Immune-related conditions and subsequent risk of brain cancer in a cohort of 4.5 million male US veterans.

BACKGROUND: Case-control studies have reported an inverse association between self-reported history of allergy and risk of glioma, but cohort data are limited. Our objectives were to evaluate the associations of major groups of medically diagnosed immune-related conditions (allergy/atopy, autoimmune disease, diabetes, infectious/inflammatory disease) and to explore associations with specific conditions in relation to subsequent diagnosis of brain cancer in a large cohort study. METHODS: We used hospital discharge records for a cohort of 4.5 million male US veterans, of whom 4383 developed primary brain cancer. Rate ratios (RRs) and 95% confidence intervals (CIs) were calculated using time-dependent Poisson regression. RESULTS: We found a significant trend of decreasing RRs for brain cancer with longer duration of allergy/atopy (P=0.02), but not for other conditions studied. Rate ratios of brain cancer for allergy/atopy and diabetes with duration of 10 or more years were 0.60 (95% CI: 0.43, 0.83) and 0.75 (95% CI: 0.62, 0.93), respectively. Several associations with specific conditions were found, but these did not withstand correction for multiple comparisons. CONCLUSIONS: This study lends some support to an inverse association between allergy/atopy and diabetes of long duration and brain cancer risk, but prospective studies with biological samples are needed to uncover the underlying biological mechanisms.

Risk of liver cancer among US male veterans with cirrhosis, 1969-1996.

BACKGROUND: Liver cancer incidence rates in the United States have increased for several decades for reasons that are not entirely clear. Regardless of aetiology, cirrhosis is a strong risk factor for liver cancer. As mortality from cirrhosis has been declining in recent decades, it is possible that the risk of liver cancer among persons with cirrhosis has been affected. METHODS: Data from the US Veterans Affairs medical records database were analysed after adjustment for attained age, race, number of hospital visits, obesity, diabetes, and chronic obstructive pulmonary disease. Hazard ratio (HR) and 95% confidence interval (95% CI) were calculated using Cox proportional hazards modelling. Survival analyses were conducted using age as the time metric and incidence of cirrhosis as a time-dependent covariate. RESULTS: Among 103 257 men with incident cirrhosis, 788 liver cancers developed. The HR of liver cancer was highest among men with viral-related cirrhosis (HR=37.59, 95% CI: 22.57-62.61), lowest among men with alcohol-related cirrhosis (HR=8.20, 95% CI: 7.55-8.91) and intermediate among men with idiopathic cirrhosis (HR=10.45, 95% CI: 8.52-12.81), when compared with those without cirrhosis. Regardless of cirrhosis type, white men had higher HRs than black men. The HR of developing liver cancer increased from 6.40 (95% CI: 4.40-9.33) in 1969-1973 to 34.71 (95% CI: 23.10-52.16) in 1992-1996 for those with cirrhosis compared with those without. CONCLUSION: In conclusion, the significantly increased HR of developing liver cancer among men with cirrhosis compared with men without cirrhosis in the United States may be contributing to the increasing incidence of liver cancer.

Rise in prostatic cancer incidence associated with increased use of transurethral resection.

We examined the association between prostatic cancer incidence rates and the rates of transurethral prostatectomy to explore reasons for the nationally reported dramatic increases in incidence rates of prostatic cancer from 1973 through 1986. There was a strong correlation between both incidence of all stages of prostatic cancer combined and of localized disease and the increasing use of transurethral resection, a common surgical procedure usually performed to relieve urinary obstruction due to benign enlargement of the prostate. Our analyses suggest that increased detection of existing tumors via transurethral resection was the primary reason for the observed increase in incidence rates of prostatic cancer. However, analyses of mortality trends, particularly among nonwhites, and laboratory studies of the histologic nature of clinically asymptomatic tumors suggest that part of the increase may reflect changes in the real risk of prostatic cancer.

Cancer risk after hip replacement with metal implants: a population-based cohort study in Sweden.

