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Regulatory authorities from developing countries have expressed a need for guidance in locating environmental, health and safety (EHS) information on industrial chemicals. In response, possible sources were identified via a search of the Internet using relevant terms and by soliciting suggestions from more than 200 knowledgeable stakeholders. This initially identified greater than 100 databases, 41 of which were chosen for further profiling and analysis based on their size and comprehensiveness. They were divided for analysis into three distinct groups: (1) data portals that provide information seekers with an efficient simultaneous search of multiple, third-party owned and maintained databases; (2) primary EHS information sources; and (3) databases that provide only EHS-type regulatory decisions but not raw data. Descriptive evaluations of each database were performed, including: (1) scope; (2) ease of access and use; (3) breadth and depth of EHS information available; (4) quality of the underlying information; and (5) procedures to keep the information current. We conclude that, although there exists EHS information to support screening level hazard and risk assessment for the majority of the highest production volume chemicals, information gaps for lower production volume chemicals persist, and Confidential Business Information claims for some chemicals can limit the information available to the general public. A lack of information on uses and exposures to chemicals, particularly in developing countries is especially challenging. Nevertheless, there are reasons (e.g. advances in regulations, marketplace pressures, and computational toxicology science) to be optimistic that going forward information gaps can be closed at an accelerated rate.

Recently published papers have alleged that exposures to endocrine disrupting chemicals (EDCs) are causing substantial disease burdens in the EU and US and are consequently costing society hundreds of billions of dollars annually. To date, these cost estimates have not undergone adequate scientific scrutiny, but nevertheless are being used aggressively in advocacy campaigns in an attempt to fundamentally change how chemicals are tested, evaluated and regulated. Consequently, we critically evaluated the underlying methodology and assumptions employed by the chief architects of the disease burden cost estimates. Since the vast majority of their assigned disease burden costs are driven by the assumption that "loss of IQ" and "increased prevalence of intellectual disability" are caused by exposures to organophosphate pesticides (OPPs) and brominated flame retardants (PBDEs), we have taken special care in describing and evaluating the underlying toxicology and epidemiology evidence that was relied upon. Unfortunately, our review uncovered substantial flaws in the approach taken and the conclusions that were drawn. Indeed, the authors of these papers assumed causal relationships between putative exposures to EDCs and selected diseases, i.e., "loss of IQ" and "increased prevalence of intellectual disability", despite not having established them via a thorough evaluation of the strengths and weaknesses of the underlying animal toxicology and human epidemiology evidence. Consequently, the assigned disease burden costs are highly speculative and should not be considered in the weight of evidence approach underlying any serious policy discussions serving to protect the public and regulate chemicals considered as EDCs.

For the purpose of assessing the human carcinogenic potential of the chlorophenoxy herbicides MCPA, MCPP, and 2,4-DP, the relevant epidemiological and toxicological evidence is reviewed. These compounds have not produced tumours in animal studies conducted under current test guidelines, giving no reason to predict that they would be carcinogenic to humans. Epidemiological studies have been conducted on three continents; greater emphasis is placed on the studies reported from western Europe, however, as this has been the area of more use. Although several of these studies provide suggestive evidence of associations between exposure to chlorophenoxy compounds and increased risks for some uncommon cancers, it is inconsistent and far from conclusive. None of the evidence specifically implicates MCPA, MCPP, or 2,4-DP as human carcinogens.

The need to notify individuals of a possible health risk from their past exposure to potentially hazardous agents frequently extends beyond workers to include community groups. The issues to consider in community notification are frequently similar to those that are important for worker notification but may include some that are unique. This case study traces the evolution of one company's strategy for communicating with the public about possible dioxin contamination associated with its operations. Early communications tended to emphasize the technical aspects of the issues in the fashion of scientists talking to other scientists. This was interpreted by some to be symptomatic of an arrogant and uncaring attitude. Beginning in the early 1980s, the company's management recognized the need to reach out to a variety of audiences on multiple levels, and shifted to a more comprehensive communications strategy. A similar shift is now occurring throughout the chemical manufacturing industry as top managers realize that, if they expect to continue to operate, they must become more accountable and responsive to the public.

Recognizing the importance of early detection of breast cancer, the Dow Chemical Company initiated a breast cancer awareness program in 1988. Evaluation of operational aspects of mammography screening component revealed that about half (53%) of 1186 eligible women in the evaluation cohort took part, although participation was three times higher for active than for retired employees. Eleven per cent of participants were considered to have "positive" screens, ie, had roentgenogram films with suspicious areas, and at least 82% of these women had follow-up medical services within 1 year of screening, as determined by a review of group insurance claims records. Two women with positive mammograms were subsequently diagnosed and treated for breast cancer within 2 months of screening. None of the women with negative mammograms developed breast cancer in the subsequent year. The suitability of group insurance data resources for responding to health care delivery questions is discussed.

