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Biomedical subjects

R B Hayes

Publications and source records attributed to R B Hayes.

At least 109 records · Page 6Linked to original sources
PubMed1993

Exposure-response analysis of cancer mortality in a cohort of workers exposed to ethylene oxide.

The authors previously reported results from the largest cohort mortality study of ethylene oxide-exposed workers that has been conducted to date. Here they extend their previous work by quantitatively examining the relation between cancer mortality and ethylene oxide exposure. This study included workers from 13 of the 14 geographically distinct facilities that were included in the previous investigation. These facilities began regularly using ethylene oxide to sterilize medical supplies or spices sometime between 1938 and 1969. Workers were followed from first exposure through December 31, 1987. Historical exposures to ethylene oxide were estimated using a regression model. Standard life-table analysis was used to examine cancer mortality in three categories of cumulative exposure to ethylene oxide. The Cox proportional hazards model was also used to examine cumulative and other measures of ethylene oxide exposure as predictors of cancer mortality. In both the life-table analysis and the Cox model, a positive trend was observed in all lymphatic and hematopoietic cancer mortality for cumulative ethylene oxide exposure. This trend was strengthened when ethylene oxide exposures 10 years prior to death were discounted (lagged) and when the analysis was restricted to neoplasms of lymphoid cell origin. Despite limitations discussed in this paper, the authors believe that these findings provide some support for the hypothesis that exposure to ethylene oxide increases the risk of mortality from lymphatic and hematopoietic neoplasms. The authors intend to continue follow-up of this relatively young cohort, which may allow more definitive conclusions to be drawn in the future.

Cohort Studies↗
PubMed1993

Vasectomy and prostate cancer in US blacks and whites.

A large population-based case-control study was carried out to investigate the association between vasectomy and prostate cancer risk in black and in white men in the United States. Study subjects resided in the geographic areas covered by the population-based cancer registries of the Georgia Center for Cancer Statistics, or the Metropolitan Detroit Cancer Surveillance System, or in 10 counties included in the cancer registry of the New Jersey State Health Department. Cases for this study were men aged 40-79 years identified from pathology and outpatient records at hospitals covered by these registries, newly diagnosed with pathologically confirmed prostate cancer between August 1, 1986, and April 30, 1989. Population controls less than age 65 years were selected at periodic intervals by random digit dialing. Older controls were systematically selected (after a random start) from computerized records of the Health Care Finance Administration. A statistically nonsignificant excess risk (odds ratio (OR) = 1.6, 95% confidence interval (CI) 0.5-4.8) for prostate cancer associated with vasectomy was noted in blacks. Overall, the risk for prostate cancer associated with vasectomy in whites was not elevated (OR = 1.1, 95% CI 0.8-1.7). An increase in risk was found, however, for white men who had had a vasectomy 20 years or more prior to study (OR = 1.7, 95% CI 0.9-3.3) or who had had a vasectomy at less than age 35 years (OR = 2.2, 95% CI 1.0-4.4). For the total study group, the odds ratio associated with men who had a vasectomy 20 or more years prior to study was 1.5 (95% CI 0.8-2.7), and the odds ratio associated with men who had had a vasectomy at less than age 35 years was 2.0 (95% CI 1.0-4.0). Further detailed analysis showed that young age at vasectomy (less than age 35 years) was a more important risk factor than was years since vasectomy.

Adult↗
PubMed1993

Cancer mortality among jewelry workers.

