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PubMed2007

The 2nd ADAO Asbestos Conference.

On National Asbestos Awareness Day 2006, a conference was held at Mount Sinai, the home ground of Dr. Irving J. Selikoff, who, more than any other single individual, started the debate about occupational hazards in the U.S. Four decades after the pioneering conference on the Biological Effects of Asbestos was organized by Drs. Selikoff and Churg, asbestos victims and their relatives, public health campaigners, medical professionals, journalists and community representatives convened in New York City to assess the progress that had been made in raising public, professional and political awareness of asbestos-related diseases. The report which follows conveys the substance of their presentations and highlights key issues which were discussed.

Asbestos↗

PubMed1982

Malignant pericardial mesotheliomas and asbestos exposure: a case report.

Three cases of malignant pericardial mesotheliomas are presented with evidence of occupational asbestos exposure. Examination results are compared with findings from experimental and epidemiological research on biological effects of asbestos dust. There are sufficient indications that time-limited effects of asbestos dust established either by measurements or assessment of the amount of concentration after a latency of more than 20 years are apt to result in the development of mesotheliomas of the pleura and peritoneum and, moreover, the pericardium. It is suggested that malignant pericardial mesothelioma also be recognized as another form of occupational disease caused by asbestos dust.

Aged↗

PubMed1984

Retired and former asbestos workers in Hawaii.

In 1979, a pilot survey defined respiratory status and unmet health care needs of retired and former male asbestos workers in Hawaii. Of 1,401 identified subjects, 741 were contacted and 411 were interviewed. Forty-five subjects were between 39 and 54 years of age; 208, between 55 and 64; and 158, age 65 or more. They represented the main ethnic groups--Caucasian, Chinese, Filipino, Hawaiian and part-Hawaiian, and Japanese--on Oahu. Most subjects had had significant exposure to asbestos in a shipyard, and 83% were current nonsmokers (160 had never smoked, and 111 were ex-smokers for ten years or more). Taking age and ethnicity into account, our group had more chronic respiratory and gastrointestinal problems than the comparable male population of Oahu in 1979, but fewer such problems than active shipyard workers elsewhere. These problems related primarily to current smoking status and secondarily to the length of asbestos exposure. Health care was available, but former workers used it less than retirees, despite having more symptoms. Very few abnormalities were reported by the subjects on their chest X-rays, pulmonary function tests, and sputum cytology performed elsewhere. These findings are compared to those of other shipyards, and support the hypothesis that the biological effects of asbestos exposure are generally mild in Hawaii.

Adult↗

PubMed1986

Common problems in asbestos-related pulmonary diseases.

Exposure to asbestos is an important public health hazard in all industrialized societies. Although the pulmonary manifestations of prolonged asbestos fiber exposure are well known, there is considerable disagreement over specific clinical features and employment policies. Three of these controversies are the following: a) Can lung cancer be ascribed to asbestos exposure in subjects who lack evidence of asbestosis? b) Is there any clinical significance to benign asbestos pleural changes? c) Is it advisable to change jobs when evidence of asbestosis or benign pleural changes develop? The purpose of this presentation is to help develop a suitable public policy for Israel. Such a policy would have clinical importance as well as economic, legal, and social consequences for the individual and society as a whole.

Asbestos↗

PubMed1987

Historical perspective on asbestos: policies and protective measures in World War II shipbuilding.

Current public health consequences of poorly controlled utilization of asbestos in the past can be traced back, in part, to decisions made 45 or more years ago. This paper focuses on the extensive use of asbestos as a fireproofing and insulating material in shipbuilding in the 1940s, when World War II industrial expansion brought about a hitherto unprecedented rise in the amount of asbestos utilized. Twenty years after World War II, asbestos diseases began to manifest themselves, affecting thousands of shipyard workers as well as other workers who had been exposed in the 1940s and during the postwar period. By scrutinizing past actions, the paper argues that social forces, as well as science and technology, affect the setting of priorities and the determination of policy regarding needed but hazardous materials.

Asbestos↗

PubMed1994

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.

Asbestos↗

PubMed1994

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.

Adult↗

PubMed1995

Loss of heterozygosity in asbestos-induced mutations in a human mesothelioma cell line.

