BACKGROUNDStandardized mortality ratios (SMRs) and other measures of relative risk by themselves may not suffice as descriptors of occupational hazards for many audiences including decision-makers and those at direct risk from hazardous work. To explore other approaches, we calculated excess years of potential life lost and excess lifetime risk for both lung diseases and fatal injuries in a cohort of uranium miners with historical records of exposure to radon gas.METHODSWe used relatively simple life table (SMR) methods and also analyzed lung cancer mortality with Poisson regression methods permitting control for smoking.RESULTSAmong uranium miners hired after 1950, whose all-cause SMR was 1.5, 28 percent would experience premature death from lung diseases or injury in a lifetime of uranium mining. On average, each miner lost 1.5 yr of potential life due to mining-related lung cancer, or almost 3 months of life for each year employed in uranium mining. As a consequence of all excess lung disease and injury risks combined, a year of mining was associated with 5.9 months loss of potential life. For each year actually working underground, miners lost more than 8 months of potential life. When controlled for smoking (and healthy worker effect) with Poisson regression, the estimates for radon-related lung cancer effects were slightly larger. Although chronic disease deaths dominated in excess years of life lost (due to radon, silica and possibly other exposures), more years were lost on average per individual injury death (38 yr), than per excess lung cancer (20 yr) or other lung disease death (18 yr). Fatal-injury dominated the potential years of life lost up to about age 40.CONCLUSIONSYears of life lost per years employed provides another, more intuitive summary of occupational mortality risk.

BACKGROUND To evaluate the utility of expanding the number and precision of injury categories used in previous occupational mortality studies, this study reanalyzed data from four previous studies of unionized construction workers (construction laborers, ironworkers, sheet metal workers, and operating engineers), by expanding the number of injury categories from 6 to 33. METHODS Proportionate mortality ratios (PMRs) were computed using the distribution of deaths from the National Occupational Mortality Surveillance System, a mortality surveillance system from 28 states, as a comparison. A blue collar comparison group was also used in additional analyses to adjust for socioeconomic and other factors. RESULTS This reanalysis identified significantly elevated PMRs in at least one of the four worker groups for falls, motor vehicle crashes, machinery incidents, electrocutions, being struck by falling objects, being struck by flying objects, explosions, suffocation, and water transport incidents. Limiting the comparison population to deaths among blue collar workers did not change the results substantially. CONCLUSIONS This study demonstrates that increasing the precision of categories of death from injury routinely used in mortality studies will provide improved information to guide prevention. Am. J. Ind. Med. 37:364-373, 2000. Published 2000 Wiley-Liss, Inc.

One common framework for describing the evaluation and assessment of hazards in the workplace includes the four steps of hazard identification, exposure assessment, exposure-response modeling, and risk characterization (NAS, 1983). We discuss hazards for occupational injury and illness in light of this framework, and we contrast the evaluation of injury hazards with the evaluation of illness hazards. In particular, the nature of the hazards, typical exposure patterns, quantification of exposure, and the attribution of outcome to exposure are discussed. Finally, we discuss the management of occupational illness and injury hazards and issues encountered when evaluating efforts designed to mitigate the effects of occupational hazards.