BACKGROUND: Joint replacement with metal implants has been the standard procedure for surgical treatment of irreversible degeneration of hip and knee joints for more than two decades. However, reports of local malignancy after joint replacement and experimental studies that suggest a carcinogenic action of metal ions and polymethylmethacrylate (an acrylic compound used to stabilize the implant in the host) have raised concern about the possible long-term risks associated with metal implants. PURPOSE: Our aim was to study cancer risk in a Swedish cohort of patients who had hip replacement surgery during the period 1965 through 1983. METHODS: We studied the risk of cancer in a cohort of 39 154 patients (14 869 men and 24 285 women), identified in the nationwide Swedish Inpatient Register with at least one hip replacement during the period 1965 through 1983. The patients were followed through 1989 by means of record linkage to the Swedish Cancer Register. The cohort contributed a total of 327 922 person-years at risk. Standardized incidence ratios (SIRs) were computed using age-, sex-, and period-specific incidence rates derived from the entire Swedish population. RESULTS: The overall relative risk of cancer was increased by only 3%. Bone cancer--the focus of previous concerns--occurred in six cases versus 4.3 expected, and connective tissue cancer occurred in 28 cases versus 25.9 expected. Increased risks were observed for kidney cancer (SIR = 1.31; 95% confidence interval [CI] = 1.13-1.51), prostate cancer (SIR = 1.13; 95% CI = 1.04-1.22), and melanoma (SIR = 1.23; 95% CI = 1.00-1.50). The relative risk of gastric cancer steadily declined with increasing follow-up time, in both men and women (SIR = 0.58; 95% CI = 0.39-0.84 more than 10 years after hip replacement). CONCLUSION: In this study, the largest study to date to evaluate hip replacement and subsequent cancer risk, the overall cancer risk appears to be negligible from a public health perspective, and our results have not produced any strong evidence against the continued use of these devices. Nevertheless, the small but statistically significant increases in kidney and prostate cancers and the decrease in gastric cancer deserve further study.

Dietary factors in oral and pharyngeal cancer.

A population-based case-control study of oral and pharyngeal cancer conducted in four areas of the United States provided information on a number of risk factors, including diet. Interviews were obtained from 871 oral cancer patients and 979 controls among whites, frequency matched for age and sex. Consumption frequency of 61 food items was assessed in the questionnaire; attention was given to foods that are sources of vitamins A and C and carotene. The major finding was an inverse relationship between fruit intake and risk of oral and pharyngeal cancer; individuals in the highest quartile of intake had about half the risk of those in the lowest quartile. Vitamin C, carotene, or fiber in fruit did not appear to account completely for this relationship, since these nutrients in vegetables did not provide similar protection. This finding suggests the influence of other constituents in fruits, although it is possible that cooking vegetables may have a nutrient-diminishing effect. Dietary intake of other nutrients, such as the B vitamins, vitamin E, folate, and iron, showed no consistent relationship to risk of oral and pharyngeal cancer. Coffee or other hot beverage consumption did not increase risk; intake of nitrite-containing meats or cooking practices, such as smoking, pickling, or charcoal grilling, also did not increase risk. All analyses were adjusted for the effects of tobacco and alcohol, strong risk factors for oral and pharyngeal cancer. Dietary findings among the few subjects who did not use tobacco or alcohol were similar to those for all subjects.

Protein intake and risk of renal cell cancer.

BACKGROUND: Renal cell cancer, although still relatively uncommon, has been increasing in incidence in the United States and other countries around the world. PURPOSE: Since previous studies have suggested an association with high intake of meat, we sought to further examine the role of diet in renal cell cancer risk. METHODS: Patients with histologically confirmed renal cell cancer that had been diagnosed between July 1, 1988, and December 31, 1990, were identified through the Minnesota Cancer Surveillance System, a statewide cancer registry. The patients eligible for inclusion in this study were white residents of Minnesota between 20 and 79 years of age. Control subjects were selected from the general population of Minnesota residents; subjects under age 65 were selected by use of a random-digit-dialing method and those 65 years or older were sampled from the Health Care Financing Administration files. Population-based control subjects were frequency-matched to cases by sex and 5-year age groups. A total of 690 patients and 707 control subjects were interviewed. Patients and control subjects were similar in distribution by sex, age, and educational level. Usual adult dietary intakes were assessed by questionnaire, and odds ratios were calculated by logistic regression analyses. RESULTS: Significantly increased risks of renal cell cancer were observed with increasing consumption of several food groups, including red meat (P for trend = .05), high-protein foods (P = .01), and staple (grains, breads, and potatoes) foods (P = .009). When examined by macronutrient status, risks increased monotonically with the amount of protein intake, from 1.2 (95% confidence interval [CI] = 0.7-1.9) to 1.4 (95% CI = 0.8-2.5) and 1.9 (95% CI = 1.0-3.6) (P for trend = .03) in the second, third, and fourth quartiles of intake, respectively, after adjustment for age, sex, caloric intake, body mass index, and cigarette smoking. No significant or consistent associations were detected with the intake of other dietary nutrients or beverages. CONCLUSION: Although an independent effect of dietary protein has not been previously associated with renal cell cancer, high protein consumption has been related to development of other chronic renal conditions that may predispose an individual to this cancer. IMPLICATION: These findings should prompt further study of dietary protein and its potential contribution to the origins of renal cell cancer.

