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PubMed1985

Products liability issues in school asbestos litigation.

The hazards posed by deteriorating friable asbestos in the nation's schools are causing serious concerns for public health officials, school boards, parents and school employees. Reports by both the Environmental Protection Agency and the U.S. Attorney General's Office agree that both school children and school employees stand a substantially increased risk of contracting some form of asbestos-related disease as a result of exposure to deteriorating asbestos materials in school buildings. School systems plagued by the asbestos hazards are now filing suits against asbestos manufacturers alleging causes of action in breach of warranty, negligence and strict products liability in tort. Some plaintiffs in school asbestos litigation seek to recover the costs of EPA-mandated asbestos inspection and abatement programs which have already been completed. Still others request injunctions to compel the manufacturers themselves to conduct inspections and finance abatement. This Note examines the school asbestos situation from a legal perspective and focuses primarily on whether the schools' claims should be considered as economic losses or as property damage. It examines the impact of statutes of limitations on these cases under both contract and tort theories. The Note argues that school asbestos claims should be decided under a strict products liability standard.

Adult↗

PubMedDate not supplied

Asbestos bodies in fine needle aspirates of the lung.

Asbestos bodies, which are the hallmark of exposure to asbestos, were identified in cytologic preparations from fine needle aspirates of the lung in two individuals, one with considerable occupational exposure to asbestos and one for whom no source of asbestos exposure could be identified. At autopsy, large numbers of asbestos bodies were identified in the lung parenchyma in each case by use of a quantitative hypochlorite digestion-concentration technique. Scanning electron microscopy and energy-dispersive x-ray analysis demonstrated that the main types of asbestos present were the commercial amphiboles, amosite and crocidolite. We have rarely identified asbestos bodies in fine needle lung aspirates studied in our laboratories and are not aware of such reports in the literature. It is likely that the identification of asbestos bodies in fine needle aspirates of the lung is indicative of considerable occupational exposure to asbestos.

Aged↗

PubMedDate not supplied

Asbestos in Colorado schools.

Forty-one public schools in Colorado were drawn at random and surveyed for asbestos-containing materials. After bulk samples of possible asbestos materials from the schools were collected and analyzed, the K2 asbestos screening test was used to eliminate samples that did not contain asbestos. Samples with positive results on the K2 test were analyzed by an outside laboratory by polarized light microscopy. The risk of potential exposure presented by these materials was then assessed for each site from which a sample was taken. Of 113 samples collected, results were negative for asbestos for only 10.6 percent by the K2 test. Of the 101 samples for which results were positive, 56 actually contained 1 or more forms of asbestos. Twelve of these 56 samples were from sprayed material; the remaining 44 were from other materials containing asbestos. Of the 41 schools sampled, 31 had asbestos materials in one of more locations. The potential exposure values for these materials ranged from very low to very high, but the majority had high-exposure potentials. Estimates based on the survey of the 41 schools indicated that 63 to 89 percent of the public schools in Colorado have asbestos materials that present potentially serious hazards, not only to the children, teachers, and staff, but also to members of the community who use the school buildings after regular school hours.

Asbestos↗

PubMed1995

Autocrine growth stimulation by transforming growth factor alpha in asbestos-transformed rat mesothelial cells.

Although the association between asbestos exposure and mesothelioma development has been established for decades, very little is known regarding the molecular mechanism(s) by which asbestos fibers induce this disease. In this series of experiments, the potential for transforming growth factor alpha (TGF-alpha) to act as an autocrine growth factor in transformed mesothelial cells was examined in rats, a model system frequently used to assess the tumorigenic potential of fibrous particulates. Both asbestos-transformed cells and spontaneously transformed cells expressed functional EGF receptors, although only the asbestos-transformed cells expressed TGF-alpha. Expression of TGF-alpha transcripts was correlated with secretion of picogram amounts of growth factor into conditioned medium by the asbestos-transformed cells. In addition, whereas TGF-alpha inhibited the growth of spontaneously transformed mesothelial cells, it stimulated the growth of asbestos-transformed cells. Neutralizing antibody that recognized TGF-alpha secreted by the asbestos-transformed cells was able to inhibit the growth of these cells. Taken together, these data indicate that TGF-alpha acts as an autocrine growth factor for asbestos-transformed rat mesothelial cells. Therefore, in asbestos-transformed mesothelial cells, altered production and responsiveness to TGF-alpha distinguish these cells from spontaneously transformed mesothelial cells. These data suggest that differences in mesothelioma etiology may be reflected in differences in the molecular alterations present in these tumors.

