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At least 19 recordsLinked to original sources
PubMed1982

Alteration of in vitro immunoglobulin secretion by amosite asbestos.

We investigated the in vitro effects of amosite asbestos on immunoglobulin (Ig) secretion by human peripheral blood mononuclear leukocytes (MNL). Concentrations of 100 to 300 micrograms/ml of amosite asbestos reduced the number of Ig-secreting cells recovered from 6-day cultures of unstimulated MNL or MNL stimulated with Epstein Barr virus. By contrast, the Ig secretory response to pokeweed mitogen was enhanced by 10 to 100 micrograms/ml concentrations of amosite asbestos; however, amosite asbestos no longer enhanced the response to pokeweed mitogen when MNL were first partially depleted of monocytes (to less than 2%) esterase-positive cells remaining). These results indicate that amosite asbestos has multiple effects on the cells involved in Ig secretion: 1) amosite asbestos inhibits unstimulated B cell function; 2) amosite asbestos inhibits the function of B cells stimulated with the direct B cell activator Epstein Barr virus; and 3) amosite asbestos may alter regulator monocyte function allowing enhanced Ig secretion in the presence of monocyte-dependent B cell triggers such as pokeweed mitogen.

Antibody Formation↗
PubMed1983

NTP Lifetime Carcinogenesis Studies of Amosite Asbestos (CAS No. 12172-73-5) in Syrian Golden Hamsters (Feed Studies).

Carcinogenesis studies of amosite asbestos were conducted by administering diets containing 1% of the asbestos in pellets from the conception of the mothers through the lifetime of male and female Syrian golden hamsters. Control groups consisted of 127 male and 126 female hamsters and the amosite asbestos groups consisted of 252 male and 254 female hamsters. No adverse effect on body weight gain or survival was observed from treatment with amosite asbestos. Neither of the amosite asbestos groups showed increased neoplasia in any organ or tissue compared to the control groups. Under the conditions of these studies, the ingestion of amosite asbestos at a level of 1% in the diet for their lifetime was not toxic and did not cause a carcinogenic response in male and female Syrian golden hamsters. Levels of Evidence of Carcinogenicity: Male Hamsters: Negative Female Hamsters: Negative

Journal Article↗
PubMed2003

Soluble ICAM-1, MCP-1, and MIP-2 protein secretion by rat pleural mesothelial cells following exposure to amosite asbestos.

Pleural inflammation is a sequela of exposure to toxic mineral fibers such as amosite asbestos. This inflammatory response involves the influx of leukocytes from the vasculature into the pleural space. Adhesion molecules such as intercellular adhesion molecule-1 (ICAM)-1 and chemokines such as monocyte chemoattractant protein-1 (MCP)-1 and macrophage inhibitory protein-2 (MIP)-2 are known to be important in pulmonary inflammation following inhalation of particulate matter. However, little is known about their role in pleural inflammation secondary to amosite asbestos exposure. Because the pleural mesothelial cell is believed to be a key target cell of asbestos exposure, the purpose of this study was to determine if ICAM-1, MCP-1, and MIP-2 proteins were secreted by these mesothelial cells following in vitro and in vivo exposure to amosite asbestos. Increased levels of ICAM-1 and MCP-1 protein were measured following 24 or 48 hours exposure of cultured rat pleural mesothelial cells to amosite fibers (1.5 to 5.0 micro g/cm(2)). Increased levels of ICAM-1, MCP-1, and MIP-2 protein were found in pleural lavage fluid from Fischer-344 rats exposed to amosite asbestos for 4 and 12 weeks and after a 12-week recovery period (following the 12-week exposure period). These findings suggest that the secretion of ICAM-1, MCP-1, and MIP-2 by rat pleural mesothelial cells may contribute to amosite-induced pleural inflammation.

Administration, Inhalation↗
PubMed1983

Chronic effects of dietary exposure to amosite asbestos and tremolite in F344 rats.

