EPIDEMIOLOGIC REVIEWS

Copyright © 1990 by The Johns Hopkins University School of Hygiene and Public Health All rights reserved

Vol. 12, 1990 Printed in U.S.A.

EPIDEMIOLOGY OF BREAST CANCER JENNIFER L. KELSEY AND MARILIE D. GAMMON

In the 1979 review of the epidemiology of breast cancer (1), various risk factors were considered "established." These included the demographic characteristics of increasing age (in Western countries), high socioeconomic status, never having been married, having been born in North America or northern Europe, urban residence, residence in the northern part of the United States (compared with the southern part), and white race. Among reproductive variables, established risk factors included never having been pregnant, late age at fullterm pregnancy, early age at menarche, and late age at menopause (whether artificial or natural). Among postmenopausal women, obesity was associated with an elevated risk. Other factors known to increase the risk for breast cancer included a family history of breast cancer (especially if the cancer was premenopausal or bilateral in a first-degree relative), a personal history of breast, endometrial, or ovarian cancer, a history of fibrocystic breast disease, and a history of radiation to the chest in relatively large doses. This "Update" is not meant to be exhaustive, but, rather, briefly summarizes major progress since 1979; more detailed reviews may be found elsewhere (2, 3). Also, the relations of mammographic parenchymal patterns to breast cancer risk (4, 5) and of tumor estrogen receptor status to breast cancer risk factors Received for publication March 20, 1990, and in final form May 1, 1990. From the Division of Epidemiology, Columbia University School of Public Health, New York, NY. Reprint requests to Dr. Jennifer L. Kelsey, Division of Epidemiology, Columbia University School of Public Health, 600 West 168th Street, New York, NY 10032. The authors thank Drs. Virginia Ernster, Nicholas Petrakis, and Margaret Wrench for their helpful suggestions and comments on the manuscript.

(6) have been reviewed in recent volumes of Epidemiologic Reviews and the American Journal of Epidemiology and will not be covered in detail here. MAGNITUDE OF THE PROBLEM AND TRENDS WITH TIME

The American Cancer Society (7) anticipates that in the United States 44,000 women will die from breast cancer and 150,000 women will develop new breast cancer in 1990. On the basis of current incidence rates, it has been estimated by the American Cancer Society that 1 in 10 women will develop breast cancer at some time during her life (8). Although ageadjusted mortality rates have remained relatively constant since 1930, incidence rates have been rising over the past several decades. Until recently, most of the increase was observed in postmenopausal women, but now increases are also seen in premenopausal women (9). It is unclear to what extent the increases in incidence rates, especially in white women, are attributable to early case finding through screening programs and to the detection and removal of lesions that would not previously have been called cancer. Incidence rates in young black women have increased faster than those in young white women, so that at present rates are higher in white women than black women only over the age of 45 years; incidence rates are similar in blacks and whites in the 40-45 year age group, and are higher in blacks than whites below age 40 years (9). In recent years, marked rises in breast cancer incidence and mortality rates have been noted in many Asian, central European, and some South American countries, where incidence rates were previously low.

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These increases have so far been noted in women under the age of 50 years; as these younger cohorts age, these increases are expected to be seen in the postmenopausal years as well. If this expectation is correct, it is estimated that the annual incidence of breast cancer in the world will be more than 1,000,000 cases by the year 2000 (10). REPRODUCTIVE VARIABLES

Studies continue to show that early age at first full-term pregnancy protects against breast cancer. In the past, number of pregnancies and duration of lactation were not believed to affect a woman's risk of breast cancer independent of their associations with age at first full-term pregnancy. However, many recent studies (1119) have noted that an increasing number of pregnancies has an independent protective effect on the risk of breast cancer; the relative risk associated with five or more pregnancies has been found to be about 0.6 compared with women with one pregnancy (19). This protective effect of parity may apply only to breast cancer diagnosed in women of about age 50 years and older; a few studies (11,12) suggest that parity may actually be associated with an increased risk for breast cancer diagnosed in young women. Some recent studies (17, 18, 2022), although not all (15, 23), report a decreasing risk for breast cancer with increasing number of months of lactation independent of age at first birth and parity, particularly for premenopausal women. Evidence is inconsistent as to whether a history of induced or spontaneous abortion at any time during the reproductive years, or specifically prior to a woman's first fullterm pregnancy, is associated with an increased risk of breast cancer (16, 17, 2426). The difficulty in distinguishing between induced and spontaneous abortions in an interview setting makes interpretation of these studies uncertain. Several studies (27-29), although not all (30-32), indicate that infertility resulting from a hormonal abnormality is not associated

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with either an increased or decreased risk of breast cancer. Studies concerned with a history of anovulation or irregular menstrual periods have yielded inconsistent results (17, 29, 33, 34). A few studies suggest that late age at last birth (35, 36) and birth to a mother of relatively late age (37, 38) are associated with elevated risk for breast cancer, independent of a woman's own age at the time she gives birth to her first child. Further evaluation of these findings is needed. BODY BUILD

