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Data on coffee-drinking habits obtained from a case-control study conducted in Detroit were used to compare the proportions of coffee drinkers in a hospital and a population control series. The comparison was based on interviews with 262 hospitalized controls and 427 population controls. The overall proportion of coffee drinkers in the total hospital control group was similar to that in the population control group. However, the proportion of moderate-to-heavy coffee drinkers among controls hospitalized for conditions that may have caused them to alter their diet (eg, gastrointestinal disorders and cardiovascular disease) was lower than that among population controls. In contrast, the proportion of moderate-to-heavy coffee drinkers among controls hospitalized for conditions that probably did not cause a change in diet (eg, fractures) was almost identical to that among population controls. These results suggest that, in hospital-based case-control studies of the effects of coffee consumption, it would be prudent to restrict the referent group to those patients hospitalized for conditions that probably did not cause a change in diet. The magnitude of bias resulting from failure to exclude controls hospitalized for diet-altering conditions will depend on two factors that may vary between studies: (1) the distribution of diet-altering conditions among the hospital controls, and (2) the relationship of these diseases to coffee consumption.

Clues to environmental determinants can often be derived from the patterns of mortality from cancer. This review focuses on the stepwise approach of using cancer mortality maps, supplemented by correlation studies linking mortality rates with demographic and industrial data at the county level, to generate hypotheses to cancer etiology which can then be pursued by analytical epidemiological studies. Advantages and limitations of this approach and its application in the study of lung cancer in the United States are described.

To investigate the influence of cigarette smoking on mononuclear cell subsets, we determined T cell, B cell, monocyte, and HLA-DR+ subsets in a population-based, stratified, random sample of healthy Caucasians using monoclonal antibodies and flow cytometry. The study population consisted of 282 subjects 20 to 69 yr of age, including 108 smokers and 174 nonsmokers. Multivariate analysis techniques were used to assess the influence of cigarette smoking status after controlling for the effects of age and gender. Cigarette smoking was associated with a nonspecific increase in the leukocyte count involving all major cell types (smokers: 8.50 +/- 0.15 versus nonsmokers: 7.33 +/- 0.12 cells/mm3; p less than or equal to 0.0001). In addition, cigarette smokers had a selective increase in CD4+ cells (helper-inducer T cells) compared with nonsmokers (55.3 +/- 0.8 versus 52.2 +/- 0.6% of lymphoid cells; p = 0.002), resulting in a statistically significant increase in the CD4+/CD8+ (helper/suppressor) ratio (2.42 +/- 0.1 versus 2.13 +/- 0.16; p = 0.02). There was no significant difference between smokers and nonsmokers in the level of CD3+ cells (total T cells: 76.8 +/- 0.7 versus 76.1 +/- 0.5; p = 0.5), CD8+ cells (suppressor-cytotoxic T cells: 25.7 +/- 0.8 versus 27.0 +/- 0.5%; p = 0.1), CD19+ cells (B cells) (10.7 +/- 0.4 versus 10.0 +/- 0.3%; p = 0.2), CD14+ cells (monocytes) (18.0 +/- 0.6 versus 17.0 +/- 0.4%; p = 0.2), or HLA-DR+ cells (14.5 +/- 0.5 versus 14.0 +/- 0.4%; p = 0.4).(ABSTRACT TRUNCATED AT 250 WORDS)

To examine sociodemographic, menstrual, reproductive, and other factors which may influence the age at natural menopause, the authors analyzed data from a large series of women participating in a nationwide breast cancer screening program conducted between 1973 and 1980. Standard life table techniques permitted assessment of factors suspected of varying the time to menstrual cessation among 983 premenopausal women, 1091 surgically menopausal women, and 1423 naturally menopausal women. The median age at natural menopause was 51.1 years. Multivariate analysis indicated that parity, irregularity of menstrual cycles before age 25 or first livebirth, and high socioeconomic status were significantly related to menopausal age. These data provide evidence for the hypothesis that certain environmental and hormonal factors which affect ovulation during reproductive years may ultimately postpone the menopause.

The relationship between occupation and cancer of the lower urinary tract in Detroit was examined by means of a population-based case-control study conducted as part of the National Bladder Cancer Study. Three hundred three white male patients with transitional or squamous cell carcinoma of the lower urinary tract and 296 white male controls selected from the general population of the study area were interviewed to obtain lifetime occupational histories. Our findings suggested that truck drivers have a significant increased risk of lower urinary tract cancer [relative risk = 2.1; 95% confidence interval (Cl) = 1.4-4.4]. A significant trend in risk was apparent with increasing duration of employment as a truck driver (P = 0.004); the relative risk estimated for truck drivers employed at least 10 years was 5.5 (Cl = 1.8-17.3). Truck drivers with a history of operating vehicles with diesel engines experienced a significant elevated risk compared to non-truck drivers (relative risk = 11.9; Cl = 2.3-61.1), but whether the increased risk observed among truck drivers was attributable to diesel exposure could not be evaluated. Nonsignificant excess risks were also seen for tool and die makers as well as for workers in several other industries and occupations. Employment in the motor vehicle manufacturing industry was associated with no significant excess risk of lower urinary tract cancer (relative risk = 1.1; Cl = 0.8-1.5).