Mortality was investigated for the years 1950-1980 for 1,009 male members of a New York jewelry workers union, and for the years 1984-1989 among 919 men and 605 women identified as jewelry workers on death certificates from 24 states. Malignant neoplasms were excessive for male union members (proportional mortality ratio [PMR] = 1.17; 95% confidence interval [CI]: 1.02-1.33) and female jeweler deaths from the 24 states (PMR = 1.24; 95% CI: 1.07-1.42). Deaths due to nonmalignant causes were not unusual, except for excesses, in union males, of the circulatory system (PMR = 1.10; 95% CI: 1.02-1.19), including arteriosclerotic heart disease (PMR = 1.25; 95% CI: 1.14-1.37) and rheumatic heart disease (PMR = 3.02; 95% CI: 1.94-4.50). Cancers of the digestive tract were proportionally elevated among union males (proportional cancer mortality rate [PMR] = 1.13; 95% CI: 0.89-1.41) and among deaths from the 24 states (PCMR = 1.22; 95% CI: 1.01-1.47). For the 24 states, excesses for digestive cancer were found for both males (PCMR = 1.19; 95% CI: 0.90-1.54) and females (PCMR = 1.26; 95% CI: 0.96-1.62). Regarding specific sites in the digestive tract, colon cancer excesses were found in union males (PCMR = 1.53: 95% CI: 1.05-2.15), and for men (PCMR = 1.27; 95% CI: 0.82-1.88) and women (PCMR = 1.36; 95% CI: 0.92-3.27) in 24 states.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular Diseases↗
PubMed1993

Occupational physical activity, socioeconomic status, and risks of 15 cancer sites in Turkey.

A multiple-site case-control study of 15 cancers (stomach; colon; rectum; larynx; lung; melanoma; skin; female breast; male breast; cervix; ovary; uterus; prostate; testis; and bladder) was conducted to evaluate their association with occupational physical activity and socioeconomic status (SES). A hospital-based study population (3,486 male cases and 379 female cases, and 2,127 male and 244 female controls) was established in an oncological treatment center in Istanbul, Turkey, from 1979-84. Assessment of physical activity and SES was based on job titles held by the study subjects. Two measures of physical activity were developed based on energy expenditure and 'sitting time' during working hours. Observed risks were adjusted for age, smoking, and SES. Elevated risks were observed among workers who held sedentary jobs for cancers of the colon (odds ratio [OR] = 1.6), rectum (OR = 1.3), melanoma (OR = 1.9), male breast (OR = 1.4), prostate (OR = 5.0), and ovary (OR = 2.0). Cancers of the cervix and uterus showed significantly decreasing risks with decreased activity. Risks of cancers of the colon, rectum, larynx, ovary, and melanoma were enhanced after risks for physical activity indices were adjusted for SES, while the associations between physical activity and cancers of the prostate, cervix, and uterus were weakened after SES adjustment. Risks of melanoma rose significantly with both activity indices after SES adjustment.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1993

Are the known bladder cancer risk-factors associated with more advanced bladder cancer?

Risk factors for superficial and invasive bladder cancer were examined in a case-control study of 470 cases identified in 1967-68 in the Brockton and Boston Standard Metropolitan Areas (MA, United States) and of 500 population-based controls. Histologic specimens were reviewed and classified as superficial or invasive, following a standardized protocol. The tobacco-associated risk for superficial bladder cancer was odds ratio (OR) = 2.6 (95 percent confidence interval [CI] = 1.7-4.1) and the risk for invasive bladder cancer was OR = 1.7 (CI = 1.1-2.5). For subjects less than 60 years of age, the risks were greater for invasive tumors (OR = 4.3, CI = 1.2-15) than for superficial tumors (OR = 2.0, CI = 0.9-4.2), but this pattern for tobacco use was not found in older subjects. A strong trend of increased risk with increased amount of cigarettes smoked was shown only for invasive bladder tumors. No clear pattern of excess risk for invasive bladder tumors was seen for age at first use and years since last use of tobacco. The risk associated with occupational exposure to aromatic amine bladder carcinogens was OR = 1.7 (CI = 0.8-3.3) for superficial and OR = 1.5 (CI = 0.8-3.0) for invasive bladder cancer. For subjects less than 60 years of age, the risks were greater for invasive (OR = 12.0, CI = 2.1-65) than for superficial tumors (OR = 4.3, CI = 0.8-24), but this pattern for occupational exposure was not found in older subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1993

N-acetylation phenotype and genotype and risk of bladder cancer in benzidine-exposed workers.