OBJECTIVES:To examine the association of immune cell number and function with occupational exposure to substances contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).METHODS:A cross sectional medical survey. The exposed participants were employed at two chemical plants between 1951 and 1972 in the manufacture of 2,4,5-trichlorophenate and its derivatives. The reference group consisted of people with no occupational exposure to phenoxy herbicides who lived within the communities of the workers. Data from a total of 259 workers and 243 unexposed referents were included in the analysis of immune function. Laboratory tests for immune status included enumeration of circulating leukocyte and lymphocyte populations, proliferative responses of circulating lymphocytes to mitogens and antigens, and serum concentrations of the major immunoglobulins and complement factor C3.RESULTS:The workers had substantial exposure to substances contaminated with TCDD, as indicated by a lipid adjusted mean serum TCDD concentration of 229 ppt compared with a mean of 6 ppt in the unexposed referents. Workers were divided into categories based on their serum TCDD concentration. For all categories except the lowest, with values of serum TCDD comparable with the unexposed referents, there were increased odds of having lower counts of CD26 cells (activated T cells) (odds ratio (OR) 1.0, 95% confidence interval (95% CI) 0.5 to 1.8 for TCDD < 20 ppt; OR 1.6, 95% CI 0.8 to 3.2 for TCDD 20-51 ppt; OR 2.7, 95% CI 1.4 to 5.1 for TCDD 52-125 ppt; OR 2.6, 95% CI 1.4 to 4.9 for TCDD 125-297 ppt; OR 2.4, 95% CI 1.3 to 4.6 for TCDD 298-3389 ppt). A less consistent finding was decreased spontaneous proliferation of cultured lymphocytes. However, increases were found in proliferation of lymphocytes in response to concanavalin and pokeweed in workers in the high TCDD category. Age, cigarette smoking, and alcohol were significant predictors of several immunological outcomes.CONCLUSIONS:Associations between serum TCDD concentration and both a decrease in circulating CD26 cells and decreased spontaneous background proliferation were the major findings of this study. These results are unlikely to be of clinical importance but may reflect limited evidence for an association between immunological changes in workers and high serum concentrations of TCDD, or chance findings resulting from the evaluation of multiple immunological variables.

Cervical cancer remains an important health problem for women. Few published studies have examined cervical cancer with respect to a woman's occupation. This study examines the association of cervical cancer mortality and occupation in a large national database. The purpose of the study is to recommend which occupations may most require health promotion activities. Mortality data from the National Occupational Mortality Surveillance System were used to calculate the proportion of deaths from cervical cancer according to occupation. This study is based on standardized death certificate data for almost 2 million deaths among women in 27 states, covering the period 1985-1990. Our results are consistent with those in previous studies, with service and apparel manufacturing workers showing elevated risk. Data presented show a difference in cervical cancer mortality by occupational group. Identification of these occupations suggests which women could be targeted for preventive services. Women in occupations with low socioeconomic status are less likely to have access to health promotion programs. Resources should be directed to these women.

This study evaluated the relationship between benzene exposure and low white blood cell (WBC) and red blood cell (RBC) counts. Hematologic screening data collected over a 35 year period at a rubber hydrochloride manufacturing plant were analyzed; an increased risk of leukemia had been demonstrated previously among workers at the plant [Infante et al. (1977).' Lancet 2:76-78; Rinsky et al. (1981): Am J Ind Med 2:217-45 (1987): NEJM 316:1044-1050/. Hematologic screening data were available for 657 of 1,037 (63.3%) individuals employed at the plant from 1939 through 1976. There was a total of 21. 710 blood test records (range per individual 1-354). The study utilized a case-control design and estimated benzene exposures using the job exposure matrix developed by Rinsky et al. (1987): NEJM 316:1044-1050]. The effects of benzene exposure in the 30, 90, and 180 days before the blood test date, as well as cumulative exposure up until the blood test date, were examined using conditional logistic regression. For WBCs there was a strong exposure response and all of the exposure metrics selected showed a significant relationship with low blood count. For RBCs there was a weak positive exposure-response, which was significant (p = 0.03) for one of the dose metrics. The finding of an exposure-response relationship in the range of exposures represented in this study, where the maximum daily benzene exposure estimate was 34 ppm, is consistent with findings of several animal studies demonstrating a decrease in peripheral lymphocyte counts at benzene exposures as low as 10 ppm, and a stronger effect of benzene exposure on lymphocytes (as reflected in total WBC count) than on red cells. There was no evidence for a threshold for the hematologic effects of benzene exposure, suggesting that even exposure to relatively low levels of benzene (e.g., <5 ppm) may result in hematologic suppression.