The fecapentaenes are potent mutagens found in high concentrations in the stools of some individuals. These compounds are produced in vivo by common species of the colonic microflora, from precursors of unknown origin. The fecapentaenes have been postulated to increase the risk of colorectal cancer. To test this hypothesis, we measured fecapentaene excretion in 69 patients with adenocarcinoma of the colon or rectum, newly diagnosed at three Washington, DC area hospitals. The cases were compared with 114 surgical controls, frequency matched to the cases on age, sex, and hospital. We attempted to measure fecapentaene excretion 4 times for each subject: before surgery; and at 1 mo; 3 mo; and 6 mo following surgery. Contrary to our study hypothesis, we found fecapentaene excretion during the four study periods to be similar or even lower in cases compared to controls. An indirect measurement of fecapentaene precursors also tended to be lower in cases. The case-control differences could not be explained as effects of bleeding or of the colorectal diagnostic workup, which was assessed in a separate group of 86 patients. We conclude from these data that the excretion of fecapentaenes does not increase the risk of colorectal cancer, at least when measured near the time of diagnosis.

Published studies of the cancer experiences of children vaccinated with Bacillus Calmette-Guérin in antituberculosis programs were reviewed and the strengths and weaknesses of each evaluated. There is little evidence that vaccination outside of the neonatal period is effective. If there is an effect of neonatal vaccination, it must convey only a small amount of "protection." Follow-up studies adequate to assess the long-term effects of such vaccination, particularly the risk of lymphoma, have not been done, and recent evidence indicates that such evaluation is warranted.

The risk of second primary cancer was evaluated in more than 25,000 women with cancer of the genital organs diagnosed between 1935 and 1982 in Connecticut. Significant excesses of subsequent cancers were observed following cancers of the cervix (35%, n = 656), uterine corpus (16%, n = 1,060), and ovary (58%, n = 366). When observed and expected second cancers of the female genital tract were excluded, these excesses became 40%, 30%, and 59% after cervix, uterine corpus, and ovary, respectively. Among women with either cancer of the cervix or uterine corpus, the risk of developing a second cancer rose with increasing duration of follow-up, reaching an excess of 61 and 34%, respectively, after 20 years. In contrast, among patients with ovarian cancer, the second cancer risk decreased over time to 41% after 10 years. Cancers related to smoking, i.e., oral cavity and pharynx, esophagus, and respiratory system, were notably increased among cervical cancer patients. The twofold to threefold risks observed for these second cancers are consistent with recent evidence linking cervical cancer to cigarette smoking and seem too large to be artifacts of confounding by low socioeconomic status. An increased incidence of second cancer of the abdominal organs (colon, rectum, kidney, bladder, ovaries) was generally observed for each gynecologic site. However, only rectal cancer was consistently linked with radiation treatment for the first primary cancer. Leukemia occurred in excess after cancers of the uterine corpus and ovary, but not after cervical cancer. The predominant cell type was acute nonlymphocytic leukemia, and the excess was associated with radiotherapy for uterine corpus cancer and with chemotherapy for ovarian cancer. Cancers of the breast and colon were increased following uterine corpus and ovarian cancer and vice versa, which supports the notion that these sites share a common etiology, perhaps related to dietary or hormonal factors. Cervical cancer patients experienced a deficit of subsequent breast cancer, possibly due to ovarian removal or ablation by radiation. Investigators need to explore further the association between the smoking-related cancer sites and cervical cancer, to clarify the role of radiotherapy and chemotherapy in relation to excess cancers, and to define more fully the etiologic factors that link cancers of the breast, colon, uterine corpus, and ovary.

To investigate the influence of age, race, and gender on the cellular immune system, we determined T-cell, B-cell, monocyte, natural killer (NK)-cell, and HLA-DR+-cell subsets in 266 nonsmokers from a population-based random sample of healthy adults using monoclonal antibodies and flow cytometry. Blacks had a lower total white blood-cell count than whites (P less than or equal to 0.0001), due primarily to a decrease in granulocytes. There was no significant difference in absolute lymphocyte count between blacks and whites. Blacks had a higher proportion of CD19+ cells (Leu 12+ B cells) and a lower proportion of CD3+ cells (OKT3+ T cells) than whites (P less than or equal to 0.01). Female sex and increasing age were independently associated with an increased percentage of CD4+ cells (OKT4A+ helper-inducer T-cell subset), resulting in a higher helper/suppressor ratio among women and older individuals (P less than or equal to 0.05). Black race and increasing age were independently associated with an increased proportion of HLA-DR+ cells (P less than or equal to 0.0001) which was not attributable to B cells or monocytes. No significant age, race, or gender effects were observed for CD14+ cells (Leu M3+ monocytes) or CD16+ cells (Leu 11A+ natural killer cells). These data demonstrate that age, race, and gender are each associated with significant differences in peripheral blood mononuclear-cell subsets. Population-based data such as these provide an important foundation for future design and interpretation of human flow cytometry data.