Several studies in subjects occupationally exposed to arylamine carcinogens have shown increased risks for bladder cancer associated with the slow acetylator phenotype. To follow up these reports, a case-control study of N-acetylation and bladder cancer risk was carried out among subjects occupationally exposed to benzidine, in benzidine dye production and use facilities in China. Thirty-eight bladder cancer cases and 43 controls from these factories were included for study of acetylation phenotype, by dapsone administration, and for polymorphisms in the NAT2 gene, by a polymerase chain reaction (PCR)-based test. In contrast to previous studies, no increase in bladder cancer risk was found for the slow N-acetylation phenotype (OR = 0.3; 95% CI = 0.1-1.3) or for slow N-acetylation-associated double mutations in NAT2 (OR = 0.5; 95% CI = 0.1-1.8). Examination of specific mutations and adjustment for age, weight, city and tobacco use did not alter the results. When examined by level of benzidine exposure in the cases, the bladder cancer risks associated with low (OR = 0.3, 95% CI = 0.0-2.2), medium (OR = 0.7, 95% CI = 0.1-4.5) and high (OR = 0.6, 95% CI = 0.1-3.5) exposure showed no interaction between genotype and benzidine exposure, within the range of exposures experienced by subjects in this study. This study, which is the first to incorporate phenotypic and genotypic analyses, provides evidence that the NAT2-related slow N-acetylation polymorphism is not associated with an increased risk of bladder cancer in workers exposed to benzidine, and may have a protective effect.

Acetylation↗
PubMed1993

Correlation between N-acetyltransferase activity and NAT2 genotype in Chinese males.

Eighty-four healthy Chinese male control subjects derived from an occupation-based case-control study of bladder cancer were evaluated for hepatic N-acetyltransferase activity by dapsone and for NAT2 genotype using allele-specific amplification of peripheral leukocyte DNA by the polymerase chain reaction. Fifty-nine percent of the overall variation in acetylation activity was explained by genotype (p < 0.0001). The remaining variation in acetylation was not associated with dapsone N-hydroxylation activity, age, current smoking status, or weight in the study population, or within any genotype subgroup. Although acetylation activity in the homozygous mutant group did not overlap with the other genotype categories, there was moderate overlap in acetylation between the heterozygous mutant and wildtype groups, and substantial variation in acetylation within them. Considering all subjects with the identical NAT2 genotype as phenotypically similar and all subjects with differing NAT2 genotypes as phenotypically distinct may result in misclassification of metabolic risk factors in epidemiological investigations. As such, it would seem prudent, where possible, to collect both acetylation phenotype and NAT2 genotype data, since the advantages and limitations of these two sources of information complement, and serve to assess the accuracy of each other.

Aged↗
PubMed1992

Mortality and incidence of bladder cancer in benzidine-exposed workers in China.

We examined bladder cancer mortality and incidence to 1981 in 1,972 workers employed in benzidine-exposed jobs in Tianjin, Shanghai, and Jilin, China, between 1972 and 1977, and in 1,974 unexposed workers employed during the same time period. In comparison to general population rates, in the benzidine-exposed group the ratio of observed to expected deaths (SMR) was 17.5 (95% C.I.: 7.5-34.5) and the ratio of observed to expected incident cases (SIR) was 25.0 (95% C.I.: 16.9-35.7). No excess was noted in the unexposed group. The 25-fold increase in bladder cancer incidence in the exposed group was related to level of exposure, with the SIR rising from 4.8 for low exposure to 36.2 for medium exposure, and 158.4 for high exposure. Risks were elevated both for producers of benzidine (SIR = 45.7; 95% C.I.: 20.9-86.8) and for users (SIR = 20.9; 95% C.I.: 12.9-32.0) of benzidine dyes. Benzidine-exposed workers who smoked tobacco had a 31-fold risk (95% C.I.: 20.4-46.4), while non-smoking workers had an 11-fold risk (95% C.I.: 3.6-25.8), suggestive of a multiplicative relationship between these two carcinogens.

Air Pollutants, Occupational↗
PubMed1992

Physical characteristics and factors related to sexual development and behaviour and the risk for prostatic cancer.