In postmenopausal women, body weight and various indicators of weight for height are positively associated with breast cancer risk; more recently a negative association has been noted between weight and breast cancer risk in premenopausal women (17, 39-44). One recent study reported a negative association between adolescent body mass and risk for premenopausal breast cancer (40). Some studies (39, 40, 45), although not all (46), have found that adult weight gain increases the risk of breast cancer. Whether regional distribution of adipose tissue (i.e., ratio of central to peripheral fat deposition) affects breast cancer risk is unclear at present (47-49). Also, conflicting results have been obtained as to whether height affects risk independently of weight (39, 41-44, 46, 50). ORAL CONTRACEPTIVES

Many studies have found that in most women use of oral contraceptives does not affect breast cancer risk, regardless of the dose, brand, or type of estrogen or progestin in the compound used, or the length of time since last use (51). Individual studies have reported various subgroups of women to be at elevated risk if they use oral contraceptives, but most of these isolated findings are probably attributable to chance. Subgroups in which at least a few studies have shown positive associations between oral contraceptives and risk for breast cancer are women with a history of biopsy-

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confirmed benign breast disorders (52-54), women with a family history of breast cancer (53, 55, 56), women who use oral contraceptives at an especially late age (46-55 years of age) (17, 57), women who use oral contraceptives when younger than about 25 years of age (58-61) and/or before their first full-term pregnancy (59, 62), and nulliparous women with long-term use (60,6365). Taken together, these subgroups include a large number of women, but fortunately, many studies do not find that women in these subgroups are at high risk (53-56, 60, 66-75). The finding that has received the most support is that long-term use of oral contraceptives at an early age (or before the first full-term pregnancy) increases the risk of breast cancer in women up to about 45 years of age (53, 58-60, 62, 64, 76-78), although other studies have failed to find this association (53, 56, 57, 66-69, 75, 7981). There are methodologically sound studies among both those that have supported and among those that have not supported this association, so it is difficult to reach any firm conclusion at this time. Nevertheless, there is concern that as this cohort ages, risk among long-term oral contraceptive users will also be elevated in women at older ages. Studies of long-term use at an early age thus continue to be an area of high priority for further research. DEPOT-MEDROXYPROGESTERONE ACETATE (DMPA)

Most studies have not found an association between the injectable progestational contraceptive depot-medroxyprogesterone acetate (DMPA) and breast cancer risk (71, 82-84). ESTROGEN REPLACEMENT THERAPY

As in 1979, no firm conclusions can be drawn about the risk for breast cancer associated with use of estrogen replacement therapy; results have continued to be inconsistent (85-95). Two recent studies (88,89) have suggested that use for 15-20 years or

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more may be associated relative risks of around 1.5 to 2.0. A few studies (86, 94, 95) have suggested slightly increased risks with increasing doses of estrogen. One recent study from Sweden (96) noted a positive association when progestin and estrogen were used in combination; the number of study subjects, however, was much too small for firm conclusions to be drawn. Thus, current evidence suggests either no effect of breast cancer risk from estrogen replacement therapy or an elevation in risk of less than twofold with very long-term use or relatively high doses. Additional studies that include large numbers of women who have used estrogen for 15 years or more are needed. Also, studies of the effect of progestin used in conjunction with estrogen are of high priority. DlETHYLSTILBESTROL (DES)

Several studies (97-100) have found that women who used diethylstilbestrol (DES) during pregnancy have an increased risk for breast cancer, with relative risks in these studies mostly around 1.5. Although in some studies it was not possible to separate the effect of diethylstilbestrol from the reason for which it was prescribed (prevention of spontaneous abortion in most instances), the general consistency of the results and the presence of a dose-response relation are suggestive of a causal association. DIET

Although dietary fat has long been thought to be involved in breast cancer etiology on the basis of ecologic correlations and animal studies, most epidemiologic case-control and cohort studies, including recent ones, have found weak associations (either positive or negative) or no association between total fat, saturated fat, or animal fat intake in adulthood or childhood and subsequent breast cancer risk (101115). The effect of diet on endogenous hormones that may be involved in the pathogenesis of breast cancer has been con-