In a population-based study of 2982 bladder cancer patients and 5782 population controls from 10 geographical areas of the US, no excess risk was associated with medications used for tuberculosis treatment or prophylaxis (relative risk (RR) = 0.95). The findings agree with other epidemiological studies that have not confirmed earlier reports linking isoniazid (INH) exposure to bladder cancer.

Breast cancer risk among 1,362 cases and 1,250 controls participating in a large multicenter screening program was examined in relation to hypertension and the use of rauwolfia derivatives. A previous diagnosis of hypertension, reported by 22% of the cases and 23% of the controls, was not associated with an increased risk of breast cancer [odds ratio (OR) = 0.9]; nor was there any excess risk for long-term hypertensives. In addition, there was no significant increase in risk associated with use of either rauwolfia derivatives (OR = 1.2), thiazide preparations (OR = 1.2), or methyldopa (OR = 1.1). However, there were significant excess risks among long-term users and those with extended intervals since first use of rauwolfia. Rauwolfia users of 10 or more years' duration or those whose initial use occurred greater than or equal to 10 years before diagnosis had risk ratios of 4.5 (95% Cl, 1.2-19.8) and 3.8 (95% Cl, 2.3-11.6), respectively. These results suggest that women exposed to long-term rauwolfia use have an elevated risk of developing breast cancer, although the results fail to support previous observations of a generalized adverse effect.

The relation between methylxanthine consumption and biopsied benign breast disease was investigated by using data from a case-control study which included 1,569 cases and 1,846 controls identified between 1973 and 1980 through a nationwide screening program. There was no evidence of an association between methylxanthine consumption and benign breast disease in the total study population. When histologic types of benign breast disease were examined, there were no trends in risk according to methylxanthine consumption among the 813 cases with fibrocystic disease, the 508 cases for whom detailed pathology data were not available, the 172 cases with benign neoplasms, or the 156 cases with other benign conditions. When cases with fibrocystic disease were examined according to presence of atypia, hyperplasia, sclerosing adenosis, or cysts, there was, again, no association between methylxanthine consumption and risk of disease. In addition, no relation was found between methylxanthine consumption and menstrual breast tenderness among premenopausal women with fibrocystic disease or unknown conditions.

To determine why the incidence rate of transitional cell bladder cancer in whites in the United States is approximately twice that in blacks, the authors examined data from a large population-based case-control study of bladder cancer conducted in 1978 involving 2,982 cases and 5,782 controls. The relative risk of transitional cell carcinoma for whites compared with blacks was 1.9 before adjustment for the major bladder cancer risk factors, whereas after adjustment for cigarette smoking and occupation it was 1.6 (95% confidence interval (CI): 1.3-2.1). Further adjustment for other risk factors, including history of a bladder infection and a family history of urinary tract cancer, did not alter this estimate. The elevated risk of white compared with blacks was limited, however, to cases whose disease was confined to the mucosa and submucosa. Among cases whose disease had extended to the bladder musculature or beyond, whites were at slightly reduced risk compared with blacks. This suggests that whites may be diagnosed with conditions that go undetected in blacks but that are unlikely as a group to progress to more extensive disease. Because of the population-based nature of the study, it was possible to determine that if bladder cancer incidence among whites of both sexes was reduced to the level among blacks, total incidence in the United States would fall by 36 per cent.

The risk of leukemia was evaluated in 9,170 2-or-more-year survivors of childhood cancer in the 13 institutions of the Late Effects Study Group. Secondary leukemia occurred in 22 nonreferred individuals compared to 1.52 expected, based on general population rates [relative risk (RR) = 14; 95% confidence interval (CI), 9-22]. The influence of therapy for the first cancer on subsequent leukemia risk was determined by a case-control study conducted on 25 cases and 90 matched controls. Treatment with alkylating agents was associated with a significantly elevated risk of leukemia (RR = 4.8; 95% CI, 1.2-18.9). A strong dose-response relationship was also observed between leukemia risk and total dose of alkylating agents, estimated by an alkylator score. The RR of leukemia reached 23 in the highest dose category. Radiation therapy, however, did not increase risk. Although doxorubicin was also identified as a possible risk factor, the excess risk of leukemia following treatment for childhood cancer appears almost entirely due to alkylating agents.