ably moderate the greater or lesser risk of women of different ages and with different reproductive histories. Therefore, it is biologically plausible that exogenous hormones, such as the synthetic estrogens and progestins found in oral contraceptives, have analogous effects. One should be prepared to find qualitatively and/or quantitatively different effects of exogenous hormones in older and younger women, and among women at any age with different reproductive histories.

Human studies of the effects of oral contraceptive use on breast cancer incidence have been complicated by the relatively short history of such use and a lack of stability of oral contraceptive formulations and usage patterns. Studies have collected and analyzed information only about relatively short-term exposures in women who started use as teenagers and about longer-term exposures among those who began to use the pill when they were in their 20s or early 30s. Both groups of women have had varied patterns of starting and stopping oral contraceptive use, and a majority have used two or more different formulations. (Oral contraceptives can vary in the types, amount, and ratios of hormones they contain.)

The utility of results of existing epidemiological studies in defining the relationship of oral contraceptives and breast cancer depends on whether they include exposures and follow-up intervals that are biologically feasible for identifying associations of both initiating and promoting events. Ideally, they should provide information about the dose, consistency, and duration of use, as well as the timing relative to reproductive physiological events (i.e., menarche, pregnancy, menopause) that perturb endogenous hormone levels.

There is considerable agreement about the consistency of results of the existing, prospective epidemiological studies. Thus far, the women in those studies have had no increases in breast cancer as they entered early postmenopausal years. Relatively few (about 10) additional years of follow-up are needed to determine whether the findings hold for later postmenopausal years. This follow-up, as well as a dedicated effort to prepare the results of existing cohort studies for pooled analysis, should be enough to confirm the existing consensus and put statistical limits on the upper bounds of measured safety with respect to the risk of breast cancer. There may also be sufficient data from this effort to determine whether oral contraceptive exposure of these virtually first users has had any impact in their postmenopausal years. The lack of an association between oral contraceptive use and postmenopausal breast cancer in these women would be an encouraging finding that will need to be confirmed

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