, MA. Dr Kreger is with the Section of Preventive Medicine and Epidemiology, The Evans Memorial Department of Clinical Research, Boston University Medical Center, Boston, MA. Address correspondence to Dr Zhang, Department of Epidemiology and Biostatistics, School of Public Health, Boston University, 80 East Concord Street, Boston, MA, 02118-2394, USA.     

Abortion and breast cancer risk in seven countries

Epidemiologic studies have been inconsistent in suggesting an association between abortion and breast cancer risk. Whether the protection provided by a full-term pregnancy also results from a short-term pregnancy or whether a prematurely terminated pregnancy could increase the risk of breast cancer is unclear. Data from a large, international collaborative study were used to evaluate the association between abortions, whether spontaneous or induced, and breast cancer risk. The data from seven countries included 3,958 breast cancer cases and 11,538 hospital controls with information on abortion history obtained through interviews. Compared with nulliparous women with no abortion (baseline), the odds ratios (OR) and 95 percent confidence intervals (CI) were: for nulliparous women with a history of prior abortion, 0,86 (CI=0.68–1.08); for parous women with no history of abortion, 0.63 (CI=0.57–0.69); for parous women with abortion before first birth, 0.82 (CI=0.69–0.97); and, for parous women with abortion only after first birth, 0.70 (CI=0.63–0.79). When restricting analysis to parous women, those with a history of abortion exhibited an elevated OR suggesting a 29 percent risk increase if the incomplete pregnancy occurred before first birth (CI=1.16–1.36) and an 11 percent risk increase for abortion only after first birth (CI=1.02–1.20) compared with women without such history. The associations observed were stronger among the youngest women. These results do not support a large overall association between abortion and breast cancer risk.Ms Michels and Drs Hsieh, Trichopoulos, and Willett are with the Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. Dr Willett is also affiliated with the Department of Nutrition, Harvard School of Public Health, and Channing Laboratory, Department of Medicine, brigham and Women's Hospital and Harvard Medical School, Boston, MA. Address correspondence to Ms Michels, Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA.     

Recent oral contraceptive use and risk of breast cancer (United States)

We examined the association between recent oral contraceptive (OC) use and the risk of breast cancer in data from a large population-based case-control study in the United States. Cases (n=6,751) were women less than 75 years old who had breast cancer identified from statewide tumor registries in Wisconsin, Massachusetts, Maine, and New Hampshire. Controls (n=9,311) were selected randomly from lists of licensed drivers (if aged under 65 years) and from lists of Medicare beneficiaries (if aged 65 through 74 years). Information on OC use, reproductive experiences, and family and medical history was obtained by telephone interview. After adjustment for parity, age at first delivery, and other risk factors, women who had ever used OCs were at similar risk of breast cancer as never-users (relative risk [RR]=1.1, 95 percent confidence interval [CI]=10–1.2). Total duration of usealso was not related to risk. There was a suggestion that more recent use was associated with an increased risk of breast cancer; use less than two years ago was associated with an RR of 1.3 (CI=0.9–1.9). However, only among women aged 35 to 45 years at diagnosis was the increase in risk among recent users statistically significantly elevated (RR=2.0, CI=1.1–3.9). Use prior to the first pregnancy or among nulliparous women was not associated with increased risk. Among recent users of OCs, the risk associated with use was greatest among non-obese women, e.g., among women with body mass index (kg/m²) less than 20.4, RR=1.7, CI=1.1–2.8. While these results suggest that, in general, breast cancer risk is not increased substantially among women who have used OCs, they also are consistent with a slight increased risk among subgroups of recent users.Authors are with the University of Wisconsin Comprehensive Cancer Center, Madison, WI, USA (Dr Newcomb, Ms Trentham Dietz); NIEHS Epidemiology Branch, Research Triangle Park, NC (Dr Longnecker); Fred Hutchinson Cancer Research Center, Seattle, WA (Dr Surer); Department of Obstetrics and Gynecology, Pritzker School of Medicine, The University of Chicago, Chicago, IL (Dr Mittendorf); Department of Community and Family Medicine, Dartmouth Medical School, Hanover, NH (Dr Baron); Boston University, School of Public Health, Boston, MA (Dr Clapp); Department of Epidemiology and Department of Nutrition, Harvard School of Public Health, and Channing Laboratory, Harvard Medical School and Department of Medicine, Brigham and Women's Hospital, Boston, MA (Dr Willett). Address correspondence to: Dr Polly A. Newcomb, University of Wisconsin-Madison Comprehensive Cancer Center, 1300 University Ave., #4780, Madison, WI 53706, USA. Supported by Public Health Service (National Cancer Institute) grants R01 CA 47147 and R01 CA 47305.     