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sidered in some studies, again with inconsistent or inconclusive results (116-119). Studies of the associations of dietary vitamin A, /3-carotene, and retinol, of serum vitamin A, vitamin E, retinol, and retinolbinding protein, and of plasma retinol and /3-carotene have also produced inconsistent results (102, 109, 114, 120-123), and, at most, individual studies show slight protective effects of one or the other of these micronutrients. The hypothesis (124) that low dietary selenium intake is associated with an increased risk for breast cancer has not been supported by epidemiologic studies (125, 126). It is also plausible that total caloric intake is the most important dietary attribute (127, 128). Total calories could influence risk through its effect on obesity and age at menarche. In short, our understanding of the role of diet in breast cancer etiology has not progressed much since the time of the 1979 review, except, perhaps, for the realization that any elevation in risk or protection from the dietary constituents studied so far is likely to be small at most. Not only are the roles of specific dietary constituents unclear, but the age at which they might have their effect is unknown. A more detailed summary of the literature on diet and breast cancer has been published by Willett (129). ALCOHOL CONSUMPTION

A modest positive association between alcohol consumption and risk of breast cancer has been observed in many (130-142), but not all (105, 143-148), epidemiologic studies. However, results have varied as to whether the risk differs according to the type of beverage used or the pattern of consumption. Also, the risk estimates associated with the level of consumption (e.g., number of drinks per week) have differed considerably among studies. A few studies have indicated that the increase in risk is associated with alcohol consumption specifically early in life (132, 141, 149); this finding needs to be evaluated further. Although certain biologic mechanisms for an

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association have been suggested, such as interference with cell membrane permeability in breast tissue (150), exposure to circulating cytotoxic products of ethanol (151), and altered hepatic function (152, 153), none is generally accepted. The question remains as to whether the increased risk is attributable to the alcohol or to some other characteristic of women who drink alcoholic beverages compared with those who do not. Also, constituents of drinks other than the alcohol itself could be responsible for the increased risk. OTHER LIFESTYLE VARIABLES AND ELECTRIC POWER USE

Although some studies have suggested a positive association between caffeine consumption and breast cancer risk (154,155), and either a negative (133,156) or a positive (146, 157) association between cigarette smoking and breast cancer risk, most evidence suggests no association for either of these substances (143,146,157-169). Physical activity has been associated with a reduced risk for breast cancer in two studies (170, 171); further evaluation of this association is needed. Physical activity could influence breast cancer risk through its effect on endogenous hormones. One study (172) suggests that even moderate physical activity at an early age decreases the frequency of ovulatory menstrual cycles, and another (173) indicates that moderate physical activity in young adults decreases luteal progesterone levels; also, amenorrheic runners have been observed to have lower levels of estradiol (174). Breast cancer risk has been hypothesized to be increased by exposure to the magnetic fields produced by electric power (175); one study reported a positive relation between residential exposure to electromagnetic fields and breast cancer (176) while another study found no association (177). BENIGN BREAST CONDITIONS

Benign breast disorders have long been accepted as breast cancer risk factors, but current evidence suggests that the elevation in risk occurs mostly in women with prolif-

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erative lesions (178-181). Biopsied tissues that show atypical hyperplasia, in particular, are associated with about a fivefold increase in risk of breast cancer, while hyperplasia characterized as moderate, florid, solid, or papillary, as well as papilloma with a fibrovascular core and sclerosing adenosis, are probably associated with relative risks of about 1.5 to 2.0 (178,180,182,183). Calcification in the biopsy specimens may be associated with an increased risk (178, 180). Several retrospective cohort studies are currently under way to evaluate further the risks associated with specific subtypes of benign breast conditions; results of these studies should be forthcoming shortly. FAMILIAL AGGREGATION AND HEREDITY

Studies continue to show that women with both a mother and a sister who have had breast cancer have a very high risk for the disease; one recent study (184) reported the risk for breast cancer in women with an affected mother and sister to be 50 percent by 65 years of age. Women with one affected first degree relative are still found to have a risk that is two to three times greater than the risk in women without an affected first degree relative. However, it is now uncertain whether the risk is higher if the relative had breast cancer diagnosed at a young age or if the relative had bilateral disease (185-188). The recent finding (189) that families with ataxiatelangiectasia, an autosomal recessive syndrome, have an excess risk of breast cancer lends further credence to the hypothesis of an hereditary component in some families. The extent to which the familial aggregation of most breast cancer is attributable to hereditary or environmental factors is not fully known. However, through complex segregation analysis of nuclear families of cases identified through two population-based cancer registries, Newman et al. (190) found evidence of autosomal dominant transmission of a susceptibility allele with high penetrance in 4 percent of families. Identification of highrisk families with evidence of susceptibility

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genes should help in the identification and mapping of such genes. This, in turn, should lead to a much better understanding of the role of heredity and its interaction with environmental risk factors. RADIATION