Risk of urinary tract cancers following kidney or ureter stones.

BACKGROUND: A relationship has been suggested between kidney or ureter stones and the development of urinary tract cancers. In this study, a population-based cohort of patients hospitalized for kidney or ureter stones in Sweden was followed for up to 25 years to examine subsequent risks for developing renal cell, renal pelvis/ureter, or bladder cancer. METHODS: Data from the national Swedish In-patient Register and the national Swedish Cancer Registry were linked to follow 61,144 patients who were hospitalized for kidney or ureter stones from 1965 through 1983. Standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) were computed on the basis of nationwide cancer incidence rates, after adjustment for age, sex, and calendar year. RESULTS: Risk of renal cell cancer was not elevated in this cohort. Significant excesses of renal pelvis/ureter cancer (SIR = 2.5; 95% CI = 1.8-3.3) and bladder cancer (SIR = 1.4; 95% CI = 1.3-1.6) were observed, but the SIRs for women were more than twice those for men. Risks varied little by age or duration of follow-up. Risks of renal pelvis/ureter cancer and bladder cancer among patients with an associated diagnosis of urinary tract infection were more than double those among patients without such infection, although the risks were significantly elevated in both groups. CONCLUSIONS: Individuals hospitalized for kidney or ureter stones are at increased risk of developing renal pelvis/ureter or bladder cancer, even beyond 10 years of follow-up. Chronic irritation and infection may play a role, since kidney or ureter stones were located on the same side of the body as the tumors in most patients with renal pelvis/ureter cancer evaluated in our study.

Pancreatitis and pancreatic cancer: a population-based study.

BACKGROUND: Little is known about the etiology of cancer of the exocrine portion of the pancreas, which produces a variety of digestive enzymes. Smoking, certain dietary factors, and diabetes mellitus are considered to be risk factors, although the risk estimates are modest in most instances. A recent cohort study of patients with chronic pancreatitis indicated a ninefold to 16-fold increased risk for pancreatic cancer. PURPOSE: Our purpose was to evaluate the relationship between various clinical types of pancreatitis and pancreatic cancer. METHODS: Data for this study were collected from all inpatient medical institutions in Sweden from 1965 until 1983 by the Swedish National Board of Health and Welfare. Data were recorded on individual hospital admissions and discharges in the Inpatient Register. All patients with records in the Inpatient Register coded for acute, chronic, or unspecified pancreatitis were considered for inclusion in the study. A population-based cohort of 7956 patients with at least one discharge diagnosis of pancreatitis was monitored (up to 19 years of follow-up) for the occurrence of pancreatic cancer by record linkages to the Swedish Cancer Registry and Registry of Causes of Death. RESULTS: A total of 46 pancreatic cancers were diagnosed during follow-up compared with 21 expected (standardized incidence ratio [SIR] of 2.2; 95% confidence interval [CI] 1.6-2.9) for the Uppsala Health Care Region. The excess risk for women and men was similar--most pronounced during the first period of follow-up (2-4 years) after discharge and close to unity after more than 10 years of follow-up. Patients with chronic pancreatitis and patients with more than one discharge diagnosis of either acute or unspecified pancreatitis were at higher risk (SIR = 3.8; 95% CI 1.4-8.2 and SIR = 4.8; 95% CI 1.9-9.9, respectively) compared with those with only one discharge of acute (SIR = 1.6; 95% CI 0.9-2.7) or unspecified (SIR = 2.1; 95% CI 1.2-3.2) pancreatitis. CONCLUSIONS: Our finding of a moderate excess of pancreatic cancer among patients with pancreatitis, especially the chronic or recurrent forms, supports some earlier clinical and case-control studies, but it is not consistent with the ninefold to 16-fold risk reported in a recent cohort study. The absence of an increased risk 10 years or more after first discharge for pancreatitis argues against a straight-forward causal relationship. Because of the relatively short interval between diagnosis of pancreatitis and pancreatic cancer, it is possible that some forms of pancreatitis are a precursor to pancreatic cancer or that shared risk factors for both diseases (e.g., cigarette smoking) may also be involved.