Reproductive factors and family history of breast cancer in relation to plasma estrogen and prolactin levels in postmenopausal women in the Nurses' Health Study (United States)

Parity, age at first birth, age at menarche, and a family history of breast cancer have each been associated consistently with breast cancer risk. Whether this increase in risk is mediated, at least in part, through changes in endogenous hormone levels is unclear. We conducted a cross-sectional study of the relationships between these factors and plasma hormone levels in 216 healthy postmenopausal women in the Nurses' Health Study (United States). The hormones evaluated were estradiol, percent and total free estradiol, percent and total bioavailable estradiol, estrone, estrone sulfate, and prolactin. After controlling for age, body mass index (weight/height²), and alcohol use, we observed inverse associations between estrone sulfate and parity (r=–0.15, P=0.03) and between percent bioavailable estradiol and age at first birth (r=–0.17, P=0.02). Although women with a family history of breast cancer tended to have higher estrogen levels compared with women without such history, the differences were not statistically significant. Age at menarche was not related significantly to any of the hormones. These data provide some additional evidence that the inverse relationship observed between parity and breast cancer risk may be mediated, at least in part, through decreased estrogen levels. Our data do not support a substantial influence of either family history of breast cancer or age at menarche on postmenopausal estrogen or prolactin levels.Authors are with the Channing Laboratory (Drs Hankinson, Colditz, Hunter, Manson, Willett, Stampfer, Speizer) and Divislon of Preventive Medicine (Dr Manson), Brigham and Women's Hospital and Harvard Medical School, Boston, MA (USA); Departments of Nutrition (Drs Willett, Stampfer), and Epidemiology (Drs Hankinson, Colditz, Hunter, Willett, Stampfer), Harvard School of Public Health, Boston, MA; and the Departments of Obstetrics and Gynecology and Medicine, University of Massachusetts Medical School, Worcester, MA (Dr Longcope). Address correspondence to Dr Hankinson, Channing Laboratory, 180 Longwood Ave., Boston, MA 02115, USA. This research was supported by research grants CA40356 and CA49449 from the US National Institutes of Health, Bethesda, MD. Dr Manson is a recipient of a Merk/Society for Epidemiologic Research grant award.     

Recall and selection bias in reporting past alcohol consumption among breast cancer cases

Recall and selection bias are well-recognized potential problems in case-control studies of alcohol and cancer, but few analyses have attempted to assess the direction and the magnitude of these potential biases. We thus examined alcohol consumption in relation to risk of breast cancer using dietary questionnaires administered both before and after the diagnosis of breast cancer in the Nurses' Health Study (United States). Among cohort members who completed a dietary questionnaire in 1986 and who were free of cancer, 616 were diagnosed with breast cancer during follow-up to December 1989. These cases and 1,277 controls (a random sample of cohort members who did not develop cancer up to 1990) then were sent another questionnaire inquiring about their diet in 1985. Four hundred and ninety-four cases (80.2 percent) and 999 controls (78.2 percent) responded to the second questionnaire. The analysis based on the prospective (1986) questionnaire demonstrated an elevated risk of breast cancer among women who drank 30 or more g of alcohol daily (about two drinks) relative to nondrinkers (odds ratio [OR]=1.55, 95 percent confidence interval [CI]=1.01–2.39). The analysis based on the retrospective questionnaire also indicated a similar but slightly attenuated elevation of risk of breast cancer among women who drank at least 30 g daily (OR=1.42, CI=0.85–2.40). In these data, bias due to selection and recall had only minor effects on reported intake of alcohol consumption.Drs Giovannucci, Stampfer, Colditz, Manson, Rosner, Speizer, and Willett are with Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA. Drs Colditz, Stampfer, and Willett are also with the Harvard School of Public Health, Boston, MA, USA. Dr Longnecker is with the University of California School of Public Health, Los Angeles, CA, USA. Address correspondence to Dr Giovannucci, Channing Laboratory, 180 Longwood Avenue, Boston, MA 02115, USA. The project was supported by research grant number CA 40935 and CA 55075 from the US National Institutes of Health.     

Histologic types and hormone receptors in breast cancer in men: a population-based study in 282 United States men

