Philip E. Enterline

Asbestos and cancer: a cohort followed up to death.

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.

ASBESTOS EXPOSURE: FACTORS ASSOCIATED WITH EXCESS CANCER AND RESPIRATORY DISEASE MORTALITY

A cohort of 1075 men who completed their working lifetimes with an asbestos company, worked at a facility in the United States, and retired with a company pension during the period 1941--67 was updated for deaths through 1973. The average length of employment was 25 years, and all had been exposed to asbestos dust. Respiratory cancer and pneumoconiosis-pulmonary fibrosis mortalities were examined in relation to cumulative dust exposure and to other factors after taking into account cumulative dust exposure. Men who worked in the production of asbestos cement pipe exhibited a higher risk of respiratory cancer, as did men with some crocidolite asbestos exposure. Because these two groups overlap, we could not be certain that crocidolite asbestos was responsible for the increased risk. Men working in general plant maintenance displayed a striking lack of deaths due to pneumoconiosis-pulmonary fibrosis, as compared with production workers and with maintenance personnel assigned to specific departments. Five mesothelioma deaths were observed at age 65 and over. Three of these deaths occurred during the period 1970--3.

Mortality among a cohort of US man-made mineral fiber workers: 1985 follow-up.

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.

Type of asbestos and respiratory cancer in the asbestos industry.

Differences in the physical properties and chemical composition of the various types of asbestos indicate that there should be differences in their carcinogenic potentials. This study of the mortality experience of 1,348 retirees from the asbestos industry shows that, after adjustment for cumulative dust exposure, men exposed only to chrysotile asbestos had a respiratory cancer mortality rate 2.4 times the expected, whereas men exposed to a combination of chrysotile and crocidolite asbestos had a mortality rate 5.3 times the expected. Since crocidolite was used largely in the asbestos cement industry, this was studied separately. Men who manufactured asbestos cement shingles and sheets containing only chrysotile asbestos had a respiratory cancer risk 1.4 times the expected, whereas men who manufactured asbestos cement pipe containing both chrysotile and crocidolite asbestos had a respiratory cancer risk 6.1 times the expected.

Respiratory cancer in relation to occupational exposures among retired asbestos workers

Enterline, P., de Coufle, P., and Henderson, V. (1973).British Journal of Industrial Medicine,30, 162-166. Respiratory cancer in relation to occupational exposures among retired asbestos worker. A cohort of 1 348 men who completed their working lifetime in the asbestos industry and retired with an industry pension during the period 1941-67 was observed through 1969 for deaths. The average length of employment in the asbestos industry for these men was 25 years and all had exposures to asbestos dust. In some instances these exposures were very high and continued for many years. Mortality for this cohort of men after age 65 was 14·7% higher than for the entire population of United States white men living at the same ages and time periods. This excess was due almost entirely to cancer and respiratory disease. The cancer excess was chiefly due to respiratory cancer where mortality was 2·7 times the expected. The respiratory disease excess was entirely due to asbestosis. A time-weighted measure of asbestos dust exposure at the time of retirement was calculated for each man. This was made up of the summed products of dust levels for each job (expressed in mppcf) and years at each level. This measure was directly related to the respiratory cancer excess at ages 65 and over, ranging from 1·7 times expected for men with less than 125 mppcf-years exposure to 5·6 times expected for men with 750 or more mppcf-years exposure. There appeared to be no direct relationship between asbestos dust exposure and respiratory cancer below 125 mppcf-years. Important increments in respiratory cancer mortality apparently occurred somewhere between 100 and 200 mppcf-years exposure. Separation of the effects of time from the effects of average dust level on respiratory cancer mortality showed that the contribution of each was about the same and that a time-weighted measure of asbestos dust appears to be an appropriate method for predicting respiratory cancer effects.

Lung cancer among women residing close to an arsenic emitting copper smelter.

Lung cancer deaths occurring between 1935 and 1969 among women residing near an arsenic emitting smelter were examined. For three geographically defined exposure groups, the observed and expected number of lung cancer deaths were compared. In none of the exposure groups did the observed number of deaths exceed the expected. However, an index of exposure based on distance of residence from the smelter and duration of residence in the area was 27% higher for cases than for age-matched controls (p = .10). Adjusting for a latency of 20 yr, case exposures were 23% higher than for controls (p = .07). Dividing individuals into quintiles of exposure yielded odds ratios ranging from 1 to 1.6 (test of trend, p = .07).

The health of retired fibrous glass workers.

A total of 416 men, retiring during the period 1945 to 1972 from six plants engaged mainly in the manufacture of fibrous glass insulation, were studied to see how their mortality experience compared with that of white men in the entire United States living in comparable age and time intervals. The mean follow-up period from first exposure was about 30 years. Overall mortality was low and there was no evidence of an excess in respiratory cancer mortality. No mesotheliomas were noted. For 115 men retiring from the same six plants during the period 1945 to 1972 due to a disability the distribution of disabilities by cause was compared with an expected distribution based on the experience of the Social Security Administration. This comparison showed no evidence of any unusual health hazards among fibrous glass workers, except a possible excess in chronic bronchitis.

Cancer Produced by Nonoccupational Asbestos Exposure in the United States

There is considerable evidence of asbestos fibers in the general environment, and asbestos fibers can be found In the lungs of most adults In urban areas of the western world. Concentrations in large urban areas appear to average around 3 ng/m3 of air and in rural areas around 0.1 ng/m3 of air. For the entire U.S. population it can be estimated that the average population exposure is 1.5 ng/m3. Based on the results of case control and other studies, It is estimated that about a third of the 1000 or so cases of malignant mesothelloma that occur In the U.S. each year appear to be related to this type of nonoccupational asbestos exposure. This Is a lifetime risk of 100 per million population. Lung cancer caused by asbestos In the general environment can be estimated from linear extrapolations of dose-response data arising from occupational studies. Using data from a study of retired asbestos products workers it Is estimated that the lifetime risk of lung cancer due to continuous asbestos exposure at 1.5 ng/m...

Evaluating cancer clusters

We have had considerable success in identifying cancer causing agents in the workplace using epidemiologic methods. This success had made us very sensitive to the occurrence of cancer clusters among workers in the belief that identification of some common exposure could reveal the presence of a carcinogen and lead to preventive measures. This intense surveillance is both a blessing and a curse. On the one hand, it is a proven way of discovering environmental causes of cancer. On the other, it leads to false alarms or does not always lead to identification of a causal agent. It is easy to demonstrate, using tables of random number 5, how clusters can occur by chance and to demonstrate that when the number of comparisons made in identifying clusters is known there is a basis for their evaluation. Unfortunately, in most instances, when cancer clusters are detected in the workplace the number of comparisons made is unknown and the statistical significance of the cluster cannot be evaluated. Moreover, it is not usually recognized that in this situation when a study is made as a result of discovering a cluster in a particular population, the cases that make up the cluster cannot be included in a data set which tests the hypothesis that a cluster exists. This paper illustrates the above points by actual experiences.

Mortality of workers potentially exposed to epichlorohydrin.

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.