Mortality was updated another 11 years through 1986 for a previously studied cohort of 2904 male chemical workers who were potentially exposed to styrene and related materials for a year or more between 1937 and 1971. Substantial deficits in mortality from all causes and total cancer were observed in the cohort when it was compared with white males in the United States, and also other chemical workers who were unexposed to styrene-based products. Mortality from leukemia was slightly less than expected during the updated period, in contrast to an excess of lymphatic leukemia observed in the original period. Yet small elevations in risk of other types of lymphatic cancer, particularly multiple myeloma, persisted. The risk of these cancers did not increase with estimated intensity or duration of styrene exposure. The findings are discussed in context with those of studies of similarly exposed workers in related industries.

To estimate prevalence of back pain and joint problems in employees of a chemical manufacturing company, a questionnaire was administered during medical surveillance examinations between 1987 and 1989. Among 5903 employees completing the questionnaire 35.4% reported back or joint pain during the past year. Back pain lasting 30 days or more occurred in 5.3% of employees, while joint pain and/or swelling occurred in 19.3% of employees. A physician visit was involved for 10.5% and 11.1% of employees reporting back pain and joint problems respectively. A trend of increasing prevalence with increasing age was significant (P less than .001) for all musculoskeletal outcomes. Unadjusted prevalence of back pain and joint problems was significantly higher among men and among whites. After adjusting for age, race, and occupation using logistic regression, the difference in prevalence for the two sexes was diminished or reversed. Similarly, differences in race were diminished when other variables were controlled. Differences in prevalence by occupation were attenuated after adjustment for age, gender, and race. Back pain tended to be reported more frequently for managers, back pain and joint problems for technicians, and back pain requiring physician visit for craftsmen. Self-reported back pain and joint problems during the previous year vary more by age and occupation and less by gender and race in this employed population.

Cohort mortality and nested case-control studies were conducted involving 2,901 men employed 1 year or more between 1940 and 1986 at any of four California facilities of a major chemical company. Employees experienced fewer deaths from each of the major causes than were expected based on U.S., California, and local county mortality rates. Respiratory cancer was significantly elevated in one socioeconomic category comprised of operators (SMR = 157, 95% CI = 109-220). The 34 cases who died from respiratory cancer and 136 matched controls, all of whom were operators, were included in a nested case-control study. Departments in which subjects had worked were grouped into 13 work assignment or product categories by an industrial hygienist without knowledge of case-control status. Smoking habits and other occupational exposures were ascertained by telephone interview from subjects or surrogate-responders. As expected, current cigarette smoking was strongly related to respiratory cancer. After adjustment for smoking, cases were significantly more likely than controls to have ever worked in one of the 13 work areas (supervision, services, and business support). However, no dose-response relationship was evident with duration of employment in this work area and the departments involved were associated with plant security and not chemical production. Results were similar when a 15-year latency period was assumed. These findings suggest that the excess of respiratory cancer mortality among operators was most likely due to differences in cigarette smoking or other factors not ascertained, rather than to a specific occupational exposure.

We tested the predictive utility of the health belief model (HBM) for adherence with a complex, ongoing medical regimen in the context of a chronically ill youthful population (56 adolescent outpatients with insulin-dependent diabetes mellitus; mean age = 14 years). A three-construct model of health beliefs was tested: Threat (perceived susceptibility combined with severity), Benefits-Costs, and Cues to seek treatment. Multiple indicators of compliance were used, and metabolic control was measured by glycosylated hemoglobin. The Benefits-Costs and Cues constructs were related to compliance in the theoretically expected positive direction. Threat interacted with Benefits-Costs in the prediction of compliance and with Cues in the prediction of metabolic control. The greatest compliance was achieved with low perceived Threat and high perceived Benefits-Costs. Poor metabolic control was associated with high Threat and Cues. As age increased, adherence to the exercise, injection, and frequency components of the regimen decreased.

