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[Assessment of asbestos exposure, mortality study, and health intervention in workers formerly exposed to asbestos in a small factory making drying machines for textile finishing and the paper mill industry in Pistoia, Italy].

BACKGROUND AND OBJECTIVES: Three malignant pleural mesotheliomas occurred among workers of a small factory that manufactured drying machines for the textile and paper mill industries using asbestos cement (crocidolite, amosite and chrysotile) as insulating panels. The Occupational Medicine Unit of the Local Health Unit of Pistoia, Italy, carried out an intervention programme in the plant in order to 1) assess past asbestos exposure via analysis of the fibre content of samples from drying machines, and of dust samples collected in the factory. Information on the characteristics of occupational exposure was also collected; 2) investigate cancer mortality by means of a mortality study of the employees and, 3) carry out a health intervention programme in workers formally exposed to asbestos in the past. METHODS: Samples from the drying machines and dust samples collected in the factory were analysed using X-ray diffractometric methods. Information on the characteristics of occupational exposure were collected by interviewing plant workers. Two-hundred and fifty employees who had worked in the factory between 1962 and 2000 were included in the mortality study. Follow-up was performed from 1962 to 2002. Health intervention in workers exposed to asbestos in the past involved general practitioners and occupational physicians (first level medical examinations); pneumologists and radiologists (second level medical examinations) of the local health unit. RESULTS: Asbestos fibres were found both in samples from drying machines and in dust samples collected in the factory. Interviews with workers showed that asbestos exposure varied considerably. The SMR for mesothelioma and lung cancer in 234 male workers were 37.0 (95%CI: 4.47-130.0), and 1.29 (95%CI: 0.26-3.78), respectively, based on mortality rates for Tuscany region. Sixty-two workers underwent first level medical examinations; 57 second level examinations. Chronic obstructive lung disease was found in 3 workers; restrictive lung disease was found in 3 employees, one of whom had pleural plaques. CONCLUSIONS: Further investigation is needed in order to identify unknown asbestos exposures in small metal engineering factories.

Acquired Immunodeficiency Syndrome↗

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.

Aged↗

Asbestos and cancer: human natural killer cell activity is suppressed by asbestos fibers but can be restored by recombinant interleukin-2.

Inhalation of asbestos fibers is associated with a marked increase in the risk of developing pulmonary malignancy, particularly bronchogenic carcinoma. As natural killer (NK) cells are specialized lymphocytes that are considered to have an important in vivo role in the recognition and destruction of malignant cells, we examined the capacity of asbestos fibers (chrysotile, amosite, and crocidolite) to interfere with the NK activity of nylon wool-nonadherent, human blood lymphocytes (51Cr-release assay, K562 target cells, 14 h effector-to-target ratio = 50:1). Final asbestos concentrations used were 1 to 1,000 micrograms/ml. None of the fibers altered spontaneous target cell lysis or lymphocyte viability. All types of asbestos suppressed NK activity in a dose-dependent fashion. This effect was most marked with chrysotile, which exerted a profound inhibitory effect on blood NK cell activity; at 100 micrograms/ml, NK activity was inhibited 84 +/- 2% (p less than 0.001). The suppressive effects of asbestos were exerted directly on the NK cells (large granular lymphocytes, 91 +/- 2% inhibition at 100 micrograms/ml; p less than 0.001). Exposure of lymphocytes to recombinant interleukin-2 (IL-2, 150 units/ml) for 24 h prior to exposure to asbestos restored the level of activity to 99 +/- 6% of the original value (p less than 0.001), and lung lymphocytes that were exposed to IL-2 in vivo (active sarcoidosis) were resistant to suppression by asbestos. Similar results were observed in a group of patients with asbestosis. This suppression of NK activity may contribute to the increased susceptibility of asbestos-exposed persons to the development of pulmonary malignancy.

Asbestos↗

Asbestos exposure and asbestos-related pleural and parenchymal disease. Associations with immune imbalance.