The relationship between occupational or environmental exposure to asbestos and the development of mesothelioma, typically after prolonged latency, has been accepted as one of cause and effect. Most studies have concluded that asbestos is not mutagenic to mammalian cells in vitro. We have studied the potential of crocidolite asbestos to induce mutations in a stable mesothelioma cell line, using a mutation assay that measures mutation at the autosomal HLA-A locus and permits clonal growth of mutant cells. The mesothelioma cell line chosen is more akin to the in vivo target cells of asbestos than human peripheral blood lymphocytes used in previous studies. Exposure of mesothelioma cells in culture to both 200 micrograms/ml and 50 micrograms/ml crocidolite for 72 hr did not result in a statistically significant difference in the mutation frequency (MF) in the HLA-A assay when compared to the spontaneous MF in these cells. Mutations in the mesothelioma cells were classified according to their molecular basis. Notwithstanding the lack of statistically significant change in overall MF, molecular analysis of mutants obtained following exposure of mesothelioma cells to crocidolite demonstrated a statistically significant increase in the class of mutations arising from loss of heterozygosity (LOH) events involving the selection locus (HLA-A) and more distal loci. Mutations following exposure to 200 micrograms/ml and 50 micrograms/ml crocidolite showed a greater frequency of LOH than did spontaneous mutants (P < 0.01 and P < 0.001, respectively). These results correlate with those obtained in an earlier study using lymphocytes. The mesothelioma cell-based assay may be useful in detecting the mutagenicity of other asbestiform fibers and man-made fibers.

Asbestos, Crocidolite↗

PubMed1990

Asbestos exposure and histologic cell types of lung cancer in surgical and autopsy series.

A case-control study was carried out on 41 surgical and 106 autopsy histological tissue samples of lung cancer in men, in order to investigate the relationships between asbestos exposure and cell type of pulmonary carcinoma. Both occupational history (obtained by interviews of surgical patients or of the next-of-kin for deceased subjects) and lung asbestos body content (determined by optical count after hypochlorite digestion and membrane filtration of lung tissues) were considered as asbestos exposure indicators. No significant relationships were found in the surgical series after adjustment for smoking. The autopsy series showed a trend towards an association between lung adenocarcinoma and asbestos exposure indicators and a markedly higher agreement between the 2 kinds of indicators than that observed in the surgical series.

Adenocarcinoma↗

PubMed1990

Inhibition of alveolar macrophage cytotoxicity by asbestos: possible role of prostaglandins.

Asbestosis and silicosis are chronic, fibrosing lung diseases due to prolonged inhalation of asbestos fibers or silica particles. However, little is known about the implication of these toxic dusts on cell-mediated cytotoxicity. Among the first types of cells that are in contact with the dusts are the alveolar macrophages (AM). We studied the effect of different concentrations of UICC chrysotile asbestos and silica on 18-h cytotoxicity of AM against tumor necrosis factor (TNF)-resistant P815 target cells or TNF-sensitive L929 target cells. Rat AM, obtained by bronchoalveolar lavage, were incubated for 2 h with 20, 50, or 100 micrograms/ml chrysotile or silica before the addition of target cells. AM cytotoxicity was significantly inhibited at greater than 20 micrograms/ml of chrysotile. In contrast, silica did not inhibit AM-mediated cytotoxicity at any concentration used. Asbestos, but not silica, caused significant production of PGE2 by macrophages and target cells. Addition of the cyclooxygenase inhibitor indomethacin to our system abolished all inhibition by asbestos. These results suggest that the inhibition of AM-mediated cytotoxicity by chrysotile was caused by prostaglandins, and that fibrogenic particles differ in their capacity to modulate AM function.

Animals↗

PubMed1993

Bidirectional modulation of TNF-alpha production by alveolar macrophages in asbestos-induced pulmonary fibrosis.

Bronchoalveolar lavage (BAL) cells were isolated from rats 1, 3, and 6 weeks after a single intratracheal instillation of saline, UICC chrysotile asbestos (5 mg), or silica (5 mg). In asbestos-exposed rats, the pulmonary response was characterized by a significant increase in the number of alveolar macrophages (AMs) and the appearance of fibrotic lesions within 1 week. By contrast, mixed macrophage and neutrophil accumulations were observed in the silica group without evidence of fibrosis. Tumor necrosis factor-alpha (TNF-alpha) production by lipopolysaccharide (LPS)-stimulated BAL cells from asbestos-treated rats was significantly lower than controls 1 and 3 weeks after exposure. However, by 6 weeks higher levels of TNF-alpha production were noticeable in this group. Decreases in LPS-induced TNF-alpha production were also observed with BAL cells from silica-treated animals at all time points studied. Lower levels of TNF-alpha were not related to decreased BAL cell viability or the presence of a significant proportion of neutrophils in the silica group. Furthermore, biphasic changes in TNF-alpha production seen in the asbestos group were correlated with concomitant decreases (3 weeks) and increases (6 weeks) in levels of TNF-alpha mRNA in AMs. These data indicate that lower levels of TNF-alpha resulted from inhibition at the gene expression level and provide evidence for bidirectional modulation of TNF-alpha production by AMs during inflammatory reactions.

