Search

Purpose: Use of specific antihypertensive medications (AHTs) has been hypothesized to increase breast cancer risk, but results across published studies are inconsistent., Methods: We re-evaluated the relationship between AHT use and breast cancer risk in a prospective cohort of 3,201 women ≥65 years of age at recruitment now with more than double the length of follow-up (12 vs. 5 years) and substantially more breast cancer diagnoses (188 compared with 75 cases). We estimated the association between AHT use overall as well as use of specific formulations (based on data collected annually) and breast cancer risk using multivariate-adjusted Cox regression., Results: Compared with women who reported no use of AHTs, women who had used calcium channel blockers (CCB) within the past two years had a 1.6-fold increased risk of breast cancer (95 % confidence interval (CI): 1.0-2.5), and in particular, recent users of immediate-release CCBs had a 2.4-fold increased risk (95 % CI: 1.3-4.5). Neither ever nor recent use of any other type of AHT was associated with breast cancer risk., Conclusions: While the observed association between immediate-release CCBs and breast cancer risk is based on a small sample size and needs to be interpreted cautiously, this result is consistent with others in the literature. However, given declines in use of these preparations in favor of sustained-release CCBs, which was not related to risk, the potential clinical and public health impact of this association is limited. This study also adds to the evidence that other commonly used AHTs are not strongly related to breast cancer risk.

Racial differences in breast cancer risk, including the risks of hormone receptor subtypes of breast cancer, have been previously reported. We evaluated whether variation in genes related to estrogen metabolism (COMT, CYP1A1, CYP1B1, CYP17A1, CYP19A1, ESR1, GSTM1, GSTP1, GSTT1, HSD17B1, SULT1A1, and UGT1A1) contributes to breast cancer risk and/or racial differences in risk within the CARE study, a multi-centered, population-based case-control study of breast cancer. Genetic variation was assessed as single nucleotide polymorphisms (SNPs), haplotypes, and SNP-hormone therapy (HT) interactions within a subset of 1,644 cases and 1,451 controls, including 949 Black women (493 cases and 456 controls), sampled from the CARE study population. No appreciable associations with breast cancer risk were detected for single SNPs or haplotypes in women overall. We detected SNP-HT interactions in women overall within CYP1B1 (rs1800440; p (het) = 0.003) and within CYP17A1 (rs743572; p (het) = 0.009) in which never users of HT were at a decreased risk of breast cancer, while ever users were at a non-significant increased risk. When investigated among racial groups, we detected evidence of an SNP-HT interaction with CYP1B1 in White women (p value = 0.02) and with CYP17A1 in Black women (p value = 0.04). This analysis suggests that HT use may modify the effect of variation in estrogen-related genes on breast cancer risk, which may affect Black and White women to a different extent.

Objective: Differences in cervical cancer incidence rates by race/ethnicity persist in the United States. We examined these differences by histologic type and by various patient and socioeconomic characteristics., Methods: Thirteen U.S. cancer registries were used to identify women 20-79 years of age diagnosed from 1992 to 2003 with invasive cervical cancer. Age-adjusted incidence rates and annual percent changes were calculated for four different races/ethnicities (Non-Hispanic whites, Hispanic whites, African-Americans, and Asians/Pacific Islanders) for cervical cancer overall, squamous cell carcinoma (SCC), and adenocarcinoma (AC)., Results: Hispanic whites had the highest incidence rate of cervical cancer overall (24.2/100,000), SCC (18.3/100,000), and AC (4.6/100,000). Non-Hispanic whites had the lowest rates of cervical cancer overall (10.8/100,000) and SCC (7.2/100,000), while African-Americans had the lowest rate of AC (2.3/100,000). Incidence rates of cervical cancer overall and SCC declined across all racial/ethnic groups. Numerous variations in incidence rates and annual percent changes were observed when analyses were stratified by county level socioeconomic characteristics., Conclusions: Variations in screening utilization and socioeconomic status may account for the majority of racial/ethnic disparities in cervical cancer incidence. Targeting groups with the greatest burdens of cervical cancer is of public health importance, particularly as we enter the human papillomavirus vaccine era.