Cancer incidence in a population-based cohort of patients hospitalized with diabetes mellitus in Denmark.

BACKGROUND: Diabetes has been associated with an increased risk of several cancers, notably cancers of the pancreas, liver, endometrium, and kidney. Since most previous studies have involved a limited sample size or focused on specific cancer sites, we conducted a comprehensive assessment of the risk of cancer in a nationwide cohort of diabetics in Denmark. METHODS: Discharge records of 109581 individuals hospitalized with a diagnosis of diabetes from 1977 through 1989 were linked with national cancer registry records through 1993. Standardized incidence ratios (SIRs) were calculated for specific cancer sites. RESULTS: The SIRs for primary liver cancer were 4.0 (95% confidence interval [CI] = 3.5-4.6) in males and 2.1 (95% CI = 1.6-2.7) in females. These SIRs remained elevated with increasing years of follow-up and after exclusion of patients with reported risk factors (e.g., cirrhosis and hepatitis) or patients whose cancers were diagnosed at autopsy. Kidney cancer risk was also elevated, with SIRs of 1.4 (95% CI = 1.2-1.6) in males and 1.7 (95% CI = 1.4-1.9) in females. For both sexes combined, the SIR for pancreatic cancer was 2.1 (95% CI = 1.9-2.4), with a follow-up time of 1-4 years; this SIR declined to 1.3 (95% CI = 1.1-1.6) after 5-9 years of follow-up. Excess risks were also observed for biliary tract and endometrial cancers. The SIRs for kidney and endometrial cancers declined somewhat after exclusion of diabetics with reported obesity. CONCLUSIONS: Patients hospitalized with a diagnosis of diabetes appear to be at higher risk of developing cancers of the liver, biliary tract, pancreas, endometrium, and kidney. The elevated risks of endometrial and kidney cancers, however, may be confounded by obesity.

Dietary carotene and vitamin A and risk of lung cancer among white men in New Jersey.

A population-based incident case-control study of lung cancer in white males was conducted during 1980-81 in six high-risk areas of New Jersey. Interviews were completed with 763 cases and 900 controls or with their next of kin. In order to assess whether dietary intake of carotene, preformed retinol, or total vitamin A modified the risk of lung cancer, subjects were asked about their usual frequency of consumption, several years earlier, of 44 food items, which provides 83% of the vitamin A in the American diet, and about their use of vitamin supplements. The men in the lowest quartile of carotene intake had 1.3 the risk (P-value for trend = .05) of those in the highest quartile after adjustment was made for smoking duration and intensity and education. No association was seen for retinol (P-value for trend = .11) or total vitamin A (P-value for trend = .30). The inverse association between carotene intake and lung cancer was most compelling for squamous cell carcinoma, with the smoking-and education-adjusted risk of those in the lowest quartile reaching 1.4 (P-value for trend = .03) the risk of those men in the highest quartile. Risk of lung adenocarcinoma was not related to carotene intake. The reduction in risk of squamous cell lung cancer with increasing carotene intake was noted in pipe and cigar smokers and cigarette smokers of different intensities. Among nonsmokers adenocarcinoma predominated. The inverse association between carotene and risk of squamous cell lung cancer was not especially strong or graded in response; but it was consistent and could be noted in each stratum when the subjects were divided by education, age, or mode of interview (direct vs. next of kin). The results of the other 4 case-control and 3 cohort studies that have looked at diet and risk of lung cancer are not consistent, and the question whether dietary carotene or total vitamin A reduces the risk of lung cancer is not yet resolved.

Incidence of cancer among patients with rheumatoid arthritis.