OBJECTIVES:To examine the effects of occupational exposure to substances contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on cytochrome P-4501A2 activity in a cross sectional medical survey. METHODS:The exposed workers had been employed at two chemical plants > 15 years earlier in the manufacture of 2,4, 5-trichlorophenol and its derivatives. The control group consisted of people with no occupational exposure to phenoxy herbicides and who lived within the communities of the exposed workers. A total of 58 workers and 125 unexposed controls participated in the analysis. Cytochrome P-450 activity was assessed with test that measures caffeine metabolites in the urine. A ratio of metabolites of caffeine (CMR) constituted a measure of P-4501A2 activity. RESULTS:Compared with the control group in multivariate logistic regression, raised non-significant associations were found for three of four categories of TCDD in exposed workers (TCDD < 20 pg/g, odds ratio (OR) 1.7, 95% confidence interval (95% CI) 0.6 to 5.0, TCDD 20-66, OR 0.3, 95% CI 0.0 to 1.7; TCDD 67-147, OR 2.3, 95% CI 0.6 to 8.8; TCDD > or = 148, OR 3.1, 95% CI 0.8 to 12.5). We found a strongly significant association of CMR and urinary cotinine, a measure of smoking, and urinary free ethanol. We found weak non-significant associations between P-4501A2 activity and increased serum TCDD among workers. CONCLUSIONS:The absence of an association between serum TCDD and cytochrome P-4501A2 may be due to the size of the study, insensitivity of the CMR to assess cytochrome P-4501A2 activity, or inadequate levels of exposure, although these were among the highest in human groups tested.

Construction, one of the larger industries in the United States, employs 7.6 million workers, many in skilled trades occupations. Previously published data about potential worksite exposures and mortality of construction site workers are limited. We analyzed occupation and industry codes on death certificates from 19 U.S. states to evaluate mortality risks among men and women usually employed in construction occupations. Proportionate mortality ratios (PMRs) for cancer and several other chronic diseases were significantly elevated among 61,682 white male construction workers who died between 1984 and 1986. Men younger than age 65, who were probably still employed immediately prior to death, had significantly elevated PMRs for cancer, asbestos-related diseases, mental disorders, alcohol-related disease, digestive diseases, falls, poisonings, traumatic fatalities that are usually work-related, and homicides. Elevated PMRs for many of the same causes were observed to a lesser degree for black men and white women whose usual industry was construction. In addition, women experienced excess cancer of the connective tissue and suicide mortality. Various skilled construction trades had elevated PMRs for specific sites, such as bone cancer and melanoma in brickmasons, stomach cancer in roofers and brickmasons, kidney and bone cancer in concrete/terrazzo finishers, nasal cancer in plumbers, pulmonary tuberculosis in laborers, scrotal cancer and aplastic anemia in electricians, acute myeloid leukemia in boilermakers, rectal cancer and multiple sclerosis in electrical power installers, and lung cancer in structural metal workers. Using a standard population of blue collar workers did not result in fewer elevated PMRs for construction workers. Despite lifestyle differences and other limitations of the study, the large numbers of excess deaths observed in this study indicate the need for preventive action for construction workers.

A cohort mortality study was conducted among 9028 (3042 women, 5986 men) workers potentially exposed to chlorinated naphthalenes (chloracnegens structurally similar to dioxins) and asbestos in the manufacture of Navy cable during World War II. Based on mortality through December 31, 1985, standardized mortality ratios (SMRs) for all cancers was 1.03 in women (95% confidence interval [CI] = 0.9 to 1.17) and 1.18 in men (95% CI = 1.10 to 1.26). There were no significant elevations in causes of death hypothesized a prior to be associated with chlorinated naphthalene exposure (malignant neoplasms [MN] of connective tissue, liver, and lymphatic and hematopoietic organs). An excess of MN of the connective tissue was suggested for workers with over 1 year of exposure and 25 years of latency (SMR = 3.54; 95% CI = 0.97 to 9.07). Among cancer sites not hypothesized to be related a priori, three showed concordant excesses among both genders (MN of stomach; rectum; and trachea, bronchus, and lung). No significant elevations occurred in hormonally related cancers among women. Cancer mortality among 460 individuals with chloracne (431 men, 29 women) was similar to that of the entire cohort, although the chloracne subcohort showed significant excesses in two rare causes of death (MN of esophagus, SMR = 3.26; "benign and unspecified neoplasms," SMR = 4.93). Use of county referent rates decreased SMRs for stomach, rectal, and buccal cavity cancer, suggesting a role for nonoccupational risk factors. It is difficult to draw conclusions about carcinogenicity of chlorinated naphthalenes because of study limitations, most importantly, concomitant asbestos exposure and the relatively short duration of exposure to chlorinated naphthalenes among most of the cohort.

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.

