Retention of Asbestos Bodies in the Lungs of Welders

Examination of asbestos bodies (AB) retained in the lungs is a useful way of assessing past occupational exposure to this material. AB retention has been extensively studied in workers directly exposed to asbestos, but less so in those end users, such as welders, who use asbestos-containing products. We therefore retrospectively studied AB retention in 211 welders, for whom biological testing procedures had been requested by a chest physician, between 1988 and 1991. Optical microscopy of AB was performed on samples of sputum (40 subjects), bronchoalveolar lavage fluid (BAL) (147 subjects), and lung tissue obtained after thoracotomy (38 subjects). Information on previous jobs and exposure was obtained using a questionnaire (the mean duration of welding activities was 16.6 years). Eighty-two subjects (38.9%) had elevated lung retention of AB in all the samples studied. Significant AB retention occurred in only 30% of sputum samples, but in 40.1% of BAL samples and 39.5% of lung tissue samples. The duration of welding activities correlated with the density of AB in BAL or lung tissue (r = 0.31, p < 0.01 and r = 0.49, p < 0.05, respectively). On the basis of the questionnaire, only two of the welders with significant AB retention had other occupational exposure to asbestos. Our findings suggest that welding activities may increase lung retention of AB, and consequently might produce higher risks of fibrotic and/or malignant pulmonary diseases. These potential risks need to be brought to the attention of doctors; a longitudinal follow-up may also be warranted in such populations, even after individuals have ceased their welding jobs.     

Role of occupational asbestos exposure in Hungarian lung cancer patients

Objective: What is the frequency of occupational asbestos exposure among patients suffering from malignant respiratory tumours and how many of these tumours are associated with asbestos in Hungary? Methods: An internationally established questionnaire with 29 questions, covering the most characteristic activities of asbestos exposure at the workplace was completed for 300 patients with respiratory malignancies, i.e. 297 patients with lung cancer and three with mesothelioma of the pleura. From the questionnaire, the smoking habits were estimated and cumulative asbestos exposure was assessed in fibre-years. Additionally, lung X-rays were classified and the national data on the incidence of malignant pleura mesothelioma were analysed. Results: A cumulative asbestos exposure of 25?fibre-years or more was detected in 11 patients with lung cancer (4%) and in each of the three patients with pleural mesothelioma (100%). In a further 72 patients (24%), cumulative occupational asbestos exposure was assessed as below 25?fibre-years (between 0.01 and 23.9?fibre-years). In this group, car and truck mechanics, and installation and construction workers using asbestos-cement were registered. Among patients with an asbestos exposure of 25?fibre-years or more, six asbestos-cement production workers were observed, among them the three mesothelioma cases. A weak but significant association between positive X-ray findings and exposure estimates could be demonstrated. Additionally, results of the lung tissue fibre counts by scanning transmission electron microscopy were available for 25 of the lung cancer patients. A good correlation was observed between the asbestos fibre counts and the assessment of cumulative asbestos exposure. In Hungary, 84 cases of pleural mesothelioma were registered in 1997 and 73 in 1998. These numbers correspond to an annual incidence of about one new case per 100,000 inhabitants older than 15?years. Conclusions: The annual incidence of lung cancer in Hungary is about 6,000. Since in our series of lung cancer patients about 4% were observed, which could be accepted as representing occupational disease because of a cumulative exposure to 25?fibre-years or more, the annual asbestos related lung tumour incidences may be estimated to be approximately 150 or more. The proportion of nearly two estimated cases of lung cancer per case of pleural mesothelioma corresponds to international experience. Up to now, lung cancer cases only exceptionally have been registered as occupational diseases, i.e. they were seriously under-diagnosed in Hungary. For improving this situation, diagnostic assistance by a self-interview with a questionnaire covering the working history for all newly diagnosed lung cancer patients would be helpful.     