Animals↗

PubMed1995

Use of asbestos in expected and unexpected places in Israel.

The main human exposures to asbestos in Israel were in manufacturing and processing of asbestos-cement products, removing and fixing brakes and clutches for vehicles, removing old insulation containing asbestos in various plants, and in preparing and using textile products containing asbestos. Asbestos is still used in Israel, even though its health hazards are well described in the medical literature. In this paper current asbestos use in Israel is described. We emphasize the "less expected" places where asbestos was found in Israel. The detection of asbestos in unexpected places requires that we stay alert and constantly search for asbestos in every workplace and residence and in the environment.

Asbestos↗

PubMed1994

[Comparative evaluation of fibrogenesis and toxicity of asbestos-containing heat-proof materials].

The article deals with the results of studies analyzing the fibrogenic activity and toxicity of asbestos-containing heat insulators exemplified by asbestos board, vulcanite and asbestos vermiculite. Physical and chemical parameters of the studied dust are presented. All studied dust types have the distinct fibrogenic activity, the highest one was seen in asbestos board. The studied dust types could be classified according to the acute toxicity: asbestos board (DL50-3.2 +/- 0.09 g/kg), chrysotile asbestos (DL50-2.0 +/- 0.08 g/kg), vulcanite (DL50-1.9 +/- 0.08 g/kg) and asbestos vermiculite (DL50-0.7 +/- 0.04 g/kg). The article touches upon the probable acting mechanism of acute toxicity of asbestos and asbestos-containing dust.

Animals↗

PubMed1994

Asbestos stimulates IL-8 production from human lung epithelial cells.

Studies have indicated that soluble products, including chemotactic factors, released by activated lung macrophages and fibroblasts are critical mediators in the pathogenesis of asbestos-induced pulmonary fibrosis. We provide evidence that mediators produced by lung epithelial cells in response to asbestos may also contribute to lung disease. In the present study, the carcinogenic and fibrogenic fibers, chrysotile and crocidolite asbestos, were shown to directly stimulate the human pulmonary type-II epithelial cell line, A549, and to a lesser degree primary human bronchial epithelial cells, to elicit the chemotactic cytokine IL-8 in the absence of endogenous stimuli such as IL-1 and TNF. That the membrane signaling events responsible for asbestos-induced IL-8 production are distinct from those responsible for IL-8 induction by cytokines was confirmed by using membrane-stabilizing agents and protein synthesis inhibitors. Stimulation was not observed with nonfibrogenic fibers, wollastonite and titanium dioxide, and was the direct result of asbestos-induced initiation of transcription. Asbestos failed to stimulate the release of TNF, IL-1 beta, or monocyte chemoattractant protein-1 in A549 or primary bronchial epithelial cells, indicating that cytokine secretion by asbestos is highly selective. However, a slight release of IL-1 alpha, probably preformed, was released in human bronchial epithelial cells. These data suggest that epithelial cells may, in addition to macrophages and fibroblasts, be an important effector cell in the immunopathogenesis of asbestos-associated diseases and in particular, in the neutrophilic infiltration that is commonly observed after asbestos exposure.

Asbestos, Serpentine↗

PubMed1995

Effects of cigarette smoke and asbestos on airway, vascular and mesothelial cell proliferation.