Objective: To estimate breast cancer risk associated with short-term (<6 months) oral contraceptive use, and explore variation in estimates by use characteristics and medical, menstrual, and reproductive history., Methods: We analyzed data from the Women's Contraceptive and Reproductive Experiences Study. Case subjects were white women and black women, 35-64 years old, diagnosed with invasive breast cancer in July 1994-April 1998. Control subjects identified by random-digit dialing were matched to case subjects by age, race, and study site. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs)., Results: Overall, short-term oral contraceptive use was not associated with breast cancer risk (OR = 1.0; 95% CI = 0.8-1.1). However, significant interaction between short-term use and menopausal status led to an observed increased breast cancer risk in pre-menopausal women (OR = 1.3; 95% CI = 1.0-1.7) and a reduced risk in post-menopausal women (OR = 0.8; 95% CI = 0.6-1.0) associated with short-term use. The association was more pronounced in women with non-contraceptive reasons for use and underlying risk factors for breast cancer., Conclusions: These associations may result from underlying characteristics of users or unmeasured factors influencing duration of use and breast cancer risk.

Objective: To assess interactions between use of estrogen plus progestin hormone therapy (EPHT) and body mass index (BMI) in relation to risks of different types of breast cancer, based on histology and hormone receptor status., Methods: We conducted a population-based case-control study that compared 975 postmenopausal breast cancer cases to 1,007 controls. Interactions between menopausal hormone therapy (HT) and BMI in relation to risk of different breast cancer types were evaluated using logistic regression., Results: Obese (BMI > or = 30.0 kg/m2) never users of HT had 1.7-fold to 2.3-fold elevated risks of ductal and ER+/PR+ tumors, respectively, compared to thinner women. BMI was not related to breast cancer risk among current HT users. Current EPHT users for > or = 5 years had 2.1 to 9.6-fold elevated risks of lobular and ER+/PR+ tumors compared to never users of HT regardless of BMI. Current EPHT users for > or = 5 years with a BMI < or = 24.9 kg/m2 also had a 2.6-fold elevated risk of ductal carcinoma. However, none of the interactions between BMI and HT use evaluated reached statistical significance., Conclusions: While interactions between HT and BMI are well established, they appear to only be present among certain breast cancer types. Since obesity is related to breast cancer risk only among never users of HT, as HT use declines the relative impact of obesity on breast cancer incidence may grow.

Results from studies evaluating the relationship between cigarette smoking and breast cancer have been inconsistent. Though most studies have found that smoking does not alter risk, others have observed both increased and decreased risks associated with smoking. The reasons for these inconsistencies are unclear, but they may be related to differences in study populations, designs, and exposure definitions. In particular, this relationship may vary by age, and few studies have focused on older women many of whom have smoked for very long durations. We conducted a population-based case-control study (975 cases/1007 controls) of women 65-79 years of age in western Washington State. Women who were current smokers, smoked for > or =40 years, had > or =11 pack-years of lifetime smoking, or started smoking before their first full-term birth each had 30-40% elevated risks of breast cancer (p < 0.05). Recency, length, and intensity of smoking are all associated with modest increased risks of breast cancer. A further understanding of the timing of smoking, and its interaction with other factors, may enhance our knowledge of whether and by what mechanisms smoking alters breast cancer risk.

Objective: We examined breast cancer risk related to lifetime exposure to oral contraceptives (OCs) and hormone replacement therapy (HRT) in postmenopausal women., Methods: The Women's Contraceptive and Reproductive Experiences (CARE) Study was a population-based case-control study that included 1847 postmenopausal women with incident invasive breast cancer, and 1932 control subjects, identified using random digit dialing., Results: 45% of cases and 49% of controls used both OCs and HRT. OC users were not at increased risk regardless of subsequent HRT exposure. HRT users who had used OCs previously did not have a higher risk of breast cancer than women with no exposure to OCs. We observed a negative interaction (p-value: 0.032) of combined hormone replacement therapy (CHRT) and past OC use. The increase in risk with CHRT was stronger in women who had never used OCs in the past (odds ratio: 1.05; 95% confidence interval: 1.01-1.10 per year of exclusive CHRT use) than in women who had used OCs (odds ratio: 1.00; 95% confidence interval: 0.97-1.03)., Conclusions: We found no indication that adverse effects of exposure to OCs or HRT appeared only in the presence of the other hormone or were exacerbated by exposure to the other hormone.