The role of smoking and exposure to asbestos and man-made vitreous fibers in a questionable case of mesothelioma

A remaining uncertainty in the U.S. cohort study of man-made vitreous fiber (MMVF) workers is whether asbestos exposure contributed to 10 questionable cases of mesothelioma. We report further details on one case from our previous mesothelioma investigation, including results of a recent lung tissue analysis. Case is a 68 year-old white male employed 1951-54 in a rock/slag wool plant where asbestos-containing products were manufactured. Cause of death was recorded as "mesothelioma, malignant, right pleural cavity" (ICD9: 163.9). Analysis for presence of asbestos bodies identified 18,300 asbestos bodies per gram of wet lung tissue (AB/gm), which greatly exceeds the normal range of 0-20 AB/gm. No MMVFs were identified in this sample. We conclude that this patient's tumor was not a mesothelioma, but a carcinoma possibly arising in the lung or mediastinum, and that this case supports the view that the few suspected mesotheliomas found in the U.S. cohort may have been caused by asbestos exposure.     

Occupational asbestos exposure among respiratory cancer patients in Lithuania

BACKGROUND: Despite intensive use of asbestos, no cancer case has ever been diagnosed as asbestos related in Lithuania. This paper attempts to estimate the proportion of those occupationally exposed to asbestos among respiratory cancer patients. MATERIAL AND METHODS: Occupational exposure to asbestos was assessed retrospectively for 298 lung cancer and four mesothelioma patients, admitted to the Institute of Oncology, Vilnius. The evaluation was based on personal interview data using an internationally established questionnaire covering most likely activities of asbestos exposure at the workplace. Cumulative exposure to asbestos at work was estimated in fiber years. Lung tissue asbestos fiber burden analysis was conducted by scanning transmission electron microscopy on 23 samples. RESULTS: A cumulative asbestos exposure of > or =25 fiber years was found for 10 lung cancer patients (3.4%). They worked in foundries, construction, installation, shipyard, power plant, railway, asbestos cement, glass and chemical industry. In a further 56 lung cancer patients (18.8%) and for one (25%) mesothelioma patient, a cumulative exposure from 5 to 24.9 fiber years was assessed. Asbestos fibers were detected in 18 cases, the burden ranged from 0.1 to 4.1 million fibers/g dry lung tissue; concentrations exceeding 1 million f/g dry lung tissue were found in four cases. All fibers were chrysotile. CONCLUSIONS: Findings indicate that a fraction (3.4%) of the lung cancer cases could be attributed to heavy occupational exposure to asbestos using the Helsinki criterion of > or =25 fiber years. Therefore, approximately 50 lung cancer cases per year in Lithuania could be asbestos-related compensable occupational diseases.     

Quantitative assessment of the risk of lung cancer and pleural mesothelioma among automobile mechanics

BACKGROUND: A quantitative assessment of the risk of lung cancer and pleural mesothelioma among mechanics exposed to dust released from automobile asbestos-containing parts was performed. METHODS: The population of automobile mechanics in France, according to profession and industrial sectors codes, was estimated from the data of the 1999 census. Risks were computed for a total male population of 242,360 automobile mechanics aged 16 to 60 years. Exposure to asbestos among these workers comes from maintenance tasks involving asbestos-containing parts produced before 1997 (date of the asbestos ban in France). Airborne asbestos concentration data available from the literature were highly variable. No data reporting the distribution of time spent for such tasks over a typical week of work were available. Therefore, different weekly exposure profiles were simulated, based on data from the 1994 SUMER survey. Risk models were those used for assessing asbestos health effects by all national and international agencies. Exposure scenarios mixed different levels of exposure, periods of time, proportions of exposed workers and dates of the "natural" disappearance of the automobile fleet built before asbestos was banned in brakes and other parts. The most realistic scenario hypothesizes that all automobile mechanics were exposed to asbestos, that the exposure levels ranged from 0.06 and 0.25 fibers/liter per week for the period before 1997, and between 0.01 and 0.06 fibers/liter per week afterwards until 2010. RESULTS: According to this scenario, the number of lifelong cancer deaths (lung and pleura) induced by asbestos exposure in this population is estimated at 602 "unavoidable" cases, due to exposure experienced before 2003; 43 other cases will occur if asbestos is not removed from existing automobiles.     

The presence of asbestos bodies in induced sputum as an indicator of asbestos exposure

BACKGROUND: Very few references on the usability of presence of asbestos bodies (AB) in induced sputum as an indicator of asbestos exposure are to be found in the scientific literature. OBJECTIVES: The purpose of this study was to prove whether the presence of AB in induced sputum is a valid assessor of asbestos exposure. METHOD: This was achieved by comparing the above-mentioned method with the search for AB in bronchoalveolar lavage (BAL) fluid and repeating the trials over time in order to study the reproducibility of the results. Results: There was good agreement of results for the presence/absence of AB in induced sputum and in BAL among subjects who were environmentally exposed and those with 'a medium-high risk occupational exposure (100%), and poor agreement (66%) among subjects with a low risk occupational exposure. Agreement of results regarding the amount of particles per test was low. The method showed a sufficient reproducibility level (Cohen K=0.5). CONCLUSION: Although the presence of asbestos bodies in induced sputum cannot replace bronchoalveolar lavage, it can however be used as a screening test for selecting subjects who should undergo BAL.     