In order to determine whether exposure to both cigarette smoke and asbestos leads to enhanced cell proliferation, and whether pleura cell proliferation reflects the presence of fibres at or near the pleura, rats were exposed to air (control), daily cigarette smoke, a single intratracheal instillation of amosite asbestos, or a combination of smoke and asbestos. Dividing cells were labelled with bromodeoxyuridine (BrdU) and animals were sacrificed at 1, 2, 7 or 14 days. Both cigarette smoke and asbestos produced increases in the labelling index of small airway wall, epithelial cells and pulmonary artery cells. In the small airways there was a brief marked positive synergistic interaction between these two agents, but synergism was not seen in the vessels. Cigarette smoke did not increase the labelling of mesothelial or submesothelial cells, whereas asbestos caused a persisting increase in mesothelial cell labelling. There was no correlation between the number of BrdU labelled mesothelial or submesothelial cells and the number of fibres touching the pleura, or located within 180 microns of the pleura. We conclude that the combination of cigarette smoke and asbestos exposure produces a complex set of interactions and has the potential to markedly increase cell proliferation in the parenchyma, an effect that may be important in both fibrogenesis and carcinogenesis. In contrast to the diminishing effects over time of a single dose of asbestos on cell proliferation in the small airways and vessels, the same dose of asbestos leads to sustained mesothelial cell proliferation. However, the latter process does not correlate with local accumulation of asbestos fibres.

Animals↗

PubMed1996

[Environmental and indoor air exposure to asbestos fiber dust as a risk and causal factor of diffuse malignant pleural mesothelioma].

In an interdisciplinary, multicentre case control study of the causal factors of the diffuse malignant mesothelioma (DMM) standardised histories where taken from n = 324 Patients suffering from DMM, n = 315 hospital control patients (KK) and n = 182 population controls (PK). For 66 DMM, 149 KK and 107 PK a risk from asbestos fibre dust at the workplace was not detectable. For latter persons indoor and outdoor asbestos exposure outside of the workplace were investigated. The following factors were examined: neighbourhood exposure from companies using asbestos, living in big cities and nearby main traffic roads, building materials containing asbestos, electric storage heaters and household contacts. For using electric storage heaters a statistically significant increased odds ratio (OR) was observed for DMM as well in comparison with KK (OR = 2.42; 95%-CI: 1.01-5.72) and in comparison for PK (OR = 2.91; 95%-CI: 1.08-7.80). Only outside of Hamburg an increased OR compared to KK was observed for people living in the neighbourhood of asbestos factories (OR = 16.3; 95%-CI: 1.35-196.8) and also, but only in Hamburg, compared to PK living nearby main traffic roads. There is only a trend for a mesothelioma-risk for household-contacts based on a few cases. In one DMM-patient without an occupational asbestos exposure the lung dust fibre analysis yielded 2.912 FB and 1.459 x 10(3) crocydolithe fibres per gram dried lung tissue. As a child he lived in the immediate vicinity of the blue asbestos mine in Wittenoom, Australia. Therefore in special cases a para-occupational asbestos or a neighbourhood asbestos exposure can be demonstrated as a risk factor of diffuse malignant mesothelioma.

Adult↗

PubMed1998

[Mineral analysis and study of asbestos pathology].

Several tools are available for the evaluation of the exposure to asbestos, particularly occupational questionnaire and mineralogical analysis of biological samples. These analysis allow quantification of the level of retention of asbestos fibres in the respiratory tract. Two groups of analysis may be used: quantification of asbestos bodies in sputum, bronchoalveolar lavage fluid or lung tissue samples using light microscopy; quantification and identification of asbestos fibres in bronchoalveolar lavage fluid or lung tissue using analytical electron microscopy. Profiles of lung retention of asbestos bodies or asbestos fibres have been described in various asbestos-related disorders, and reference values are available in control populations mainly for asbestos bodies using light microscopy. Mineralogical analysis of biological samples is not required for compensation of occupational asbestos-related diseases. However, this type of analysis may prove to be useful to the chest physician when looking for the etiology of some nonspecific respiratory diseases (interstitial pulmonary fibrosis, lung cancer), particularly when the occupational questionnaire is not contributive. As they are quite easier and less expensive, analysis using light microscopy will be performed first.

Asbestos↗

PubMed1998

[The assessment of asbestos exposure].