The phenoxy herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) is widely used to control the growth of weeds and broadleaf plants. We convened a panel of 13 scientists to weigh the evidence on the human carcinogenicity of 2,4-D. The panel based its findings on a review of the toxicological and epidemiological literature on 2,4-D and related phenoxy herbicides. The toxicological data do not provide a strong basis for predicting that 2,4-D is a human carcinogen. Although a cause-effect relationship is far from being established, the epidemiological evidence for an association between exposure to 2,4-D and non-Hodgkin's lymphoma is suggestive and requires further investigation. There is little evidence of an association between use of 2,4-D and soft-tissue sarcoma or Hodgkin's disease, and no evidence of an association between 2,4-D use and any other form of cancer. Scientists on the panel were asked to categorize 2,4-D as a "known," "probable," "possible," or "unlikely" carcinogen or as a noncarcinogen in humans. The predominant opinion among the panel members was that the weight of the evidence indicates that it is possible that exposure to 2,4-D can cause cancer in humans, although not all of the panelists believed the possibility was equally likely: one thought the possibility was strong, leaning toward probable, and five thought the possibility was remote, leaning toward unlikely. Two panelists believed it unlikely that 2,4-D can cause cancer in humans.

Background: This 5-year study of the Dow Chemical Texas Operations 1984-1985 Smoking Cessation Incentive Program (SCIP) evaluated the smoking habits of 1,097 participants and 1,174 nonparticipants., Results: We observed, via questionnaire and saliva cotinine data, that participants were 2.3 times more likely to be long-term (greater than or equal to 5 years) nonusers of tobacco than nonparticipants (10.2% vs 4.4%, P less than or equal to 0.01). However, smoking cessation rates for 3-4 years, 1-2 years, and less than 1 year were similar for participants who remained smokers at the conclusion of SCIP and nonparticipants. Age and the interaction between the management job category and having quit smoking for at least 30 days sometime prior to the worksite program were important predictors of smoking cessation among participants. Thirty-six percent of the participants who were considered exsmokers of 6 months duration at the conclusion of the program in 1985 remained long-term quitters 5 years later. Stress and enjoyment of smoking were the two most important reasons provided by participants for recidivism., Conclusions: The results of this 5-year evaluation demonstrate the heterogeneity of employee participation and success with a worksite smoking cessation program.

There are few epidemiologic data available to address the question of potential carcinogenic effects of hydrogen chloride (HCl) exposure on humans. An opportunity arose to augment a nominal HCl exposure classification that had been done earlier for a nested case-control study of lung cancer among a cohort of chemical manufacturing employees. Working from first-hand knowledge of the relevant chemical processes and limited HCl monitoring data, a certified industrial hygienist estimated average exposures for each of the job assignments of 308 lung cancer cases and 616 comparison workers. The risk of lung cancer was then analyzed in relation to several measures of HCl exposure, including duration, a cumulative exposure score, highest average exposure, and latency. None showed evidence of an association between HCl exposure and lung cancer. This is consistent with the limited rodent bioassay data, which also failed to find a tumorigenic response from HCl. Thus, even at high level occupational exposures (up to 3000 micrograms/m3 for several years) there is no evidence that HCl is a human carcinogen.

Nonparticipants in general population health surveys have been found to be less healthy than participants, but data on nonparticipants in work-site health surveys have been more scarce. We compared cause-specific mortality among 11,156 male employees of The Dow Chemical Company who participated in at least one work-site health examination between 1967 and 1978 with 6915 employees who did not participate. The nonparticipants experienced higher mortality rates for nearly every cause of death examined but particularly from smoking and alcohol-abuse related diseases. This was especially true during the first 5 years of follow-up, suggesting that some employees do not participate because they are already ill. These findings have important implications for the use of examination data for both primary and secondary disease prevention purposes, and these are discussed.

This paper identifies the parties to which epidemiologists are obligated and explores the areas in which potential conflicts of obligations can occur. It is concluded that all epidemiologists, regardless of the organizational context in which they operate, share similar obligations to their subjects, society, their employer or funding agency, and their colleagues. The fundamental principals inherent to an epidemiologist's obligation to protect the public health is to identify real health problems and promote their resolution. It is in everyone's interest, including private industry, to respect those principals, and an industry supported epidemiology program can be an effective means for accomplishing that. These programs can be innovatively designed to protect those fundamental principles and thereby avoid conflicts of interest. This is illustrated with some examples from the epidemiology program operated at The Dow Chemical Company.