A retrospective cohort mortality study with 5529 nitroglycerin, 4989 dinitrotoluene, and 5136 unexposed workers compared the mortality of the exposed groups with that of the United States population and that of the unexposed group with life-table analysis and Poisson regression. Mortality from ischemic heart disease was close to that expected, and mortality from cerebrovascular disease was slightly less than that expected, for the workers with both nitroglycerin and dinitrotoluene exposure and for those with dinitrotoluene exposure only. A significant interaction between age and nitroglycerin exposure was detected in the Poisson regression analyses for ischemic heart disease, particularly for workers actively exposed to nitroglycerin. The rate ratio for the workers under 45 years of age and actively exposed to nitroglycerin was 3.30 (95% confidence interval 129-8.48). This study did not show a chronic effect of nitroglycerin or dinitrotoluene exposure on cardiovascular disease risk. Potential biases related to the company's medical screening program may have limited the ability to detect chronic cardiovascular effects.

An analysis of OSHA fatality investigations for 1984-1987 found 104 work-related deaths in children. The largest category (30%) involved industrial vehicles and equipment, followed by electrocution (17%) and falls (11%). Forty-three deaths (41%) occurred while engaged in types of work prohibited for children by the Fair Labor Standards Act (FLSA). Three deaths involved work with conveyors, an activity currently permitted for child workers under FLSA. OSHA issued citations for safety violations in 70% of deaths. Since OSHA investigates only some work-related deaths, the actual number of child labor fatalities during the four year period was probably higher. Using information from OSHA and from death certificate data, we estimate that there are at least 100 work-related deaths in the United States in children under 18 each year. Hazardous child labor continues to occur even in industries regulated by OSHA and FLSA.

A retrospective cohort study of the incidence of bladder cancer was conducted in response to a union request for an evaluation of a possible excess number of cases of bladder cancer at a chemical plant in western New York State. Workers at the plant were exposed to two potential bladder carcinogens-ortho-toluidine (o-toluidine) and aniline. Incidence rates of bladder cancer among workers at the plant were compared with those of the population of New York State (excluding New York City). Among all 1749 workers at the plant, 13 cases of bladder cancer were observed versus 3.61 expected [standardized incidence ratio (SIR) = 3.60; 90% confidence interval (CI) = 2.13-5.73]. Among the 708 workers who worked in areas in which o-toluidine and aniline were used, 7 cases were observed versus 1.08 expected (SIR = 6.48; 90% CI = 3.04-12.2). Among the 288 maintenance, shipping, and janitorial workers thought to have been possibly exposed, 4 cases were observed versus 1.09 expected (SIR = 3.66; 90% CI = 1.25-8.37). Among the remaining 753 workers who were probably not exposed, 2 bladder cancers were observed versus 1.43 expected (SIR = 1.39; 90% CI = 0.25-4.39). Increased risk of bladder cancer was strongly associated with increased duration of employment in the department where o-toluidine and aniline were used (P < .001). Among workers with 10 or more years of employment in the department, the SIR was 27.2 (90% CI = 11.8-53.7). o-Toluidine is an animal carcinogen more potent than aniline and is known to produce bladder tumors in rats; hence, it is more likely that o-toluidine is responsible for the observed excess number of cases of bladder cancer, although aniline may have played a role.

A bladder cancer incidence study was conducted among 540 workers exposed to the potential bladder carcinogen 4,4'-methylenebis(2-chloroaniline) from 1969 to 1979. Among the 385 workers who participated in a urine screening examination, none had suspicious or positive cytology. Twenty-one workers had at least one reading of atypia and 60 had either a positive dipstick for heme or greater than five red blood cells per low power field. The study protocol initially involved referral to private physicians for follow-up of any suspicious laboratory results. However, the diagnosis by cystoscopy of a bladder tumor in a nonsmoking man less than 30 years old with low-level hematuria prompted us to offer cystoscopy to all members of the cohort. A total of three tumors were identified in 200 persons who received cystoscopy. All were low-grade, papillary tumors and two occurred in men with completely normal urine screening results. These findings suggest that cystoscopy of asymptomatic persons should be considered in designing bladder cancer screening programs in high-risk cohorts.