The study hypothesis was that asbestos exposure and asbestos-related pleural plaques and interstitial disease are associated with (1) immune imbalances favoring helper-inducer T-cell subsets in blood and bronchoalveolar lavage (BAL) and (2) T-lymphocyte accumulation in BAL. One hundred twenty-two asbestos-exposed subsets (AES), including 27 nonsmokers (NS), were evaluated and compared with 10 unexposed normal subjects. Data were collected on medical, smoking, and occupational histories, physical examination, spirometry, lung volumes, single-breath DLCO, chest films read by a "B" reader, and T-lymphocyte characterization in blood and BAL using flow cytometry analysis of monoclonal-antibody-treated cells. On average, AES were 47 yr of age and had 23 yr of asbestos exposure. Fifty-eight (48%) had pleural thickening, and seven (6%) had profusion greater than or equal to 1/0. In blood, asbestos-exposed NS had lower total and percent CD8 and lower total CD3 than did normal subjects. In BAL, asbestos-exposed NS had higher total CD3 than did normal subjects. Among AES, increased asbestos exposure was associated with increased percent CD8 in BAL and decreases in both percent lymphocytes and total CD8 in blood. Increase in CD4/CD8 ratio in BAL were associated with pleural thickening. In those seven with profusion greater than or equal to 1/0, there was increased percent CD4 in blood and decreased percent CD8 in BAL. These results suggest immune imbalance favoring helper-inducer T-cell subsets in association with asbestos exposure systemically and with pleural plaques in BAL.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The trend in airborne asbestos concentrations at plants manufacturing asbestos-containing products in Japan.

In Japan, chrysotile is still permitted to use under the Ordinance on Prevention of Hazards due to Specified Chemical Substances. In recent years many countries have introduced a policy of prohibiting the use of asbestos, based on clinical and epidemiological studies. In light of this, it is important to evaluate the airborne asbestos concentrations in workplaces and also estimate the number of related disease cases in order to discuss the ban of asbestos use. The survey covered 528 workplaces in 145 plants and included 2795 asbestos handling workers from 1985 to 1998. These plants were belonging to the Japan Asbestos Association (JAA) as member companies. In Japan, nearly all of the asbestos using manufacturing companies are members of JAA. In our study, all of the workplaces were divided under each separate manufacturing process and classified into 3 categories of Control Classes. Of the 454/528 (86.0%) workplaces classified as Control Class 1 are improved to 376/378 (99.5%). Though in the cases of small enterprises, other factors such as a shift in product lines, and the economic recession, as well as efforts, contributed to improvements in working conditions. JAA recommended self-administered concentrations of 1.0 f/ml (compatible to <0.3 f/ml in personal exposure level) in 1991 to promote further improvements of the work environment. From this point of view, exposure limits can almost be technically achieved in Japan, and it is expected that asbestos related disease could be expected to decrease in 20 to 30 years later. This survey will become basic material for verifications whether we could control asbestos related diseases enough in such well-controlled work environment.

Air Pollutants, Occupational↗

Asbestos-related diseases and asbestos types used in the former GDR.

In the period from 1960 to 1990 about 1.4 million tonnes of asbestos were imported by the former German Democratic Republic (GDR) and mainly processed into asbestos-cement products for the building industry. The production was concentrated in the former counties of Magdeburg and Dresden. In the past, asbestos was primarily used as insulation and fire prevention material, etc. in the large-scale chemical industry. Chrysotile was predominantly imported from the former Soviet Union, partly from Canada. Very small amounts of amphiboles came from Mozambique, but they were not processed in the counties of Magdeburg and Halle. In the German Federal State of Saxony-Anhalt, approx. 600 asbestoses, almost 2,700 pleural changes caused by asbestos, 843 asbestos-induced mesotheliomas and 787 bronchial and laryngeal carcinomas caused by asbestos were recorded in the period from 1960 to 1990. A considerable percentage of the mesotheliomas are solely due to exposure to chrysotile asbestos.

Asbestos↗

Relationship between Asbestos Exposures and 8-Hydroxydeoxyguanosine Levels in Leukocytic DNA of Workers at a Chinese Asbestos-material Plant.