The purpose of this study was to investigate the determinants of spermatogenesis recovery among 30 azoospermic and 17 oligospermic workers who had a maximum of 18 months of exposure to 1,2-dibromo-3-chloropropane during 1976 to 1977. A maximum of 11 years of follow-up data were examined. Of the 26 azoospermic subjects who voluntarily participated in follow-up, 19 (73.0%) showed evidence of spermatogenesis recovery. Thirteen azoospermic subjects recovered to normospermic levels; however, their mean most recent sperm count (44.4 million/mL) was significantly lower (P less than .01) than the mean (88.8 million/mL) of the 17 oligospermic subjects who recovered to normospermic levels. The lack of spermatogenesis recovery was definitively shown to be job (drumming and canning) and, possibly, age related. Duration of exposure and the initial 1977 categorization of exposure (high, moderate, and low) were not predictive of recovery. Testicular atrophy was observed with azoospermia, and the testicles subsequently increased in size among those azoospermic subjects who returned to normospermic levels. The follicle-stimulating hormone level in 1977 was significantly associated with azoospermia as well as the likelihood of return to normospermia among the azoospermic subjects.

Worksite smoking cessation intervention programs have become increasingly popular, although program evaluations are often unavailable. In 1984, the Texas Operations of Dow Chemical USA offered a Smoking Cessation Incentive Program (SCIP) to its employees. SCIP was a highly publicized, upbeat program that had the active support of management and union. Altogether, 7,516 employees (95.4% of all employees) were surveyed about their smoking habits; 28.3% identified themselves as smokers. A total of 1,113 employees voluntarily enrolled in SCIP from March 1, 1984, through March 1, 1985. Smoking cessation methods included a buddy program, nicotine-containing chewing gum, American Lung Association self-help material and group clinics, and incentive prizes. SCIP registrants, compared to employees identified as smokers in a pre-program survey who did not participate in SCIP, were significantly (P less than .01) more often females, whites, administrators, professionals, heavier smokers, and smokers who had tried to quit at least two times prior to SCIP. There were 326 (29.3%) SCIP participants who quit smoking for at least one month during SCIP. A total of 265 (23.8%) succeeded at quitting for at least six months and remained ex-smokers at the end of the program. Logistic regression analysis showed administrators had significantly higher six-month or more rates of quitting than did professionals, craftsmen, operators or clerical workers.(ABSTRACT TRUNCATED AT 250 WORDS)

A recent cohort mortality study of male, hourly wage employees of a large Michigan chemical production and research facility had found a greater than expected number of deaths coded to liver and biliary tract cancer. In response, an additional investigation was then undertaken of the 44 liver and biliary tract cancer deaths observed between 1940 and 1982. A random sample (N = 1,888) of subjects was selected from the total cohort (N = 21,437) to serve as referents. Company work history records were used to classify cases and referents by work area assignment and potential for exposure to 11 selected chemical agents which have been shown to produce cancer of the liver or biliary passages in experimental animals. Statistically significant associations in both positive and negative directions were found for several work areas within the facility. A suggestive association was found for vinyl chloride monomer, based on five cases with presumed exposure.

This study evaluated the concordance between occupation and industry listed on death certificates with actual work history information for a group (n = 5,882) of long-term (10 years or more) workers at a chemical company. Match rates were calculated as the percent of death certificate occupation and company entries that were confirmed by work history data using 3-digit 1980 U.S. Census Bureau group codes. The concordance rate for industry differed by employment status at death: employed, 94.9%; inactive, 30.8%; and retired, 91.1%. Concordance on occupation was analyzed for employed (n = 467) and retired (n = 932) subjects who had computerized work histories (randomly done prior to the study) and who had matched on the company on the death certificate. Concordance ranged from 0 to 50% for the first job, to 50 to 70% for the last job, longest job, and longest job in the last 10 years of company employment. The most consistent predictor of concordance was job duration. Misclassification was reviewed by occupational category. Results from this and other investigations lead to the inevitable conclusion that usual occupation data from death certificates are grossly inadequate for studies of occupational risks.

A plant-based case-control study was undertaken to investigate a possible excess of brain tumor mortality identified at a Texas Chemical plant from a sample-based cohort study. Work histories and presumptive exposures of 28 former employees who had died of primary intracranial neoplasms were contrasted with those of two matched comparison groups in an effort to identify a possible etiologic agent. Because the sample-based cohort study suggested they might be at increased risk, those employees hired prior to 1945, those employed from one to four years and those employed for 20 or more years were studied separately. No statistically significant associations were found, although an elevated risk was suggested for employment in the machine shop prior to 1945 based on three exposed cases.

A general mortality survey was done on a 5% random-start systematic sample (N = 1,666) of present and former white male employees of a Texas chemical plant. The purpose was to determine whether there were any unusual patterns of cause-specific mortality that would require further research with case-control studies. Mortality risks were examined by duration of employment and year of hire as surrogates for more specific exposure data. Among all employees in the sample, there was significant excess mortality due to All Cancer, Ill-Defined Conditions, and All External Causes of Death, and a significant deficit from All Circulatory Diseases. The excess mortality from All Cancer was primarily attributable to excess cancers of the kidney, lung, and pancreas. The excesses for lung and kidney cancer were statistically significant. Those employed for 1 year or more experienced significantly lower mortality from All Causes than those employed for less than 1 year.