Risk of cancer in locations containing asbestos: myth or reality?

The risk of cancer induced by asbestos is proportional to the 'dose' inhaled (level X duration of exposure). Airborne asbestos fibre concentrations in buildings with sprayed asbestos insulation are very low. The estimation of life-long risk of cancer for people working continuously in this kind of buildings was made according to the Hughes and Weill's model. The lung cancer and mesothelioma mortality increase, attributable to asbestos, would be less than 0.1%, which means less than one death by century for all employees working in these buildings, in Switzerland. On the other hand, maintenance employees lying electric cables, pipes, etc., inside the asbestos-containing sprayed insulation, or workers transforming or pulling down these buildings, may be exposed to high asbestos fibre levels and should wear protective equipment.     

Asbestos bodies in bronchoalveolar lavage fluid in relation to occupational history

Concentrations of asbestos bodies (AB) were assessed by optical microscopy of 10 ml iron-stained samples and compared with the exposure history acquired by personal interview for 156 patients. Concentrations equalling or exceeding 1 AB/ml were found in 85% of patients who had been heavily exposed to asbestos and only 7% of those who were unlikely to have been exposed. Elevated AB concentrations were observed among primary asbestos, shipyard and construction workers. Smoking was not found to affect the AB concentrations. The use of Papanicolaou-stained cytological Millipore preparations during routine screening was a less sensitive method for the assessment of AB concentrations than that involving iron-stained preparations. The expression of AB concentration as AB/ml or AB/million cells were found to be equally useful indicators of exposure. The correlation between AB concentration and exposure history was greater than in earlier studies on workers exposed to chrysotile. Concentrations exceeding 1 AB/ml were indicative of a nontrivial exposure to asbestos. Despite the observed correlation between AB concentration and exposure history, the individual variability of AB counts, methodological differences and laboratory-bound reference values are important in the interpretation of AB concentrations in bronchoalveolar lavage (BAL) fluid at individual level.     

Measurement of asbestos fibre concentrations in fluid of repeated bro-choalveolar lavages of exposed workers

OBJECTIVES: The aim of this study was to assess the reliability of asbestos fibre concentration in bronchoalveolar lavage fluid (BALF) by carrying out the mineralogical analysis of BALF at different times in the same patient and comparing the results. METHODS: Twenty two patients underwent diagnostic fibreoptic bronchoscopy twice: the first was to assess the past asbestos exposure and the second for different clinical reasons. Mineralogical analysis of BALF was carried out. RESULTS: In 16 patients (72.7%), a reduction of concentration in BALF of all asbestos fibres was observed. The concentrations of both chrysotile and amphiboles in the first bronchoalveolar lavage (BAL) were related to their concentrations in the second BAL and the observed differences were not statistically significant. A significant decrease in asbestos body concentration between the first and the second BAL was found (Wilcoxon test, P < 0.01). CONCLUSIONS: The reliability of the fibre concentration in BALF as a marker of past asbestos exposure seems quite good. In most cases, it allows us to distinguish workers in different classes of exposure and gives useful information on the pattern of exposure. Uncertainties related in general to lung residues and in particular to mineralogical analysis of BALF (mainly due to the high coefficient of variation (CV) at low fibre concentrations and the results of the statistical analysis on total fibres) suggest that this biomarker is more likely suitable for a qualitative/categorical approach to exposure assessment than a quantitative one.     