Histologic slides from 282 incident cases of breast cancer in men, that were identified in 10 population-based cancer registries in the United States, were reviewed by a single pathologist. Breast cancer more often presented in the noninvasive stage in men (10.8 percent of all cases) than would be expected among women. All noninvasive carcinomas were of the ductal type. Of invasive carcinomas, compared with women, men had smaller proportions of lobular and mucinous types and larger proportions of ductal and papillary types and Paget's disease. No case of tubular or medullary carcinoma was seen. The breast in men is composed only of ducts and normally contains no lobules, and the histologic types of breast carcinomas that predominate in men are likely of ductal origin. Estrogen and progesterone receptors were present in 86.7 percent and 76.3 percent of invasive carcinomas, respectively, which are higher proportions than would be expected among women. Also, unlike findings in women, receptor content was not associated with patient age at diagnosis.Dr Stalsberg is with the Institute of Medical Biology, University of Tromsø, Tromsø, Norway, and Drs Thomas, Rosenblatt, Jimenez, and McTiernan are with the Program in Epidemiology, Fred Hutchinson Cancer Research Center, Seattle, WA, USA, Authors also are affiliated with the University of Illinois, Champaign, IL, USA (Dr Rosenblatt); the Institutio Regional de Investigacion en Salud Publica, Guadalajara, Mexico (Dr Jimenez); the University of Washington School of Medicine, Seattle, WA, USA (Dr McTiernan); the Pharmaceutical Division, CIBAGEIGY Corp., Summit, NJ, USA (Dr Stembagen); the University of Southern Maine, Portland, ME, USA (Dr Thompson); the Connecticut Cancer Epidemiology Unit, New Haven, CT, USA (Dr McCrea Curnen); the School of Public Health, University of California, Berkeley, CA, USA (Dr Satariano); the Resource for Cancer Epidemiology, Department of Health Services, Emeryville, CA, USA (Dr Austin); the School of Public Health, Emory University, Atlanta, GA, USA (Dr Greenberg); the New Mexico Tumor Registry, Albuquerque, NM, USA (Dr Key); the Epidemiology Program, Cancer Research Center of Hawaii, Honolulu, HI, USA (Dr Kolonel); the Northern California Cancer Center, Alameda, CA, USA (Dr West). Address correspondence to Dr Stalsberg, Institute of Medical Biology, University of Tromsø, N-9037 Tromsø, Norway. This study was funded by grant number RO1 CA35653 from the US National Cancer Institute.     

A meta-analysis of alcoholic beverage consumption in relation to risk of colorectal cancer

Quantitative methods were used to review epidemiologic data relating consumption of alcoholic beverages to risk of colorectal cancer. The data (27 studies) supported the presence of a weak association. For consumption of two alcoholic beverages daily, on average the relative risk of colorectal cancer was 1.10 (95% confidence interval 1.05–1.14). Other findings were: (1) the association did not vary according to gender or site within the large bowel; (2) results from follow-up studies (relative risk 1.32, 95% confidence interval 1.16–1.51) suggested a stronger relationship than those from case-control studies (relative risk 1.07, 95% confidence interval 1.02–1.12); and (3) the evidence supporting beverage specificity was not conclusive, although the results were consistent with a stronger association with consumption of beer (relative risk 1.26, 95% confidence interval 1.13–1.41) than with consumption of wine (relative risk 1.11, 95% confidence interval 0.91–1.36) or liquor (relative risk 1.13, 95% confidence interval 0.99–1.29). Because the magnitude of the association between alcohol consumption and risk of colorectal cancer was small, the findings regarding a causal role of alcohol were inconclusive.Dr Longnecker is in the Department of Epidemiology, UCLA School of Public Health, 10833 Le Conte Avenue, Los Angeles, CA 90024. At the time of this work be was a Medical Foundation Research Fellow in the Department of Epidemiology, Harvard School of Public Health, supported by the Medical Foundation, Inc., Boston, MA. Mss Orza, Adams, and Dr Chalmers are with the Technology Assessment Group, Harvard School of Public Health. Dr Vioque is with the Department of Epidemiology, Harvard School of Public Health and is supported by a grant from the FIS 89/0827 (Spain). The research was supported by a grant from the International Life Sciences Institute. Address reprint requests to Dr Longnecker.     

Diet,alcohol, and smoking and the occurrence of hyperplastic polyps of the colon and rectum (United States)

