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OBJECTIVE: This is an update of an earlier study on the relation between exposure to arsenic in air and deaths from respiratory cancer. The purpose was to verify earlier findings of a supralinear dose response relation and to examine relations with other cancers, particularly those reported in studies on drinking water. METHODS: An earlier study of 2802 men who worked at a copper smelter for a year or more during the period 1940-64 and who were followed up for deaths during the period 1941-76 was updated until 1986. Estimates of exposure for the period 1977-1984 were added. RESULTS AND CONCLUSIONS: The additional follow up confirms the earlier finding that at low doses the increments in death rates for respiratory cancer for a given increment in dose are greater than at high doses. The additional follow up also shows significant increases in cancer of the large intestine and bone, and SMRs > 150 for cancer of the buccal cavity and pharynx, rectal cancer, and kidney cancer. There was a positive relation between exposure to arsenic in air and kidney and bone cancer, but none for the other cancers, except respiratory.

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Four new or updated epidemiologic studies were presented at a meeting on the health effects of gasoline exposure held in Miami, Florida, November 5-8, 1991. A focus of these studies was whether there is a relationship between gasoline exposure and kidney cancer and leukemia. For gasoline distribution workers, who have a relatively high exposure, there was some evidence for a kidney cancer relationship in three studies but none in the fourth. There was evidence for an acute myelocytic leukemia relationship in three studies. The fourth study dealt only with kidney cancer. It is possible that the benzene content of gasoline was responsible for the leukemia findings. It is uncertain whether gasoline exposure is a cause of kidney cancer.

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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.

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Literature published in the years 1934-1965 was reviewed to determine attitudes and opinions of scientists as to whether asbestos is a cause of cancer. In Germany, the issue was decided in 1943 when the government decreed that lung cancer, when associated with asbestosis (of any degree), was an occupational disease. In the United States, however, there was no consensus on the issue until 1964. Opinions of scientists over a 22 year period are shown and the contributions of various cultural, social, economic and political factors to these opinions are discussed. A lack of experimental and epidemiological evidence played a major role in delaying a consensus. Other important factors included a rejection of science conducted outside of the U.S. during this period, particularly a rejection of German scientific thought during and after WWII, and a rejection of clinical evidence in favor of epidemiological investigations. Individual writers rarely changed their minds on the subject of asbestos as a cause of cancer.

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A historical cohort study was conducted to evaluate the mortality experience of 6,831 employees of the Shell Oil Company, Deer Park, Texas, petroleum refinery and chemical plant with emphasis on cancer mortality. Subjects were all workers with potential plant exposure who were employed for at least 3 months during 1948-72. Vital status was determined as of 12/31/83 for 98% of the cohort and death certificates were obtained for 95.4% of 1,180 observed deaths. The statistical analyses excluded 159 female study members. For all causes of death combined, all cancers combined, and for most of the nonmalignant disease categories examined, there were deficits in mortality among refinery workers, chemical plant workers, and workers with experience in both areas. These deficits were generally most pronounced for chemical plant workers. An analysis of specific cancer sites revealed patterns of increased risk suggestive of a possible relationship between occupational exposures in the refinery and lympho-reticulosarcoma. Patterns of increased risk were also observed among chemical plant workers for a category of lymphopoietic tissue cancers, including multiple myeloma, myelofibrosis, polycythemia vera, and certain non-Hodgkin's lymphomas. Some very limited evidence of a possible workplace association was also found among refinery workers for leukemia and cancers of the central nervous system and biliary passages/liver. No evidence was found of an increased risk for cancer of the respiratory system or stomach or for malignant melanoma. A work history review of all suspect cancer excesses failed to identify any common work areas, job assignments, or exposure potentials, although the lack of detailed data on specific chemical exposures precluded accurate assessments of exposure-response.

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In the cohort of American MMMF workers reported by ENTERLINE et al. [Ann. occup. Hyg. 31, 625-656 (1987)] autopsies were recorded in 652 (13.5%) of 4840 deaths. Lung tissue samples were sought from all pathologists and obtained in 145 (22.2%), together with similar samples from 124 matched referents. Lung fibre counts by phase contrast microscopy were 60% higher (P less than 0.05) in workers than referents. Electron microscopy (ATEM) also showed more fibres of all kinds--MMMF, asbestos and other--but no convincing excess of any one type. Lung samples of only 26% of workers contained any MMMF, almost all siliceous in nature and in low concentration. There were too few cases of lung cancer (19) for any useful conclusion; however, in the plant with the highest lung cancer SMR (200), and a probable mesothelioma, amosite at greater than 1.0 fibres per micrograms (f micrograms-1) was found in four of six workers but in none of their matched referents. Although our findings contribute little to the interpretation of the results obtained by ENTERLINE et al. they indicate the potential value of tissue analyses in monitoring epidemiological studies of MMMF exposure.