Asbestos content of lung tissue in asbestos associated diseases: a study of 110 cases

Diseases associated with asbestos exposure include asbestosis, malignant mesothelioma, carcinoma of the lung, and parietal pleural plaques. In this study the asbestos content of lung tissue was examined in groups of cases representing each of these diseases and in several cases with non-occupational idiopathic pulmonary fibrosis. Asbestos bodies (AB), which are the hallmark of asbestos exposure, were present in the lungs of virtually everyone in the general population and present at increased levels in individuals with asbestos associated diseases. The highest numbers of AB occurred in individuals with asbestosis, all of whom had levels greater than or equal to 2000 ABs/g wet lung tissue. Every case with a content of 100,000 ABs/g or higher had asbestosis. Intermediate levels occurred in individuals with malignant mesothelioma and the lowest levels in patients with parietal pleural plaques. There was no overlap between the asbestos content of lung tissue from patients with asbestosis and those with idiopathic pulmonary fibrosis. Lung cancer was present in half the patients with asbestosis, and the distribution of histological patterns did not differ from that in patients with lung cancer without asbestosis. The asbestos body content in patients with lung cancer was highly variable. Control cases had values within our previously established normal range (0-20 ABs/g). There was a significant correlation (p less than 0.001) between AB counted by light microscope and AB and uncoated fibres counted by scanning electron microscopy. The previous observation that the vast majority of asbestos bodies isolated from human tissues have an amphibole core was confirmed.     

Asbestos content of lung tissue in asbestos associated diseases: a study of 110 cases.

Diseases associated with asbestos exposure include asbestosis, malignant mesothelioma, carcinoma of the lung, and parietal pleural plaques. In this study the asbestos content of lung tissue was examined in groups of cases representing each of these diseases and in several cases with non-occupational idiopathic pulmonary fibrosis. Asbestos bodies (AB), which are the hallmark of asbestos exposure, were present in the lungs of virtually everyone in the general population and present at increased levels in individuals with asbestos associated diseases. The highest numbers of AB occurred in individuals with asbestosis, all of whom had levels greater than or equal to 2000 ABs/g wet lung tissue. Every case with a content of 100,000 ABs/g or higher had asbestosis. Intermediate levels occurred in individuals with malignant mesothelioma and the lowest levels in patients with parietal pleural plaques. There was no overlap between the asbestos content of lung tissue from patients with asbestosis and those with idiopathic pulmonary fibrosis. Lung cancer was present in half the patients with asbestosis, and the distribution of histological patterns did not differ from that in patients with lung cancer without asbestosis. The asbestos body content in patients with lung cancer was highly variable. Control cases had values within our previously established normal range (0-20 ABs/g). There was a significant correlation (p less than 0.001) between AB counted by light microscope and AB and uncoated fibres counted by scanning electron microscopy. The previous observation that the vast majority of asbestos bodies isolated from human tissues have an amphibole core was confirmed.     

An index of past asbestos exposure as applied to car and bus mechanics

Different ways to describe historic fibre exposure from asbestos-containing friction materials were studied and compared for a group of 103 car and bus mechanics with more than 20 years employment and 15 years of asbestos exposure. A model was constructed to calculate cumulative asbestos exposure from friction materials including duration, intensity and exposure last year. The model is a combination of an additive and a multiplicative model, where an asbestos index was constructed that takes both near field and far field exposure into consideration. The model was based upon data from the international literature and quantitative asbestos measurements performed 1976–1988 in Swedish car repair workshops. The fibres were counted by phase-contrast microscopy with fibre criteria of length >5 μm and aspect ratio ≥3:1. The mechanics' fibre exposure at 398 repair workshops during a period of 48 years were calculated using the model. The mean cumulative exposure was estimated to be 2.6 f ml⁻¹1 year. The annual cumulative exposure was highest for truck mechanics in the early 1960s. The car mechanics had a time-weighted average fibre exposure range of 0.11 – 0.41 f ml⁻¹ (mean 0.21 f ml⁻¹) in 1965 compared to 0.003 – 0.08 f ml⁻¹ (mean 0.021 f ml⁻¹ in 1985. In order to validate the model, the mechanics' fibre exposure estimated using the model were compared with representative asbestos exposure measurements for car mechanics during the 1960s and the 1970s (correlation coefficient = 0.69). Five lung physiological variables (FVC, TLC, FEV₁, TL_co and CV%) were used to study exposure-response relationships. None of the exposure parameters suggested any significant relationship between exposure and decrease in lung function.     

