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Purpose: Alcohol intake is associated with increased risk of breast cancer. In contrast, the relation between alcohol consumption and breast cancer survival is less clear., Patients and Methods: We assessed pre- and postdiagnostic alcohol intake in a cohort of 22,890 women with incident invasive breast cancer who were residents of Wisconsin, Massachusetts, or New Hampshire and diagnosed from 198 to 200 at ages 20 to 79 years. All women reported on prediagnostic intake; a subsample of 4,881 reported on postdiagnostic intake., Results: During a median follow-up of 11.3 years from diagnosis, 7,780 deaths occurred, including 3,484 resulting from breast cancer. Hazard ratios (HR) and 95% CIs were estimated. Based on a quadratic analysis, moderate alcohol consumption before diagnosis was modestly associated with disease-specific survival (compared with nondrinkers, HR = 0.93 [95% CI, 0.85 to 1.02], 0.85 [95% CI, 0.75 to 0.95], 0.88 [95% CI, 0.75 to 1.02], and 0.89 [95% CI, 0.77 to 1.04] for two or more, three to six, seven to nine, and ≥ 10 drinks/wk, respectively). Alcohol consumption after diagnosis was not associated with disease-specific survival (compared with nondrinkers, HR = 0.88 [95% CI, 0.61 to 1.27], 0.80 [95% CI, 0.49 to 1.32], 1.01 [95% CI, 0.55 to 1.87], and 0.83 [95% CI, 0.45 to 1.54] for two or more, three to six, seven to nine, and ≥ 10 drinks/wk, respectively). Results did not vary by beverage type. Women consuming moderate levels of alcohol, either before or after diagnosis, experienced better cardiovascular and overall survival than nondrinkers., Conclusion: Overall alcohol consumption before diagnosis was not associated with disease-specific survival, but we found a suggestion favoring moderate consumption. There was no evidence for an association with postdiagnosis alcohol intake and breast cancer survival. This study, however, does provide support for a benefit of limited alcohol intake for cardiovascular and overall survival in women with breast cancer.

Bilateral oophorectomy is often performed during hysterectomy for benign conditions and can reduce breast cancer risk by 20%-50% when performed at younger ages. Accuracy of estimating the decrease in breast cancer risk associated with bilateral oophorectomy could be affected by common conditions that lead to surgery, such as uterine fibroids or endometriosis. The authors examined the potential for confounding by nonmalignant indications for surgery on breast cancer risk estimates in a population-based case-control study of invasive breast cancer newly diagnosed in 1992-1995. Breast cancer cases (N = 4,935) aged 50-79 years were identified from Wisconsin, Massachusetts, and New Hampshire tumor registries; similarly aged controls (N = 5,111) were selected from driver's license and Medicare lists. Reproductive and medical history was obtained from structured telephone interviews. Odds ratios and 95% confidence intervals were estimated with multivariate logistic regression. Women who underwent bilateral oophorectomy with hysterectomy at age ≤ 40 years had significantly reduced odds of breast cancer (odds ratio = 0.74, 95% confidence interval: 0.60, 0.90) compared with women with intact ovaries and uterus. Effect estimates were virtually unchanged after adjustment for uterine fibroids or endometriosis history. Results indicate that breast cancer risk reductions conferred by bilateral oophorectomy are not strongly confounded by failure to account for nonmalignant indications for surgery.

Early life exposures, such as being breastfed in infancy, may influence the risk of breast cancer in adulthood. We evaluated the risk of breast cancer in relation to ever having been breastfed in infancy among 9,442 women who participated in a population-based, case-control study. Cases were identified through cancer registries in three states (Massachusetts, New Hampshire, and Wisconsin); controls were identified through statewide drivers' license lists or medicare lists. Data on known and suspected risk factors were obtained through telephone interview. We used unconditional logistic regression to assess the relation of breast cancer with ever having been breastfed and with breastfeeding duration (available for only 19% of breastfed women) in premenopausal women (1,986 cases and 1,760 controls) and postmenopausal women (2,600 cases and 2,493 controls). We found no evidence that ever having been breastfed in infancy was associated with breast cancer risk in either premenopausal women (odds ratio [OR] = 0.96; 95% confidence interval [CI] = 0.83-1.10) or postmenopausal women (OR = 0.98; 95% CI = 0.87-1.10). The association did not differ according to breast cancer stage, mother's history of breast cancer, or any other reproductive factor assessed. Likewise, we found no association between breastfeeding duration and risk of breast cancer. Our results did not support the hypothesis that exposure to breast milk in infancy influences the risk of adult breast cancer.

