Exposure of UK industrial plumbers to asbestos, Part I: Monitoring of exposure using personal passive samplers

Epidemiological data suggest that there has been and may continue to be a significant risk to maintenance workers, who through their work may disturb asbestos-containing materials (ACM). The sampling and assessment of maintenance workers' exposure is a particular problem because they may not know that they are working with ACM. A strategy to monitor their true exposure has been developed and applied to one group of workers. The asbestos exposure of industrial plumbers was measured using personal passive samplers developed at the Health and Safety Laboratory (HSL). The light-weight samplers, which collect particles by electrostatic attraction, are simple to use and do not require prior knowledge that asbestos is to be disturbed as does conventional sampling. The samplers were issued by post and analysed, after return, using transmission electron microscopy (TEM). The strategy was found to be a reasonably efficient and cost-effective way to obtain data on maintenance worker's exposure to asbestos. The results of the TEM analysis of the passive samplers showed that the percentage of workers exposed to >5 microm long asbestos fibres was 62% in Round 1 and 58% in Round 2. For phase contrast microscopy equivalent (PCME) asbestos fibres, the values were 46 and 29%, respectively. The three samples with the highest numbers of fibres were followed up and were associated with plumbers working in areas which had supposedly been stripped of asbestos just prior to their starting work, suggesting that poor removal, clean-up and clearance practice presents a significant part of the risk to plumbers. Although flow rates will vary with conditions and time, an approximate average sampling rate from previous comparisons was used to calculate the concentration. This gave an average exposure to regulated PCME fibres of 0.009 f ml-1 for amphibole asbestos and 0.049 f ml-1 for chrysotile. The calculate risk based on the PCME fibre types collected and their estimated concentrations, showed that the risk from airborne amphibole fibres was approximately 6 times greater than from chrysotile fibres. If representative, the estimated lifetime risk of death from an asbestos related cancer for an exposure from age 20 for 40 years would be 68 per 100,000, which equates to an annual risk of death of the order of 10 per million.     

Environmental asbestos exposure in rural Turkey and risk of lung cancer

The aim of this study was to determine the risk of lung cancer in a cohort of villagers with environmental asbestos exposure. The study was carried out as a field-based epidemiological study. Information from 3143 individuals in 15 asbestos exposed villages and 2175 individuals in 12 control villages was obtained. Asbestos fiber type to which villagers were exposed mainly was tremolite or tremolite, actinolite, chrysotile mixtures. The cumulative fiber count of the villagers during their lifespan ranged from 0.19 to 4.61 fiber-years/ml. The annual average incidence ratio of lung cancer was 135.21/100,000 persons/year in men and 47.28 in women in the asbestos exposed villages. For the control villages, this ratio was 60.15/100,000 person/year in men and 15.06 in women. Being a male, advanced age, smoking and asbestos exposure were established to increase the risk of lung cancer. Environmental asbestos exposure in rural area is a risk factor for lung cancer independent of smoking.     

Pleural plaques and exposure to mineral fibres in a male urban necropsy population.

OBJECTIVES--The study aimed to evaluate the risk of pleural plaques according to the degree of past exposure to asbestos, type of amphibole asbestos, and smoking, as well as to estimate the aetiologic fraction of asbestos as a cause of plaques among urban men. METHODS--The occurrence and extent of pleural plaques were recorded at necropsies of 288 urban men aged 33 to 69 years. The pulmonary concentration of asbestos and other mineral fibres was analysed with scanning electron microscopy. The probability of past exposure was estimated from the last occupation. RESULTS--Pleural plaques were detected in 58% of the cases and their frequency increased with age, probability of past occupational exposure to asbestos, pulmonary concentration of asbestos fibres, and smoking. The risk of both moderate and widespread plaques was raised among asbestos exposed cases, and the risk estimates were higher for widespread plaques than for moderate plaques. The age adjusted risk was higher for high concentrations of crocidolite/amosite fibres than for anthophyllite fibres. The aetiologic fraction of pulmonary concentration of asbestos fibres exceeding 0.1 million fibres/g was 43% for widespread plaques and 24% for all plaques. The median pulmonary concentrations of asbestos fibres were about threefold greater among cases with widespread plaques than among those without plaques. No increased risk of pleural plaques was associated with raised total concentrations of non-asbestos fibres. CONCLUSION--The occurrence of pleural plaques correlated closely with past exposure to asbestos. The risk was dependent on the intensity of exposure. Due to methodological difficulties in detecting past exposures to chrysotile and such low exposures that may still pose a risk of plaques, the aetiologic fractions calculated in the study probably underestimate the role of asbestos.     