Objective: To investigate the relationship between allergy and risk of breast cancer in women 45 years of age and younger., Methods: Data were analyzed from a population-based case-control study of breast cancer in western Washington. Cases were women born after 1944 who were diagnosed with invasive breast cancer (n = 747) between January 1983 and April 1990. Controls (n = 958) were similarly aged women ascertained through random-digit dialing. Cases and controls were interviewed about their history of doctor diagnosed allergies, including detailed information on the specific types of allergies and the age of onset. Using logistic regression we examined the associations between allergy history and breast cancer., Results: A history of allergies was associated with a reduced risk of breast cancer for women older than 35 (odds ratio (OR) = 0.77; 95% confidence interval (CI) = 0.60-0.99), but not for women 35 years or younger (OR = 1.30; 95% CI = 0.94-1.81). There was little difference in effect when age of first allergy onset was examined. No specific type of allergy was associated with breast cancer risk., Conclusion: Our results provide some evidence that a history of allergy may be associated with a reduced risk of breast cancer for women who develop breast cancer between 35 and 45 years of age. Future studies are needed to verify the relationship between immune responses and breast cancer risk.

Objective: To examine the relation between breast cancer risk and job history among women 20-44 years of age who participated in a multi-center, population-based, case-control study., Methods: Participants consisted of women newly diagnosed with breast cancer (1642) and controls identified by random-digit dialing (1494). Details about the three longest jobs were collected and coded by an industrial hygienist. Odds ratios and 95% confidence intervals were calculated and adjusted for age, study site, and other breast cancer risk factors., Results: Several occupational and industrial categories were found to influence breast cancer risk. Stratification of the study population by parity revealed differences in breast cancer risk between the two groups for several occupational categories, including teachers, librarians or counselors (increased risk only among parous women) and natural scientists and mathematicians (decreased risk only among nulliparous women)., Conclusions: This is among the first population-based case-control studies to examine occupational history and breast cancer risk in young women, with the ability to consider a wide array of potential confounders, including reproductive characteristics. This study provides further evidence of an increased breast cancer risk for several occupations and industries. Other findings were not as strongly supported by previous investigations.

Objective: Postmenopausal hormone use and risk of breast cancer by histopathology was examined in a large multi-centered population-based case-control study., Methods: Women younger than 75 years newly diagnosed with invasive breast cancer between 1988 and 1991 were identified from statewide tumour registries in Wisconsin, Massachusetts, New Hampshire, and Maine. Only postmenopausal women were included in this analysis. Breast cancer cases (lobular (n = 219), ductal, NOS (n = 2172), and specific ductal subtypes (n = 242)) were compared with randomly selected population controls (n = 3179) using adjusted multi-variable polytomous logistic regression to estimate odds ratios (OR) and 95% confidence intervals (95%CI) for each histology., Results: Lobular carcinoma was associated with recent (within 2 years) estrogen therapy (OR: 1.8, 95% CI: 1.0-3.4) and recent use of combined estrogen-plus-progestin therapy (OR:3.6, 95%CI: 1.8-7.6). Risk of ductal carcinoma was not associated with recent use of either estrogen alone (OR: 0.9, 95% CI: 0.7-1.2) or combined therapy (OR:0.9, 95% CI: 0.6-1.3). No associations were found with ductal subtypes., Conclusions: The association between postmenopausal hormone use and risk of breast cancer may depend on histopathology. Of particular interest is the association between combined hormone therapy and increased risk of lobular carcinoma. This lesion is increasingly common but, nonetheless, comprises fewer than 10% of invasive breast cancers.