Carcinogenesis bioassays of blocky (nonfibrous) tremolite and amosite asbestos alone or in combination with the intestinal carcinogen 1,2-dimethylhydrazine dihydrochloride (DMH) were conducted with male and female Fischer 344 rats. The minerals were administered at a concentration of 1% in pelleted diet for the entire lifetime of the rats starting with the dams of the test animals. One group of amosite rats also received chrysotile asbestos via gavage during lactation. Group sizes varied from 100 to 250 animals. The offspring from mothers exposed to tremolite or amosite asbestos were smaller at weaning than those from untreated mothers and remained smaller throughout their life. The administration of dimethylhydrazine (DMH) did not affect body weight gain, either in amosite-exposed or nonexposed animals. Survival was comparable in the tremolite and control groups. The amosite-exposed rats showed enhanced survival compared to the untreated controls. DMH exposure reduced survival by approximately one year, although the amosite plus DMH groups survived slightly better than the DMH alone groups. No toxicity or increase in neoplasia was observed in the tremolite-exposed rats compared to the controls. Significant increases (p less than 0.05) in the rates of C-cell carcinomas of the thyroid and monocytic (mononuclear cell) leukemia in male rats were observed in amosite-exposed groups. However, the biological significance of the C-cell carcinomas in relation to amosite asbestos exposure is discounted because of a lack of significance when C-cell adenomas and carcinomas were combined and the positive effect was not observed in the amosite plus preweaning gavage group. The biological significance of an increased incidence of mononuclear cell leukemia is questionable, because of a lack of statistical significance in the amosite group when evaluated using life table analysis, lack of significance when compared to the tremolite control group, and the fact that no toxic or neoplastic lesions were observed in the target organs, i.e., gastrointestinal tract and mesothelium. DMH caused a high rate of (62-74%) of intestinal neoplasia in amosite and nonamosite-exposed groups. Neither an enhanced carcinogenic nor protective effect was demonstrated by exposure to amosite asbestos.

1,2-Dimethylhydrazine↗
PubMed1983

Acute lung response to amosite asbestos: a morphological study.

The acute morphological response to amosite asbestos in the guinea pig was studied by light microscopy and by transmission, scanning, and scanning transmission electron microscopy. Fiber identification was carried out by energy dispersive X-ray analysis. Animals were studied at postinjection intervals of 2, 4, and 12 hr and 1-7 days. Three groups of test animals were studied for each time interval. These consisted of a vascularly perfused parenchymal group and a free cell lavaged group. The information obtained was compared with saline-injected and normal control animals. The acute tissue response was characterized by intraalveolar, not interstitial, events. The early phagocytic response was shared between polymorphs and macrophages, while in the longer intervals, the macrophages were the phagocytic cell type. Packaging differences within the two types of phagocytes were seen. Endothelial stability was noted, while some edematous type I pneumocytes were observed. Fibrotic involvement was limited to some intraalveolar fibrin deposits. It is suggested that the term "free asbestos fibers" refers to an extracellular event, while intracellular fibers are coated with either a membranous sheath, a siderosome, or a classical ferruginous coating.

Acute Disease↗
PubMed1995

Differential release of superoxide anions by macrophages treated with long and short fibre amosite asbestos is a consequence of differential affinity for opsonin.

OBJECTIVE: To investigate the ability of short and long fibre samples of amosite asbestos to stimulate superoxide production in isolated rat alveolar macrophages, and to determine how opsonisation with rat immunoglobulin might modify this response. METHODS: Macrophages were isolated from rat lung by bronchoalveolar lavage and challenged with both opsonised and non-opsonised long and short fibres of amosite asbestos. Release of superoxide anions was measured by the spectrophotometric reduction of cytochrome c, in the presence and absence of superoxide dismutase. RESULTS: Both long and short fibre samples of amosite asbestos without opsonisation were ineffective in stimulating isolated rat alveolar macrophages to release superoxide anions in vitro. After opsonisation with immunoglobulin, however, a dramatic enhancement of release of superoxide anion was seen with long fibres, but not short, which confirms the importance of fibre length in mediating biological effects. The increased biological activity of the long fibre sample is explained by increased binding of the opsonin to the fibre surface as, at equal mass, the long fibres bound threefold more immunoglobulin than the short fibres. CONCLUSION: Opsonisation is an important factor in modulation of the biological activity of fibres at the cellular level. Differences in binding of opsonin to samples of fibre previously considered to be identical apart from length, suggest that surface reactivity needs to be taken into account when fibres are compared. Binding of biological molecules, in vivo, may thus be an important modifying factor in the pathological processes initiated by fibres.