Dispersion of asbestos fibers and artificial mineral fibers (MMMF) inside truck cabs: a possible exposure of truck drivers]

Tests on samples of braided asbestos cord used in truck exhaust systems revealed a constant presence of chrysotile. Amosite fibres were also observed in many of the samples. Following a case of asbestosis in a truck driver, it was assumed that asbestos fibres could reach the driver's cab through the openings of the ventilation and heating system and also through the spaces between the bonnet and the floor of the driver's cab. Dust samples taken in the driver's cab of 10 (no.) trucks revealed the presence of asbestos fibres in 3 cases; MMMF were present in 7 cases, very likely originating from the noise insulation panelling. It is therefore suggested that there is a possible risk for truck drivers of exposure to asbestos and MMMF fibres dispersed inside the driver's cab.     

Lung cancer and mesothelioma in the pleura and peritoneum among Swedish insulation workers

OBJECTIVES: To estimate the risk of cancer and death in Swedish insulation workers some years after their exposure to asbestos had stopped. One hypothesis was that the risk of lung cancer would tend to decrease some years after the exposure had ended. METHODS: In a cohort study the cancer morbidity and cause of death was investigated in 248 insulation workers and compared with the corresponding morbidity and mortality in the general population. Due to stringent regulations, exposure to asbestos of all types had almost ended in Sweden in the mid- 1970s. Through a questionnaire, surviving insulation workers were asked about their exposure to asbestos and their smoking habits. RESULTS: Between 1970 and 1994 there were 86 deaths compared with the 46.0 expected (standardised incidence ratio (SIR) 1.9; 95% confidence interval (95% CI) 1.5 to 2.3), the increase was mainly due to an increased cancer mortality. The morbidity was increased for lung cancer (11 cases v 2.5 expected (SIR 4.4; 95% CI 2.2 to 7.9)), peritoneal mesothelioma (seven cases; no expected incidence could be calculated as the occurrence is too rare in the general population), cancer in pancreas (five cases v 0.7 expected (SIR 7.1; 95% CI 2.3 to 16.7)). No cases of pleural mesothelioma were found. The risk of lung cancer did not tend to approach that of the general population after the exposure to asbestos decreased. CONCLUSIONS: In the 1980s and the early 1990s, Swedish insulation workers still have a highly increased risk of diseases related to asbestos. The attributable risk for death and cancer was about 50%. The study also confirms the previous finding that mesothelioma in insulation workers seems to be situated in the peritoneum more often than in the pleura.     

Applying quality criteria to exposure in asbestos epidemiology increases the estimated risk

Mesothelioma deaths due to environmental exposure to asbestos in The Netherlands led to parliamentary concern that exposure guidelines were not strict enough. The Health Council of the Netherlands was asked for advice. Its report has recently been published. The question of quality of the exposure estimates was studied more systematically than in previous asbestos meta-analyses. Five criteria of quality of exposure information were applied, and cohort studies that failed to meet these were excluded. For lung cancer, this decreased the number of cohorts included from 19 to 3 and increased the risk estimate 3- to 6-fold, with the requirements for good historical data on exposure and job history having the largest effects. It also suggested that the apparent differences in lung cancer potency between amphiboles and chrysotile may be produced by lower quality studies. A similar pattern was seen for mesothelioma. As a result, the Health Council has proposed that the occupational exposure limit be reduced from 10 000 fibres m(-3) (all types) to 250 f m(-3) (amphiboles), 1300 f m(-3) (mixed fibres), and 2000 f m(-3) (chrysotile). The process illustrates the importance of evaluating quality of exposure in epidemiology since poor quality of exposure data will lead to underestimated risk.     

Lung cancer risk in male workers occupationally exposed to diesel motor emissions in Germany.