Background: Factors related to improving outcomes in breast cancer survivors are of increasing public health significance. We examined postdiagnosis weight change in relation to mortality risk in a cohort of breast cancer survivors., Methods: We analyzed data from a cohort of 3,993 women with ages 20 to 79 years living in New Hampshire, Massachusetts, or Wisconsin with invasive nonmetastatic breast cancers diagnosed in 1988 to 1999 identified through state registries. Participants completed a structured telephone interview 1 to 2 years after diagnosis and returned a mailed follow-up questionnaire in 1998 to 2001 that addressed postdiagnosis weight and other factors. Vital status information was obtained from the National Death Index through December 2005. Hazard ratios and 95% confidence intervals were estimated from Cox proportional hazards models and adjusted for prediagnosis weight, age, stage, smoking, physical activity, and other important covariates., Results: During an average 6.3 years of follow-up from the postdiagnosis questionnaire, we identified 421 total deaths, including 121 deaths from breast cancer and 95 deaths from cardiovascular disease. Increasing postdiagnosis weight gain and weight loss were each associated with greater all-cause mortality. Among women who gained weight after breast cancer diagnosis, each 5-kg gain was associated with a 12% increase in all-cause mortality (P = 0.004), a 13% increase in breast cancer-specific mortality (P = 0.01), and a 19% increase in cardiovascular disease mortality (P = 0.04). Associations with breast cancer mortality were not modified by prediagnosis menopausal status, cigarette smoking, or body mass index., Conclusion: These findings suggest that efforts to minimize weight gain after a breast cancer diagnosis may improve survival.

The purpose of this study was to examine the risk of premenopausal breast cancer for women in relation to childbearing recency and whether this association differs by breast-feeding history and/or the amount of weight gained during pregnancy. This analysis was based on data from a population-based case-control study composed of 1,706 incident cases of invasive breast cancer and 1,756 population controls from Wisconsin, New Hampshire, and Massachusetts. In a telephone interview conducted from 1996 to 2001, information was gathered on established breast cancer risk factors, as well as reproductive history, including amount of weight gained during the last full-term pregnancy and whether the child was breast-fed. Unconditional logistic regression was used to estimate odds ratios and Wald 95% confidence intervals for the risk of breast cancer. When compared with nulliparous women, women that had given birth within the past 5 years before breast cancer diagnosis in the cases or a comparable period in controls had a nonsignificant 35% increased risk of invasive breast cancer (odds ratio, 1.35; 95% confidence interval, 0.90-2.04), adjusting for age and known breast cancer risk factors (Ptrend = 0.14). We did not find a significant interaction with breast-feeding (Pinteraction = 0.30) or pregnancy weight gain (Pinteraction = 0.09).

A number of breast cancer risk factors are modifiable later in life, yet the combined impact of the population changes in these risk factors on breast cancer incidence is not known to have been evaluated. The population attributable risk (PAR) associated with individual risk factors and the summary PAR for sets of modifiable and nonmodifiable risk factors were estimated by using data on 3,499 invasive breast cancer cases and 4,213 controls from a population-based study in Wisconsin, Massachusetts, and New Hampshire, conducted from 1997 to 2001. The summary PAR for factors modifiable after menopause, including current postmenopausal hormone use, recent alcohol consumption, adult weight gain, and recent recreational physical activity, was 40.7%. Of the individual modifiable factors, the highest PARs were observed for weight gain (21.3%) and recreational physical activity (15.7%), which together showed a summary PAR of 33.6%. The summary PAR for factors not modifiable after menopause, including family history of breast cancer, personal history of benign breast disease, height at age 25 years, age at menarche, age at menopause, age at first birth, and parity, was 57.3%. These findings suggest that a substantial fraction of postmenopausal breast cancer may be avoided by purposeful changes in lifestyle later in life.