Animals↗
PubMed1992

Comparison of the pulmonary responses to chrysotile and amosite asbestos administered intratracheally. I) Early phase of cellular reactions.

To clarify whether serpentine and amphibole asbestos have different effects on the lung, UICC chrysotile and amosite asbestos were injected intratracheally into hamster lung, and the lungs were examined at 30 min, 1, 4, 8, and 24 h, and 2 and 4 days after asbestos application by light and scanning electron microscopy. A leukocyte and macrophage reaction appeared at 4 h and increased up to 2 days, and the cell reaction was stronger and more prolonged after application of chrysotile than after application of amosite asbestos. Furthermore, chrysotile induced more prominent cell (leukocytes or/and macrophages) necrosis and alveolar wall thickening. These findings indicate that chrysotile asbestos induces more stronger cell reactions in the alveolar wall, and is more noxious than amosite.

Animals↗
PubMed1993

Absence of amosite asbestos in airway mucosa of non-smoking long term workers with occupational exposure to asbestos.

There is considerable experimental evidence that asbestos fibres are taken up by epithelial cells, and that uptake of fibres is associated with various deleterious, particularly mutagenic, effects. It is not known, however, if asbestos fibres are taken up by human bronchial epithelial cells in vivo. To investigate this question, the amosite asbestos content of the mucosa of seven different airways and four parenchymal sites supplied by these airways in six necropsy lungs from heavily exposed never-smoking long term shipyard and insulation workers without asbestosis was examined. Amosite asbestos was readily found in moderately high concentration in all parenchymal samples, but 33 of 40 airway samples that could be evaluated showed no amosite fibres. The seven positive airways had fibre concentrations that were always much lower than the parenchymal concentrations, and these very few fibres may have been contaminants from the parenchyma. These data suggest that, at least in non-smokers, amosite asbestos either does not penetrate into or does not accumulate in human airway mucosa. These findings also call into question the idea that asbestos acts as a direct airway carcinogen in humans.

Aged↗
PubMed1993

Malignant mesothelioma induced in baboons by inhalation of amosite asbestos.

Ten out of 12 South African baboons (Papio ursinus) survived exposure to amosite asbestos dust for periods ranging from 242 days to 898 days at an aerosol level ranging between 1,100 and 1,200 fibers per milliliter. After exposure, they were kept under observation until they died; the total residence time of amosite varied from 1.2-10.2 years. All underwent detailed postmortem necropsy examinations. All baboons had asbestosis. Five of the baboons developed malignant diffuse mesothelioma; three peritoneal, and two pleural with peritoneal invasion. These results indicate that amosite is highly carcinogenic. Since it is difficult to accomplish follow-up of persons exposed to amosite asbestos because of the geographic location of the amosite mines and mills in South Africa (a majority of the workers being migrant laborers from countries bordering on the Transvaal), it is therefore probable that cases of peritoneal mesothelioma have been missed. If human beings are likely to react to amosite as do baboons, epidemiological follow-up should include identification of abdominal as well as thoracic neoplasms.

Animals↗
PubMed1995

Cytogenetic and pathogenic effects of long and short amosite asbestos.

This study utilized two samples of amosite asbestos which differ in their length, but not in their diameter and which have been shown previously to have very different abilities to cause pathology in rats exposed by instillation or inhalation. The activity of these amosite samples in causing chromosomal aberrations in Chinese hamster ovary cells in culture was examined, along with the effect of the glutathione (GSH) synthesis-inhibiting agent buthionine sulphoximine. The incidence of chromosomal aberrations in cells treated with the short fibre sample was similar to control levels; the long amosite sample caused significantly more chromosomal aberrations than the short fibre sample. When cells were treated with buthionine sulphoximine to decrease the levels of intracellular glutathione, the incidence of chromosomal aberrations was increased in the control cells, but also on treatment with both short and long amosite, the long sample again being considerably more active than the short. The pathogenicity of the long amosite may result from the ability of the fibres to cause chromosome damage, while the enhancement of this damage caused by decreasing intracellular glutathione suggests that the asbestos fibres may impose an oxidant stress on the cells which contributes to these aberrations.