BACKGROUND: Although in several epidemiological studies exposure to diesel motor emissions (DME) shows an elevated lung cancer risk, it is still controversial whether DME is a human carcinogen. METHODS: In a pooled analysis of two case-control studies on lung cancer in Germany a total of 3498 male cases with histologically or cytologically ascertained lung cancer and 3541 male population controls were included. Information about lifelong occupational and smoking history was obtained by questionnaire. Drivers of lorries, buses, taxies, diesel locomotives and forklift trucks, bulldozers, graders, excavators, and tractors, were considered as exposed to DME and their cumulative exposure was estimated. All odds ratios were adjusted for smoking and asbestos exposure. RESULTS: The evaluation of lung cancer risk for all jobs with DME-exposure combined showed an odds ratio of OR=1.43 (95%-CI: 1.23-1.67). Most pronounced was the increase in lung cancer risk in heavy equipment operators (OR=2. 31 95%-CI: 1.44-3.70). The risk of tractor drivers increased with length of employment and reached statistical significance for exposures longer than 30 years (OR=6.81, 95%-CI: 1.17-39.51). The group of professional drivers (e.g., trucks, buses, and taxies), showed an increased risk only in West Germany (OR=1.44, 95%-CI: 1. 18-1.76), but not in East Germany (OR=0.83, 95%-CI: 0.60-1.14). DME-exposure in other traffic related jobs (e.g., diesel engine locomotive drivers, switchmen, forklift operators) was associated with an odds ratio of OR=1.53 (95%-CI: 1.04-2.24). CONCLUSIONS: The study provides further evidence that occupational exposure to diesel motor emissions is associated with an increased lung cancer risk.     

Exposure and mineralogical correlates of pulmonary fibrosis in chrysotile asbestos workers.

OBJECTIVES: The relation between lifetime cumulative exposure to asbestos, pathological grade of pulmonary fibrosis, and lung burden of asbestos at death, was explored in a necropsy population of former workers in a chrysotile asbestos textile plant in South Carolina. METHODS: Estimates of cumulative, mean, and peak exposures to asbestos were available for 54 workers. Necropsy records and lung tissue samples were obtained from hospital files. Matched control cases were selected from consecutive necropsies performed at the same hospitals. The extent and severity of pulmonary fibrosis was graded on tissue sections. Mineral fibres in lung tissue were characterised by transmission electron microscopy combined with x ray spectroscopy. RESULTS: A significant positive correlation (r = 0.67, P < 0.0001) was found between lifetime cumulative exposure to asbestos and total lung burden of asbestos fibres. This relation was also found for the individual types of asbestos associated with the exposure: chrysotile and tremolite. Pulmonary fibrosis was correlated with both cumulative exposure to asbestos (r = 0.60, P < 0.01) and the concentration of asbestos fibres in the lung (r = 0.62, P < 0.0001). The concentration of tremolite fibres in the lung provided a better estimate of lung fibrosis than did the concentration of chrysotile. Asbestosis was usually present in asbestos textile workers with more than 20 fibre-years cumulative exposure. The lengths and aspect ratios of chrysotile asbestos, but not amphibole asbestos, were greater in the lungs of asbestos fibre workers than in the control population. Textile workers with lung cancer had significantly greater cumulative exposures and fibrosis scores than workers without lung cancer. CONCLUSIONS: Both cumulative exposure to asbestos and lung fibre burden are strongly correlated with severity of asbestosis. The data also support the hypothesis that the high prevalence of asbestosis and lung cancer in this population resulted from exposure to long fibres of chrysotile asbestos in the workplace.     