Hyperplastic polyps of the colon reveal a geographic distribution similar to that of colorectal cancer and adenomatous polyps. However, unlike adenomas—known precursors of colorectal cancer—little is known about the etiology or clinical significance of the hyperplastic polyp. In this prospective study, we set out to determine the main dietary and other lifestyle factors in the United States that might be associated with this lesion. Hyperplastic polyps of the distal colon and rectum were diagnosed in 219 of 12,922 men of the Health Professionals Follow-up Study having had an endoscopic procedure between 1986 and 1992, and 175 of 15,339 women of the Nurses' Health Study who had undergone an endoscopy for a variety of reasons between 1980 and 1990. After adjusting for age, family history of colon cancer, history of previous endoscopy, and total energy intake using multiple logistic regression, those consuming 30 g or more of alcohol per day were at increased risk relative to nondrinkers among men (relative risk [RR]=1.69; 95 percent confidence interval [CI]=1.01–2.80) and women (RR=1.79, CI=1.02–3.15). Current smoking also was found to be associated strongly positively with hyperplastic polyps in men (RR=2.45, CI=1.59–3.75) and women (RR=1.96, CI=1.16–2.86). High intake of folate was associated inversely with risk in both men (RR=0.74, CI=0.49–1.11, between high and low intakes of folate) and women (RR=0.45, CI=0.28–0.74, between high and low intakes of folate). Among macronutrients, a suggestive increase in risk existed with intake of animal fat, although this was attenuated in the full multivariate model (RR[men]=1.48, CI=0.94–2.41, and RR [women]=1.22, CI=0.77–1.94) between high and low quantities of animal fat intake. These prospective data provide evidence of associations between low folate intake, alcohol consumption, and current cigarette smoking, and risk of hyperplastic polyps of the distal colon and rectum. These same factors also have been found to be related to adenoma and cancer of the colon. The hyperplastic polyp is an indicator of populations at high risk for colorectal carcinoma, and it also may serve as a marker for factors that influence neoplastic evolution.Drs Giovannucci, Stampfer, Colditz, and Willett are with the Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA. Authors also are affiliated with: the Department of Nutrition, Harvard School of Public Health, Boston, MA (Drs Kearney, Rimm, Stampfer, Ascherio, and Willett); the Department of Epidemiology, Harvard School of Public Health (Drs Rimm, Stampfer, Colditz, Ascherio, and Willett); and the Department of Surgery, New England Deaconess Hospital, Boston, MA (Dr Bleday). Address correspondence to Dr Giovannucci, Channing Laboratory, 180 Longwood Avenue, Boston, MA 02115, USA. This project was supported by research grants number CA 55075 and HL 35464 from the National Institutes of Health and Special Institution Grant No. 18 from the American Cancer Society. Dr Colditz. was supported by a Faculty Research Award (FRA-398) from the American Cancer Society.     

Liveborn children and risk of hepatocellular carcinoma

Clinical, animal, and epidemiologic evidence indicates that exogenous steroids influence the risk of hepatocellular carcinoma (HCC) and a recent study suggested that parity also may increase the risk of this tumor in women. The latter hypothesis was evaluated in the data from a case-control study which was carried out in Athens and covered 166 male and 19 female cases of HCC, and 381 male and 51 female hospital controls. Among males, there was no association between the number of liveborn children and risk of HCC, whereas among women, there was a suggestive positive association. Compared with women with one or two children, the relative risk for HCC was 0.6 among nulliparous women, 1.3 among those with three or four children and 1.7 among those with five or more children. The association of parity with risk of HCC was limited to women who were positive for hepatitis-B surface antigen (HBsAg) and was not confounded by hepatitis-C virus infection or tobacco smoking. The small number of HCC cases does not permit firm conclusions. If confirmed, however, these results would provide the foundation for a practical preventive advice that could be given to women who are positive for HBsAg.Drs Tzonou and Zavitsanos are with the Department of Hygiene and Epidemiology, University of Athens, Medical School, 11527 Athens, Greece. Drs Hsieh and Trichopoulos are with the Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA. Address correspondence to Dr Trichopoulos. This work was supported in Athens by a grant to the University of Athens from the Greek Ministry of Health, and in Boston by a grant to Harvard University from the Leon Lemos Foundation.     

Physical activity, obesity, and risk of colorectal adenoma in women (United States)

The relationship between physical inactivity, body mass index (BMI) (wt[kg]/ht[m]²), and pattern of adipose distribution with risk of colorectal adenomas (precursors of cancer) was examined in 13,057 female nurses in the United States, 40 to 65 years of age in 1986, who had an endoscopy between 1986 and 1992. From 1986 to 1992, 439 participants were newly diagnosed with adenomas of the distal colorectum. After controlling for age, prior endoscopy, parental history of-colorectal cancer, smoking, aspirin, and intakes of animal fat, dietary fiber, folate, methionine, and alcohol, physical activity was associated inversely with risk of large (1 cm) adenomas in the distal colon (relative risk [RR]=0.57,95 percent confidence interval [CI]=0.30–1.08, comparing high and low quintiles of average weekly energy expenditure from leisure-time activities; P trend = 0.05). Much of the benefit came from activities of moderate intensity such as brisk walking. In addition, BMI was associated directly with risk of large adenomas in the distal colon (multivariate RR=2.21 [CI=1.18–4.16], P trend = 0.0001, for BMI 29 cf <21 kg/m²). Waist circumference and the waist-to-hip ratio (WHR) were not related significantly to adenoma independently of BMI, but women with both a high BMI and high WHR were at greater risk of large colon adenoma (multivariate RR=1.99, CI=0.98–4.05) than women with high BMI but relatively low WHR (multivariate RR=1.35, CI=0.61–2.97). BMI was not related to small (<1 cm) adenoma risk but physical activity had an inverse association with small adenomas in the distal colon (multivariate RR=0.68, CI=0.40–1.15, P trend = 0.03). The relationships between BMI or physical activity were considerably weaker and inconsistent for rectal adenomas. These results, in women, support an inverse association between physical activity and occurrence or progression of ademonas in the distal colon; obesity is associated with an elevated risk of large adenomas.The authors are with the Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA. The authors are also affiliated with the Department of Nutrition, Harvard School of Public Health, Boston, MA (Drs Giovannucci, Stampfer, and Willett), and the Department of Epidemiology, Harvard School of Public Health, Boston, MA (Drs Colditz, Stampfer, and Willett). Address correspondence to Dr Giovannucci, Channing Laboratory, 180 Longwood Avenue, Boston, MA 02115, USA. The work was supported by research grant numbers CA 40935 and CA 55075 from the US National Institutes of Health. Dr Colditz is supported by a Faculty Research Award (FRA-398) from the American Cancer Society.     