This cohort study evaluated mortality patterns, 1940 through 1982, of 2,192 chemical workers who, having engaged in the manufacture of higher chlorinated phenols and derivative products, had potential occupational exposures to chlorinated dioxins. Relative to United States white male mortality experience, there were no statistically significant deviations from expected for the following categories: all causes, total malignant neoplasms, or specific malignancies of particular interest: stomach cancer, liver cancer, connective and other soft-tissue cancer, the lymphomas, or nasal and nasopharyngeal cancer. For the cirrhosis of the liver category, internal comparisons demonstrated increasing trends associated with duration of employment in the Chlorophenol Production and Finishing areas; but available evidence suggests this finding was related to alcohol abuse. The study does not support a causal association between chronic human disease as measured by mortality and exposures to the higher chlorinated phenols, derivative products, or their unwanted contaminants, the chlorinated dioxins.

Mortality was updated through 1982 for 611 arsenic-exposed employees originally studied through 1973. In the earlier report, total mortality was observed to have been below the comparable U.S. population; however, mortality was significantly elevated for respiratory cancer. The focus of the update was on respiratory cancer and of special interest was whether the risk of respiratory cancer remained in excess for individuals alive as of the end of the last study. In the update, 9 additional respiratory cancers were observed subsequent to 1973, the end of the follow-up in the original study, versus 7.8 expected. The risk ratio for the time-interval 1974-1982 (standardized mortality ratio SMR = 116) was diminished compared to that reported in the original study (SMR = 330). When the entire study period was analyzed, the risk of respiratory cancer did not appear to decline with interval since exposure cessation. Analyses by duration of arsenic exposure and interval since first exposure did not reveal any obvious dose-response relationships.

Forty-four asymptomatic male subjects were examined for their nasal carriage of strains of Staphylococcus aureus capable of producing staphylococcal toxic shock antigen (TSA), an exotoxin implicated in the pathogenesis of toxic shock syndrome. In addition, the levels of antibody to TSA in sera from these subjects were determined by an enzyme-linked immunosorbent assay. S. aureus was isolated from the anterior nares of 23 subjects. Of those 23 isolates of S. aureus, 9 were found to produce TSA. All individuals carrying strains of S. aureus capable of producing TSA had high to moderate levels of antibody to TSA. In contrast, those individuals carrying strains not producing TSA had levels of antibody to TSA ranging from high to nondetectable. A second examination of nasal samples from 42 of these subjects revealed that 86% of those carrying S. aureus initially still carried S. aureus after a period of 3 months; all subjects found to carry TSA-producing strains initially and that were examined a second time yielded TSA-producing strains once again.

A nested case-control study conducted among a cohort of chemical manufacturing employees provided an opportunity to test the hypothesis that lung cancer risk is inversely related to dietary intake of vitamin A. Eligible for study were 308 former male employees who had died of lung cancer between 1940 and 1980. Two control groups, one a decedent and the other a "living" series, were individually matched to the cases one-for-one. Interviews were completed with 734 subjects or their next-of-kin and included a food frequency list. A vitamin A index was developed for each subject based on the frequency of consumption of 29 food items. After adjustment for a number of potentially confounding variables (e.g., smoking, educational level, and use of vitamin supplements), there was evidence that vitamin A intake was inversely associated with lung cancer risk. The effect was most pronounced in the comparisons with the "living" controls and appeared strongest among cigarette smokers. Subjects in the lowest tertile of vitamin A intake had approximately twice the risk of lung cancer as those in the highest. Analyses of an index of carotenoids and of individual food items suggested that plant sources of vitamin A may play a more important role in producing the effect than do animal sources.

A recent cohort mortality study of 19,608 male employees of a major Texas chemical production facility had suggested that they might be at higher risk of lung cancer compared with the male population of the United States or Texas but not with the male population of the five-county area in which they reside. An occupational exposure was a possible explanation for this pattern, and a nested case-control study was undertaken of the 308 lung cancer deaths observed between 1940 and 1981. Two control groups, one a decedent and the other a "living" series, were individually matched to cases one-for-one. Interviews were conducted with subjects or their next of kin to collect information on smoking and other potential confounders. These data were combined with employee work history records and industrial hygiene data to form the basis of the analyses. Traditional stratification methods and conditional logistic regression were employed to examine for effect modification and to control confounding. Statistically significant, positive and negative associations were found for assignment to several work areas within the facility. Suggestive associations were observed for exposure to sulfur dioxide and heat. These and additional associations are discussed relative to evidence from other studies.

