Esophageal cancer among black men in Washington, D.C. I. Alcohol, tobacco, and other risk factors.

A case-control study involving interviews with the next of kin or close friends of 120 black males who recently died of esophageal cancer and 250 similarly aged black males who died of other causes was undertaken to discover reasons for the exceptionally high mortality from this cancer in Washington, D.C. The age-adjusted annual death rate in Washington, D.C., for nonwhite males, 1970-75, was 28.6/100,000, far higher than the national rate of 12.4/100,000 and the rates in other metropolitan areas of the country. The major factor responsible for the excess was alcoholic beverage consumption, with an estimated 81% of the esophageal cancers attributed to its use; high use of alcoholic beverages was also found among the controls. The relative risk (RR) of esophageal cancer associated with use of alcoholic beverages was 6.4 (95% confidence interval=2.5, 16.4). The RR increased with amount of ethanol consumed and was highest among drinkers of hard liquor, although the risk was also elevated among consumers of wine and/or beer only. The RR associated with cigarette smoking was 1.9 (1.0, 3.5) when controls with smoking-related causes of death were excluded but declined to 1.5 (0.7, 3.0) when adjusted for ethanol consumption. Significant differences of approximately twofold were found between low and high levels of a) consumption of fresh or frozen meat and fish, fruits and vegetables, and dairy products and eggs and b) relative weight (wt/ht2). The inverse trends with these general measures of nutritional status were not explained by alcoholic beverage consumption or socioeconomic status as measured by educational level.

Esophageal cancer among black men in Washington, D.C. II. Role of nutrition.

A case-control study of esophageal cancer was conducted among the black male residents of Washington, D.C., to find reasons for the exceptionally high risk in this population. The next of kin of 120 esophageal cancer cases who died during 1975-77 and of 250 D.C. black males who died of other causes were interviewed. Five indicators of general nutritional status--fresh or frozen meat and fish consumption, dairy product and egg consumption, fruit and vegetable consumption, relative weight (wt/ht2), and number of meals eaten per day--were each significantly and inversely correlated with the relative risk of esophageal cancer. Associations with other food groups were not apparent. The least nourished third of the study population, defined by any of these five measures, was at twice the risk of the most nourished third. None of these associations was markedly reduced by controlling for ethanol consumption, the other major risk factor in this population; smoking; socioeconomic status; or the other nutrition measures. When the three food group consumption measures were combined into a single overall index of general nutritional status, the relative risk of esophageal cancer between extremes was 14. Estimates of the intake of vitamin A, carotene, vitamin C, thiamin, and riboflavin were inversely associated with relative risk; but each micronutrient index was less strongly associated with risk than were the broad food groups that provide most of the micronutrient. Thus no specific micronutrient deficiency was identified. Instead, generally poor nutrition was the major dietary predictor of risk and may partially explain the susceptibility of urban black men to esophageal cancer.

Testicular cancer risk among young men: role of cryptorchidism and inguinal hernia.

The role of cryptorchidism (undescended testis) and inguinal hernia in the etiology of testicular cancer among men aged 18-42 years was evaluated in a case-control study of 271 cases and 259 controls referred to three collaborating medical centers in the Washington, DC, area. The relative risk of testicular cancer for men who reported a history of an undescended testis was 3.7 (95% confidence interval = 1.6-8.6). The risk increased with increasing age at correction; the risk was highest for those men whose cryptorchid testis was never corrected. Among unilateral cryptorchids, no increased risk of testicular cancer was observed for the normally descended testis. There was only a slight excess risk for men without cryptorchidism who had a herniorrhaphy; however, those who underwent a hernia operation after age 7 had a significantly elevated risk of testicular cancer on the same side as the hernia. This case-control study is the first one to support the clinical recommendations for early surgical correction of cryptorchidism and inguinal hernia. Data from this study suggest that the excess cancer risk associated with cryptorchidism is due to internal factors that affect the undescended testis rather than to some underlying developmental abnormality.

Are racial differences in squamous cell esophageal cancer explained by alcohol and tobacco use?