Differences between Black and White patients with cancer of the uterine corpus in interval from symptom recognition to initial medical consultation (United States)

To determine whether Black women with symptoms of uterine corpus cancer had longer times from symptom recognition to initial medical consultation than did White women in the United States, 331 newly diagnosed patients living in Atlanta (GA), New Orleans (LA), and San Francisco/Oakland (CA) during 1985–87 were interviewed to collect information on symptoms, dates of recognition and consultation, and other factors that might affect the interval. Data were analyzed to estimate medical consultation rates and rate ratios following sysptom recognition. Median recalled times between symptom recognition and consultation were 16 days for Black women and 14 days for White women. Although poverty, having no usual source of healthcare, and other factors were associated with lower consultation rates, the adjusted rate among Black women was only somewhat lower (0.87) than among White women, and the 95 percent confidence interval (CI=0.58–1.31) was consistent with no true difference between the races. In addition, the median time to consultation for women with stage IV cancer was only 15 days longer than the time (14 days) for the women with stage I cancer. These results suggest that time from symptom recognition to initial medical consultation does not contribute importantly to the more advanced stage cancer of the uterine corpus commonly found among Black women.Drs Coates and Eley and Ms Click are with the Department of Epidemiology, Rollins School of Public Health of Emory University, Atlanta, GA (USA). Authors are also with the Division of Cancer Prevention & Control, National Cancer Institute, Rockville, MD (Drs Harlan and Edwards); Department of Pathology Obstetrics and Gynecology, Duke University Medical Center, Durham, NC (Dr Robboy); Forsyth Medical Park, Winston-Salem, NC (Dr Barrett); Environmental Epidemiology Section, California State Department of Health Services, Emeryville, CA (Dr Reynolds); Department of Pathology, Louisiana State University Medical Center, New Orleans, LA (Dr Chen); School of Public Health, University of Massachusetts, Amberst, MA (Dr Darity); Office of the President, Northeastern Ohio Universities College of Medicine, Rootstown, OH (Dr Blacklow). Address correspondence to Dr Coates, Department of Epidemiology, Rollins School of Public Health of Emory University, 1518 Clifton Road, NE, Atlanta, GA 30322, USA. This research was supported in part by contracts N01CN-35042-46, N01CN-05227, N01CN-45174, and N01CN-45176 from the National Cancer Institute, US National Institutes of Health.     

Nutrients and pancreatic cancer: a population-based case-control study

A case-control study was conducted in the Minneapolis-St Paul (Minnesota, United States) area to assess the role of dietary factors in the etiology of pancreatic cancer. Cases were White males aged 40 to 84 whose death certificate listed pancreatic cancer (exocrine only). White male controls were ascertained through random-digit dialing. Family members were interviewed about the subject's dietary usage in the two years prior to death (cases, n=212) or prior to interview (controls, n=220). Energy-adjusted,nutrient-intake, risk estimates were calculated. Among all respondents, negative trends were observed for polyunsaturated fat, linoleic acid, vitamin C, and -carotene. Positive trends were observed for riboflavin and retinol. Point estimates were, in general, comparable between the analyses of all respondents and spouse-only respondents. The nutrients associated with a decreased risk for pancreatic cancer occur primarily in vegetables and fruits, of which the consumption of cruciferous and -carotene-rich vegetables and citrus fruits provided the greatest reduction in risk.Authors are at the University of Minnesota. Drs Olsen and Schuman are at the School of Public Health, Division of Epidemiology, Minneapolis, MN, USA. Dr Mandel is with the Division of Environmental and Occupational Health, School of Public Health. Dr Gibson is at the School of Medicine, Department of Behavioral Sciences. Dr Wattenberg is at the School of Medicine, Department of Laboratory Medicine and Pathology. Address correspondence to Dr Olsen, The Dow Chemical Company, Health and Environmental Sciences, Epidemiology, 1803 Building, Midland, MI 48674, USA. This study was supported by grant SIG5 from the American Cancer Society.     