Asbestos as reference material for fibre-induced cancer

The objective of this paper is to review published data on the carcinogenicity of asbestos fibres with regard to the elucidation of a potential risk originating from exposure to man-made vitreous fibres (MMVF). Steps in the comparison of the two fibre classes are characterization of the fibres, pulmonary deposition, biodurability and biopersistence and a review of the cancer risk from asbestos fibres after inhalation in rats and humans. Various dust samples of chrysotile, crocidolite, and amosite were used as reference materials in studies with experimental animals. These fibres are normally thinner and shorter than MMVF. These differences in dimensions cause differences in the deposition in the airways. In addition, significant dissimilarities exist in the deposition pattern between rats and humans. Data from biopersistence studies show that focusing only on fibres longer than 20 wm and using weighted half-time for a characterization of risk may be misleading. Inhalation experiments with rats need fibre exposure concentrations over 100 times higher to match the lung cancer risk of asbestos workers, and about 1000 times higher to reach the same mesothelioma risk. Also, the striking difference between the low lung burden of amphibole fibres of asbestos workers with mesothelioma and the more than 1000 times higher lung burden of rats with a low mesothelioma risk demonstrates the low sensitivity of the inhalation test model for the carcinogenic potency even of crocidolite fibres. It can be concluded that the rat inhalation model is also not sensitive enough to predict the cancer risk of other fibre types for humans.     

Mesothelioma associated with environmental exposures

BACKGROUND: The main sources of environmental, non-occupational exposure to asbestos or asbestiform fibres are: a) industrial plants in which asbestos was used in the production process; b) asbestos "in place" (mainly in buildings); c) contaminated soils. The association of these exposures with increasing risk of mesothelioma has been documented since 1960 in many places. OBJECTIVES AND METHODS: The present paper is aimed at describing the main results of studies performed in the locations with soils naturally contaminated with asbestos or asbestiform fibres. Environmental exposure data and asbestos-related health outcomes, mainly mesothelioma, are analyzed through a review of the literature. RESULTS: The sites with asbestos or other mesotheliomatogenous fibres in soils are characterized by low concentration levels of airborne fibres. Furthermore, exposure levels may increase when specific activities are carried out (mainly related to building construction), involving mechanical disturbance of fibre-containing materials. The type of fibres found are mainly amphiboles (tremolite). The population at risk of exposure is the general population, which can be exposed from birth. In these sites, the sex ratio of mesothelioma cases is close to 1.0 and the average age of cases ranges from 50 to 60 years. CONCLUSIONS: Both "natural"and industrial environmental asbestos or asbestiform fibre exposures increase potential risk for mesothelioma. Strategies of environmental reclamation and risk communication should be implemented in these areas.     

Health effects of asbestos exposure in humans: a quantitative assessment

Asbestos causes four diseases in humans: Lung fibrosis (asbestosis) follows heavy exposure and, in industrialized countries, is mainly a relic of past working conditions. The risk of pleural fibrosis and plaques is likely to be linearly dependent from time since first exposure and is present for all types of asbestos fibres. The diagnostic uncertainties regarding pleural plaques and the substantial degree of misclassification make it difficult to precisely estimate the shape of the dose-response relationship. The risk of lung cancer seems to be linearly related to cumulative asbestos exposure, with an estimated increase in risk of 1% for each fibre/ml-year of exposure. All fibre types seem to exert a similar effect on lung cancer risk; a multiplicative interaction with tobacco smoking has been suggested. Pleural mesothelioma is a malignant neoplasm which is specifically associated with asbestos exposure: the risk is linked with the cubic power of time since first exposure, after allowing for a latency period of 10 years, and depends on the fibre type, as the risk is about three times higher for amphiboles as compared to chrysotile. Environmental exposure to asbestos is also associated with mesothelioma risk.     

Airborne fibre concentrations and lung burden compared to the tumour response in rats and humans exposed to asbestos

The excess risk of tumours exposed to asbestos were previously compared with the results of rat inhalation experiments. It could be demonstrated that humans at the workplace suffer from a tumour risk at fibre concentrations which are 300 times lower than those needed in the rat inhalation model to produce the same risk. However, the estimation of human risk was based on the study of workers at a chrysotile textile factory, whereas animal experimental results were related to exposure to amphiboles. Since for this comparison the risk of cancer due to exposure to amosite or crocidolite fibres at the workplace is of interest, quantitative exposure-response relationships for lung cancer and mesothelioma for the white workforce of South African amosite and crocidolite mines were discussed. On comparing the risk of lung cancer in this study with the risk of lung cancer for chrysotile textile workers, it can be concluded, that the risk of lung cancer and mesothelioma from crocidolite and amosite was higher than in the chrysotile textile factory.It could be also demonstrated, on the basis of a study of the lung burden of mesothelioma cases and of controls, that a significantly increased odds ratio of about 5 was established at amphibole concentrations of between 0.1 and 0.2 f μg⁻¹ dry lung (WHO fibres longer than 5 μm from TEM analysis). On the other hand, carcinogenic response was observed at a fibre concentration 6000 times higher in animal inhalation experiments with crocidolite asbestos (SEM analysis of WHO fibres). As a result of these findings, it has been concluded that inhalation studies in rats are not sufficiently sensitive for the detection of hazards and risks to humans exposed to man-made fibres.     