A case-control study of prostatic cancer was carried out to examine the association between selected physical characteristics and factors related to sexual development and behaviour and the risk for this disease. In consideration of an endocrinologic mechanism for these putative risk factors, the association between selected factors and serum hormone level in a comparison group, free of prostate cancer, was also examined. One-hundred cases and 113 controls were included for study. An elevated risk for prostatic cancer was found for those currently married (odds ratio (OR) = 4.0), those who had been married once (OR = 2.8), and those who were currently practising a religion (OR = 2.0). Compared to subjects with one child, those with more than one child and those with no children were more common among cases than controls. Prostatic cancer risk was associated with large body size and, in particular, with greater weight (p < 0.01). Early age at attainment of adult height was also associated with prostatic cancer risk (p < 0.01). Only moderate associations were found between increased frequency of sexual intercourse and prostatic cancer risk. The levels of testosterone (T), dihydrotestosterone, salivary testosterone and T/SHBG (sex hormone binding globulin) did not vary with age. Older men had higher oestradiol levels. Further, little association between hormone levels and risk factors was found, except for married subjects having increased serum androgens (p < 0.05) and heavy subjects having decreased serum androgens (not significant).

Age Factors↗
PubMed1992

Determination of CYP1A2 and NAT2 phenotypes in human populations by analysis of caffeine urinary metabolites.

The wide variations in urinary bladder and colo-rectal cancer incidence in humans have been attributed in part to metabolic factors associated with exposure to carcinogenic aromatic and heterocyclic amines. Cytochrome P-4501A2 (CYP1A2), which catalyses N-oxidation, and acetyltransferase (NAT2) which catalyses N- and O-acetylation, both appear to be polymorphically distributed in human populations; and slow and rapid NAT2 phenotypes have been implicated as risk factors for these cancers. Caffeine has also been shown to undergo 3-demethylation by CYP1A2, and it is further acetylated to 5-acetylamino-6-formylamino-3-methyluracil (AFMU) by the polymorphic NAT2. In this report, we describe a metabolic phenotyping procedure that can be used to determine concomitantly the hepatic CYP1A2 and NAT2 phenotypes. For the NAT2 phenotype, we confirm the valid use of the urinary molar ratio of AFMU/1-methylxanthine, even in alkaline urines. For the CYP1A2 phenotype, the urinary molar ratio of [1,7-dimethylxanthine + 1,7-dimethyluric acid]/caffeine, taken at 4-5 h after caffeine ingestion, was identified from pharmacokinetic analyses of 12 subjects as being better correlated (r = 0.73; p = 0.007) with the rate constant for caffeine 3-demethylation than other previously suggested ratios. This procedure was then used to determine the CYP1A2 phenotype in subjects from Arkansas (n = 101), Italy (n = 95), and China (n = 78). Statistical and probit analyses of nonsmokers indicated that the CYP1A2 activity was not normally distributed and appeared trimodal. This trimodality allowed arbitrary designation of slow, intermediate, and rapid phenotypes, which ranged from 12-13% slow, 51-67% intermediate, and 20-37% rapid, in the different populations. A reproducibility study of 13 subjects over a 5 day or 5 week period showed that, with one exception, intraindividual variability did not alter this CYP1A2 phenotypic classification. Induction of CYP1A2 by cigarette smoking was also confirmed by the increased caffeine metabolite ratios observed in the Arkansas and Italian smokers (blonde tobacco). However, Italian smokers of black tobacco and Chinese smokers did not appear to be induced. Furthermore, probit analyses of Arkansas and Italian blonde tobacco smokers could not discriminate between phenotypes, apparently as a consequence of enzyme induction.

Adult↗
PubMed1992

Biomarkers in occupational cancer epidemiology: considerations in study design.

Epidemiologic studies of occupational groups have been central to the identification of human carcinogens. The incorporation of a biochemical component into occupational studies of cancer can expand the possibilities for identifying human carcinogens and for understanding the disease process. Two epidemiologic studies of occupation and cancer which include evaluation of biomarkers are described. The association of acetylator phenotype with bladder cancer risk was studied in benzidine-exposed workers. The association of benzene-related leukopenia with leukemia is being studied in benzene-exposed workers. These investigations illustrate issues in the use of biomarkers in epidemiologic studies of cancer risk. Such studies require the identification and characterization of the population at risk. Disease susceptibility factors are amenable for inclusion in these studies and can be statistically modeled as exposure-effect modifiers. Biomarkers of exposure are mainly of importance in short-term longitudinal and cross-sectional studies of exposure and intermediate outcomes and for validation of other data sources. Several sources of error can affect the results of molecular epidemiologic studies. Aside from minimizing laboratory error, consideration must be given in the design and execution of these studies to potential problems in subject selection and field collection of biologic samples and other relevant data.