The objective of the study was to evaluate the level of 8-hydroxydeoxyguanosine (8-OHdG) in DNA of peripheral-blood leukocytes as a biological marker of asbestos exposure and/or its fibrotic effects in an occupational population exposed to asbestos. The setting was a large-scale asbestos plant in China producing brake linings, asbestos rubber, and textile using chrysotile. From a base population of active and retired workers with various levels of cumulative exposure to asbestos and grades of asbestosis, 39 study subjects were randomly selected to reflect incremental grades of asbestosis based on Chinese diagnostic standards. They consisted of 19 "normal" (control) and ten "suspected" and ten "definite" asbestosis-grade subjects, group-matched for age and sex. Leukocytic DNA was extracted from 5-mL samples of peripheral blood and 8-OHdG level measured by high-pressure liquid chromatography. A cumulative asbestos exposure index (CEI) was calculated for each subject as the summed product of duration and level of asbestos exposure per job, incorporating a job-exposure matrix. Geometric mean 8-OHdG levels showed a positive gradient in relation to increasing grades of asbestosis (control: 1.78, suspected: 2.21, definite: 2.58), with a significant difference between the control and definite-asbestosis subgroups (p < 0.05). The 8-OHdG level of the two subgroups combined as one "asbestosis" group was significantly higher than that of the control group (control: 1.78, asbestosis: 2.39, p = 0.01). Further, 8-OHdG levels were moderately correlated with CEIs for all subjects (r = 0.35, p < 0.05) and with grades of asbestosis for all (r = 0.47, p < 0.01) and for male subjects (r = 0.43, p < 0.05). In multiple regression analyses, grade of asbestosis explained 27% of the total variation in 8-OHdG and was a better predictor than CEI or duration of exposure. Thus, the 8-OHdG level in leukocytic DNA is related to grade of asbestosis and to individual cumulative exposure and may serve as a biologic marker reflecting the status of oxidative DNA damage by asbestos.

Journal Article↗

Asbestos exposure and retention as determinants of airway disease and asbestos alveolitis.

To evaluate the relationships of asbestos exposure, retention, airway response, and the asbestos alveolitis, we exposed 2 groups of sheep every 2 wk for 3 yr to either 100 ml phosphate-buffered saline (PBS) or 100 mg UICC chrysotile fibers in 100 ml PBS. The sheep were evaluated periodically by pulmonary function tests (PFT), chest radiograph (CR), bronchoalveolar lavage (BAL), and transbronchial lung biopsy (TLB). At Month 24 of the study, all asbestos-exposed sheep had significant increases in lung resistance and upstream resistance. However, only 9 of the 16 asbestos-exposed sheep had significant changes in TLB, CR, Cst, and VC, which clearly separated them from the other 6 sheep in these parameters. The 2 groups, however, had similar air-flow limitation. At lung biopsy, all asbestos-exposed sheep had significant peribronchiolar fibrosis, with significant alveolitis only in the group of 9 sheep with radiographic and functional changes of early asbestosis. The 9 sheep also had significant changes in BAL cellularity and biochemical profile, which differentiated them from the other 6 asbestos-exposed sheep. Analysis of BAL fiber content at that point revealed that despite identical exposure, the group with interstitial lung disease had significantly more fiber retention (p less than 0.01). The data demonstrate that whereas asbestos airway disease appears to be primarily an exposure-dose-related response, the lung response appears to be more closely related to alveolar retention of the dust.

Airway Resistance↗

Effects of cigarette smoke on the clearance of short asbestos fibres from the lung and a comparison with the clearance of long asbestos fibres.

Long asbestos fibres are generally considered to have greater disease-producing potential than short asbestos fibres. However, recent reports have suggested that short fibre asbestos appears to be as effective an inducer of macrophage growth factors and toxic oxygen species as long fibre asbestos, but that short fibres are readily removed from lung and do not gain access to tissues. Because smoke is believed to impair the clearance of asbestos fibres from lung, we examined the clearance of a short (geometric mean length 1.3 microns) amosite preparation administered by intratracheal instillation to guinea-pigs. Half the animals in each group were exposed to the smoke of 10 cigarettes daily. Animals were sacrificed 1 day, 1 week, or 1 month later, the macrophages recovered by lavage, and fibre concentrations and sizes determined by analytical electron microscopy in macrophages and lung tissue. A 30-fold increase was seen in total numbers of fibres retained in macrophages in smokers compared to non-smokers by 1 month, and there was an eightfold increase in retention of short fibres in the lung tissue by 1 month. By contrast, a long fibre amosite preparation (geometric mean length 8.9 microns) showed approximately the same increase in fibre retention in macrophages, but only a twofold increase in tissue retention. We conclude that (1) cigarette smoke markedly impairs the clearance of short amosite fibres from the lung with enhanced retention of fibres in both macrophages and tissue; (2) the effects of smoke on short fibre tissue retention appear to be greater than those on long fibre retention; (3) with the long fibre preparation, smoke causes increased tissue retention of relatively shorter fibres; (4) for both fibre size experiments, the increase in total fibres in macrophages in smoke-exposed animals reflects an increase in the total number of fibre-containing macrophages, rather than an increase in the number of fibres phagocytized per macrophage; (5) enhanced short fibre retention markedly increases total fibre surface area, a parameter which has been suggested as a measure of fibre toxicity, to the point where short fibres might under some circumstances have roughly the same potential toxicity as long fibres. These observations suggest that short asbestos fibres could play an important role in the pathogenesis of some types of asbestos-related disease in cigarette smokers.