Animals↗
PubMed1999

Studies on the inhalation toxicology of two fiberglasses and amosite asbestos in the Syrian golden hamster. Part II. Results of chronic exposure.

Fiberglass (FG) is the largest category of man-made mineral fibers (MMVFs). Many types of FG are manufactured for specific uses building insulation, air handling, filtration, and sound absorption. In the United States, > 95% of FG produced is for building insulation. Several inhalation studies in rodents of FG building insulation have shown no indication of pulmonary fibrosis or carcinogenic activity. However, because of increasing use and potential for widespread human exposure, a chronic toxicity/carcinogenicity inhalation study of a typical building insulation FG (MMVF 10a) was conducted in hamsters, which were shown to be highly sensitive to the induction of mesotheliomas with another MMVF. A special-application FG (MMVF 33) and amosite asbestos were used for comparative purposes. Groups of 140 weanling male Syrian golden hamsters were exposed via nose-only inhalation for 6 h/day, 5 days/wk for 78 wk to either filtered air (chamber controls) or MMVF 10a, MMVF 33, or amosite asbestos at 250-300 WHO fibers/cm(3) with two additional amosite asbestos groups at 25 and 125 WHO fibers/cm(3). They were then held unexposed for 6 wk until approximately 10-20% survival. After 13, 26, 52, and 78 wk, various pulmonary parameters and lung fiber burdens were evaluated. Groups hamsters were removed from exposure at 13 and 52 wk and were held until 78 wk (recovery groups). Initial lung deposition of long fibers (>20 microm in length) after a single 6-h exposure was similar for all 3 fibers exposed to 250-300 fibers/cm(3). MMVF 10a lungs showed inflammation (which regressed in recovery hamsters) but no pulmonary or pleural fibrosis or neoplasms. MMVF 33 induced more severe inflammation and mild interstitial and pleural fibrosis by 26 wk that progressed in severity until 52 wk, after which it plateaued. While the inflammatory lesions regressed in the recovery animals, pulmonary or pleural fibrosis did not. A single multicentric mesothelioma was observed at 32 wk. No neoplasms were found in the remainder of the study. Amosite asbestos produced dose-related inflammation and pulmonary and pleural fibrosis as early as 13 wk in all 3 exposure levels. The lesions progressed during the course of the study, and at 78 wk severe pulmonary fibrosis with large areas of consolidation was observed in the highest 2 exposure groups. Progressive pleural fibrosis with mesothelial hypertrophy and hyperplasia was present in the thoracic wall and diaphragm in most animals and increased with time in the recovery hamsters. While no pulmonary neoplasms were observed in the amosite exposed hamsters, a large number of mesotheliomas were found; 25 fibers/cm(3), 3.6%; 125 fibers/cm(3), 25.9%; and 250 fibers/cm(3), 19.5%. For the 3 fiber types, the severity of the lung and pleural lesions generally paralleled the cumulative fiber burden, especially those >20 microm length, in the lung, thoracic wall, and diaphragm. They also inversely paralleled the in vitro dissolution rates; that is, the faster the dissolution, the lower were the cumulative lung burdens and the less severe the effects.

Animals↗
PubMed2000

Pathogenicity of a special-purpose glass microfiber (E glass) relative to another glass microfiber and amosite asbestos.