American Journal of Industrial MedicineVolume 13, Issue 1 p. 1-4 Article Control of smoking in occupational epidemiologic studies: Methods and needs Dr. Aaron Blair PhD, Corresponding Author Dr. Aaron Blair PhD Occupational Studies Section, National Cancer Institute, Bethesda, MDOccupational Studies Section, National Cancer Institute, Landow Building, Room 4C16, Bethesda, MD 20892Search for more papers by this authorKyle Steenland PhD, Kyle Steenland PhD Industry-wide Studies Branch, National Institute for Occupational Safety and Health, Cincinnati, OHSearch for more papers by this authorCarl Shy MD, Carl Shy MD Department of Epidemiology, University of North Carolina School of Public Health, Chapel HillSearch for more papers by this authorMaureen O'Berg PhD, Maureen O'Berg PhD E.I. DuPont de Nemours and Co., Inc., Wilmington, DESearch for more papers by this authorWilliam Halperin MD, William Halperin MD Industry-wide Studies Branch, National Institute for Occupational Safety and Health, Cincinnati, OHSearch for more papers by this authorTerry Thomas PhD, Terry Thomas PhD Occupational Studies Section, National Cancer Institute, Bethesda, MD Organizing Committee for Workshop on Obtaining and Using Information on Smoking in Occupational Epidemiologic Studies, sponsored by the National Cancer Institute and the National Institute for Occupational Safety and Health, December 15–16, 1986, in Bethesda, Maryland.Search for more papers by this author Dr. Aaron Blair PhD, Corresponding Author Dr. Aaron Blair PhD Occupational Studies Section, National Cancer Institute, Bethesda, MDOccupational Studies Section, National Cancer Institute, Landow Building, Room 4C16, Bethesda, MD 20892Search for more papers by this authorKyle Steenland PhD, Kyle Steenland PhD Industry-wide Studies Branch, National Institute for Occupational Safety and Health, Cincinnati, OHSearch for more papers by this authorCarl Shy MD, Carl Shy MD Department of Epidemiology, University of North Carolina School of Public Health, Chapel HillSearch for more papers by this authorMaureen O'Berg PhD, Maureen O'Berg PhD E.I. DuPont de Nemours and Co., Inc., Wilmington, DESearch for more papers by this authorWilliam Halperin MD, William Halperin MD Industry-wide Studies Branch, National Institute for Occupational Safety and Health, Cincinnati, OHSearch for more papers by this authorTerry Thomas PhD, Terry Thomas PhD Occupational Studies Section, National Cancer Institute, Bethesda, MD Organizing Committee for Workshop on Obtaining and Using Information on Smoking in Occupational Epidemiologic Studies, sponsored by the National Cancer Institute and the National Institute for Occupational Safety and Health, December 15–16, 1986, in Bethesda, Maryland.Search for more papers by this author First published: 1988 https://doi.org/10.1002/ajim.4700130102Citations: 26 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume13, Issue1Special Issue: Smoking and Occupation in Epidemiologic Studies1988Pages 1-4 RelatedInformation

In order to assess the possible human carcinogenicity of formaldehyde we conducted a retrospective cohort mortality study of workers exposed for at least three months to formaldehyde in three garment facilities which produced permanent press garments. A total of 11,030 workers contributing 188,025 person-years were included in the study. Vital status was successfully ascertained through 1982 for over 96% of the cohort. The average (TWA) formaldehyde exposure at the three plants monitored in 1981 and 1984 by NIOSH was 0.15 ppm but past exposures may have been substantially higher. In general, mortality from nonmalignant causes was less than expected. A statistically significant excess in mortality from cancers of the buccal cavity (SMR = 343) and connective tissue (SMR = 364) was observed. Statistically nonsignificant excesses in mortality were observed for cancers of the trachea, bronchus and lung (SMR = 114), pharynx (SMR = 112), bladder (SMR = 145), leukemia and aleukemia (SMR = 113), and other lymphopoietic neoplasms (SMR = 170). Mortality from cancers of the trachea, bronchus and lung was inversely related to duration of exposure and latency. In contrast, mortality from cancers of the buccal cavity, leukemias, and other lymphopoietic neoplasms increased with duration of formaldehyde exposure and/or latency. These neoplasms also were found to be highest among workers first exposed during a time period of high potential formaldehyde exposures in this industry (1955-1962). However, it should be recognized that these findings are based on relatively small numbers and that confounding by other factors may still exist. The results from this investigation, although far from conclusive, do provide evidence of a possible relationship between formaldehyde exposure and the development of upper respiratory cancers (buccal), leukemias, and other lymphopoietic neoplasms in humans.