The effect of asbestosis on lung cancer risk beyond the dose related effect of asbestos alone

Aims: To determine if the presence of asbestosis is a prerequisite for lung cancer in subjects with known exposure to blue asbestos (crocidolite). Methods: Former workers and residents of Wittenoom with known amounts of asbestos exposure (duration, intensity, and time since first exposure), current chest x ray and smoking information, participating in a cancer prevention programme (n = 1988) were studied. The first plain chest radiograph taken at the time of recruitment into the cancer prevention programme was examined for radiographic evidence of asbestosis according to the UICC (ILO) classification. Cox proportional hazards modelling was used to relate asbestosis, asbestos exposure, and lung cancer. Results: Between 1990 and 2002 there were 58 cases of lung cancer. Thirty six per cent of cases had radiographic evidence of asbestosis compared to 12% of study participants. Smoking status was the strongest predictor of lung cancer, with current smokers (OR = 26.5, 95% CI 3.5 to 198) having the greatest risk. Radiographic asbestosis (OR = 1.94, 95% CI 1.09 to 3.46) and asbestos exposure (OR = 1.21 per f/ml-year, 95% CI 1.02 to 1.42) were significantly associated with an increased risk of lung cancer. There was an increased risk of lung cancer with increasing exposure in those without asbestosis. Conclusion: In this cohort of former workers and residents of Wittenoom, asbestosis is not a mandatory precursor for asbestos related lung cancer. These findings support the hypothesis that it is the asbestos fibres per se that cause lung cancer, which can develop with or without the presence of asbestosis.     

Asbestos and colon cancer: lack of association in a large case-control study.

Previous studies linking exposure to asbestos with human colon cancer have used mortality rather than incidence as their endpoint and have neither assessed nor controlled for confounding by diet, genetic factors, or other risk factors for colon cancer. A case-control study of 746 histologically confirmed cases of colon cancer and 746 matched neighborhood controls was conducted in Los Angeles County, California. In univariate analyses of the 419 male pairs, a weak association was found between asbestos exposure and colon cancer (odds ratio (OR) = 1.16, 95% confidence interval (CI) 0.80-1.69). When confounding by family history of large bowel cancer, diet, body weight, and physical activity was controlled, there was no association between colon cancer and exposure to asbestos among males (OR = 0.99, 95% CI 0.66-1.50). When asbestos exposure was restricted to occurrences preceding diagnosis by more than 15 years, there was no clear association between such exposure and colon cancer, either before (OR = 1.14, 95% CI 0.76-1.70) or after confounding was controlled (OR = 0.93, 95% CI 0.60-1.44). Further analyses by frequency and duration of exposure failed to show any association between asbestos and risk of colon cancer, but did show a consistent pattern of confounding by nonoccupational factors that, when controlled, invariably produced a weak protective effect of asbestos exposure. Among the 327 female pairs, only 6 cases and 11 controls reported asbestos exposure (OR = 0.55, 95% CI 0.20-1.48), and there was no evidence of risk increasing as the frequency or duration of exposure increased. This study suggests not only that occupational exposure to asbestos is not a risk factor for colon cancer in the general population of Los Angeles, but also that observed associations between asbestos and colon cancer should not be interpreted as causal unless confounding by nonoccupational factors has been evaluated and controlled.     