The aim of the study is to present the principles of assessing asbestos exposure in two different contexts: that of a patient suffering from pleuropulmonary pathology that could be attributed to asbestos and that of a group possible exposed to asbestos. In the first case this evaluation concerns past exposure and depends typically on information obtained during the course of an interview with the patient. In the second case, the exposure is assessed by atmospheric analysis. Jobs in which occupational exposure to asbestos occurs should be examined, the tasks which entail this exposure and objects containing asbestos are discussed in the first part of the article. The accent is placed on the source of exposure, and the use of materials containing asbestos outside the asbestos industry. Some guidelines enabling the appreciation of the intensity of asbestos exposure as a function of the jobs involved and the objects handled are suggested. Regulations and the principle of quantifying asbestos in the atmosphere during direct exposure in the working environment of the one hand and during the course of passive exposure in the environment of the other are discussed in the second part of the article.

Air Pollutants↗

PubMed1989

Induction of angiogenesis by intraperitoneal injection of asbestos fibers.

Tumors and activated macrophages release angiogenic factors that stimulate migration and proliferation of capillaries. We studied the development of angiogenesis before the appearance of mesotheliomas in C57B1/6 mice. Weekly i.p. injections of crocidolite asbestos fibers produced mesotheliomas after 30-50 wk. The initial histologic response to asbestos fibers was a nodular lesion on the peritoneal lining composed of clusters of fibers, activated macrophages, and proliferating mesenchymal cells. The earliest visible evidence of angiogenesis was seen surrounding 7% of these lesions 14 days after a single injection of 200 micrograms of crocidolite asbestos fibers. After six weekly injections, 30% of the lesions containing asbestos fibers were surrounded by a capillary network radiating toward the center of the lesion. Other mineral fibers, including chrysotile asbestos and fiberglass, also induced angiogenesis after six weekly injections. In contrast, only 8% of the lesions containing short asbestos fibers (90.6% less than or equal to 2.0 microns) and 9% of the lesions containing silica particles showed evidence of angiogenesis. We conclude that tumorigenic mineral fibers induce angiogenesis in the peritoneal lining, whereas nontumorigenic mineral particles or short asbestos fibers are less effective. Ingrowth of new blood vessels around clusters of asbestos fibers may facilitate the later emergence of mesotheliomas at these sites.

Animals↗

PubMed1983

Chronic effects of dietary exposure to amosite and chrysotile asbestos in Syrian golden hamsters.

Bioassays of amosite, short-range (SR), intermediate-range (IR) or intermediate-range chrysotile asbestos in combination with the intestinal carcinogen 1,2-dimethylhydrazine dihydrochloride (DMH) were conducted with male and female Syrian golden hamsters. Amosite and both forms of chrysotile asbestos were administered at a concentration of 1% in pelleted diet for the entire lifetime of the hamsters starting with mothers of the test animals. Group sizes varied from 125-254. There was no adverse effect on body weight gain or survival by either type of asbestos or by IR chrysotile asbestos in combination with DMH. A significant increase (p less than 0.05) in adrenal cortical tumors was observed in male hamsters exposed to SR and IR chrysotile asbestos and in females treated with IR chrysotile asbestos when compared to the pooled control groups. However, statistical significance (p less than 0.05) was lost when these dosed groups were compared with temporal control groups. Neither of the male or female amosite asbestos groups showed increased neoplasia in any tissue or organ compared to the control groups. The cocarcinogen studies using IR chrysotile asbestos and 1,2-dimethylhydrazine dihydrochloride were considered inadequate because there was no increase in intestinal neoplasia in the DMH group.

1,2-Dimethylhydrazine↗

PubMed1992

The effects of asbestos inhalation on the distribution and enhancement of immunoassociated antigen expression of alveolar macrophage subpopulation.