Objective: We conducted a population-based case-control study to investigate the association between hormone therapy (HT) and ovarian cancer incidence, and followed all these cancer cases to determine the association of HT use with ovarian cancer mortality., Methods: Seven hundred fifty-one incident cases of invasive epithelial ovarian cancer aged 40-79 years were diagnosed in Massachusetts and Wisconsin between 1993-1995 and 1998-2001 and matched to similarly aged controls (n = 5,808). Study subjects were interviewed by telephone, which ascertained information on HT use and specific preparation, estrogen alone (E-alone) or estrogen plus progestin (EP). Ovarian cancer cases were followed-up for mortality through December 2005. Multivariate logistic regression was used to estimate odds ratios and 95% confidence intervals (CI) for ovarian cancer incidence, and Cox proportional hazards modeling was used to estimate hazard ratios and corresponding confidence intervals for ovarian cancer mortality., Results: Ever use of HT was significantly associated with an increased risk of ovarian cancer (odds ratio 1.57, 95% CI 1.31-1.87). The excess risk was confined to women who used E-alone preparations (OR 2.33, 95% CI 1.85-2.95). No significant associations were detected between pre-diagnosis HT use and ovarian cancer survival., Conclusions: Hormone therapy increases risk of ovarian cancer among E-alone users, but there is no substantial impact on survival after diagnosis.

Numerous studies have observed reduced breast cancer risk with increasing levels of physical activity, yet these findings have been inconsistent about optimal times of activity and effect modification by other factors. We investigated the association between recreational and occupational physical activity and breast cancer risk in a population-based case-control study in Massachusetts, New Hampshire, and Wisconsin. During structured telephone interviews, 7,630 controls, 1,689 in situ, and 6,391 invasive breast cancer cases, ages 20 to 69 years, reported lifetime history of recreational physical activity and occupation. Neither lifetime recreational nor strenuous occupational physical activity appeared to be associated with risk of breast carcinoma in situ. In contrast, recreational physical activity was associated with a reduced risk of invasive breast cancer. After adjustment for potentially confounding factors, women averaging >6 h per week of strenuous recreational activity over their lifetime had a 23% reduction in the odds ratio of invasive breast cancer when compared with women reporting no recreational activity (95% confidence interval, 0.65-0.92; P(trend) = 0.05). However, this reduction in risk was limited to women without a first-degree family history of breast cancer (P(interaction) = 0.02). Inverse associations were observed for physical activity early in life, in the postmenopausal years, and in the recent past, but these findings were confined to women without a family history of breast cancer. Lifetime strenuous occupational activity was not associated with invasive breast cancer risk. These results provide further evidence that, for most women, physical activity may reduce the risk of invasive breast cancer.

Alcohol consumption has been investigated as a possible risk factor for ovarian cancer in several epidemiological studies, with inconsistent findings. Recent studies have suggested that the association between alcohol consumption and ovarian cancer may vary according to histologic subtype of ovarian cancer and type of alcohol consumed (e.g., wine, beer, or liquor). We examined these associations in a population-based case-control study comprised of 762 incident cases of epithelial ovarian cancer and 6,271 population controls from Massachusetts and Wisconsin aged 40-79 years. Women reported their usual alcohol consumption as young adults (20-30 years of age) and in the recent past. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. There was no significant association of ovarian cancer with increasing alcohol consumption either during ages 20-30 years (p trend 0.42) or in the recent past (p trend 0.83). Regular drinking of beer (1 drink/day or more) during ages 20-30 (OR 1.55, 95% CI 1.07-2.26), though not liquor (OR 1.35, 95% CI 0.86-2.11) or wine (OR 0.99, 95% CI 0.49-2.00), was associated with a statistically significant increase in risk of invasive tumors, whereas no significant relationships were observed for recent drinking, regardless of alcohol type. The elevated risk for early adult regular drinking was confined to serous invasive tumors (OR 1.52, 95% CI 1.01-2.30), though results for other subtypes were based on sparse data and results were imprecise. In this study, neither total alcohol consumption as a young adult nor recently was associated with an increase in the risk of ovarian cancer.