Breastfeeding and breast cancer risk

A population-based case-control study of breast cancer with a focus on premenopausal women under 45 years of age, conducted in three geographic regions of the United States, enabled the evaluation of risk in relation to varying breastfeeding practices. Among premenopausal parous women (1,211 cases, 1,120 random-digit-dialing controls), a history of breastfeeding for two or more weeks was associated with a relative risk (RR) of 0.87 (95 percent confidence interval [CI]=0.7–1.0). This relationship was not altered substantially by removing from the reference group women who had problems with breastfeeding in the first two weeks, including those with insufficient milk production. Risk was not related substantially to number of children breastfed or length of breastfeeding, although a relatively low risk was observed among those breastfeeding for the longest duration examined (RR=0.67, CI=0.4–1.1 for an average period per child of 72 or more weeks). Women who began to breastfeed at a young age (<22 years) experienced the greatest reduction in risk, but other timing parameters (e.g., interval since first or last breastfeeding) were not predictive of risk. Risks were not modified substantially by age or menopause status, although the number of menopausal subjects examined was limited. Use of medications to stop breast milk was unrelated to risk (RR=1.04). The results of this study do not support the notion that breastfeeding substantially reduces breast cancer risk; however, this may reflect the fact that most of our study subjects breastfed only for limited periods of time (average breastfeeding per child of 30 weeks). Further studies are needed to clarify the relationship of breastfeeding to breast cancer risk, and to determine possible etiologic mechanisms underlying any observed associations.Drs Brinton, Potischman, and Swanson are with the Environmental Epidemiology Branch, National Cancer Institute, Betbesda, MD, USA. Authors also are affiliated with the Special Epidemiology Program, New Jersey State Department of Health, Trenton, NJ, USA (Ms Schoenberg); Rollins School of Public Health, Emory University, Atlanta, GA, USA (Dr Coates); the Division of Epidemiology, Columbia University School of Public Health, New York, NY, USA (Dr Gammon); and the Fred Hutchinson Cancer Research Center, University of Washington, Seattle, WA (Drs Malone, Stanford, Daling). Address correspondence to Dr Brinton, Environmental Epidemiology Branch, National Cancer Institute, Executive Plaza North, Room 443, Bethesda, MS 20892, USA.     

Melanoma: linked temporal and latitude changes in the United States

The rise in the incidence and mortality from melanoma of the skin is slowing down in younger age groups in the United States. In many White populations, including that of the US, melanoma incidence and mortality rates increase according to proximity of residence to the Equator. Variations with age in this gradient do not seem to have been examined. We examined how the influence of latitude on melanoma rates varied with age. Estimates of age-specific trends by time and by latitude for natural logarithm (Ln) melanoma incidence-rates from the Surveillance, Epidemiology and End Results (SEER) programs, and Ln melanoma mortality rates from the US Vital Statistics were derived from fitted regression equations. Unexpectedly, a decline from old age to youth in the influence of latitude was found for both incidence and mortality from melanoma of the skin in males, and for mortality in females. Further, these changes in the relationship to latitude with age correlated with the changes in time trends with age. The link with exposure suggests that the time trends in melanoma are driven by variations in damage to melanocytes in early life that increases sensitivity to sunlight. This has implications for the general understanding of melanoma etiology and for health education.Dr Lee is at the School of Public Health, University of Washington, Seattle, WA, USA. Dr Scotto is with the Division of Biostatistics & Epidemiology, Georgetown University, Washington, DC, USA. Address correspondence to Dr Lee, Department of Epidemiology SC 36, School of Public Health, University of Washington, Seattle, WA 98195, USA.     

Passive smoking and diet in the etiology of lung cancer among non-smokets

A case-control study was undertaken in Athens to explore the role of passive smoking and diet in the causation of lung cancer, by histologic type, in non-smoking women. Among 160 women with lung cancer admitted to one of seven major hospitats in Greater Athens between 1987 and 1989, 154 were interviewed in person; of those interviewed, 91 were life-long non-smokers. Among 160 identified controls with fractures or other orthopedic conditions, 145 were interviewed in person; of those interviewed, 120 were life-long non-smokers. Marriage of a non-smoking woman to a smoket was associated with a relative risk for lung cancer of 2.1 (95% confidence interval [CI] 1.1–4.1); number of cigarettes smoked daily by the husband and years of exposure to husband's smoking were positively, but not significantly, related to lung cancer risk. There was no evidence of any association with exposure to smoking of other household members, and the association with exposure to passive smoking at work was small and not statistically significant. Dietary data collected through a semi-quantitative food-frequency questionnaire indicated that high consumption of fruits was inversely related to the risk of lung cancer (the relative risk between extreme quartiles was 0.27 (CI 0.10–0.74)). Neither vegetables nor any other food group had an additional protective effect; futthermore, the apparent protective effect of vegetables was not due to carotenoid vitamin A content and was only partly explained in terms of vitamin C. The associations of lung cancer risk with passive smoking and reduced fruit intake were independent and did not confound each other. Passive smoking was associated with an increase of the risk of all histologic types of cancer, although the elevation was more modest for adenocarcinoma.Drs kalandidi, Katsouyanni, Voropoulou, and Bastas are in the Department of Hygiene and Epidemiology, University of Athens Medical School, Athens, Greece. Dr Saracci is at the International Agency for Research on Cancer, Lyon, France. Dr Trichopoulos is in the Department of Epidemiology, Harvard School of Public Health. Reprint requests should be sent to Dr Trichopoulos at 655 Huntington Avenue, Boston, MA 02115, USA. The research was supported by the International Agency for Research on Cancer and the Commission of the European Communities. It is part of the EUROPASS collaborative EEC project.     