Objective: To assess risk factors for breast cancer among very young compared to older premenopausal women., Methods: Between 1990 and 1992 a population-based case-control study conducted in Atlanta, GA, Seattle/Puget Sound, WA, and central NJ interviewed 3307 premenopausal women aged 20-54 years. Logistic regression models estimated adjusted relative risks (RR) and 95% confidence intervals (CI) for each of three 10-year age groups., Results: Among the youngest age group (<35 years, n = 545), significant predictors of risk included African-American race (RR = 2.66: 95% CI 1.4-4.9) and recent use of oral contraceptives (RR = 2.26; 95% CI 1.4-3.6). Although these relationships were strongest for estrogen receptor-negative (ER-) tumors (RRs of 3.30 for race and 3.56 for recent oral contraceptive use), these associations were also apparent for young women with ER+ tumors. Delayed childbearing was a risk factor for ER+ tumors among the older premenopausal women (Ptrend < 0.01), but not for women <35 years in whom early childbearing was associated with an increased risk, reflecting a short-term increase in risk immediately following a birth. Family history of early-onset breast cancer was more strongly associated with risk among women <35 years (RR = 3.22) than those 45-54 years (RR = 1.51). Risk factors for premenopausal breast cancer not significantly modified by age at diagnosis included early age at menarche, low body mass index, and heavy alcohol consumption., Conclusion: These findings suggest the possibility that women who develop breast cancers at very young ages may be etiologically as well as clinically distinct.

Objectives: To evaluate the associations of dietary macronutrients, food groups, and eating patterns with risk of breast cancer in a population-based case-control study., Methods: In this study among women 20-44 years of age, 568 cases with breast cancer and 1451 population-based controls were included. They completed a detailed in-person interview, a self-administered food-frequency questionnaire and were measured for anthropometric indices. Logistic regression was used to estimate odds ratios (OR) and their 95% confidence intervals (CI) of breast cancer, adjusted for age, study site, race, education, alcohol consumption, oral contraceptive usage, smoking status, and body mass index., Results: There was no association between breast cancer risk and intake of calories, macronutrients, or types of fat. Risk of breast cancer was unrelated to intakes of a variety of food groups, including red meats, dairy, high-fat snacks and desserts, or foods high in animal fat. Increased risk was observed for high intake of a food group composed of sweet items, particularly sodas and desserts. Risk increased linearly with percent of calories from sweets and frequency of sweets intake. Consumption of sweets 9.8 or more times per week compared with <2.8 times per week was associated with an adjusted OR of 1.32 (95% CI = 1.0-1.8). This association did not appear to be due to the high-fat foods or carbonated beverages that comprised the food group. Compared with women reporting one or two meals and snacks per day, reduced risks were noted for women reporting six or more (OR = 0.69, 95% CI = 0.4-1.1)., Conclusions: These data suggest a modest relationship between intakes of sweet items with risk of in-situ and localized breast cancer in young women. This relation is consistent with the hypothesized link of high insulin exposure and risk of breast cancer. There was some suggestion that women who ate many times during the day were at reduced risk of disease, which is also consistent with an insulin-related mechanism.

Objective: Exercise has been hypothesized to influence cancer risk through a variety of mechanisms including hormonal, metabolic and immunologic effects, yet its relation with the risk of thyroid cancer has not been examined. We conducted a population-based case-control study in women aged 18-64 in three counties of western Washington State to assess the relation of recreational physical activity with risk of papillary thyroid cancer., Methods: Of 558 women with thyroid cancer of the follicular epithelium diagnosed during 1988-1994 who were identified as eligible, 468 (83.9%) were interviewed; this analysis was restricted to women with papillary histology (n = 410). Controls (n = 574) were identified by random digit dialing, with a response proportion of 73.6%. Logistic regression was used to calculate odds ratios (OR) and associated confidence intervals (CI) estimating the relative risk of papillary thyroid cancer associated with various aspects of recreational exercise., Results: Risk of thyroid cancer was reduced among women who reported that they engaged in regular recreational exercise during the 2 years before diagnosis relative to women who did not report exercise during that time period (OR = 0.76, 95% CI 0.59-0.98). A similar risk reduction was noted among women who reported having exercised regularly between ages 12 and 21 (OR = 0.83, 95% CI 0.64-1.1). However, no clear associations with aspects of recreational activity, including average hours exercised per week or weekly energy expenditure, were observed., Conclusions: These results provide some initial support for the hypothesis that physical activity may reduce risk of thyroid cancer.