Objective: To examine the relationship between anthropometric measures and ovarian cancer by menopausal status., Methods: We analyzed data from a population-based case-control study comprised of 700 incident cases of epithelial ovarian cancer and 5,943 population controls from Massachusetts and Wisconsin enrolled between 1993 and 2001. In a telephone interview, information was gathered on established ovarian cancer risk factors, as well as adult height and age-specific body weight. Logistic regression was used to estimate multivariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for body mass index (BMI) throughout life., Results: Recent BMI had no significant association with ovarian cancer risk (P-trend 0.14 for continuous BMI), after adjustment for age and other ovarian cancer risk factors. However, a non-significant positive association (overall P-trend 0.08) was observed for BMI at age 20; the risk estimate comparing a body mass of >25 kg/m2 to the lowest quintile (

The intrauterine environment appears to play a role in the development of adult diseases, including several prominent cancers. Our study aims to characterize the relationship between birth weight, a measure of the intrauterine environment, and adult obesity. A population-based sample of women aged 50-79, living in the states of Massachusetts, New Hampshire or Wisconsin, were randomly selected from lists of licensed drivers and Medicare beneficiaries to participate as controls in a case-control study of breast cancer. Information on birth weight, adult height and adult weight were collected through structured telephone interviews from 1992-1995. Our analysis was based on 1,850 interviews. A U-shaped relationship between birth weight and adult BMI was observed. Median adult BMI for the birth weight categories (in kilograms) <2.3, 2.3<2.5, 2.5<3.2, 3.2<3.9, 3.9<4.5 and > or =4.5 were 26.6, 24.4, 25.1, 25.5, 25.4 and 26.6 kg/m respectively. Compared to women 2.5<3.2 kg at birth, women in highest birth weight category (> or =4.5 kg) had an odds ratio of 1.99 (95% CI 1.13-3.48) of being obese (> or =30 kg/m(2)) as adults. The odds ratio for women in the <2.3 kg birth weight category was 1.67 (95% CI 1.01-2.76). These data suggest that both low and high birth weights are associated with higher adult BMI and support the hypothesis that fetal experience may influence adult obesity with potential consequences for risk of several major cancers., (Copyright 2002 Wiley-Liss, Inc.)

Epidemiological evidence now consistently supports a modest increase in breast cancer risk among women using postmenopausal hormones, usually estrogens. Less is known regarding how the addition of progestin affects breast cancer risk. The objective of this study was to investigate the type and duration of postmenopausal therapy and breast cancer risk. We performed a multicenter population-based case-control study set in Massachusetts, New Hampshire, and Wisconsin. The subjects were 5298 postmenopausal women (age range, 50-79 years) with a new diagnosis of invasive breast cancer from statewide tumor registries. For comparison, 5571 controls were randomly selected from population lists. Participants completed a structured telephone interview covering hormone use and breast cancer risk factors. Multivariable regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CIs). The RR for breast cancer increased with longer durations of hormone use, about 2%/year for estrogen alone (RR, 1.02; 95% CI, 1.01-1.03) and 4%/year for estrogen-progestin use (RR, 1.04; 95% CI, 1.01-1.08). Estrogen-progestin use that was both recent and long term (>5 years in duration) was more strongly associated with breast cancer risk (RR, 1.57; 95% CI, 1.15-2.14) than similar use of estrogen alone (RR, 1.39; 95% CI, 1.17-1.65). In estrogen-progestin users, risks were similar for sequential and continuous use regimens but perhaps stronger for lobular than ductal breast cancer. Use of progestin alone was associated with a doubling of risk (RR, 2.09; 95% CI, 1.07-4.07 for ever use versus nonuse). Estrogen-progestin use, both sequential and continuous, appears to be more strongly associated with risk of breast cancer than use of estrogen alone.