Environmental exposure to asbestos in the area around Goor has been established as the cause of pleural mesothelioma in women

OBJECTIVE: To determine whether a disease cluster of 22 additional cases of pleural mesothelioma among women could be attributed to environmental asbestos exposure due to asbestos fibers from waste material on roads and property yards. The women studied were observed in an area with substantial environmental exposure to asbestos during the period 1989-2002. DESIGN: Ecological study. METHOD: In the study period of 1989-2002, all cases of mesothelioma among women, based on a strict histopathologic definition, occurring in the region of Twente, The Netherlands (n = 59) were provided by the regional cancer register. Additional information was collected on the occupational histories of the cases and their partners and addresses of residence through medical records, general practitioners, and next-of-kin. Environmental asbestos exposure was assigned to all cases that had had a long-term stay in a house in the area around Goor with demonstrated local environmental asbestos pollution and where any contact with asbestos through occupation or in the household had been excluded. RESULTS: In the risk area around Goor, out ofa total of 28 cases ofwomen with pleural mesothelioma, asbestos in the environment was found to be the only source of asbestos exposure for to women. In a further 4 women, environmental asbestos exposure was found to be the most likely cause of pleural mesothelioma. The average cumulative exposure was around 0.11 fiber/ml x exposure years. The observed extra incidence of 22 cases was attributed to the environmental exposure to asbestos in 64% (14/22) of cases. CONCLUSION: The environmental pollution to asbestos waste materials in the area around Goor was the main cause of the strongly increased incidence of pleural mesothelioma among women in this area. Taking into account an equal risk among men, the consequences of asbestos exposure in the area around Goor in the next 25 years are likely to result in 2 cases of pleural mesothelioma each year.     

Exposure to asbestos fibres during gasket removal

In the chemical industry, asbestos gaskets have been used extensively to prevent leakage between solid surfaces. The purpose of this study was to assess the potential personal exposure to asbestos fibres during gasket removal and thus to determine what is reasonably required in terms of protective regime and work method. Two groups were studied: group A, who only removed gaskets if they could be removed easily and without breaking; and group B, who removed gaskets which were left by the first group. For both groups, the gasket was first made wet before removal. The samples were analysed using phase-contrast microscopy and transmission electron microscopy. The average exposure to fibres for group A, averaged over the work period, was 0.04–0.242 fibres ml⁻¹ as determined by phase-contrast microscopy. On further analysis with transmission electron microscopy it was found that only four of the 11 samples contained asbestos in very low concentrations and that most of the fibres, which were identified using phase-contrast microscopy, probably originated from the glass fibre lagging around the pipes. For group B the average fibre concentration, averaged over the work period, as determined by phase-contrast microscopy, ranged between below the detection limit and 0.02 fibres ml⁻¹. The subsequent transmission electron microscopy analysis shows that the exposure to asbestos fibres ranged between below the limit of detection to 0.004 fibres ml⁻¹. This study shows that the exposure to asbestos fibres during gasket removal activities was well within the 8-h average exposure limit of 0.3 fibres ml⁻¹.     

Occupational exposures and lung cancer in New Caledonia

Aims: To study the associations between occupational exposures and the risk of lung cancer in New Caledonia.

Methods: All cases diagnosed between January 1993 and December 1995 (228 lung cancers) and 305 population controls were included. Detailed information on lifetime job history, smoking, and other potential risk factors was collected by interview. Occupational exposures were assessed from the questionnaires by an industrial hygienist, without knowledge of case-control status.

Results: No significant association was found with exposures related to nickel mining and refining, the main industrial activity in the territory. Among men, an excess risk of lung cancer was found for bus and truck drivers. Increased risks were also observed in men with the highest level of cumulative exposure to cleaning products and inorganic fertilisers. Exposure to field dust was associated with lung cancer risk in both sexes, and risk increased with cumulative exposure level. In some areas tremolite asbestos derived from local outcroppings was used as a whitewash. The association between exposure to field dust and lung cancer was limited to men and women exposed to this whitewash—that is, living in areas where the soil may contain tremolite.

Conclusion: This study shows several associations between occupational exposures and lung cancer. The findings suggest that exposure to tremolite fibres from cultivated fields may increase the risk of lung cancer in New Caledonia.

     

Asbestos, cement, and cancer in the right part of the colon.