Benzene↗
PubMed1991

Peripheral hormone levels in controls and patients with prostatic cancer or benign prostatic hyperplasia: results from the Dutch-Japanese case-control study.

The possible relationship between changes in peripheral hormone levels and the occurrence of prostatic pathology was studied in a case-control study, involving estimation of various plasma hormones in 368 Dutch and 258 Japanese men, who were grouped as controls and patients with benign prostatic hyperplasia, focal prostatic carcinoma, or clinically evident prostatic carcinoma. Results of a number of previous, smaller studies concerning interrelationships between hormone levels in elderly men were confirmed within the Dutch and Japanese groups. Plasma levels of testosterone and estradiol were significantly lower in the Japanese men, when compared with those in Dutch men. Probably as a result of this difference in testosterone levels, the ratio between serum levels of testosterone and sex hormone-binding globulin (SHBG) was decreased in the Japanese men, while the ratio between the concentrations of dihydrotestosterone and testosterone was increased. These differences were also found when results from Japanese subgroups (controls and patients with prostate pathology) were compared with those from the Dutch subgroups. There were no significant differences in plasma androgen levels between Japanese or Dutch prostate cancer cases and their respective control subgroups. These findings do not support a correlation between the lower plasma testosterone levels and a lower incidence of prostate cancer in the Japanese men. Furthermore, no significant differences were found between salivary levels of testosterone or the ratio between testosterone and SHBG in the various Dutch subgroups. In Japanese benign prostatic hyperplasia patients, the testosterone to SHBG ratio was significantly increased. In conclusion, the results of this retrospective, cross-sectional study do not indicate that hormonal levels play a primary role in the origin or promotion of prostatic abnormalities. The finding of a lower plasma testosterone in the Japanese men, however, remains suggestive, warranting a more extensive prospective study.

Age Factors↗
PubMed1991

Testicular cancer in young men and parental occupational exposure.

To investigate whether parental occupation, especially during the 12 month period before birth, could be responsible for elevated rates of testicular cancer in young men, we used data from a case-control study of 223 cases and 212 controls conducted in the Washington, DC area. For all histologic types of testicular cancer combined, no significant associations were found for specific occupations, nor for the broad occupational categories of professional, other white collar, or blue collar workers. However, for cases with seminomas, excess risks were seen for those with parents employed in the following occupations: mothers in health-related occupations, O.R. = 4.6 (1.1-19.1), and fathers working in automobile service stations, O.R. = 4.0 (0.6-24.5), manufacturing industries, O.R. = 2.2 (1.0-4.2), and aircraft production and maintenance, O.R. = 5.3 (0.7-24.1). Although these findings for seminoma are intriguing, they do not explain the increase of testicular cancer in young men.

Adolescent↗
PubMed1991

O(6)-methylguanine-DNA methyltransferase and uracil DNA glycosylase in human broncho-alveolar lavage cells and peripheral blood mononuclear cells from tobacco smokers and non-smokers.

Because interindividual variations in the activities of DNA repair enzymes may be a risk factor in the pathogenesis of lung diseases, O(6)-methylguanine-DNA methyltransferase (O(6)-MT) and uracil DNA glycosylase (UDG) were measured in broncho-alveolar lavage cell (BALC) and peripheral blood mononuclear cell (PBM) samples from 57 healthy volunteers (25 smokers and 32 non-smokers). According to cotinine determination in 39 cases where serum for this was available, 38% of the self-acclaimed non-smokers had greater than 10 ng/ml of cotinine in their serum. Whether grouped into smokers and non-smokers according to clinical history or by serum cotinine, there were no statistically significant differences between these groups in O(6)-MT or UDG in either of the cell types. However, a tendency towards lower values in smokers was seen. The highest intraindividual variation in O(6)-MT activity was 7-fold, while the highest interindividual variation reached 18-fold. For UDG, the respective values were 24- and 307-fold. Although the distribution of O(6)-MT in BALC was different from that in PBM, the data are consistent with unimodality in both of the cell types. These findings suggest that exposure to cigarette smoke is not entirely responsible for the wide interindividual variation in O(6)-MT and UDG DNA repair activities.