Background: Breast and thyroid cancer have been observed to occur more frequently than expected as multiple primary tumors in women. The study presented herein focuses on the effects of age at diagnosis and treatment for the first cancer on the development of the second cancer., Methods: This retrospective cohort study used a study population consisting of 38,632 women diagnosed with primary invasive breast cancer and 2189 women diagnosed with primary invasive thyroid cancer between 1974 and 1994. Cases were identified from records of the Cancer Surveillance System of western Washington and followed for subsequent cancer development through 1995., Results: Seventy-one women were diagnosed during their lives with both breast and thyroid cancers. Including cancers diagnosed during the same month as or after the initial cancer, the relative risk (RR) of breast cancer among women with thyroid cancer was 1.5 (95% confidence interval [CI] 1.1-2.0), and the RR of thyroid cancer among women with breast cancer was 1.5 (95% CI 1.1-2.2). Among women with thyroid cancer, risk of breast cancer was greatest when the latter cancer was diagnosed under 45 years of age (RR = 2.3, 95% CI 1.1-4.4). First course of treatment, including radiation or hormonal therapy to treat thyroid cancer, and radiation, chemotherapy, or hormonal therapy to treat breast cancer, did not alter a woman's risk of developing the second cancer., Conclusions: The data suggest that the incidence of breast and thyroid cancer may be related, and that in particular women with thyroid cancer may be at a moderately increased risk of developing breast cancer before age 45.

Objectives: The reported mutagenic and carcinogenic effects of some chemicals present in hair dyes have raised concern that hair dye use could increase breast cancer risk. This case-control study evaluated how detailed aspects of hair coloring and hair spray application by reproductive-age women may affect breast cancer risk., Methods: Cases were white female residents of three counties of western Washington state 45 years of age or less, who were diagnosed with breast cancer between 1983 and 1990 (n = 844). A sample of similarly aged women residing in the same counties served as controls (n = 960). Information on hair coloring and hair spray use, as well as other exposures, was ascertained during in-person interviews., Results: Breast cancer cases were slightly more likely than controls to report ever having used some type of hair coloring application, including use of rinses, semi-permanent or permanent dyes, as well as bleaching then dyeing or frosting their hair (relative risk [RR] = 1.3, 95% CI = 1.0-1.6, adjusted for age, fullterm pregnancies, family history of breast cancer, and weight). In subgroup analyses, women with exclusive use of just one of these methods of hair coloring application had no elevation in risk (similarly adjusted RR = 1.1, 95% CI = 0.9-1.3), whereas women who used two or more of these methods did have an elevated risk (RR = 1.9, 95% CI = 1.4-2.5). Hair spray use was not related to the risk of breast cancer (ever versus never users: RR = 1.0, 95% CI = 0.8- 1.3)., Conclusion: The lack of an association between exclusive use of a single type of hair coloring application and breast cancer risk argues that hair coloring application does not influence breast cancer risk among reproductive-age women. Thus, the results of the present study, as well as negative ones from most (but not all) prior studies, are most consistent with the conclusion that neither hair coloring application nor hair spray application influences breast cancer risk.

Objectives: Greater incidence of thyroid cancer in women than men, particularly evident during the reproductive years, has led to the suggestion that female hormones may increase risk of this disease. We conducted a population-based case-control study in women aged 18 to 64 years in three counties of western Washington State (United States) to assess the relation of use of exogenous hormones, including oral contraceptives (OC) and hormone replacement therapy (HRT), to risk of papillary thyroid cancer., Methods: Of 558 women with thyroid cancer of the follicular epithelium diagnosed during 1988-94 who were identified as eligible, 468 (83.9 percent) were interviewed; this analysis was restricted to women with papillary histology (n = 410). Controls (n = 574) were identified by random digit dialing, with a response proportion of 73.6 percent. Logistic regression was used to calculate odds ratios (OR) and associated 95 percent confidence intervals (CI) estimating the relative risk of papillary thyroid cancer among users of exogenous hormones., Results: Among women aged 45 to 64 years, we observed no association of use of OCs or HRT with risk of papillary thyroid cancer. Among women less than 45 years of age, risk of papillary thyroid cancer was reduced in women who had ever used OCs (OR = 0.6, CI = 0.4-0.9); beyond the relation with ever-use, there was no further association with specific aspects of exposure such as estrogenic potency, latency, recency, age at first or last use, or use at the reference date., Conclusions: Our data do not support the hypothesis that use of exogenous estrogens increases the risk of female thyroid cancer.