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This 1983 to 1985 update of an earlier study examined the mortality experience of 16,661 man-made mineral fiber workers employed 1 year or more (6 months for two plants) during 1945 to 1963 (1940 to 1963 for one plant) at one or more of 17 US manufacturing plants. Using local death rates to estimate expected deaths there was a small statistically significant (P less than .05) excess in all malignant neoplasms (standardized mortality ratio [SMR] = 108.3) and in respiratory cancer (SMR = 112.1) for the total period 1946 to 1985. For respiratory cancer the excess was greatest for mineral wool workers. For glass wool workers and glass filament workers respiratory cancer SMR values were much lower. For workers exposed in the production of small-diameter fibers, the overall respiratory cancer SMR was slightly elevated but lower than in earlier reports. A total of four malignant mesotheliomas have now been noted on death certificates. Two of these were coded to the International Classification of Disease rubrics used to estimate 1.45 expected mesothelioma deaths for the total study. Overall, the evidence of a relationship between exposure to man-made mineral fibers and respiratory cancer appears to be somewhat weaker than in the previous update.

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Race is an important determinant of disease frequency, yet the race of subjects in retrospective epidemiologic studies is frequently unknown. If addresses are available, the race of study subjects may be estimated from the racial composition of the blocks on which they have resided. Such information can be obtained from census block statistics for Standard Metropolitan Statistical Areas and, with the 1990 Census, probably for the entire United States. The authors assigned black race to persons on blocks with greater than 60% black residents and white race to those residing on blocks containing less than 40% blacks. The validity of the procedure was tested on 341 decedents of known race who resided at the time of death within the Detroit, Michigan, Standard Metropolitan Statistical Area. Thirteen individuals who lived on blocks with 40-60% blacks were excluded from analysis, as well as 18 others for whom racial composition of blocks could not be ascertained. In 293 (94%) of the remaining 310 persons, race assigned on the basis of census information agreed with race obtained from death certificates. This method should prove useful for assigning race to study subjects lacking racial identification.

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An epidemiological study was undertaken to determine whether the animal carcinogen, epichlorohydrin (ECH), produces cancer in man. A total of 863 workers with probable exposure to ECH at two chemical plants during 1948-65 were followed up for deaths up to 1983. Twenty years or more after first exposure the all cancer SMR was 112.2 (22 deaths) and the SMR for leukaemia was 500.0 (three deaths), which is statistically significant. All cancer, leukaemia, and most other causes of death were related to estimated levels of exposure to ECH, except violence. The most consistent (both plants) relation was between exposure level and heart disease. Overall, the heart disease SMR 20 years or more after first exposure was 39.2 (five deaths) for low exposure and 105.4 (17 deaths) for high exposure. Limited evidence of a cardiovascular disease relation to ECH production in one other epidemiological study is supported by this study. Allyl chloride used in the production of ECH may play a part. The relation of heart disease and exposure does not appear to be an artifact, although the fact that many other causes of death were also related to exposure argues against a causal relation.

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Multistage modeling incorporating a time-dependent exposure pattern is applied to lung cancer mortality data obtained from a cohort of 2802 arsenic-exposed copper-smelter workers who worked 1 or more years during the period 1940-1964 at a copper smelter at Tacoma, Washington. The workers were followed for death through 1976. There were 100 deaths due to lung cancer during the follow-up period. Exposures to air arsenic levels measured in micrograms/m3 were estimated from departmental air arsenic and workers urinary arsenic measurements. Relationships of different temporal variables with excess death rates are examined to judge qualitatively the implications of the multistage cancer process. Analysis to date indicates a late stage effect of arsenic although an additional early stage effect cannot be ruled out.

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A cross-sectional study of 788 male employees of an aluminum production company examined the relationship of radiographic abnormalities to smoking and dust exposure from the mining and refining of bauxite to alumina. Among the aluminas produced were low temperature range transitional forms. The present analyses were limited to nonsmokers and current smokers. Two National Institute of Occupational Safety and Health (NIOSH)-certified "B" readers interpreted the radiographs. The predominant radiographic abnormalities noted were scanty, small, irregular opacities in the lower zones of profusion 0/1 to 1/1. Rounded opacities were rare. Among nonsmokers with low dust exposures, the prevalence of opacities greater than or equal to 1/0 showed no trend with increasing age and duration of exposure, suggesting no relationship between age and prevalence of opacities of Category 1 or more in this cohort (p greater than 0.10). Nonsmokers who had accumulated higher dust exposures showed a trend of increasing prevalence of opacities with increasing duration, suggesting an effect of occupational exposure at higher cumulative exposure levels (p less than 0.05). In most exposure categories, smokers exceeded nonsmokers in their prevalence of opacities greater than or equal to 1/0; the overall prevalence among smokers being 12 and 11% according to Readers A and B, respectively, compared with 4% in nonsmokers (p less than 0.01). In conclusion, 7 to 8% of aluminum workers in this cohort had radiographic findings of scanty, small, irregular opacities, the prevalence of which was increased among smokers (p less than 0.01). There was a moderate increase in the prevalence of opacities with increasing tenure in nonsmokers with high cumulative exposures (p less than 0.05).