BACKGROUND: To evaluate hypotheses about the relationship between immune alterations and cancer, several investigators have determined cancer incidence in groups of patients with rheumatoid arthritis (RA), a chronic autoimmune disease. The primary finding has been an increased risk of hematopoietic cancers. PURPOSE: In this study, we have attempted to refine estimates of the association between RA and subsequent development of specific cancers. METHODS: We investigated site-specific cancer risk associated with RA in a population-based cohort study of 11683 Swedish men and women with a hospital (inpatient) diagnosis of RA. These case patients were identified from 1965 to 1983 and had follow-up through 1984 by computer linkage of the Swedish Hospital Inpatient Register to the National Swedish Cancer Registry (840 case patients with cancer) and the Swedish Registry of Causes of Death. Cancer risk was estimated by standardized incidence ratios (SIRs) for specific cancers. RESULTS: For men and women overall, there were decreased risks for cancers of the colon (SIR = 0.63; 95% confidence interval [CI] = 0.5-0.9), rectum (SIR = 0.72; 95% CI = 0.5-1.1), and stomach (SIR = 0.63; 95% CI = 0.5-0.9) and an increased risk for lymphomas (SIR = 1.98; 95% CI = 1.5-2.6). CONCLUSIONS: The reduced risk for colorectal cancer in patients with RA is consistent with previous studies of RA patients and with reports which state that use of nonsteroidal anti-inflammatory drugs may protect against the development of large bowel cancers. The excess of lymphomas also confirms a number of earlier investigations of RA patients.

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.

Diet in the etiology of oral and pharyngeal cancer among women from the southern United States.

A case-control interview study involving 227 women in North Carolina with oral cavity or pharyngeal cancer and 405 matched controls showed a protective effect of a usual adult diet high in fruits and vegetables. The relative risks of 0.65 for moderate and 0.52 for high (relative to 1.0 for infrequent) consumption of fruits and vegetables were statistically significant and remained after controlling for demographic characteristics, tobacco and alcohol use, relative weight, and intake of other food groups. Risks were lower with higher bread and cereal intake but higher for those women with the lightest weights, adjusted for height. The inverse associations between oral and pharyngeal cancer and intake of fruits and vegetables and intake of breads and cereals could not be attributed to an association with general nutritional status, since meat and fish consumption was related to an increased risk of oral and pharynx cancer. Moreover, dairy and egg consumption was generally unrelated to cancer risk. The reduction in risk with greater fruit and vegetable consumption is consistent with the hypothesis that vitamin C and/or beta-carotene intake is associated with a reduced risk of oral and pharyngeal cancer.

Diet, tobacco use, and fatal prostate cancer: results from the Lutheran Brotherhood Cohort Study.

A cohort of 17,633 white males age 35 and older responded to a mailed epidemiological questionnaire in 1966 and was followed until 1986 to determine the risk of cancer associated with diet, tobacco use, and other factors. During the 20-year follow-up, 149 fatal prostate cancer cases were identified. Relative risks for prostate cancer were significantly elevated among cigarette smokers (relative risk, 1.8; 95% confidence interval, 1.1-2.9) and users of smokeless tobacco (relative risk, 2.1; 95% confidence interval, 1.1-4.1). No significant associations were found with frequency of consumption of meats, dairy products, fruits, or vegetables. There were no overall significant associations between consumption of vitamin A from animal sources (retinol) and provitamin A from plant sources (carotene) and risk, but positive trends were seen for ages under 75, while inverse associations were found at older ages. Beverage consumption, including drinking coffee and alcohol, was unrelated to risk. Marital status, education, rural/urban status, and farming residence were also unrelated to the risk of fatal prostate cancer. The findings add to limited evidence that tobacco may be a risk factor for prostate cancer, but fail to provide clues to dietary or other risk factors.

Does chronic fatigue syndrome predispose to non-Hodgkin's lymphoma?

Chronic fatigue syndrome, an illness that frequently is associated with abnormalities of cellular immunity, has been reported anecdotally to be associated with an increased incidence of lymphoid hyperplasia and malignancy. This report describes an initial analysis of population-based cancer incidence data in Nevada, focusing on the patterns of non-Hodgkin's lymphoma prior to and subsequent to well described, documented outbreaks of chronic fatigue syndrome during 1984-1986. In a study of time trends in four age groups, the observed time trends were consistent with the national trends reported in the Surveillance, Epidemiology, and End Results Program. No statistically significant increase attributable to the chronic fatigue syndrome outbreak was identified at the state level. Additional studies are in progress analyzing the data at the country level, reviewing patterns in other malignancies, and continuing to monitor the cancer patterns over subsequent years.

Cancer risk in a population-based cohort of patients hospitalized for psoriasis in Sweden.