It has been hypothesized that women who participate in vigorous physical activity may have lower risk of breast cancer due to lower lifetime exposure to ovarian hormones. A population-based case-control study was conducted to investigate the association between leisure-time physical activity and risk of breast cancer among women aged 21 to 45 years. Cases were 747 women diagnosed with invasive breast cancer between 1983 and 1990 in three counties of western Washington state (United States), and were identified through the Seattle-Puget Sound Surveillance, Epidemiology, and End Results (SEER) registry. Controls were 961 women selected from the same area by random-digit telephone dialing. Physical activity was assessed through personal interview, with questions on frequency and duration of each type of recreational activity during the two-year period immediately prior to reference data (date of diagnosis for cases and a comparable assigned date for controls) and between ages 12 and 21. For the two-year time period before diagnosis, there was no association with frequency of activity (age-adjusted odds ratio [OR] = 0.93, 95 percent confidence interval [CI] = 0.71-1.22 for four or more episodes per week cf none), total hours spent in physical activity (age-adjusted OR = 0.92, CI = 0.71-1.22 for four or more hours per week cf none) or MET (metabolic equivalent energy expenditure unit) (age-adjusted OR = 0.95, CI = 0.73-1.23 for 18 or more METs per week of none), nor any trend is risk with increasing activity levels. Similarly, there was no association between leisure activity during adolescence and breast cancer risk. These results were not confounded further by body mass index (wt/ht2), age at menarche, age at first full-term pregnancy, parity, family history of breast cancer, or other measured health behaviors. Our findings do not support a protective effect of leisure-time physical activity either in the adolescent years or in adulthood on breast cancer in young women.

Because of the reduced risk of ovarian cancer related to prior full-term pregnancies, we sought to determine whether there was any association with a history of one or more incomplete pregnancies. White female residents of three counties in Washington State (United States) diagnosed with ovarian cancer during 1986-88 (n = 322), and a random sample of control women selected from these same counties (n = 426), were interviewed regarding their pregnancy and childbearing histories. Among women who had given birth to at least one child, an additional incomplete pregnancy was not associated with the risk of ovarian cancer (relative risk [RR] = 1.1, 95 percent confidence interval [CI] = 0.8-1.6, adjusting for age, oral contraceptive use, and number of births). For those who had never given birth, a somewhat smaller proportion of cases had a history of incomplete pregnancy than controls (RR = 0.8, CI = 0.4-1.7). In an analysis restricted to ever-pregnant women, a prior induced or spontaneous abortion was not found to be associated with the incidence of ovarian tumors (RR = 1.0, CI = 0.6-1.7, and RR = 1.3, CI = 0.8-1.9, respectively). Other studies of the possible relation between incomplete pregnancies and ovarian cancer generally have observed either a weak negative association or no association at all. It is possible that if incomplete pregnancies do affect the risk of ovarian cancer, their impact might be too small to be identified reliably through epidemiologic studies.

To evaluate predictors of contralateral breast cancer risk, we examined data from a nested case-control study of second primary cancers among a cohort of women in western Washington (United States) diagnosed with breast cancer during 1978 through 1990 and identified through a population-based cancer registry. Cases included all women in the cohort who subsequently developed contralateral breast cancer at least six months after the initial diagnosis, but prior to 1992 (n = 234). Controls were sampled randomly from the cohort, matched to cases on age, stage, and year of initial breast cancer diagnosis. Information on potential risk factors for second primary cancer was obtained through medical record abstractions and physician questionnaires. Women who were postmenopausal due to a bilateral oophorectomy (i.e., a surgical menopause) at initial breast cancer diagnosis had a reduction in contralateral breast cancer risk compared with premenopausal women (matched odds ratio [mOR] = 0.25, 95 percent confidence interval [CI] = 0.09-0.68), whereas no reduction in risk was noted among postmenopausal women who had had a natural menopause (mOR = 0.90, CI = 0.39-2.09). Among postmenopausal women, there was a suggestion of a lower risk associated with relatively high parity (2+). A family history of breast cancer was associated with an increased risk (mOR = 1.96, CI = 1.22-5.15) and varied little by menopausal status. Having an initial tumor with a lobular component (c.f. a ductal histology) was not related strongly to risk (mOR = 1.47, CI = 0.79-2.74). The results of the present and earlier studies argue that we have limited ability to predict the occurrence of a contralateral breast tumor. Better predictors will be required before diagnostic and preventive interventions can be targeted to subgroups of patients with unilateral breast cancer.