Animals↗

Asbestos body formation and iron accumulation in mouse peritoneal granulomas after the introduction of crocidolite asbestos fibers.

This report describes the cell biology of the development of asbestos bodies after a single intraperitoneal injection of a suspension of crocidolite asbestos fibers into the mouse peritoneal cavity. The majority of the infected fibers were found in aggregates of peritoneal macrophages, exudate cells, and fibrous tissue. These aggregates developed into granulomas containing not only numerous asbestos fibers, but also cells of various types, including macrophages, multinucleated giant cells, fibroblasts, plasma cells, granulocytes, and mast cells. Cytoplasmic ferritin was abundantly present in macrophages and giant cells. In addition, iron-rich inclusion bodies were detected. The results of this study show that asbestos body formation can occur outside the pleural cavity. Asbestos body formation occurred in the granulomas after periods of 1 month and longer. On the basis of morphologic criteria, various types of asbestos body were distinguished. X-ray microanalysis showed that variations in the density of the coat could attributed to the presence of chemical elements in various concentrations. Evidence is presented that asbestos body formation is an extracellular phenomenon.

Animals↗

The CARET asbestos-exposed cohort: baseline characteristics and comparison to other asbestos-exposed cohorts.

The Carotene and Retinol Efficacy Trial (CARET) was a double-blind, placebo-controlled trial of the daily administration of 25,000 IU vitamin A and 30 mg beta-carotene for the prevention of lung cancer. Of close to 18,500 participants, more than 4,000 were asbestos-exposed men recruited from shipyard and construction trades at five study centers in the United States. While the primary endpoint of the trial was the incidence of lung cancer, a number of questions about the natural history of asbestos-related disease will also be addressed. The mean age at entry into the trial was 57 years and the mean duration of follow-up on active intervention was 4 years. With the exception of 133 never-smoker pilot participants (3%), all subjects recruited were by intention current (38%) or ex-smokers (58%), with a mean cumulative smoking exposure at entry of 43 pack-years. Mean years from first asbestos exposure were 35, and mean duration of asbestos exposure in a high-risk trade was 19 years. The distribution of radiographic abnormalities was as follows: normal, 34%; parenchymal opacities (ILO profusion score > 1/0) alone, 18%; pleural thickening alone, 27%; both parenchymal opacities and pleural thickening, 21%. The CARET cohort, when compared to previously reported asbestos-exposed cohorts, is characterized by substantial asbestos exposure and high proportion of asbestos-related radiographic findings. The active intervention was halted in 1996, after a mean duration of 40 years. Passive follow-up of the cohort will continue until the year 2000.

Asbestos↗

Pulmonary asbestos body counts and electron probe analysis of asbestos body cores in patients with mesothelioma: a study of 25 cases.

Malignant mesotheliomas of the pleura and peritoneum are well-recognized risks of asbestos exposure. We determined the asbestos body content of the lungs from 24 cases of malignant mesothelioma (19 pleural, five peritoneal) and compared such to the content of lungs from 50 consecutive adult autopsies and four cases of overt asbestosis using a Clorox-digestion concentration technique. The cores of 90 asbestos bodies were examined by energy dispersive x-ray analysis and compared with similar data from 120 standard asbestos fibers and 20 fiberglass fibers. The malignant mesothelioma patients had asbestos body counts intermediate between those of the general population and those of patients with asbestosis, although some of the mesothelioma cases overlapped with the general population. These latter cases often lacked an identifiable occupational exposure to asbestos. EDXA studies demonstrated an amphibole core in 88 of the 90 asbestos bodies (amosite or crocidolite in 80 of 88, anthophyllite or tremolite in eight of 88), and chrysotile in two instances.

Adult↗

Comments on the Health Effects Institute-Asbestos Research (HEI-AR) report: "Asbestos in public and commercial buildings," with emphasis on risk assessment methods used.