To determine the relation between exposure to acid mist and laryngeal cancer, the smoking habits, drinking habits, and incidence of laryngeal cancer of 879 male steelworkers exposed to acid mists during pickling operations was ascertained. Sulphuric acid mist was the primary exposure for most men in this cohort. These men had all worked in a pickling operation for a minimum of six months before 1965, with an average duration of exposure of 9.5 years. Exposures to sulphuric acid in the 1970s averaged about 0.2 mg/m3, and earlier exposures were probably similar. Interviews were conducted with all cohort members or their next of kin in 1986 and medical records of decedents were reviewed. Nine workers were identified who had been diagnosed as having laryngeal cancer, using a conservative case definition that required medical record confirmation for any case among decedents and confirmation by a physician for any case among live individuals. Using data from national surveys of cancer incidence as referent rates, 3.44 laryngeal cancers would have been expected. Excess smoking by the exposed cohort compared with the United States population resulted in an upward adjustment of the expected number of cases of laryngeal cancer to 3.92. The standardised incidence rate ratio for laryngeal cancer was 2.30 (9/3.92), with a one sided p value of 0.01 (assuming a Poisson distribution). The finding of excess laryngeal cancer in this cohort is consistent with four other studies published since 1981.

Workers' compensation claims in Ohio were evaluated as a source of surveillance data for identifying workplaces at high risk of cumulative trauma disorders (CTDs) and analyzed for their demographic and industrial characteristics. During a 5-year period (1980 to 1984), 6,849 workers' compensation claims met the case criteria for CTDs. Tenosynovitis due to continuous motion was the most frequently reported condition (58%), and the wrist was the body part most frequently affected (48%). The highest case rate was observed for female workers in the 36 to 45 age group. Incidence rates for individual companies were determined and those with the highest rates for CTDs were identified. The employer-specific rates for CTDs based on workers' compensation claims data can be used as an effective surveillance tool in locating high-risk operations where ergonomic interventions can be implemented to reduce CTD hazards.

MBOCA (4,4' methylenebis (2-chloroaniline) is a structural analogue of benzidine and is carcinogenic in mice, rats, and dogs. MBOCA has not yet been demonstrated to be carcinogenic in humans and is not regulated as an occupational carcinogen in the United States. We report two noninvasive papillary tumors of the bladder identified in a screening study of 540 workers exposed to MBOCA during its production at a Michigan chemical plant from 1968 to 1979. Both tumors occurred in men under 30 years old who had never smoked. Although the prevalence of grade 1-2 tumors among asymptomatic males in this age group is unknown, the incidence of clinically apparent tumors on U.S. males aged 25-29 is only 1 per 100,000 per year. The detection of the two tumors in young, nonsmoking males is consistent with the hypothesis that MBOCA induces bladder neoplasms in humans.

To assess the mortality experience of a cohort of chemical workers in the Kanawha Valley of West Virginia, 29,139 males who worked at any one of three facilities over a 39-year period were followed-up for vital status. The facilities include two chemical manufacturing plants and a research and development center. From this cohort, 5,785 men were found to have died as of the study end, December 31, 1978. This was less than the 6,148.5 men expected to have died, based upon the United States white male population (standardized mortality ratio (SMR) = 94, 95% confidence interval (CI) = 92-96). Eighty-six specific causes of death were examined. Statistically significant increased deaths were observed for two causes; cancers of the liver (not specified as primary or secondary) (SMR = 174; CI = 102-280) and lympho- and reticulosarcoma (SMR = 140; CI = 104-187). When all biliary and liver cancer was examined by duration and time since initial employment, the SMR for those who worked at least 25 years and whose deaths occurred 30 years or more after first employment was 301 (95% confidence limit = 168-497). The identification and follow-up of this complete cohort provides the basis for future study of subcohorts with specific chemical and process exposures and case control studies of specific causes of death.