Respiratory cancer in chrysotile textile and mining industries: exposure inferences from lung analysis

In an attempt to explain the much greater risk of respiratory cancer at the same cumulative exposure in asbestos textile workers in Charleston, South Carolina, than in Quebec miners and millers, both exposed to chrysotile from the same source, 161 lung tissue samples taken at necropsy from dead cohort members were analysed by transmission electron microscopy. Altogether 1828 chrysotile and 3270 tremolite fibres were identified; in both cohorts tremolite predominated and fibre dimensions were closely similar. Lung fibre concentrations were analysed statistically (a) in 32 paired subjects matched for duration of employment and time from last employment to death and (b) in 136 subjects stratified by the same time variables. Both analyses indicated that the Quebec/Charleston ratios for chrysotile fibre concentration in lung tissue were even higher than the corresponding ratios of estimated exposure intensity (mpcf). After allowance for the fact that regression analyses suggested that the proportion of tremolite in dust was probably 2.5 times higher in Thetford Mines, Quebec, than in Charleston, the results from both matched pair and stratification analyses of tremolite fibre concentrations in lung were almost the same as for chrysotile. It is concluded that neither fibre dimensional differences nor errors in estimation of exposure can explain the higher risks of lung cancer observed in asbestos textile workers. The possible co-carcinogenic role of mineral oil used in the past in asbestos textile plants to control dust provides an alternative hypothesis deserving consideration.     

Respiratory cancer in chrysotile textile and mining industries: exposure inferences from lung analysis.

In an attempt to explain the much greater risk of respiratory cancer at the same cumulative exposure in asbestos textile workers in Charleston, South Carolina, than in Quebec miners and millers, both exposed to chrysotile from the same source, 161 lung tissue samples taken at necropsy from dead cohort members were analysed by transmission electron microscopy. Altogether 1828 chrysotile and 3270 tremolite fibres were identified; in both cohorts tremolite predominated and fibre dimensions were closely similar. Lung fibre concentrations were analysed statistically (a) in 32 paired subjects matched for duration of employment and time from last employment to death and (b) in 136 subjects stratified by the same time variables. Both analyses indicated that the Quebec/Charleston ratios for chrysotile fibre concentration in lung tissue were even higher than the corresponding ratios of estimated exposure intensity (mpcf). After allowance for the fact that regression analyses suggested that the proportion of tremolite in dust was probably 2.5 times higher in Thetford Mines, Quebec, than in Charleston, the results from both matched pair and stratification analyses of tremolite fibre concentrations in lung were almost the same as for chrysotile. It is concluded that neither fibre dimensional differences nor errors in estimation of exposure can explain the higher risks of lung cancer observed in asbestos textile workers. The possible co-carcinogenic role of mineral oil used in the past in asbestos textile plants to control dust provides an alternative hypothesis deserving consideration.     

Asbestos exposure, manganese superoxide dismutase (MnSOD) genotype, and lung cancer risk

To assess whether differences in genetic susceptibility to oxidative stress modify asbestos-related lung cancer risk (caused by lung inflammation, free radical production), we examined possible interactions between manganese superoxide dismutase (MnSOD) genotypes and asbestos in a hospital-based case-control study of 811 white lung cancer cases and 957 friend/spouse controls. Cumulative lifetime asbestos exposure score (AES) was calculated from self-reported duration and intensity of occupational and nonoccupational exposures. A total of 13.5% of cases and 10% of controls had "high" AES (determined by a priori cut point). The homozygous variant MnSOD genotype was associated with increased lung cancer risk among individuals with zero or "low" AES (odds ratio [OR], 2.14; 95% confidence interval [CI], 1.52-3.01) and no association (OR = 1.00; 95% CI = 0.36-2.73) among the "high" AES group. We observed no statistically significant interaction between MnSOD genotype and asbestos exposure for lung cancer risk.     

Mesothelioma in an individual following exposure to crocidolite-containing gaskets as a teenager

Mesothelioma is considered a signal tumor for asbestos exposure and typically occurs decades after first exposure to asbestos. Tissue analysis often indicates past exposure to mixed types of asbestos. This report describes the case of a 58-year-old man who developed mesothelioma after reported exposure to crocidolite from asbestos-containing gaskets beginning at age 16 during three summers during high school and for approximately four hours per day during the last semester of his senior year. He had no further known exposure to asbestos. Analytical transmission electron microscopy analysis of digested tissue samples revealed elevated levels of crocidolite asbestos fibers and the presence of crocidolite cored ferruginous bodies. This case is unique in that it establishes that relatively short and/or intense exposures to crocidolite asbestos traumatically released from a previously classified Category 1 nonfriable asbestos-containing material (NESHAP) was confirmed via tissue burden analysis years following the historically defined exposures.     