Tobacco smoking,alcohol consumption,and risk of oral cancer: a case-control study in Beijing,People's Republic of China

A case-control study of oral cancer was conducted in Beijing, People's Republic of China (PRC). The study was hospital-based and controls were hospital in-patients matched for age and gender with the cases. The response rates for cases and controls were 100 percent and 404 case/control pairs were interviewed. Tobacco smoking and alcohol consumption emerged as independent risk factors for oral cancer. For tobacco smoking, the association was considerably stronger for smokers of pipes than for smokers of cigarettes. For all kinds of tobacco, expressed as cigarette equivalents, the odds ratio (OR) for total pack-years smoked, among males, rose from 1.0 in never-smokers to 3.7 (95 percent confidence interval, 1.8–7.4) in the highest quintile of exposure. Similar results were found for females. The association with tobacco consumption was strong for squamous cell carcinoma but there was no trend in risk associated with tobacco for adenocarcinomas and other histologic types. So few women reported consuming alcohol that this variable could be examined only in male. Risk in the highest category of total lifetime intake of alcohol relative to than in lifetime abstainers was 2.3 (1.1–4.8) with a significant trend in risk with increasing dose (P<0.002). The combined effects of tobacco and alcohol appear to be approximately multiplicative in males. The attributable risk of oral cancer for tobacco among tobacco smokers was estimated as 34 percent (45 percent among males and 21 percent among females); for alcohol consumption in males the estimate was 23 percent.Drs Zheng, Hu, and Niu are from the Department of Epidemiology, National Institute for Enviromental Health and Engineering, Chinese Academy of Pieventive Medicine, Beijing, People's Republic of China. Dr Boyle is with the Unit of Analytical Epidemiology, Internationat Agency for Research on Cancer, Lyon, France, where Dr Zheng beld a fellowship. Dr Duan is with the Beijing Union Hospital. Dr Jian is with the Cancer Institute, Chinese Academy of Medical Sciences. Dr Ma is with the Beijing Medical University Stomatological Hospital, Dr Shui is with the Beijing Municipal Stomatological Hospital, Dr MacMabon is in the Department of Epidemiology, Harvard School of Public Health where Dr Zbeng was a graduate student. Address reprint requests to Dr Zheng at the Cancer Prevention Research Unit, Department of Epidemiology and Public Health, Yale University, School of Medicine, B.O. Box 3333, New Haven, CT 06310, USA, Dr Zbeng was supported, in part by a grant from the DuPont Company.     

Maternal risk of breast cancer following multiple births: a nationwide study in Sweden

The association between multiple births and subsequent maternal breast cancer risk was explored in a nested case-control study in Sweden encompassing 19,368 parous women with breast cancer diagnosed up to age 65 years, and 100,459 parous controls. Among cases and controls, there were 329 and 2,031 women, respectively, with a history of at least one live multiple birth. Compared with singleton mothers, breast cancer risk was 12 percent lower (odds ratio=0.088, 95 percent confidence interval=0.78–0.99) in women who had had a multiple birth. After stratification for age at diagnosis, evidence of a significant inverse association was found only in women aged 54 years or younger. Birth order of the multiple pregnancy had no apparent risk-modifying effect. Age at earliest multiple birth was unrelated to breast cancer risk. The inverse association between twinning and breast cancer risk may reflect protective physiological features of twin pregnancies. Further research is needed to investigate the role, if any, of in creased levels of steroid hormone-binding globulins in mothers of twins and the proposed inhibitory effects of human chorionic gonadotropin and -fetoprotein, both of which are increased during multiple gestations, on breast carcinogenesis. Breast feeding patterns in mothers of twins also may modify their risk of developing breast cancer.Ambors are with the Department of Cancer Epidemiology (Drs Lambe Ekbom, Adami) and Department of Social Medicine (Lambe), University Hospital, Uppsala, Sweden: Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA (Drs Hsieb, Tsilib, Adami, Ekbom, Trichopoulos); UMASS Cancer Center, Worcester, MA, USA (Dr Hsieb). Address correspondece to Dr Lambe, Department of Cancer Epidemiology, University Hospital, S-751 85 Uppsala, Sweden. This project is funded by grants from the Swedish Cencer Societv. the Swedish Societv of Medicine. and the Wahlmarks Fund at Uppsala City Council.     