Objective: To evaluate the association between dietary intake of carotenoids and vitamin A and the incidence of ovarian cancer., Methods: We conducted a population-based case-control study of ovarian cancer in Massachusetts and Wisconsin. Incident cases diagnosed between 1991 and 1994 were identified through statewide tumor registries. We selected community controls at random from lists of licensed drivers and Medicare recipients; 327 cases and 3129 controls were included in the analysis. Data were collected by telephone interview, which included an abbreviated food and supplement list to quantify typical consumption of carotenoids (lutein/zeaxanthin, alpha-carotene, beta-carotene), retinol and total vitamin A at 5 years prior to diagnosis in cases, or to a comparable reference date in controls. Results were adjusted for age, state, and other risk factors., Results: Participants with the highest dietary intake of lutein/zeaxanthin (> or =24,000 microg/week) experienced a 40% lower risk of ovarian cancer (95% CI = 0.36-0.99) compared to those with the lowest intake. Intake of alpha-carotene, beta-carotene, retinol and total vitamin A was unrelated to risk. Among foods, we observed non-significantly lower risks with high consumption of spinach, carrots, skim/lowfat milk and liver., Conclusion: These results support previous findings suggesting an inverse relationship between carotenoid intake and ovarian cancer risk.

Objective: Although many studies have shown that higher weight increases the risk of postmenopausal breast cancer, some aspects of this association are unclear. In order to examine the risk associated with different patterns of weight change, we analyzed data from a large case-control study of postmenopausal breast cancer., Methods: Participants included women aged 50 79 years (n = 5031) who are newly diagnosed with invasive breast cancer in Massachusetts, New Hampshire, and Wisconsin. Similarly-aged population controls (n = 5255) were selected at random from driver's license files and Medicare beneficiary lists. Height, weight, and information on other breast cancer risk factors were ascertained by structured telephone interviews from 1992 to 1995, and logistic regression was used to estimate multivariable-adjusted odds ratios (OR) and 95% confidence intervals (CI)., Results: Women in the top quintile groups for height at age 20, recent weight, and recent body mass index had significantly increased risks of breast cancer. Among women who reached their highest adult weight at younger ages (<45 years), increasing weight loss since that age was associated with a reduced risk of postmenopausal breast cancer (OR 0.90, CI 0.84 0.98, per 5 kg). However, weight loss among women whose highest weight occurred after age 45 was not associated with risk (OR 1.00, CI 0.95 1.05, per 5 kg). Weight gain since the lowest adult weight increased risk by 8% for each 5 kg of gain (OR 1.08, CI 1.06-1. 11). Temporary weight cycling (weight loss followed by weight gain) was not associated with increased risk., Conclusions: Weight gain clearly increased risk of postmenopausal breast cancer. These data lend further support to efforts aimed at helping women avoid weight gain as they age.

Background: There is considerable interest in the possibility of an infectious etiology for human breast cancer. Although studies have shown that certain strains of mice transmit mammary tumor virus via breast milk, few epidemiologic studies have addressed this topic in humans., Methods: We evaluated the relationship between having been breast-fed as an infant and breast cancer risk among 8299 women who participated in a population-based, case-control study of breast cancer in women aged 50 years or more. Case women were identified through cancer registries in three states (Massachusetts, New Hampshire, and Wisconsin); control women were identified through statewide driver's license lists (age <65 years) or Medicare lists (ages 65-79 years). Information on epidemiologic risk factors was obtained through telephone interview. We used multiple logistic regression to assess having been breast-fed and maternal history of breast cancer in relation to breast cancer occurrence both in premenopausal women (205 case women; 220 control women) and in postmenopausal women (3803 case women; 4071 control women)., Results: We found no evidence that having been breast-fed increased breast cancer risk in either premenopausal women (odds ratio [OR] = 0.65; 95% confidence interval [CI] = 0.41-1.04) or postmenopausal women (OR = 0.95; 95% CI = 0.85-1.07). In addition, breast cancer risk was not increased by having been breast-fed by a mother who later developed breast cancer., Conclusion: Our results do not support the hypothesis that a transmissible agent in breast milk increases breast cancer risk. Because premenopausal women were not well represented in our study population, our findings with regard to this group may not be generalizable and should be viewed with caution.