An in-plant case-control study of 26 renal cancer deaths was conducted to determine whether an occupational exposure may be related to an apparent increase in mortality from this disease observed among a sample of employees at a multiple process chemical production facility. None was found that explained the excess. Elevated odds ratios were identified for employment in the cell maintenance area of chlorine production and with those presumptive exposures considered to occur in this job, asbestos and caustic, but not chlorine. While an association between renal cancer and asbestos has been previously reported, an association with caustic, per se, is not consistent with prior observations made by others. Diminished risk estimates were observed for employment in magnesium production and for exposures in this process to sulfur dioxide and heat. Both the increased and decreased risks, while statistically significant, are based on small numbers of exposed subjects and may be spurious owing to the problem of multiple comparisons.

Recent studies have reported an increased risk of death from primary intracranial neoplasms among employees in the petrochemical industry. One of them, a NIOSH/OSHA county-based case-control study, suggested a twofold risk for having ever been employed at the Texas Division of Dow Chemical U.S.A. Using the case-control approach, we compared 24 brain tumor cases among employees at this large, diverse chemical plant in Texas with two sets of age-, race-, and sex-matched controls to determine if a risk could be associated with job assignment in a particular process area, with presumptive exposure to a major process chemical, or with a number of other occupationally related and unrelated variables. Results implicated no specific area or chemical. The only significant findings were an elevated odds for being hired prior to 1950 and a negative correlation with employment greater than 10 years. Further, preliminary calculations of expected deaths from primary intracranial neoplasms among the employee cohort suggested there was no excessive risk.

There have been many investigations of cognitive development in older hearing-impaired children, but few with preschool hearing-impaired children. The performance of 40 hearing and 40 hearing-impaired children of preschool age (2 1/2 to 5 1/2 years) was compared on five nonverbal cognitive tasks and three subtests from the Perceptual Performance subscale of the McCarthy Scales of Children's Abilities (1972). For this set of tasks there was a significant effect of age consistent with a developmental change. A one-way MANCOVA on all dependent measures with age as the covariate revealed no significant differences between the hearing-impaired and hearing children. The results suggest that despite a deficiency in language abilities, the cognitive development of young hearing-impaired children is comparable to that of hearing children of the same age.

The question as to whether or not any or all of the phenoxy herbicides are carcinogenic to humans continues to be evaluated. We review the evidence available from the retrospective cohort and case-control epidemiology studies. Graphs of the individual probability densities for the odds ratios from the eight case-control studies of soft-tissue sarcoma, Hodgkin's disease, or non-Hodgkin's lymphoma demonstrate gross inconsistencies which are not likely to be attributable to chance. Early studies, conducted in Sweden, had indicated strong associations, but subsequent work from New Zealand and the United States has failed to substantiate those findings. The reasons for the discordant results may relate more to methodologic problems in the earlier studies than to qualitative or quantitative differences in the exposures of the underlying populations. The retrospective cohort studies offer the advantage of having focused on occupational groups believed to have had the highest exposures, although they have been criticized as being individually too small to assess the risks of the rarer forms of cancer. Consideration of the combined cohort studies of workers exposed to the phenoxy herbicides per se provides little or no evidence of carcinogenicity. Thus, the total weight of evidence currently available does not support a conclusion that the phenoxy herbicides present a carcinogenic hazard to humans.

Available medical and morbidity surveillance findings from 1976 to 1978 for two employee cohorts potentially exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were compared with those of matched unexposed employees. The medical surveillance findings were derived from a screening programme offered to all active employees and included an analysis of various medical history questions and blood chemistry results. Group medical insurance claims served as the source of morbidity surveillance data and the period prevalence of selected diseases was analysed. Few significant differences between the exposed and unexposed were detected. Among the cohort of employees potentially exposed during the manufacture of 2,4,5-trichlorophenoxyacetic acid (2,4,5,-T), a significantly greater frequency of x-ray proved ulcer was reported and significantly more members of this group had diseases of the digestive system diagnosed. Such findings were absent in the more highly TCDD-exposed cohort engaged in 2,4,5-trichlorophenol production, making it unlikely that dioxin was a cause.