A Health Effects Institute--Asbestos Research Report calculates the risk of exposure to environmental asbestos fibers (EAF) by downward extrapolation from the mortality of workers exposed for 20 years. This extrapolation is improper because 1) relative risks of asbestos exposure very likely are not linearly progressive; 2) the composition of EAF may not be equivalent to that in mining or fabricating; 3) the same environmental asbestos concentration probably represents different exposure doses for different populations; and 4) health effects of asbestos exposure on children, seniors, patients, the institutionalized, the handicapped, and the chronically ill may not be the same as those of healthy workers. Evidence of asbestos-related disease among family members of exposed workers demonstrates that the risk observed for EAF is substantially larger than that estimated from downward extrapolation and suggests a basis for an alternative approach to estimating asbestos-related health risks. Such epidemiologic procedures are well established and ought to form the basis for detecting the health effects of EAF. It is also unclear which industry supports HEI-AR.

Academies and Institutes↗

Production of nitric oxide elevates nitrosothiol formation resulting in decreased glutathione in macrophages exposed to asbestos or asbestos substitutes.

The purpose of this study was to investigate the effects of pneumoconiogenic particles, such as asbestos, on nitrosothiol formation in macrophages. In addition, the effects of man-made mineral fibers (MMMFs) were also evaluated, because they have come into heavy use as substitutes for asbestos. RAW264.7 cells and J774 cells of murine macrophage cell lines were cultured with chrysotile B (CH) asbestos, crocidolite (CR) asbestos, or MMMFs comprised of glass wool (GW), rock wool (RW), or ceramic (RF1). All of these fibers significantly increased nitric oxide (NO) production in the culture with macrophages. Chrysotile B, CR, and GW significantly decreased the level of reduced glutathione (GSH) in RAW264.7 cells. S-nitrosothiol (RS-NO) formation was increased by both types of cells on exposure to every fiber. A large portion of this increased RS-NO may be in the form of S-nitrosoglutathione (GS-NO), because GSH is the most abundant thiol substance in the cell. Both CH and GW significantly increased superoxide anion in the media cultured of RAW264.7 cells. These results indicate that macrophages exposed to asbestos or MMMFs are subject to oxidative stress, not only through the generation of reactive oxygen and nitrogen species, but also through decreases in the level of the cellular antioxidant, GSH, by GS-NO formation. The increase of RS-NO in macrophages exposed to asbestos or MMMFs may deserve more attention as the indicator of continuous oxidative stress by NO on cells and tissues, which causes inflammation and involves the development of asbestos-induced diseases.

Animals↗

Asbestos exposure and radiological abnormalities among maintenance and custodian workers in buildings with friable asbestos-containing materials.

OBJECTIVES: Few studies have been carried out to evaluate the respiratory effects of asbestos exposure of custodian and maintenance workers. METHODS: By a multicentre cross-sectional study, 277 custodian and maintenance employees working in buildings with friable asbestos-containing materials and 87 unexposed subjects were studied for radiological abnormalities by use of the International Labour Office (ILO) classification of radiographs of pneumoconiosis, in relation to parameters of asbestos exposure. RESULTS: The cumulative asbestos exposure index was generally low (fewer than 5 fibres/ml x years in 82.3% of exposed workers). On multivariate analysis, pleural thickening was significantly related to latency since onset of exposure to asbestos in exposed workers, after adjustment for age, body mass index and tobacco smoking. CONCLUSIONS: Asbestos exposure of custodian and maintenance employees in buildings with friable asbestos-containing materials might be associated with an excess of pleural thickening on chest X-rays.

Adult↗

Asbestos fibers and trace metals in the blood of cattle grazing in fields inundated by asbestos-rich sediments.

During a major storm in 1975, a pasture was inundated with serpentinitic sediments which are rich in asbestos fibers and trace metals. Little natural revegetation has occurred at the site and dairy and beef cattle which continue to graze in and around the contaminated site are exposed to asbestos fibers by inhalation and ingestion. The effect of this material on the cattle was investigated in this study by analyzing blood samples from exposed and control animals for asbestos fibers, trace metals, and general blood chemistry. The analysis showed that at the time of exposure Ni and Mn values were significantly higher in the exposed animals than in the controls, and in six out of seven samples asbestos fibers were present as determined by STEM analysis. Once the animals were removed from the site, trace metal levels returned to normal but asbestos fibers were still present in three out of seven animals. Two of the control animals unaffected by the sediments also showed asbestos fibers and there were no relationships between the magnitude of fibers and trace metal content. This suggests that the sediments influence the blood chemistry of animals but the presence and magnitude of asbestos fibers in the blood can be influenced by other factors as well.