A case-control study of alcoholic beverage consumption in relation to risk of cancer of the right colon and rectum in men

To examine the relation between alcoholic beverage consumption and risk of cancer of the right colon and rectum, 644 male cases and 992 male community controls were interviewed by telephone. The risks of cancer at these sites associated with alcohol consumption five years in the past were similar; using subjects with right colon cancer for reference, the adjusted relative risk (RR) of rectal cancer associated with five or more drinks per day was 0.9 (95% confidence limits = 0.4, 1.7). Alcohol consumption 20 years in the past was associated with a greater risk of rectal cancer (RR for five or more drinks per day = 1.8 [1.0, 3.3]). Analyses based on a community controls provided weaker evidence, consistent with previous findings, that heavy consumption of alcohol five years in the past, and possibly of beer in particular, was associated with moderately increased risk of colorectal cancer (RR of cancer of the right colon associated with consumption of five or more alcoholic drinks per day was 1.8 [1.0, 3.2], and of cancer of the rectum was 1.5 [0.9, 2.5]).At the time of this work Dr Longnecker was a Medical Foundation Research Fellow in the Department of Epidemiology, Harvard School of Public Health, supported by the Medical Foundation, Boston, Massachusetts. His current address, to which reprint requests should be sent, is Department of Epidemiology, UCLA School of Public Health, 10833 Le Conte Avenue, Los Angeles, CA, USA 90024-1772. The research was supported by a grant from the Alcoholic Beverage Medical Research Foundation, Baltimore MD.     

Eating frequency—a neglected risk factor for colon cancer?

Eating frequency was examined in relation to risk of cancer of the colon and rectum in a population-based case-control study conducted in Stockholm, Sweden in 1986–88. In the present analysis, 328 cases and 500 controls were included. The adjusted relative risk (RR) of colon cancer per daily eating occasion was 1.2 (95 percent confidence interval [CI]=1.1–1.4, adjusted for year of birth, sex, intake of energy, fat, protein, and fiber, browning of meat surface, physical activity, and body mass index). The corresponding RR for rectal cancer was 1.0 (CI=0.9–1.2). The frequency of eating snacks was related to risk of colon cancer (RR per snack = 1.6, CI=1.2–1.9), while the frequency of eating meals (breakfast, lunch, or dinner) was not (RR per meal = 0.8, CI=0.6–1.1). The results are consistent with findings in two other case-control studies in which eating frequency was found to be a risk factor for colon cancer.Dr Gerhardsson de Verdier is with the Department of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden, and the Department of Preventive Medicine, University of Southern California School of Medicine, Los Angeles, CA, USA. Dr Longnecker is with the Department of Epidemiology, UCLA School of Public Health, Los Angeles, CA, USA. Address correspondence to Dr Gerhardsson de Verdier at the Institute of Environmental Medicine, Department of Epidemiology, Box 60208, S-104 01, Stockholm, Sweden. The study was supported by two grants (2228-B86-013XA; 2228-B87-02XA) from the Swedish National Cancer Society. Dr Longnecker is the recipient of a Junior Faculty Research Award from the American Cancer Society.     

Type of postmenopausal hormone use and risk of breast cancer: 12-year follow-up from the Nurses' Health Study

We prospectively examined the use of hormone replacement therapy in relation to breast cancer incidence in a cohort of women 30 to 55 years of age in 1976. During 12 years of follow-up (480,665 person-years) among postmenopausal women, 1,050 incident cases of breast cancer were documented. Overall, past users of replacement estrogen were not at increased risk. After adjustment for established risk factors, type of menopause, age at menopause, and current age, the rate ratio (RR) was 0.91, 95 percent confidence interval (CI) = 0.78–1.07. the risk of breast cancer was elevated significantly among current users (RR = 1.33, CI = 1.12–1.57); after adjusting for age, we observed no evidence of increasing risk with increasing duration of use among current users (P trend = 0.41), or among past users (P trend = 0.46). Women currently using unopposed estrogen (RR = 1.42, CI = 1.19–1.70), estrogen and progesterone (RR = 1.54, CI = 0.99–2.39), or progesterone alone (RR = 2.52, CI = 0.66–9.63), were all at increased risk of breast cancer compared with never users. These data suggest that long-term past use of estrogen replacement therapy is not related to risk, that current estrogen use increases risk of breast cancer to a modest degree, and that the addition of progesterone does not remove the increased risk observed with current use of unopposed estrogen.The authors are with the Nurses' Health Study, Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, MA; and Harvard Medical School, Boston, MA, USA. Address correspondence to Dr Colditz, Channing Laboratory, 180 Longwood Ave., Boston, MA 02115-5899, USA. Supported by research grant CA40356 from the National Cancer Institute, NIH, Department of Health and Human Services. Dr Colditz is supported by an American Cancer Society Faculty Research Award FRA-398.