Studies of clinical series of psoriasis patients have suggested an increased risk of nonmelanoma skin cancer and melanoma; the risk of other neoplasms has rarely been studied. In order to assess the incidence of cancer in a nationwide series of psoriasis patients from Sweden, we followed up, for the years 1965-89, 9773 patients with a hospital discharge diagnosis of psoriasis made during 1965-83, who were alive and free from malignancy 1 y after first discharge. We compared their incidence of neoplasms with that of the national population by computing standardized incidence ratios (SIR). We observed a total of 789 neoplasms [SIR 1.37, 95% confidence interval (CI) 1.28, 1.47]. There was an increase in the risk of cancers of the oral cavity and pharynx (SIR 2.80, 95% CI 1.96, 3.87), liver (SIR 1.91, 95% CI 1.28, 2.74), pancreas (SIR 1.56, 95% CI 1.02, 2.23), lung (SIR 2.13, 95% CI 1.71, 2.61), skin (squamous cell carcinoma, SIR 2.46, 95% CI 1.82, 3.27), female breast (SIR 1.27, 95% CI 1.00, 1.58), vulva (SIR 3.24, 95% CI 1.18, 7.06), penis (SIR 4.66, 95% CI 1.50, 10.9), bladder (SIR 1.43, 95% CI 1.03, 1.92), and kidney (SIR 1.56, 95% CI 1.04, 2.25). The risk of malignant melanoma was decreased (SIR 0.32, 95% CI 0.10, 0.74). Despite some limitations (possible diagnostic misclassification, lack of data on treatment, relatively short follow-up), our study provides evidence against an increased risk of melanoma among patients hospitalized for psoriasis. In addition to nonmelanoma skin and genital cancers, patients hospitalized for psoriasis were at increased risk of several malignancies, in particular those associated with alcohol drinking and tobacco smoking.

Collection of dietary-supplement data and implications for analysis.

The role of nutrient intake in disease outcome is often examined in epidemiologic studies. Most such studies conducted in the United States, however, have not included fortified foods or vitamin supplements. In the United States, these are important sources of vitamins C and E, but not of beta-carotene. In addition, the importance of these nutrient sources varies by race, sex, and age. Failure to include these sources produces errors in nutrient estimates, notable misclassification of individuals with regard to their total intake, and rankings of intake that bear little or no relationship to blood concentrations of those nutrients. Implications for statistical analysis are also considered. Risk analyses in which nutrients from supplements are handled as control variables or are analyzed separately may impair the ability to detect associations between total nutrient intake and disease risk. The additional source of misclassification of nutrient status for vitamins C and E and other nutrients derived from fortified foods or supplements would make it more difficult to obtain significant and consistent results in etiologic studies of these nutrients; this has not been a factor for beta-carotene, which is derived almost exclusively from fruits and vegetables.

Dietary factors and the risk of pancreatic cancer: a case-control study in Shanghai China.

In Shanghai, China, age-adjusted incidence rates for pancreatic cancer have increased steadily, beginning in the early 1970s. To examine the effects of diet on this cancer, a population-based case-control study was conduct. Cases (n = 451) were permanent residents of Shanghai, 30-74 years of age, newly diagnosed with pancreatic cancer between October 1, 1990 and June 30, 1993. Decreased cases (19%) were excluded from the study. Controls (n = 1552) were selected among Shanghai residents, frequency matched to cases by gender and age. Information on usual adult dietary intake was obtained by trained interviewers in person, using a food frequency questionnaire. Dietary associations were measured by odds ratios and 95% confidence intervals. Risks of pancreatic cancer were inversely associated with consumption of vegetables (P for trend among men = 0.03; among women = 0.15) and fruits (P among men = 0.02; among women = 0.08). Reductions in risk were related also to intake of dietary fiber and micronutrients abundant in plant sources, such as vitamins C and E and carotene. There was also an inverse association with egg consumption (P for trend among men = 0.08; among women = 0.001). No consistent positive associations were observed with intake of other food groups, including preserved animal foods, fresh red meat, organ meat, poultry, and staple foods. On the other hand, risks increased with frequency of consumption of preserved vegetables and foods that were deep fried, grilled, cured, or smoked, providing clues to the possible role of nitrosamines, polycyclic aromatic hydrocarbons, and heterocyclic aromatic amines. The inverse associations observed with intake of dietary fat and protein in our study were unexpected, although these findings were based on consumptions well below the average intake in Western countries, where most previous studies on pancreatic cancer were conducted. Our results suggest that dietary variations have contributed little to the rising trends of pancreatic cancer in Shanghai. However, given the improving food availability and changing dietary patterns in China, further study of dietary and nutritional risk factors for pancreatic cancer appears warranted.

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.