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Previous studies of the relationship between arsenic levels and respiratory cancer among copper smelter workers have not directly accounted for possible effects of SO2 exposure and cigarette smoking. This is a report on the 1949-1980 mortality experience of 6,078 white male workers who worked at least 3 years between 1 January 1946 and 31 December 1976 at one or more of eight US copper smelters. The completeness of the cohort was verified statistically, and worker exposures to arsenic, SO2, dust, nickel, cadmium, and lead were estimated from retrospective industrial hygiene surveys reported elsewhere. By using internal controls, a dose-response relationship for lung cancer was observed with exposure to arsenic and SO2. When cigarette smoking data were included with arsenic and SO2 exposure data in a nested case-control analysis, only smoking and arsenic were statistically significant factors. The arsenic-lung cancer relationship was confined to a single smelter associated with high content feed. In the remaining smelters mortality for all causes of death and for all cancer was not high based on comparisons with national, state, and local rates.

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Deaths and death rates for mesothelioma of the pleura are presented by age, sex, and geographic area for the United States for the years 1968-81. Death rates increased with age and in every age group were roughly three times higher for males than for females. Over the period 1968-81, death rates increased for males aged 65 years or more, whereas death rates in other age-sex groupings remained fairly constant or declined slightly. It is known that asbestos is highly related to mesothelioma, and the increase in death rates among older males could be due to asbestos. Conversely, the fact that death rates in younger males and in females have not been increasing suggests some kind of background level not strongly related to the use of asbestos. When the geographic distribution of death rates was examined by state, there was considerable geographic variation with some clustering. High death rates for males appeared for the Northeastern States and along the Pacific Coast, and for Illinois, Florida, Wyoming, and Colorado. Females shared this geographic pattern to some extent. When death rates were examined by county, a relationship was seen between pleural mesothelioma deaths among males and the presence of asbestos products plants and shipbuilding facilities. Excessive death rates in some counties and states did not appear to be related to asbestos exposure. Although the similarity in geographic patterns of mortality for males and females suggests a common etiology, the trends in mortality suggest different etiologies. There may be important causes of pleural mesothelioma yet to be identified.

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The mortality experience of 1074 white men who retired from a United States asbestos company during the period 1941-67 and who were exposed to asbestos working as production and maintenance employees for the company is reported to the end of 1980 when 88% of this cohort was known to be dead. As noted in earlier reports the mortality for respiratory and gastrointestinal cancer was raised. A more detailed examination of causes of death shows that the excess in gastrointestinal cancer was largely due to a statistically significant excess in stomach cancer. A statistically significant excess was also noted for kidney cancer, cancer of the eye, and non-malignant respiratory disease. Eight deaths from malignant mesothelioma were observed, two of which were peritoneal. Asbestos exposures for these mesothelioma cases were low relative to other members of the cohort. Continuing follow up of this cohort shows a dose response relation for respiratory cancer that has become increasingly linear. Standardised mortality ratios peaked 10 to 15 years after retirement and were relatively constant at around 250 in each five year interval starting in 1950. This excess might have been detected as early as 1960 but certainly by 1965. The mortality experience of this cohort reflects the ultimate effects of asbestos since nearly all of the cohort has now died.

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This paper is a reanalysis of data on the respiratory cancer mortality experience of 2,802 men who worked one year or more during the period 1940-1964 at a copper smelter in Tacoma, Washington. Exposure estimates presented earlier have been recalculated and perhaps improved. While the previous analysis showed only a weak relation between respiratory cancer and arsenic exposure, use of new data shows a much stronger relation--but one that is concave downward and not ordinarily considered for environmental exposure and cancer. This new analysis indicates that arsenic is probably more potent as a carcinogen than indicated by other studies. It also demonstrates the distinction between airborne arsenic and the bioavailability of arsenic, and the importance of this distinction for risk assessment. When a dose-response relation is based on airborne concentrations of arsenic, it is clearly concave downward, but when based on urine concentrations, it appears to be linear.

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Partly because of the poor quality of exposure information on humans, most lifetime carcinogenic risk assessments have been based on animal data. There are, however, surrogate measures for exposure that have not been fully utilized. One of these is duration of exposure where data on mean exposure levels are available. A method is presented for the use of such data, and the method is illustrated by developing a risk assessment from the available epidemiologic literature on gasoline and kidney cancer. This risk assessment is fairly consistent across studies and close to a risk assessment based upon an experiment with rats. While there needs to be much improvement in the quality of environmental data available to epidemiologists, it is possible that a number of risk assessments can be made from existing epidemiologic data and efforts directed away from extrapolation from animal data.

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