BACKGROUND: In the United States, incidence rates of squamous cell esophageal cancer are more than five times higher among black men than among white men. Reasons that might explain this large racial disparity are being sought. PURPOSE: We evaluated whether differential use of alcohol and tobacco can fully account for the excess of squamous cell esophageal cancer among U.S. blacks. METHODS: We conducted a population-based, case-control study with in-person interviews with 373 squamous cell esophageal cancer case patients (124 white males and 249 black males) and 1364 control subjects (750 white males and 614 black males) from three U.S. geographic areas. Histologically confirmed cases of squamous cell esophageal cancer newly diagnosed from August 1, 1986, through April 30, 1989, among white and black men aged 30-79 years were included. RESULTS: Alcohol use of more than one drink per day and/or current cigarette use of at least one pack per day accounted for 92.7% (95% confidence interval [CI] = 86.8%-98.5%) of the squamous cell esophageal cancers in blacks, versus 86.3% (95% CI = 75.5%-97.1%) in whites, and for 94% of the difference between the black and white annual incidence rates. The interaction between race and the continuous drinking/smoking variable in a logistic regression analysis was statistically significant (two-sided, P = .02). Exposure rates among controls at all levels of combined alcohol and tobacco use examined were slightly higher among blacks and accounted for a small portion of the racial differences in incidence rates. CONCLUSION: Although the vast majority of esophageal cancers in both blacks and whites in our data can be explained by use of alcohol and tobacco, it is not clear why heavy consumption of alcohol and/or tobacco is responsible for 14.9 per 100,000 per year more cases of squamous cell esophageal cancer among blacks than among whites. The differences in the odds ratios appear to account for more of the racial differences in incidence rates than do the prevalences of exposure to alcohol and tobacco alone. The reasons for this apparent racial difference in carcinogenic risk from the same level of alcohol and tobacco use are unknown, but they may include qualitative differences in alcohol consumption, differences in other environmental exposures that interact with alcohol and/or tobacco to modify risks, or differences in susceptibility to these factors.

Adenocarcinoma of the esophagus: role of obesity and diet.

BACKGROUND: In the United States, the incidence of adenocarcinoma of the esophagus, including the esophagogastric junction, has been increasing rapidly over the past two decades. Except for an association with Barrett's esophagus, little is known about the etiology of these cancers. PURPOSE: Our purpose was to investigate dietary and nutritional risk factors for adenocarcinoma of the esophagus. METHODS: A population-based, case-control interview study of 174 white men with adenocarcinoma of the esophagus and 750 control subjects living in three areas of the United States was conducted during 1986 through 1989. RESULTS: Risk was significantly elevated for subjects in the heaviest quartile compared with the lightest quartile of body mass index (odds ratio [OR] = 3.1; 95% confidence interval [CI] = 1.8-5.3). No significant associations were seen with total calories from food, number of meals eaten per day, level of fat intake, or consumption of coffee and tea. Risks were highest for those consuming the least amount of vegetables, with some evidence of a dose response for the subcategories of cruciferous vegetables (P for trend < .001) and vegetables consumed raw (P for trend = .10). A significantly elevated risk was also seen for those consuming the least amount of raw fruit (P for trend = .05). No clear associations were reported for intake of particular micronutrients overall or in supplements, but a significant protective effect was associated with increasing intake of dietary fiber (P for trend = .004). CONCLUSIONS: The findings of an increased risk with obesity and decreased risks with intake of raw fruits and vegetables and dietary fiber provide useful directions to pursue in further investigations of this malignancy. IMPLICATIONS: The finding with respect to obesity is particularly noteworthy, since it may explain at least a portion of the recent epidemic increases reported in the incidence of this tumor.

Dietary and nutritional factors and pancreatic cancer: a case-control study based on direct interviews.

BACKGROUND: The relationship between diet and pancreatic cancer remains unclear. In this study, we assessed the role of diet and nutrition as risk factors for pancreatic cancer, using data obtained from direct interviews only, rather than data from less reliable interviews with next of kin. We evaluated whether dietary factors could explain the higher incidence of pancreatic cancer experienced by black Americans compared with white Americans. METHODS: We conducted a population-based case-control study of pancreatic cancer diagnosed in Atlanta (GA), Detroit (MI), and 10 New Jersey counties from August 1986 through April 1989. Reliable dietary histories were obtained for 436 patients and 2003 general-population control subjects aged 30-79 years. RESULTS: Obesity was associated with a statistically significant 50%-60% increased risk of pancreatic cancer that was consistent by sex and race. Although the magnitude of risk associated with obesity was identical in blacks and whites, a higher percentage of blacks were obese than were whites (women: 38% versus 16%; men: 27% versus 22%). A statistically significant positive trend in risk was observed with increasing caloric intake, with subjects in the highest quartile of caloric intake experiencing a 70% higher risk than those in the lowest quartile. A statistically significant interaction between body mass index (weight in kg/height in m2 for men and weight in kg/height in m1.5 for women) and total caloric intake was observed that was consistent by sex and race. Subjects in the highest quartile of both body mass index and caloric intake had a statistically significant 180% higher risk than those in the lowest quartile. CONCLUSIONS: Obesity is a risk factor for pancreatic cancer and appears to contribute to the higher risk of this disease among blacks than among whites in the United States, particularly among women. Furthermore, the interaction between body mass index and caloric intake suggests the importance of energy balance in pancreatic carcinogenesis.