Asbestos fibres in bronchoalveolar lavage fluid from asbestos workers: examination by electron microscopy

The uncoated and coated fibre load in bronchoalveolar lavage (BAL) fluid was assessed using light microscopy, scanning electron microscopy, and x ray microanalysis in 15 subjects with previous, unprotected exposure to asbestos, including three with clinical and radiological evidence of asbestosis, and in 13 urban dwelling control subjects with no known occupational exposure to asbestos. The mean ferruginous body count per ml BAL fluid in asbestos exposed subjects as determined by light microscopy was 52 (range 0-333). No ferruginous bodies were detected in control subjects. The mean fibre count per ml BAL fluid in asbestos exposed subjects as determined by electron microscopy was 793 (133-3700), significantly greater than 239 (44-544) in controls (p less than 0.05). Electron microscopic counts correlated with duration of previous exposure to asbestos (r = 0.47, p less than 0.05) and with percentage neutrophil counts (r = 0.53, p less than 0.025). There was no relation between electron microscopic fibre counts and light microscopic ferruginous body counts. In 11 asbestos exposed cases x ray microanalysis confirmed the presence of asbestos and in six the asbestos fibre type was clearly identified. Of five subjects showing no asbestos bodies by light microscopy, all showed fibres by electron microscopy, and in three cases the presence of asbestos was confirmed by microanalysis. Among control subjects, fibres were either large organic fibres or smaller particles which microanalysis showed were not asbestos. In only one control case were a few fibres identified which were confirmed as asbestos fibres on microanalysis. Electron microscopic examination of BAL fluid may confirm past exposure to asbestos and probably gives a crude quantitative estimate of asbestos load.     

Study of asbestos bodies in Japanese urban patients

To study whether low-level exposure to asbestos contributes to lung cancer risk, the asbestos body (AB) content in lung tissue was measured in 476 patients with lung cancer and 369 patients with other diseases, all from a Japanese industrialized city. Eleven patients with histologically confirmed asbestosis were included. The findings were stratified into four groups. A significant number of patients with lung cancer were seen in the groups with high counts, as compared to controls. There was no significant difference in histologic type and site of lung cancer among four groups. The patients with lung cancer in high count groups were significantly younger than those with lower counts. A significant number of smokers were seen in the groups with high AB counts among patients with lung cancer as compared to controls, even if the patients with asbestosis were excluded. These findings suggest that there may be a positive interaction of smoking and exposure to asbestos relative to the incidence of lung cancer even at a low exposure level.     

Asbestos fibres in bronchoalveolar lavage fluid from asbestos workers: examination by electron microscopy.

The uncoated and coated fibre load in bronchoalveolar lavage (BAL) fluid was assessed using light microscopy, scanning electron microscopy, and x ray microanalysis in 15 subjects with previous, unprotected exposure to asbestos, including three with clinical and radiological evidence of asbestosis, and in 13 urban dwelling control subjects with no known occupational exposure to asbestos. The mean ferruginous body count per ml BAL fluid in asbestos exposed subjects as determined by light microscopy was 52 (range 0-333). No ferruginous bodies were detected in control subjects. The mean fibre count per ml BAL fluid in asbestos exposed subjects as determined by electron microscopy was 793 (133-3700), significantly greater than 239 (44-544) in controls (p less than 0.05). Electron microscopic counts correlated with duration of previous exposure to asbestos (r = 0.47, p less than 0.05) and with percentage neutrophil counts (r = 0.53, p less than 0.025). There was no relation between electron microscopic fibre counts and light microscopic ferruginous body counts. In 11 asbestos exposed cases x ray microanalysis confirmed the presence of asbestos and in six the asbestos fibre type was clearly identified. Of five subjects showing no asbestos bodies by light microscopy, all showed fibres by electron microscopy, and in three cases the presence of asbestos was confirmed by microanalysis. Among control subjects, fibres were either large organic fibres or smaller particles which microanalysis showed were not asbestos. In only one control case were a few fibres identified which were confirmed as asbestos fibres on microanalysis. Electron microscopic examination of BAL fluid may confirm past exposure to asbestos and probably gives a crude quantitative estimate of asbestos load.     

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.