Adult↗
PubMed1991

Mortality of coke plant workers in The Netherlands.

During the production of coke, large quantities of coke oven gas are emitted. People who work on the top or on the sides of coke ovens are exposed to this oven gas, which contains a range of carcinogenic chemicals. To investigate the cancer risks under these work conditions, a retrospective study was undertaken. In total 11,399 former workers were enrolled in the study. Of these, 5639 had worked in the coke plant for at least six months between 1945 and 1969. The other 5740 had worked in another plant during the same period and formed a non-exposed group for comparison. The study group was followed up until 1984 for mortality. The causes of death were obtained from the Central Bureau of Statistics. Among the coke oven workers significantly higher death rates were found for lung cancer and non-malignant respiratory disease. Mortality in the byproduct section was similar to that expected. Among workers in the tar distillery the rate for lung cancer was higher than expected. The risk for gastric cancer and non-malignant respiratory disease among the workers of the coke shipping department was increased but the SMRs did not reach statistical significance. No data were collected about individual smoking habits or socioeconomic state of the study subjects and the possibility that the risk found could be attributed to these factors cannot be ruled out. It has been stated by other investigators, however, that the effect of not controlling for smoking tends to be modest.

Coke↗
PubMed1990

Lung cancer and the debrisoquine metabolic phenotype.

In a case-control study, we tested the hypothesis that the genetically determined ability to metabolize debrisoquine is related to risk of lung cancer. Overall, individuals who were extensive metabolizers of debrisoquine were at significantly greater risk of lung cancer than those who were poor or intermediate metabolizers (odds ratio = 6.1; 95% confidence interval = 2.2-17.1). In this study, case patients had lung cancer, and control subjects had either chronic obstructive pulmonary disease or cancers other than lung cancer. Results were adjusted for age, race, asbestos exposure, and smoking. Both black and white individuals who were extensive metabolizers of debrisoquine were at significantly increased risk after similar adjustment (for blacks, odds ratio = 4.5, 95% confidence interval = 1.1-18.1; for whites, odds ratio = 10.2, 95% confidence interval = 2.0-51.4). Significantly increased risk of lung cancer was also present for individuals who were extensive metabolizers when subjects with chronic obstructive pulmonary disease or other cancers were considered separately. These data confirm that the ability to metabolize debrisoquine is a major determinant of susceptibility to lung cancer. Evaluation of the marker in other case-control settings, further exploration of racial differences, and the prospective evaluation of this marker in subgroups at high risk of lung cancer are areas worthy of further study.

Adenocarcinoma↗
PubMed1990

Serum vitamin A and subsequent development of prostate cancer in the first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study.

The relation between serum vitamin A measurements made at baseline examination (1971-1975) and subsequent development of prostate cancer was examined in the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study (1981-1984). The analytic cohort consisted of 2440 men 50 years of age or older who were followed for a median of 10 years. A total of 84 men developed prostate cancer. The mean level of serum vitamin A was significantly lower (P less than 0.01) in prostate cancer cases than in noncases. Considered as a continuous variable or in quartiles, a statistically significant (P less than 0.005 or P less than 0.02, respectively) trend was observed for increased risk of prostate cancer with decreasing levels of serum vitamin A. Adjusted for age and race, men in the lowest quartile had a relative risk of 2.2 (95% confidence intervals, 1.1, 4.3) compared to those in the highest quartile. The elevated risk of prostate cancer associated with the lowest quartile of serum vitamin A levels did not attenuate with increasing time between blood drawing and diagnosis, suggesting that metabolic effects of early disease are an unlikely explanation of these results. The inverse association between serum vitamin A and prostate cancer incidence was independent of age at examination and several other possible confounding variables. This is the first prospective study of serum vitamin A and prostate cancer to include a large (84) number of cases.

Aged↗