OBJECTIVE--The aim was to investigate associations between exposure to mineral fibres and dust, and cancer in subsites within the large bowel. DESIGN--Pooled retrospective cohort studies. SUBJECTS AND SETTINGS--Blue collar workers, employed for at least one year in different trades; asbestos cement or cement workers (n = 2507), other industrial workers (n = 3965), and fishermen (n = 8092). MAIN OUTCOME MEASURES--Standardised incidence ratios (SIRs, national reference rates) were calculated for cause specific cancer morbidity between 1958 and 1989. The observation period began 15 years after first employment. RESULTS--The asbestos cement and cement workers had a slightly increased risk of colorectal cancer (SIR 1.5; 95% confidence interval (95% CI) 1.1-2.0). This was due to an increase only in the right part of the colon (SIR 2.5; 95% CI 1.6-3.8). The ratio of right (7th revision of the International Classification of Diseases ICD-7) 1530-1531)/left (ICD-7 1532-1533) colon cancer among the asbestos cement and cement workers of 4.8 differed significantly from the ratio both among the other blue collar workers (0.4) and among the fishermen (1.5). As the sensitivity and accuracy was insufficient, mortality data did not show the excess of cancers in the right part of the colon. CONCLUSIONS--An increased incidence of cancer in the right part of the colon was evident in the asbestos cement and cement workers. The distribution of cancers within the colon was noticeably different from that in other blue collar workers, indicating that our findings cannot be explained by socioeconomic confounding factors. A detailed and appropriate disease classification, based on incidence data, is necessary in order not to obscure or underestimate effects of exposure in epidemiological studies on colorectal cancer.     

The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure

Mortality reports on asbestos exposed cohorts which gave information on exposure levels from which (as a minimum) a cohort average cumulative exposure could be estimated were reviewed. At exposure levels seen in occupational cohorts it is concluded that the exposure specific risk of mesothelioma from the three principal commercial asbestos types is broadly in the ratio 1:100:500 for chrysotile, amosite and crocidolite respectively. For lung cancer the conclusions are less clear cut. Cohorts exposed only to crocidolite or amosite record similar exposure specific risk levels (around 5% excess lung cancer per f/ml.yr); but chrysotile exposed cohorts show a less consistent picture, with a clear discrepancy between the mortality experience of a cohort of xhrysotile textile workers in Carolina and the Quebec miners cohort. Taking account of the excess risk recorded by cohorts with mixed fibre exposures (generally<1%), the Carolina experience looks uptypically high. It is suggested that a best estimate lung cancer risk for chrysotile alone would be 0.1%, with a highest reasonable estimate of 0.5%. The risk differential between chrysotile and the two amphibole fibres for lunc cancer is thus between 1:10 and 1:50.Examination of the inter-study dose response relationship for the amphibole fibres suggests a non-linear relationship for all three cancer endpoints (pleural and peritoneal mesotheliomas, and lung cancer). The peritoneal mesothelioma risk is proportional to the square of cumulative exposure, lung cancer risk lies between a linear and square relationship and pleural mesothelioma seems to rise less than linearly with cumulative dose. Although these non-linear relationships provide a best fit ot the data, statistical and other uncertainties mean that a linear relationship remains arguable for pleural and lung tumours (but not or peritoneal tumours).Based on these considerations, and a discussion fo the associated uncertainties, a series of quantified risk summary statements for different elvels of cumulative exposure are presented.     

Asbestos and colon cancer: a weight-of-the-evidence review.

What is the evidence that exposure to asbestos causes colon cancer? This weight-of-evidence review considers epidemiologic evidence from cohort studies of asbestos-exposed workers, case-control studies of colon cancer, animal bioassays, and other corroborative evidence. The major evidence for a causal association at high exposure is a combined colorectal standardized mortality ratio (SMR) of 1.5 for asbestos cohorts where the lung cancer SMR was greater than twofold. However, misdiagnosis may spuriously elevate the SMR. The strongest evidence against a causal association between colon cancer and asbestos exposure is the lack of an exposure-response gradient in asbestos cohorts where trends for lung cancer are observed. Population-based case-control studies of colon cancer do not show any consistent risk associated with asbestos exposure. Long-term ingestion studies show no evidence of an increased incidence of colon cancer in animals by this route of exposure and do not provide biological plausibility for a causal association between asbestos exposure and colon cancer.