Cause specific mortality was surveyed among 37,682 male employees with three or more days of service between 1940 and 1982 at the Midland or Bay City, Michigan, locations of Dow Chemical USA. Vital status was ascertained through 1982 for 97.5% of the cohort members, and death certificates were obtained for 97.1% of the 7,751 decedents. Comparisons of observed mortality with expected levels based on any of three general population groups (US, Michigan, or seven local counties) consistently demonstrated lower mortality in the cohort from each of the major causes of death, including total malignant neoplasms. Unique among hourly employees was significant excess mortality in the categories of cancer of other lymphatic tissue, and motor vehicle accidents, and both hourly and salaried nonexempt employees experienced significantly higher mortality from other and ill-defined cancers. The influence of duration of employment and age at and period of hire were explored with the Mantel-Haenszel method as adapted for a cohort study. Results were evaluated both including and excluding the mortality experience of subsets of employees with past exposure to known human carcinogens (arsenic, asbestos, bis-chloromethyl ether, benzene, organic dyes, and vinyl chloride). The use of the general mortality survey in monitoring whether or not there are major health problems among the employees and in setting research priorities is emphasized.

The prevalence of selected illnesses and symptoms during 1977-85 was compared between 175 employees potentially exposed to the organophosphate insecticide chlorpyrifos and 335 matched controls with no history of exposure to organophosphates. Subjects were subdivided into three exposure intensity groups on the basis of job title and air monitoring data for dose response testing. This classification scheme was shown roughly to correlate with plasma cholinesterase inhibition in the workers. No statistically significant differences in illness or prevalence of symptoms were observed between the exposed and unexposed groups or among the three exposure subgroups. Potentially exposed employees did report symptoms of dizziness and of malaise and fatigue relatively more often than subjects from the comparison group; however, further analyses by exposure level, process area, or time did not support a relation with exposure. No cases of peripheral neuropathy were seen among the exposed workers. Although the sample size was small and the statistical power limited, the cumulative exposures likely to have been experienced by this workforce exceed those to be expected for individuals using the product as recommended. The absence of exposure related adverse effects, including neurological impairment, is reassuring.

The mortality experience of 371 employees assigned to acrylamide monomer and polymerisation operations was examined with particular emphasis on cancers at sites identified from animal studies such as the central nervous system, thyroid gland, other endocrine glands, and mesotheliomas. A total of 29 deaths was observed up until 1982 (38.0 expected). No statistically significant excesses were noted in the total cohort and no deaths were found for the hypothesised sites of cancer. The observed deaths in the total cohort for the all cancers category were somewhat in excess (11 v 7.9); however, this was due entirely to excess cancers of the digestive tract and respiratory system in the subgroup with previous exposure to organic dyes. Among those employees not exposed to organic dyes, four deaths were due to malignancies versus 6.5 expected. This study does not support a cause effect relation between exposure to acrylamide at this work site and overall mortality, total malignant neoplasms, or any specific cancers.

Mortality is reported to the end of 1982 for 878 chemical workers potentially exposed to 2,4-dichlorophenoxyacetic acid (2,4-D) at any time between 1945 and 1983. Observed mortality was compared with expected levels based on adjusted rates for United States white men and for other male employees from this manufacturing location who were not exposed to 2,4-D. Because of a recently reported increased incidence of astrocytomas in male rats fed the highest dose level of 2,4-D, special attention was given to deaths from brain neoplasms in the cohort. None was observed. The absence of an increased risk of brain cancer in people exposed to 2,4-D is supported by studies of other exposed populations and those studies are briefly reviewed. Moreover, in the present study, analyses by production area, duration of exposure, and cumulative dose showed no patterns suggestive of a causal association between 2,4-D exposure and any other particular cause of death.

Cause-specific mortality was surveyed among 19,608 male employees with 1 or more years of service between 1940 and 1980 at the Texas Operations of Dow Chemical U.S.A. Vital status was ascertained through 1980 for 97.3% of the cohort members, and death certificates were obtained for 96.4% of the 3,444 decedents. Mortality risks were found to vary, depending upon which of 3 population groups (United States, Texas, and local counties) was used for comparison, although significantly fewer than expected deaths from all causes was a common finding due to significant deficits in diabetes, diseases of the circulatory system, and cirrhosis of the liver. Significantly more deaths were from ill-defined conditions and cancers of unspecified sites. Lung cancer was significantly elevated in comparisons with the incidences in the United States and Texas, but not in comparison with those in the local counties. The influence of age at hire, period of hire, duration of employment, interval since entry into cohort, employment status, and two measures of social class--educational level and job category--were explored with the use of the Mantel-Haenszel method as adapted for a cohort study. Findings from these analyses are discussed in relation to the observations of other investigators and in the context of the possible impact of these findings on future studies of this work force.