Animals↗

PubMed1996

Differential effects of tumor necrosis factor and asbestos fibers on manganese superoxide dismutase induction and oxidant-induced cytotoxicity in human mesothelial cells.

We compared induction of manganese superoxide dismutase (MnSOD) by asbestos fibers and tumor necrosis factor alpha (TNF) using cultured human mesothelial cells. Transformed pleural mesothelial cells (MET 5A) were exposed for 48 h to amosite asbestos fibers (2 micrograms/cm2), to TNF (10 ng/ml), and to the combination of these two. TNF and amosite+TNF caused significant MnSOD mRNA upregulation. Similarly MnSOD specific activity was increased by TNF (290% increase) and the amosite+TNF combination (313% increase) but not by amosite alone. In cell injury experiments, amosite and amosite+TNF exposures caused significant cell membrane injury when assessed by lactate dehydrogenase release, which was 31% and 57% higher than in the unexposed cells. However, only the amosite+TNF combination caused significant depletion of cellular high-energy nucleotide when expressed as percentage of [14C]adenine labeling in cellular high-energy nucleotides. The nucleotide levels were 91.5 +/- 2.0% in the unexposed cells, 89.9 +/- 3.9% in amosite-exposed cells, 90.1 +/- 2.2% in TNF-exposed cells, and 79.8 +/- 9.4% in amosite+TNF-exposed cells. Amosite+TNF-exposed cells were also most sensitive to menadione (20 mumol/L, 2 h), a compound which generates superoxide radicals intracellularly. In conclusion, our data suggests that in human mesothelial cells inflammatory cytokines but not asbestos fibers alone can cause MnSOD induction. In this study, however amosite asbestos+TNF treatment rendered these cells more vulnerable to oxidant-induced cell damage despite elevated MnSOD activity.

Asbestos, Amosite↗

PubMed1990

Small-airways dysfunction in never smoking asbestos exposed Danish plumbers.

Among 701 Copenhagen plumbers we examined the lung function of 23 never smokers, who had removed asbestos insulation and intermittently been exposed to high levels of asbestos for about 25 years without being exposed to welding fume. The plumbers had significantly lower TLC, MEF25, MEF50, closing volume and closing capacity in comparison to 23 never smoking electricians without asbestos exposure. There was no reduction in TLCO. Pulmonary clearance of aerosolized 99mTc-DTPA was normal indicating that the asbestos had not induced increases in pulmonary epithelial permeability. However, in 11 of the 23 plumbers the 99mTc-DTPA ventilation scintigrams had a slightly irregular and spotty appearance, which together with the results of the lung function tests are suggestive of small airways' dysfunction. None of the subjects had symptoms or clinical signs of lung disease.

Adult↗

PubMed1991

Work load and physiological responses during asbestos removal with protective clothing.

The removal of asbestos-containing building materials requires the use of dust-repelling protective clothing and a respirator. The present study was aimed at measuring physiological responses to asbestos removal in actual work situations. The subjects were eight asbestos workers. During the work, the men wore permeable or impermeable clothing along with a powered or non-powered filtering device including a full-face or half-face mask. Environmental parameters, work postures, heart rate (HR), the skin temperature at two sites and the rectal temperature were recorded every minute during work. Perceived exertion, thermal sensation, thermal comfort, and skin wetness were rated by the subjects. The ambient temperature at work sites ranged from 19 degrees to 37.5 degrees C and relative humidity, from 21% to 50%. The mean HR ranged from 101 to 141 beats min-1. The calculated (from HR measurements) average oxygen consumption (VO2) varied from 0.9 to 1.9 l min-1, which corresponded to 27%-60% of the maximal value. The peak rectal temperature and the highest mean of two measurements of skin temperature were 37.7 degrees +/- 0.3 degree C and 34.4 degrees +/- 0.9 degree C, respectively. The sweat rate varied from 162 to 583 g h-1. Poor work posture was common during asbestos removal. The arms were elevated over shoulder level for 35% of the work time. During the work the mean physiological strain was considered to be moderate, with some heavy peak loads being registered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Mortality study of asbestos cement workers.