We have studied the effects of in vivo asbestos exposure on the surface immune-associated (Ia) antigen expression and distribution of alveolar macrophage subpopulations defined by continuous iso-osmotic Percoll gradients (density range: 1.006 to 1.123 g/ml) using a rat model of asbestos inhalation. Two groups of rats were exposed by intermittent inhalation (6 hr/day for 5 days/week over 4 weeks) to either amphibole (crocidolite) or serpentine (chrysotile) asbestos. A group of control rats was sham-exposed to clean air only. Alveolar macrophages from rats of three groups were obtained by bronchoalveolar lavage. During exposure, distinct differences appeared within 7 days of asbestos exposure, and some of these findings persisted in the crocidolite-exposed group for as long as 2 to 5 months after the cessation of exposure. Furthermore, relatively greater proportions of Ia-antigen positive cells were detected in several density fractions obtained from both asbestos-exposed groups (especially the crocidolite-exposed group). Multinucleated alveolar macrophages were seen frequently in all Percoll fractions after both types of asbestos inhalation. A significant proportion of multinucleated alveolar macrophages in these fractions expressed surface Ia-antigen positivity. The finding of enriched numbers of higher-density phagocytes in bronchoalveolar lavage cell subpopulations from asbestos-exposed rats may reflect the presence of newly recruited-immature monocytes and/or macrophages at sites of intrapulmonary asbestos deposition. Also, increased proportions of Ia-antigen positive cells suggest that a part of them were functionally activated.

Administration, Inhalation↗

PubMed1983

Analysis of depressed cell-mediated immunity in asbestos workers.

To explore the mechanisms of asbestos-related perturbations of the immune system, we evaluated the in vitro cell-mediated immunity of five asymptomatic asbestos workers with hypergammaglobulinemia and decreased T-cell numbers. These results were compared with those in 10 matched controls. Analysis of T-lymphocyte populations revealed decreased absolute numbers of OKT4+ (helper/inducer) T cells in the peripheral blood and phytohemagglutinin (PHA)-stimulated mononuclear cell cultures of the workers. When chrysotile asbestos was added to PHA cultures, expansion of OKT4+ cell populations was disproportionately inhibited in workers' cultures. Furthermore, control proliferative responses to PHA became indistinguishable from initial worker responses. These effects were incompletely explained by the cytotoxic effects of asbestos on cultured lymphocytes. We conclude that both in vivo and in vitro exposure of mononuclear cell populations to asbestos may lead to a diminution of helper-inducer T-cell numbers. In asbestos-exposed individuals, this latter lymphocyte subpopulation appears to be especially sensitive to in vitro asbestos exposure. Although the clinical implications of these findings are unclear, we hypothesize that many of the immunologic abnormalities that occur in asbestos workers could be explained by direct asbestos effects on the OKT4+ immunoregulatory population.

Asbestosis↗

PubMedDate not supplied

Clara cell protein (CC16) in serum and bronchoalveolar lavage fluid of subjects exposed to asbestos.

The Clara cell protein (CC16) is a small and readily diffusible protein of 16 kDa secreted by bronchiolar Clara cells in the distal airspaces. These epithelial cells are altered in several pulmonary pathological processes induced by various lung toxicants. In the search for a new biomarker of asbestos-induced lung impairment, we used a sensitive immunoassay to determine the levels of CC16 in bronchoalveolar fluid (BALF) and serum of subjects exposed to asbestos compared with a group of healthy controls. In the BALF of asbestos-exposed subjects there was an insignificant trend towards CC16 elevation compared with controls, with a (mean +/- SD of 0.81 +/- 0.65 mg l-1 for asbestos-exposed subjects (n = 23) versus 0.39 +/- 0.19 mg l-1 for controls (n = 11) (p = 0.09). In serum, CC16 concentration was significantly increased among asbestos-exposed subjects, with values of 27.2 +/- 24.0 micrograms l-1 for asbestos-exposed subjects (n = 34) versus 16.1 +/- 7.6 micrograms l-1 for controls (n = 34) (p = 0.01). Regarding the effects of smoking, there were significant differences between generally lower CC16 levels in serum and BALF (p = 0.05 and 0.001, respectively) of smokers compared with the higher levels in non-smokers. Serum CC16 levels positively correlated with those in BALF, which is consistent with a diffusional transfer of CC16 from the bronchoalveolar space into the serum. No association, however, emerged between the levels of CC16 in serum or BALF and either the duration of asbestos exposure or the severity of the lung impairment as assessed by chest X-ray. These findings suggest that exposure to asbestos elicits early changes in the local and, importantly, also the systemic levels of CC16. This pneumoprotein therefore appears as a promising non-invasive biomarker of asbestos-induced lung injury and occupational disease in both smoking and non-smoking exposed subjects.