Using a modification of the traditional cohort mortality methodology, risk estimates of death due to brain tumors were calculated for production and nonproduction employees of Dow Chemical U.S.A., Texas Division. A total of 25 malignant, benign and unspecified brain tumors were identified using a geographically limited record-linkage process. Expected deaths were extrapolated from 1,666 white males in a 5% sample of the 1940 through 1977 total workforce. The resulting sample-based standardized mortality ratios (which were not evaluated for statistical significance) suggest, at most, only a slight increased risk of mortality from brain tumors for the overall time period. There was, however, a probable elevated risk associated with first employment prior to 1945. To date, diminished risk has been noted for those hired during subsequent years.

There have been many studies conducted of mortality in occupational cohorts, but few of cancer incidence. Two major facilities of the Western Division of Dow Chemical USA are located fortuitously within an area covered by the population-based California Tumor Registry, which allowed linkage of records to identify incident cancers among 1,403 male workers. Using adjusted county rates for comparison, 49 new cancers were observed in the cohort from 1969 through 1983, whereas 63.0 were expected (standardized incidence ratio = 78, 95% confidence limits = 53 to 103). Nonsignificant excesses were noted for several cancer groups among some categories of workers; however, there was no predominant tumor type within the groups. The successful completion of this collaborative project suggests that using population-based tumor registries for surveillance of occupational cohorts is feasible.

This study provided 2 additional years of follow-up through 1984 for a previously studied cohort of 2192 employees potentially exposed to chlorinated dioxins. A separate analysis was done of the subgroup of 323 workers who had chloracne. No clear evidence was found for a causal association between any cause of death and potential occupational exposures to the higher chlorinated phenols, derivative products, or the chlorinated dioxins. Particular focus was directed at mortality from cancers of the stomach, liver, connective and other soft tissue, nasal and nasopharynx, and the lymphomas. Analyses by various indices of exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin and hexa- to octachlorinated dioxins did not show deaths from these cancers to have been disproportionately distributed among the workers considered to have had the highest exposures.

A retrospective cohort mortality study was conducted among men employed for one or more years, between 1940 and 1969, at an operating division of a large chemical company. Vital status follow-up for the cohort of 1,919 men was determined through 1979 and identified 390 deaths. Overall mortality in the study group and in each of eight employment subgroups was less than that of the corresponding United States white male population. Additionally, standardized mortality ratios were not significantly elevated for any of the examined cause-of-death categories. Cause-specific mortality comparisons were also made among the employment subgroups and by duration of employment in the company division using an internal analysis method. There were no relationships observed for employment duration. Several significant differences (p less than 0.05) by employment subgroup were noted; however, neither the decreases nor increases presently could be ascribed to identifiable environmental factors.

Mortality was updated to the end of 1982 for 594 employees exposed to benzene who had been studied previously and for an additional 362 exposed workers not studied previously. Cause specific mortality comparisons were made using United States white male, age, and calendar year adjusted rates. Total mortality was observed to have been significantly below expectation, and this was particularly evident for deaths from accidental causes. Mortality from skin cancer was significantly raised, although there were no unusual or common characteristics among the affected individuals which would suggest a link with exposure to benzene. A non-significant excess of total deaths from leukaemia was noted based on four observed cases; however, all four were myelogenous leukaemias and this represented a significant excess in that subcategory. These and other deaths of possible interest are reviewed in detail. Analyses by work area, duration of exposure, and cumulative dose index did not show patterns suggestive of a causal association between exposure to benzene and any particular cause of death.

Cause-specific mortality was evaluated by period of hire for 37,682 male chemical workers in order to test the hypothesis that employees hired during World War II (1941-1945) were at increased risk for selected causes of death. One recent study of refinery workers reported that those hired during the war years had experienced greater mortality from external causes (accidents, homicides, and suicides), alcoholism, and cancers of several sites relative to employees hired before or after the war. In the present study, employees were divided into three period-of-hire subcohorts: prior to 1941, 1941-1945 (World War II), and 1946 and after. Comparison of observed mortality among these subcohorts through 1982 was made with expected levels based on age- and calendar year-specific U.S. white male rats. Neither hourly nor salaried employees hired during the war showed evidence of higher mortality from homicide, suicide, alcoholism, or any of the selected cancer types suggested from the refinery study. Hourly, but not salaried, war years new hires experienced excessive mortality from only those accidents involving motor vehicles. Possible reasons for the discrepant findings between this and the earlier study of refinery workers are discussed, with methodological differences being dismissed.