We have used data from a large population-based case-control study in the United States to evaluate the effect of occupational physical activity on breast cancer risk. Women diagnosed with breast cancer identified from four state cancer registries, and controls randomly selected from lists of licensed drivers or Medicare beneficiaries, were interviewed by telephone for information on usual occupation and other factors. We classified usual occupation into one of four categories of physical activity. After excluding subjects for whom a strength rating could not be assigned, we had a final sample size of 4,863 cases and 6,783 controls. Using conditional logistic regression models, we calculated adjusted odds ratios (OR) and 95 percent confidence intervals (CI) for occupations having light, medium, and heavy activity compared with sedentary ones. Women with heavy-activity occupations had a lower risk of breast cancer than women with sedentary jobs (OR = 0.82, CI = 0.63-1.08), as did women with jobs with medium activity (OR = 0.86, CI = 0.77-0.97) or light activity (OR = 0.92, CI = 0.84-1.01). There was a significant decreasing trend in the ORs from sedentary to heavy work (P = 0.007). Although limited by exposure misclassification, these data are consistent with the hypothesis that physical activity reduces the risk of breast cancer.

The relation between body size and breast cancer remains uncertain, particularly with regard to differences between pre- and postmenopausal women. The authors examined whether height, weight, body mass index, and weight change were associated with breast cancer risk among pre- and postmenopausal women. This population-based case-control study included women aged 20-74 years (n = 6,548) who were diagnosed with invasive breast cancer during 1988-1991 in Maine, Massachusetts, New Hampshire, and Wisconsin. Similarly aged control women (n = 9,057) were selected at random from driver's license files and Health Care Financing Administration files. Height, weight, and information on other breast cancer risk factors were ascertained by telephone interview, and logistic regression was used to estimate multivariate-adjusted odds ratios and 95% confidence intervals. Among premenopausal women, the adjusted odds ratio for the upper quintile group of height relative to the lowest was 1.36 (95% confidence interval (CI) 1.05-1.76). The heaviest premenopausal women had a lower risk (odds ratio (OR) = 0.87, 95% CI 0.70-1.10). Among postmenopausal women, the adjusted odds ratios were higher for the upper quintile categories of both height (OR = 1.27, 95% CI 1.11-1.45) and weight (OR = 1.57, 95% CI 1.37-1.79). Weight gain since ages 18 and 35 years was associated with increased postmenopausal breast cancer risk, and risk was lower in women who had lost weight. These findings suggest that programs to avoid weight gain merit study as a means to reduce risk of postmenopausal breast cancer.

Data from a population-based case control study were used to estimate occupation-specific relative risks for female breast cancer, adjusted for established breast cancer risk factors. Breast cancer cases under age 75 were identified from tumor registries in four states. Controls were randomly selected from driver's license and Medicare beneficiary lists. Information on usual occupation and risk factors was obtained by telephone interview. Odds ratios from logistic regression adjusted for age, state, body mass index, benign breast disease, family history of breast cancer, menopausal status, age at menarche, parity, age of first birth, lactation history, education, and alcohol consumption were calculated for each of 26 occupational groups. Complete occupational information was obtained for 6,835 cases and 9,453 controls. Of 26 occupational groups, only "administrative support occupations" had a statistically significantly increased risk of breast cancer (OR = 1.15, 95% CI 1.06-1.24). In these data, no specific occupational group had an unusual risk of breast cancer. Increased risks reported elsewhere for nurses and teachers were not corroborated.