This article describes the activity of an E-glass microfiber (104E) during chronic inhalation and intraperitoneal injection studies in rats. Results are compared with another microfiber of similar dissolution rate (k(dis)), code 100/475, and the more durable amosite asbestos, both of which we had previously used in similar experiments (Davis et al., 1996). Rats were exposed to aerosol concentrations of 1000 fibers (longer than 5 microm)/ml, as measured by optical microscopy, for 7 h/day, 5 days/wk. Subgroups of rats were followed for mean lung burden, early and late signs of fibrosis, and tumor incidence. At the end of 12 mo of exposure, the mean number of 104E fibers of all lengths in the lungs was approximately double that for amosite but two-thirds of that for 100/475. For fibers longer than 15 microm, the mean 104E burden was similar to that for the amosite and more than twice that of the 100/475. After a 12-mo recovery period, the retained lung burdens (of fibers of all lengths) were approximately 30% of those at 12 mo for both microfibers, and somewhat higher (approximately 44%) for amosite. Amosite and 100/475 fibers longer than 15 microm were more persistent in the lungs than 104E fibers. The chemical composition of 104E fibers did not appear to have been significantly altered by up to 24 mo of residence in lung tissue, whereas the composition of 100/475 was substantially altered over the same time period. From the inhalation study, out of the pathology subgroup of 43 animals exposed to 104E microfibers, 10 had lung tumors (7 carcinoma, 3 adenoma) and 2 had mesotheliomas, whereas in 42 rats exposed to amosite asbestos, there were 16 lung tumors (7 carcinoma, 9 adenoma) and 2 mesotheliomas. The 104E- and amosite-treated animals had similar levels of fibrosis. In contrast, 38 animals treated with 100/475 had little fibrosis, 4 lung tumors (adenomas), and no mesotheliomas. The greater pathogenicity of the 104E fibers, compared to 100/475 fibers, might be partly explained by the greater numbers of long fibers retained in the lung after 12 mo of inhalation. However, we speculate that modification of surface properties by extensive selective leaching of some glass components reduces the toxic potential of 100/475. In a parallel intraperitoneal injection study, 104E caused considerably more mesotheliomas (21 rats out of 24) than 100/475 (8 rats out of 24). In addition, 104E appeared to be more active than amosite asbestos, since mesotheliomas appeared much more quickly in the 104E-treated animals. In conclusion, we have shown that two microfiber types, 100/475 and 104E, of similar dissolution rates, had markedly different pathogenicity in rats. We believe that this contrast is only partly due to differences in numbers of long fibers and that differences in surface properties of the fibers, possibly due to proportionately greater leaching of 100/475 fibers, play an important role.

Administration, Inhalation↗
PubMed1997

Progression of pleural and parenchymal disease on chest radiographs of workers exposed to amosite asbestos.

OBJECTIVES: To determine predictors of progression of pleural and parenchymal disease on the chest radiographs of workers exposed to a short term, intense exposure of amosite asbestos. METHODS: The first and last of a series of chest radiographs of 887 workers exposed to amosite was interpreted and coded according to International Labour Organisation (ILO) standards by two physicians. Significant predictors of disease progression were found by a linear stepwise regression analysis from among such variables as smoking history, latency (time since first exposure), duration and intensity of exposure, and cytology. RESULTS: Although most radiographs remained normal, some showed progression of disease with about twice as many patients with abnormalities on the last film. Various combinations of age, intensity of exposure, and time between films were significant predictors of pleural and parenchymal disease and progression of such disease. No predominance of one sided disease was noted. Cytology and smoking were unreliable predictors of disease. Most disease progression was minor, usually of less than two scoring categories. CONCLUSION: An intense, yet short, exposure to amosite asbestos can produce pleural and parenchymal changes on chest radiographs. The number of those affected roughly doubled over a period spanning 10 to 20 years after exposure. Age and intensity of exposure are the most important predictors of disease.

Adult↗
PubMed1985

A scanning electron microscopic study of the early response of lung tissue to amosite asbestos exposure.

The early response of the lung to a single exposure of amosite asbestos was examined via scanning electron microscopy and correlated light microscopy in the guinea pig model. At 2 h post-exposure, lesions consisted of discrete areas of atelectasis with influx of neutrophils and macrophages. Free asbestos fibres were evident in affected areas. By 4 h post exposure, affected regions were more extensive with phagocytic cell numbers increased both in reactive sites and in adjacent tissue. By 1 day post-exposure, the inflammatory response was well developed and encompassed wide areas of the lung. Activated phagocytes were congregated in atelectatic regions and on blood vessel walls. Numerous macrophages were present even in alveoli distant to reactive loci. The 6 day and 12 day time frames marked a subsiding of the inflammatory response in which macrophages outnumbered PMNs in the comparably fewer reactive areas. There was a notable decrease both in marginated leucocytes and in accumulations of phagocytes in tissue adjacent to affected regions.

Acute Disease↗