Familial aggregation of hematopoietic malignancies and risk of non-Hodgkin's lymphoma.

Examination of risk factors that may be responsible for the increasing incidence of non-Hodgkin's lymphoma (NHL) over the past few decades would be incomplete without considering familial aggregation of hematolymphoproliferative neoplasms and the relative contributions of heredity and environment to the etiology of NHL. Reports of families with two or more NHL cases and sometimes additional members affected by other hematopoietic malignancies (multiple-case families) are summarized, as are findings from surveys and quantitative risk estimates from population-based studies of familial aggregation. The notable occurrence of various immunological abnormalities among multiple-case family members with and without NHL or related neoplasms is underscored, as is the diversity of types of other lymphoproliferative and hematopoietic malignancies among close relatives in these families. Preliminary evidence suggesting that multiple-case families may be more susceptible to certain environmental exposures is presented. An international registry of such families (particularly those identified in population-based studies) is proposed to clarify the interrelationship of genetic, familial, and environmental factors in the etiology of NHL.

Prenatal and perinatal risk factors for testicular cancer.

In an attempt to determine the risk factors responsible for the dramatic increases in testicular cancer incidence in young adults, mothers of testicular cancer cases and controls were questioned about in utero exposures, pregnancy-related conditions, and perinatal factors during their pregnancies with the 202 cases and the 206 controls. The strongest risk factor was low birth weight with a greater than 12-fold risk (confidence interval = 2.8 to 78.1) for subjects weighing 5 lb or less at birth compared to those who weighed over 5 lb. A statistically significant 2-fold increase in risk was associated with unusual bleeding or spotting during pregnancy, regardless of whether medication was taken for this condition. Other exposures during pregnancy associated with a statistically significant increase in risk were: use of "sedatives"; alcohol consumption; and exposure to X-rays. No excess risk was associated with the use of hormones during pregnancy. The findings for birth weight and abnormal uterine bleeding suggest that significant compromise of the normal maternal-fetal environment may be associated with subsequent increase in risk of testicular cancer. However, this increase in risk is not great enough to explain the dramatic increases in testicular cancer that have occurred in young adults.

A case-control and family study of Waldenstrom's macroglobulinemia.

Waldenstrom's macroglobulinemia (WM) is a rare disorder of lymphoid and plasma cells characterized by an immunoglobulin M (IgM) monoclonal gammopathy, clinical and immunopathologic similarities with other lymphoproliferative neoplasms, but the etiology of which is unknown. We undertook the first case-control study of this disorder among 65 cases, comprising 87% of all WM patients diagnosed during 1969-1983 in the greater Baltimore, Maryland area. Compared with 213 hospital controls without cancer, cases were slightly better educated, but there were otherwise no differences in sociodemographic factors, history of prior medical conditions, medication use, cigarette smoking, alcohol consumption, specific occupational exposures, employment in any particular industries or occupations, or familial cancer history. Cases were more likely than controls to have first-degree relatives with a history of pneumonia, diphtheria, rheumatic fever, and diabetes mellitus. An exploratory evaluation of immunologic profiles of first-degree relatives of 48% of families of cases revealed that relatives of two cases had asymptomatic IgM (> 750 mg/dl) monoclonal gammopathy and close to 40% of the 109 evaluated had diverse immunologic abnormalities. Larger population-based case-control studies are needed to further evaluate the suggestive evidence of immune dysfunction among families of WM cases.

HLA and multiple myeloma among black and white men: evidence of a genetic association.