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] = 1.0-1.2). Total duration of use also 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.

A priori hypotheses suggest that cigarette smoking could either increase or decrease breast cancer incidence. To clarify these competing hypotheses, we used data from a very large population-based breast cancer case-control study to investigate the impact of smoking on breast cancer risk. Breast cancer patients less than 75 years old were identified from statewide tumor registries in Wisconsin, Massachusetts, Maine, and New Hampshire; controls were randomly selected from driver's license lists (age less than 65) or lists of Medicare beneficiaries (age 65-74). Information on reproductive history, medical history, and personal habits including cigarette smoking was obtained by telephone interview. A total of 6,888 cases and 9,529 controls were interviewed. There was virtually no relationship between current smoking and breast cancer risk (multivariate odds ratio, 1.00; 95% confidence interval, 0.92-1.09), and former smokers had a barely increased risk (odds ratio, 1.10; 95% confidence interval, 1.01-1.19). Similar results were observed among both premenopausal and postmenopausal women. There was no suggestion that heavy or long-term smoking increased or decreased risk, nor were there indications that women who began smoking at an early age were at increased risk, as has been hypothesized. The results of this large population-based study indicate that smoking does not influence the risk of breast cancer, even among heavy smokers who began smoking at an early age.

Despite extensive study, concerns remain about a possible association between long-term postmenopausal hormone treatment--particularly use of combination preparations--and risk of breast cancer. The authors evaluated the use of postmenopausal hormone replacement therapy in relation to breast cancer risk in a large multicenter, population-based case-control study. Women with a new diagnosis of breast cancer were identified through statewide tumor registries in Wisconsin, Massachusetts, Maine, and New Hampshire. Controls were randomly selected from population lists in each state. For this analysis of postmenopausal women, data were available from 3,130 breast cancer cases and 3,698 controls interviewed between 1989 and 1991. Replacement hormone use was not associated with breast cancer risk in women who had ever undergone this treatment (relative risk (RR) = 1.05, 95% confidence interval (CI) 0.93-1.18). Among women who had used replacement hormones for 15 years or more, there was no clear increase in risk, although the small sample size did not preclude the possibility of a modest association (RR = 1.11, 95% CI 0.87-1.43). Risk among women using progestins in combination with estrogens was similar to that in women using estrogens alone. Risk did not vary according to type of menopause, family history of breast cancer, history of benign breast disease, or alcohol intake. These results are consistent with the majority of reports which find no overall increased risk associated with the use of replacement hormones. However, in contrast to several other studies, this study did not find long-term use to be associated with increased risk. These results also do not support a hypothesized effect of combined progestin and estrogen use on the risk of breast cancer.

Data from a large, multicenter, population-based case-control study were analyzed to investigate the relation between multiple birth pregnancies and subsequent breast-cancer risk in the gravidas. Women less than 75 years old who had breast cancer were identified from statewide tumor registries in Wisconsin, western Massachusetts, Maine and New Hampshire. Controls aged less than 65 years were selected randomly from lists of licensed drivers, and controls aged between 65 and 74 were selected randomly from lists of Medicare beneficiaries. Information on reproductive history and other factors was obtained by means of telephone interviews. After excluding nulliparous women, 5,880 case subjects and 8,217 controls remained for analysis. Multiple birth pregnancies occurred in 146 cases and 218 controls. Adjusted for the number of full-term pregnancies and other confounders, the odds ratio (OR) for any multiple birth pregnancy was 0.94 (95% confidence interval, 0.75 to 1.17). The null association between multiple birth pregnancies and breast cancer remained if the mother's first pregnancy or last pregnancy resulted in a multiple birth. In addition, no trend in risk emerged for age at first multiple birth or time since last multiple birth. While other investigators have suggested biological mechanisms to explain both protective and detrimental effects of multiple births and subsequent development of breast cancer, this study does not support either assertion.