The present study describes cause-specific mortality of asbestos cement workers in the Emilia Romagna region of Italy. The cohort included workers in ten factories, most of which started operating between 1955 and 1965. Asbestos, mainly chrysotile, constituted 10%-20% of the dry component of the mixture. Crocidolite range between 5% and 50% of total asbestos. Asbestos concentrations up to 44 ff/cc were reported prior to 1975, while in recent years they have usually been below 0-1 ff/cc. The cohort included 3341 workers who had at some time been employed in the ten factories under study. Their mortality experience was compared with that of the population resident in Emilia Romagna. Vital status was ascertained at 1989. Seventy-three subjects were lost to follow-up (2.2%). Mortality from all causes and from all types of cancer was increased in the cohort. Malignant neoplasms of the respiratory tract showed a significant increase (SMR: 134; 90% confidence interval: 101-175; 40 observed) due to lung cancer (SMR: 124; 90% confidence interval: 91-166; 33 observed) and neoplasms of the pleura, mediastinum, and other parts of the respiratory tract (SMR: 602; 90% confidence interval 237-1267; 5 observed). The discrepancy between observed and expected mortality mainly concerned subjects with at least 20 years of employment in the factories. Five more cases of histologically confirmed mesothelioma occurred after the end of follow-up.

Asbestos↗

PubMed1987

Asbestos induced fibrosis in the omentum of rats. Immunofluorescence microscopical demonstration of collagens types I and III; laminin and fibronectin.

Fibrosis and neoplasia are evoked by asbestos fibres. Different experimental models have been used to elucidate the cellular mechanism of their pathogenesis but there is no report available dealing with the role of structural glycoproteins and collagens in the development of the fibrosis. The omentums of 20 female SPF-Sprague-Dawley rats were investigated 1, 2 and 6 months after intraperitoneal injection of 15 mg UICC reference samples of crocidolite, by light- and immunofluorescence microscopy. Using monospecific antibodies, laminin, collagens types I and III and fibronectin were localized. After 6 months typical asbestos bodies were detected. By indirect marking of the basal lamina with anti-laminin-antibodies the marked degree of vessel proliferation occurring during the development of granuloma became visible. The deposition of connective tissue which was already established after 4 weeks was mainly due to collagen type III. After 4 and 8 weeks an accumulation of fibronectin associated with larger asbestos fibres was observed. The results suggest that fibrogenesis is promoted by the opsonic activity of fibronectin for long asbestos fibres. The fibrosis may derive from activated resident fibroblasts.

Animals↗

PubMed1984

Asbestos-induced lung inflammation. Role of local macrophage-derived chemotactic factors in accumulation of neutrophils in the lungs.

In a recently developed sheep model of progressive low-dose pulmonary exposure to asbestos, initial alveolar lymphocyte and macrophage activation was followed by pulmonary neutrophilia in higher-dose exposed animals. This was observed after 18 months of exposure to intratracheal instillations of asbestos fibers and coincided with progressive alveolitis and decreased lung compliance. Alveolar macrophages from those animals were found to produce a chemotactic factor which attracted in vitro peripheral blood neutrophils. It attracted neutrophils more efficiently from higher-exposure than lower-exposure animals. Supernatants of control macrophages exposed to asbestos in vitro were also chemotactic for PMN. Similarly, bronchoalveolar lavage fluids from the animals showed chemotactic activity for peripheral blood neutrophils. It is suggested that chronic exposure to asbestos activates alveolar macrophages to produce chemotactic factors which in turn attract neutrophils from the vascular compartment and may thus contribute to the inflammatory process in asbestosis.

Animals↗

PubMed1984

The use of asbestos-cement pipe for public water supply and the incidence of cancer in selected communities in Utah.

We tested the hypothesis that there is an association between the use of asbestos-cement piping for drinking water supplies and the incidence of gastrointestinal and kidney cancer. Cancer incidence in 14 Utah communities that had used predominantly asbestos-cement piping for transporting their drinking water supplies for 20 years or more were compared to 27 Utah communities that had never used asbestos-cement piping. Cancer incidence was tabulated for 11 cancer sites for the years 1967-1976. Increased Standard Incidence Ratios (SIRs) were found for cancer of the kidney in men (SIR 192) and leukemia (a control site) in women (SIR 203). No increased SIRs were found for the opposite sex at these sites or for the other gastrointestinal sites singly or in combination. There was no increase in age-adjusted cancer incidence for the 11 sites in 4 of the 14 study communities that had used asbestos-cement piping for 30 years or more. Limitations of the study were that the water supplies were nonaggressive, and leaching from the pipes was minimal if at all. Furthermore, the latent period for observation was very short, suggesting that these results should be considered preliminary.

Adult↗