Previously, susceptibility of the breast to the carcinogenic effect of radiation was believed to be greatest between the ages of 10 and 20 years when breast tissue is rapidly developing, with little increase in risk associated with exposure before age 10 years or after age 40 years. Studies still indicate that radiation exposure after about 35 to 40 years of age has only a small effect on breast cancer risk (191, 192). However, it is now known (193-195) that women who were below the age of 10 years at the time of exposure, including during infancy (196, 197), also have an increased risk, but the excess risk was not apparent until the women had reached the ages at which breast cancer normally occurs. The increased risk associated with radiation exposure persists for at least 35 years and may well remain throughout life (191). Although a linear dose-response relation has generally been reported, no empirical data exist for estimating the risk associated with very low exposure levels (191, 192, 198-200); an almost prohibitively large sample size would be needed to estimate risks at very low exposure levels. Screening for breast cancer by mammography has been shown to reduce breast cancer deaths in women of age 50 years and older (201204) and possibly in younger women (204206). Further research is needed to determine the risk-benefit ratio for mammography in younger women, but in general, the risk of radiation-induced breast cancer is estimated to be small in relation to its benefits (206). MULTIPLE PRIMARIES

It has been known for some time that the risk of breast cancer is increased in a woman with a previous history of breast, endometrial, or ovarian cancer. Recently,

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studies have been undertaken of specific attributes of a first breast cancer that are associated with an increased risk of cancer in the contralateral breast. A positive family history of breast cancer predicts contralateral breast cancer (207-209), but other findings, including those concerned with prior radiation treatment for cancer, reproductive factors, and body build, have been inconsistent (210-215).

diol in their breast fluid (229) and parous or lactating women to have low levels (230). Concentrations of breast fluid cholesterol and its oxidation products, cholesterol epoxides, which have been reported to be mutagenic, carcinogenic, and cytotoxic, have been associated with certain breast cancer risk factors including biopsyconfirmed proliferative epithelial disorders (231, 232).

ENDOGENOUS HORMONES

MAMMOGRAPHIC PARENCHYMAL PATTERNS AND ESTROGEN RECEPTORS

For many years epidemiologists and others have studied the etiologic significance and usefulness as markers of risk of various patterns of circulating endogenous hormones and their metabolites, but as in the 1979 review, no consistent associations have been found (216-220). Among the hormones and metabolites that have recently been the focus of study are serum or urinary levels of estradiol, androstenedione, testosterone, progesterone, prolactin, and sexhormone binding globulin, as well as blood levels of selected thyroid hormones (45, 221-228). Issues regarding storage of serum samples, difficulties in the measurement of certain hormones such as the biologically active component of prolactin, and whether important interactions among these hormones are taking place may need to be resolved before further progress is made. At present, the greatest amount of interest appears to be in the possible etiologic role of nonprotein-bound and albumin-bound estradiol and of biologically active prolactin. Also of interest is whether there are certain critical time periods of a woman's life (e.g., adolescence, perimenopausal years) during which these hormones have their major influence on breast cancer risk. Some recent evidence suggests that studies of hormone levels in serum need to be supplemented by measurements of hormone levels in breast fluid, since breast fluid estrogen levels may be 5 to 45 times higher than serum levels (229, 230). Women with benign breast disorders have been found to have elevated levels of estra-

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These topics have recently been reviewed in this journal and in the American Journal of Epidemiology (4-6). In brief, the densest parenchymal patterns, DY and P2, are associated with a two- to threefold increase in risk for subsequent breast cancer. Of the many risk factors for breast cancer that have been considered, only age, parity, and body weight have repeatedly been shown to be inversely related to the proportion of dense patterns in breast tissue. Because breast cancer risk increases with age and postmenopausal body weight, the interpretation of these findings regarding age and weight is unclear. The proportion of estrogen receptor positive tumors increases with older age of the breast cancer case, is higher in white than in black cases, and may be higher in postmenopausal than premenopausal cases. Otherwise, no breast cancer risk factors have been consistently associated with estrogen receptor status or concentration. CONCLUSION

During the past decade, a few new potential etiologic factors, such as alcohol, caffeine, and cigarette consumption, as well as diethylstilbestrol exposure during pregnancy, have been considered, but only alcohol and diethylstilbestrol use are still regarded as possible risk factors. Parity and lactation, previously thought not to be important, are now emerging as possible protective factors. Knowledge about risks associated with radiation, body build, and

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benign breast disorders has been refined, while enthusiasm about diet as a possible risk factor has been dampened. Surprisingly elusive are the roles of both exogenous and endogenous hormones in breast cancer etiology, especially in view of the enormous number of studies that have been concerned with them. During the next several years, it is hoped that their significance as breast cancer risk factors will become more clear. The studies in the diethylstilbestrolexposed women and of oral contraceptive users suggest that the timing of the exposure may be critical, as the possible effect of both of these hormonal agents may be limited to specific time periods of rapid breast development. Also, since most known risk factors generally have modest relative risks, account for only a portion of breast cancer cases, and do not readily lead to preventive measures, new ideas are needed, particularly regarding exposures at critical time periods. Finally, it is hoped that susceptibility genes will be identified and lead to further progress in our understanding of genetic-environmental interactions. REFERENCES

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