Adult↗

PubMed1993

The relationship between HLA-A, B, DQ, and DR antigens and asbestos-induced lung disease.

To evaluate the relationship between human leukocyte antigen (HLA) and both asbestos-induced pulmonary fibrosis and pleural fibrosis, we obtained HLA-A, B, C, DQ, and DR phenotypes in 42 long-term asbestos-exposed workers. Among these exposed workers, 15 had asbestosis (ILO > or = 1/0) on the chest radiograph and 18 had asbestos-induced pleural fibrosis. We found that there was an increased percentage of HLA-A29, HLA-B44, and HLA-Bw4 in the subjects with asbestosis. In addition, we observed a marginally positive relationship between HLA-A29 and the severity of pulmonary fibrosis. Similarly, there was a higher prevalence of HLA-DRw53 and DQ2 in the subjects with asbestos-induced pleural fibrosis. The presence of HLA-DQ2 was significantly related to the extent and type of asbestos-induced pleural fibrosis while HLA-DRw53 was not consistently related to the type or extent of pleural disease. Importantly, we observed that HLA-A29, HLA-B44, HLA-Bw4, HLA-DRw53, and HLA-DQ2 do not have a significantly shorter duration or latency of asbestos exposure. Moreover, none of the HLA haplotypes (A29, B44, Bw4, DRw53, and DQ2) that we found to be associated with radiographic manifestations of asbestos-induced lung disease were associated with the physiologic abnormalities that have been traditionally associated with asbestos-induced lung disease. The only exception was an isolated decrease in the residual volume associated with the presence of HLA-A29. These results suggest that the HLA-A29 phenotype may be associated with the development of asbestosis and the HLA-DQ2 phenotype may be associated with the development of asbestos-induced pleural fibrosis. However, these associations are not particularly strong, physiologic correlation is lacking, and previous studies do not support our findings.

Asbestosis↗

PubMed2005

Asbestos in the non-mining industry on the Witwatersrand, South Africa.

BACKGROUND AND INTRODUCTION: For many decades, and until fairly recently, asbestos was commonly found in most sectors of South African industry. Consequently there is a large but indeterminate pool of formerly exposed workers, some of whom will present to medical practitioners for evaluation of possible asbestosis, the pneumoconiosis caused by the fibre. Fundamental to the diagnosis of asbestosis is a history of asbestos exposure sufficient to cause the disease. Attending practitioners need to be aware of the common asbestosis-inducing industries and jobs and the duration of exposure reported by patients if we are to obtain and interpret their exposures. This paper describes asbestos exposure in 141 cases of asbestosis. METHODS: Cases were identified from patient records at the Occupational Medicine Clinic of the National Institute for Occupational Health (NIOH, formerly NCOH), for the years 1980-2000. Patients were only included in the series if they had no asbestos exposure in mining, if they had been certified with asbestosis by a compensation panel, and if on re-reading of the chest radiograph a radiologist reported irregular opacities (profusion 1/0 or greater on the International Labour Organisation (ILO) scale). Asbestos exposure was taken from the patient's records. RESULTS: Only one patient was exposed in an industry where asbestos was incidental to the enterprise's operation, while 54% of cases arose from exposure in primary asbestos industries, i.e. companies selling, distributing, refining, milling or using raw asbestos to manufacture products. The mean reported duration of exposure was 17.5 years. Surprisingly, 21 cases (15%) reported less than 5 years' exposure. Unexpectedly, 7 cases had a latency period from first exposure to diagnosis of less than 6 years. CONCLUSION: The data presented should assist practitioners in the purposeful exploration of asbestos exposure and in interpretation of its significance with regard to asbestosis.

Adult↗