Animals↗

Potential source of asbestos in non-asbestos textile manufacturing company.

Recently, a worker with lung carcinoma and a metastatic brain tumor was diagnosed as having a work-related disease. He had been employed in a non-asbestos textile company for 25 years. Consequently, to identify and explore possible causative agents for lung cancer in a non-asbestos textile manufacturing company and establish a causal relationship between exposure and lung cancer, an epidemiological investigative study was conducted and the work processes the worker was engaged in were examined. Air samples were taken from the workplace and during the drilling processes, and a suspected causative material was analyzed. The study revealed that the subject had been employed in the non-asbestos textile manufacturing company for 25 years from 1973 and his responsibilities included repairing spinning machines. In particular, the subject was involved in drilling B-bushings that were used to protect against gear abrasion in the spinning machines. An analysis of the B-bushings using a transmission electron microscope equipped with an energy dispersive X-ray analyzer indicated that they contained crocidolite asbestos fibers. Air samples obtained when drilling the B-bushings clearly indicated that the subject had most likely been exposed to crocidolite fibers when installing the B-bushings in the spinning machines. The frequency and duration of the work suggested that there would be a sufficient degree of exposure to crocidolite fibers to cause lung cancer. Except for smoking and asbestos exposure, no other chemical exposure was suspected for developing lung cancer in the workplace. Smoking appeared to be more of a potentiating risk factor in conjunction with the asbestos exposure. Accordingly, this case may provide significant evidence in identifying the cause of the mesothelioma or lung carcinoma found among workers in non-asbestos textile manufacturing companies elsewhere.

Air Pollutants, Occupational↗

Quantitation of asbestos and asbestos-like fibers in human lung tissue by hot and wet ashing, and the significance of their presence for survival of lung carcinoma and mesothelioma patients.

Technical standardization on randomly chosen samples of tissue specimen is essential for the validity of interpretations derived from measurements on the presence of asbestos fibers in lung in combination with further features of the patients. Fixed non-tumorous lung tissue (2-3 g) of 150 patients after surgery for various lung diseases were either digested in 45 ml of 13% solution with sodium hypochlorite (NaClO; wet ashing) or heated in an oven at 600 degrees C for 15 min (hot ashing). After tissue disintegration asbestos and asbestos-like fibers were counted by visual inspection, and the fiber concentration in the lung parenchyma was computed. In addition, the patients' survival, and the occupational and social history were analyzed. As a result, the mean concentrations of fibers were found to be 55 f/g (fibers/gram, hot ashing) and 46 f/g (wet ashing). The difference is statistically not significant. Mesotheliomas contributed 49% (73 patients), non-small cell lung carcinomas 32% (59 patients) to the entire cohort. Eighteen patients had a non-malignant lung disease. Analysis of living habits revealed that 73 (49%) patients were heavy smokers, and 99 (66%) patients had a history of occupational asbestos exposure which lasted for 18 years on average. A statistically significant difference of the asbestos fiber concentration between the group with professional exposure and that without detectable asbestos exposure could be obtained in mesothelioma patients and non-malignant lung diseases only, and a tendency for elevated fiber presence was seen in non-small cell lung carcinoma patients. In tissue specimen of patients with non-malignant lung diseases the highest fiber concentration was measured (median 104 f/g) followed by mesothelioma patients (77 f/g), and lung carcinoma patients (62 f/g wet tissue). The difference in the fiber concentration between smokers and ex-smokers versus non-smokers was particularly high in patients with non-malignant lung diseases (103 f/g in smokers versus 33 f/g in non-smokers), still statistically significant in mesothelioma patients (100 f/g smokers versus 61 f/g non smokers), and negligible in lung carcinoma patients (58 f/g smokers versus 62 f/g non-smokers). Only 5/70 mesothelioma patients were not exposed to asbestos at work, and nearly half of the patients (36) were non-smokers. The median survival of mesothelioma patients was significantly shortened for patients with a high intrapulmonal fiber concentration greater than 70 f/g (35 weeks versus 60 weeks). This correlation was also true for lung carcinoma patients (110 weeks versus 230 weeks).

Asbestos↗