To evaluate the possibility that genetic factors contribute to the excess rates of multiple myeloma among blacks, serological typing of human leukocyte antigens (HLA) was conducted for black and white male patients and controls who participated in a large population-based case-control interview study. Forty-six black cases, 88 black controls, 85 white cases, and 122 white controls were typed for the Class I antigens (HLA-A, -B, -C) and for the Class II antigens (HLA-DR, HLA-DQ). Black cases had significantly higher gene frequencies than black controls for Bw65, Cw2, and DRw14, while white cases had higher gene frequencies than white controls for A3 and Cw2 and blanks at the DR and DQ loci. Further analysis of the association between Cw2 and multiple myeloma revealed relative risks of 5.7 (95% confidence interval = 1.5-26.6) and 2.6 (95% confidence interval = 1.0-7.2) for blacks and whites, respectively. The frequency of Cw2 in black and white controls was similar. These findings suggest that the Cw2 allele enhances the risk of myeloma in blacks and whites but do not explain the higher incidence of this cancer among blacks. The study also suggests that undefined DQ antigens may play an etiological role, supporting the need for further research into the immunogenetic determinants of myeloma.

Dietary factors and risks for prostate cancer among blacks and whites in the United States.

Prostate cancer is the most common malignancy in men in the United States, with substantially higher rates among American blacks than whites. We carried out a population-based case-control study in three geographic areas of the United States to evaluate the reasons for the racial disparity in incidence rates. A total of 932 men (449 black men and 483 white men) who had been newly diagnosed with pathologically confirmed prostate cancer and 1201 controls (543 black men and 658 white men) were interviewed in person to elicit information on potential risk factors. This report evaluates the impact of dietary factors, particularly the consumption of animal products and animal fat, on the risk of prostate cancer among blacks and whites in the United States. Increased consumption (grams/day) of foods high in animal fat was linked to prostate cancer (independent of intake of other calories) among American blacks [by quartile of intake, odds ratio (OR) = 1.0 (referent), 1.5, 2.1, and 2.0; Ptrend = 0.007], but not among American whites [by quartile of intake, OR = 1.0 (referent), 1.6, 1.5, and 1.1; Ptrend = 0.90]. However, risks for advanced prostate cancer were higher with greater intake of foods high in animal fat among blacks [by quartile of intake, OR = 1.0 (referent), 2.2, 4.2, and 3.1; Ptrend = 0.006] and whites [by quartile of intake, OR = 1.0 (referent), 2.2, 2.6, and 2.4; Ptrend = 0.02]. Increased intake of animal fat as a proportion of total caloric intake also showed positive but weaker associations with advanced prostate cancer among blacks (Ptrend = 0.13) and whites (Ptrend = 0.08). No clear associations were found with vitamin A, calcium, or specific lycopene-rich foods. The study linked greater consumption of fat from animal sources to increased risk for prostate cancer among American blacks and to advanced prostate cancer among American blacks and whites. A reduction of fat from animal sources in the diet could lead to decreased incidence and mortality rates for prostate cancer, particularly among American blacks.

Familial cancers associated with subtypes of leukemia and non-Hodgkin's lymphoma.

To investigate whether a history of hematolymphoproliferative cancers (HLP) and other cancers among a parent or sibling is a risk factor for specific subtypes of leukemia and non-Hodgkin's lymphoma (NHL), data from a population-based case-control study, in Iowa and Minnesota, of 578 leukemia cases, 622 NHL cases and 1245 controls were evaluated. Having at least one sibling with HLP significantly increased the risk for all leukemias combined (odds ratio (OR) = 2.3) and for NHL (OR = 2.7). In particular, chronic lymphocytic leukemia (CLL) was significantly increased among those reporting a sibling with leukemia (OR = 3.0) or lymphoma (OR = 4.3). Elevated risks of small lymphocytic NHL (SML) (OR = 7.3) and diffuse NHL (DIF) (OR = 5.4) were also observed among subjects who had a sibling with lymphoma (primarily Hodgkin's disease). A significantly increased risk of follicular NHL was noted among those with a sibling history of pancreatic cancer (OR = 4.8) and colorectal cancer (OR = 2.7). Parental history of HLP was not associated with any type of leukemia or NHL. A history of stomach cancer among parents was associated with a 2-fold elevation of CLL and DIF compared to controls. Increased risks of CLL and DIF were also linked to breast cancer among sisters and mothers, respectively. Prostate cancer among fathers increased the risk 2-fold for CLL and 3-fold for SML. This study confirms some familial cancer associations previously reported for leukemia and NHL, and provides new information regarding the various subtypes of leukemia and NHL.

Thyroid nodularity after childhood irradiation for lymphoid hyperplasia: a comparison of questionnaire and clinical findings.