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.

In registry-based population studies on marital status in relation to cancer, incidence rates sometimes have been calculated using marital status-specific populations that have been estimated by interpolation and extrapolation from census data as a denominator. Alternatively, other cancers from the same registry have been used to estimate the proportion of the population in each marital-status category in the calculation of the relative risk (RR) of a given cancer. Using cancer registry data from four United States populations for the years 1979-87, we compared the relative incidence estimated using each of the two methods. For selected cancers diagnosed during 1979-81, the age-adjusted risks of never-married Black persons were 1.5 to 2.2 times those of married persons when the population size was estimated from census data. The corresponding RRs were 0.7 to 1.1 when the 'control' cancers were used. Among Whites, the differences between the two methods were about 20 to 30 percent. For both races, the difference between the methods was greater still for the years for which we relied on extrapolation to estimate the population (1981-87). The differences between the risk estimates from the two methods may be related to underenumeration in the census, inconsistent definitions of marital status between cancer registries and the census, errors in the extrapolation of the population, and/or the possible association of the incidence of 'control' cancers with marital status. In the US, while each method has some potential for bias, we believe that the likelihood of bias is relatively greater using the census-based method.

The purpose of this population-based case-control study was to learn whether risk factors differ for the individual immunoglobulin types of multiple myeloma. In particular, we sought to determine whether IgA and IgG myeloma were related to a history of exposure to reported IgA- and IgG-stimulating conditions, respectively, or to a history of selected occupational and physicochemical exposures. The M-component immunoglobulin type was determined from immunoelectrophoresis as reported in medical records, and exposure status was obtained through in-person interviews. IgG (56 percent) and IgA (22 percent) M-components predominated. For 17 percent of cases, no peak was found on immunoelectrophoresis; they were presumed to have light-chain myeloma. Persons with these three types of myeloma did not differ with respect to distributions of age or race, but a somewhat higher proportion of light-chain cases were women (58 percent cf 45 percent of all other cases). Detailed analysis of the IgA and IgG subtypes provided little evidence that they differ with respect to prior immune stimulation or employment in several specific jobs. IgA myeloma, but not IgG myeloma, was associated modestly with a history of exposure to chest and dental X-rays. Our study provides little evidence that IgA and IgG myeloma differ with respect to the risk factors examined.

All British Columbia (Canada) women under 75 years of age who were diagnosed with breast cancer during 1988-89 were asked to complete a postal questionnaire which included detailed information on menopausal estrogen use. Controls were drawn from the Provincial Voters List, matched by five-year age category to the cases. The present analysis consists of 699 cases and 685 controls who were postmenopausal due to natural causes or to a hysterectomy. There was no overall increase in risk of breast cancer associated with ever-use of unopposed estrogen (odds ratio [OR] = 1.0, 95 percent confidence interval [CI] = 0.8-1.3). For estrogen use of 10 years or longer, the relative risk [RR] was 1.6 (CI = 1.1-2.5). The risk estimate for current users was somewhat elevated (OR = 1.4, CI = 1.0-2.0). Compared with women who never used hormone preparations, women who had used estrogen plus progestogen had an RR of 1.2 (CI = 0.6-2.2). Our results suggest that ever-use of estrogen, with or without progestogen, does not appreciably increase the risk of breast cancer. However, long-term and recent use of unopposed estrogen may be associated with a moderately increased risk.