Ionizing radiation is a well-established cause of thyroid cancer and nodularity, however, important questions relating to the magnitude of the risk following low-dose medical exposures remain unresolved. To address these issues, we conducted a follow-up study of 1590 individuals treated between 1938 and 1969 with X-rays for childhood lymphoid hyperplasia (av. thyroid dose = 24 cGy) and 1499 individuals treated with surgery only. Thyroid nodularity was determined from self-administered questionnaires completed by 1195 irradiated and 1063 surgically-treated subjects and from clinical examinations of 602 irradiated and 457 non-irradiated subjects. A much higher relative risk (RR) for radiation-induced thyroid nodules was estimated from the questionnaire than from the clinical examination data, 15.8 and 2.7, respectively. (The corresponding estimates of excess RR per cGy were 64 and 7%). Analysis of the examination data revealed a strong dose-response relationship, similar excess RR/cGy for males and females, and an inverse relationship with age at exposure. Although the thyroid gland is one of the most sensitive organs to the neoplastic effects of radiation, the radiation-induced risk of thyroid nodularity reported from questionnaire studies may over-estimate the true risk.

Biochemical epidemiology in community-based studies: practical lessons from a study of T-cell subsets.

Elaborate laboratory tests are increasingly being incorporated into traditional epidemiologic research designs, a concept commonly termed biochemical epidemiology. Some of the issues encountered are illustrated by a recent population-based survey of healthy individuals in the Washington, D.C. area designed to examine the effects of demographic characteristics, lifestyle, and medical conditions on peripheral blood T-cell subsets. The study was conducted in three phases: selection of households by random digit dialing (Phase I); telephone interviews (Phase II), and self-administered questionnaires and phlebotomy (Phase III). Although this design facilitated the selection of the final study population, it influenced the participation rates by offering opportunities for nonresponse at each phase. Race was the strongest determinant of response rate despite the use of highly-trained, racially-matched telephone interviewers and repeated attempts at refusal conversion. Also discussed are issues of confidentiality, and logistics of biologic specimen collection and handling. The difficulties encountered in this survey are examined, with suggestions for future population-based investigations involving biochemical epidemiology.

Testicular cancer in the United States: trends in incidence and mortality.

The patterns of incidence and mortality of testicular cancer in the United States indicate substantial differences by age, race, time period, and geographical region. An epidemic increase over time in the risk of testicular cancer is noted for young men aged 15-44, with the most recent birth cohorts showing the greatest rate of increase. Indeed, some of the evidence suggests the possibility of two separate increases, one apparent from at least the late 1930's through the late 1950's and the second appearing in the late 1970's. The incidence data for blacks also show a young adult peak, even though the rates for whites are four to five times higher than for blacks at all ages except early childhood. Mortality rates for older men consistently declined over the 30-year period, while rates for younger men showed a dramatic drop only for the most recent time period. Aetiological factors yet to be determined may be responsible for the increasing incidence of testicular cancer in young adults. Survival factors appear to explain the age-specific differences between the incidence and mortality curves over time.

Occupation and risk for testicular cancer: a case-control study.

A case-control study of 271 testicular cancer cases aged 18-42, including 60 seminomas and 206 other germinal cell tumours, and 259 controls was carried out to study the association between occupation and testicular cancer risk. Study subjects were identified at three medical centres, two of which treat military personnel. Controls were men diagnosed with a cancer other than of the genital tract. Associations were identified between professional employment (administrators, teachers and other professionals) and risk for testicular seminoma, OR = 2.8 (95% Cl: 1.4-5.4) and between employment in production work and risk for other germinal cell tumours, OR = 1.8 (95% Cl: 1.1-2.7). No specific occupations within these broad groups were responsible for observed increases. Self-reported exposure to microwave and other radio waves was associated with an excess risk for both seminomas and other germinal cell tumours. However, an assessment of radio wave exposure based on job title did not support this finding. Although testicular cancer has been increasing in recent decades among young males, occupational factors did not appear to account for a substantial proportion of testicular cancer occurrence in the population studied.

Chromosome aberrations in relation to radiation dose following partial-body exposures in three populations.

Structural chromosome aberrations were evaluated in peripheral blood samples obtained from three populations exposed to partial-body irradiation. These included 143 persons who received radiotherapy for enlarged thymus glands during infancy and 50 sibling controls; 79 persons irradiated for enlarged tonsils and 81 persons surgically treated for the same condition during childhood; and 77 women frequently exposed as young adults to fluoroscopic chest X rays during lung collapse treatment for tuberculosis (TB) and 66 women of similar ages treated for TB with other therapies. Radiation exposures occurred 30 and more years before blood was drawn. Doses to active bone marrow averaged over the entire body were 21, 6, and 14 cGy for the exposed thymic, tonsil, and TB subjects, respectively. Two hundred metaphases were scored for each subject, and the frequencies of symmetrical (stable) and asymmetrical (unstable) chromosome aberrations were quantified in 97,200 metaphases. Cells with stable aberrations were detected with greater frequency in the irradiated subjects compared with nonirradiated subjects in all three populations, and an overall test for an association between stable aberrations and partial-body ionizing radiation was highly significant (P less than 0.001). We found no evidence that radiation-induced aberrations varied by age at exposure. These data show that exposure of children or young adults to partial-body fractionated radiation can result in detectable increased frequencies of stable chromosome aberrations in circulating lymphocytes 30 years later, and that these aberrations appear to be informative as biological markers of population exposure.

Thyroid cancer after exposure to external radiation: a pooled analysis of seven studies.

The thyroid gland of children is especially vulnerable to the carcinogenic action of ionizing radiation. To provide insights into various modifying influences on risk, seven major studies with organ doses to individual subjects were evaluated. Five cohort studies (atomic bomb survivors, children treated for tinea capitis, two studies of children irradiated for enlarged tonsils, and infants irradiated for an enlarged thymus gland) and two case-control studies (patients with cervical cancer and childhood cancer) were studied. The combined studies include almost 120,000 people (approximately 58,000 exposed to a wide range of doses and 61,000 nonexposed subjects), nearly 700 thyroid cancers and 3,000,000 person years of follow-up. For persons exposed to radiation before age 15 years, linearity best described the dose response, even down to 0.10 Gy. At the highest doses (> 10 Gy), associated with cancer therapy, there appeared to be a decrease or leveling of risk. For childhood exposures, the pooled excess relative risk per Gy (ERR/Gy) was 7.7 (95% CI = 2.1, 28.7) and the excess absolute risk per 10(4) PY Gy (EAR/10(4) PY Gy) was 4.4 (95% CI = 1.9, 10.1). The attributable risk percent (AR%) at 1 Gy was 88%. However, these summary estimates were affected strongly by age at exposure even within this limited age range. The ERR was greater (P = 0.07) for females than males, but the findings from the individual studies were not consistent. The EAR was higher among women, reflecting their higher rate of naturally occurring thyroid cancer. The distribution of ERR over time followed neither a simple multiplicative nor an additive pattern in relation to background occurrence. Only two cases were seen within 5 years of exposure. The ERR began to decline about 30 years after exposure but was still elevated at 40 years. Risk also decreased significantly with increasing age at exposure, with little risk apparent after age 20 years. Based on limited data, there was a suggestion that spreading dose over time (from a few days to > 1 year) may lower risk, possibly due to the opportunity for cellular repair mechanisms to operate. The thyroid gland in children has one of the highest risk coefficients of any organ and is the only tissue with convincing evidence for risk about 1.10 Gy.

The epidemiology of multiple myeloma.

Multiple myeloma is a relatively rare cancer that primarily affects older individuals. In the United States, the highest rates of myeloma are found in black individuals and these rates continue to outpace the rate of myeloma in white individuals. The causes of myeloma are largely unknown. The strongest potential risk factors include radiation and agricultural exposures.

Testicular cancer in young men: the search for causes of the epidemic increase in the United States.

A case-control study of 271 men with testicular cancer and 259 controls was conducted in the Washington, DC area to evaluate whether suggested risk factors could be responsible for the epidemic increases in testicular cancer in young men. No substantial risks were associated with a history of groin hernia operation, the common childhood diseases, allergies, x rays below the waist, venereal disease, vasectomy, or external means of elevating the temperature of the testis. Excess risks were associated with a history of undescended testis (RR = 3.7, CI = 1.5-9.5), testicular trauma (RR = 2.6, CI = 1.6-4.2), and mumps orchitis (RR = 5.8, CI = 0.7-129.7). It is unlikely, however, that any of these conditions has increased sufficiently over time to markedly affect the testicular cancer incidence patterns. Therefore, while the risk factors identified in this paper are of epidemiological interest, they do not account for the increase in testicular cancer in young men.