asbestos--amosite and Asbestosis

The term asbestos collectively refers to a group of naturally occurring fibrous minerals which have been exploited in numerous commercial and industrial settings and applications dating to antiquity. Its myriad uses as a "miracle mineral" owe to its remarkable properties of extreme resistance to thermal and chemical breakdown, tensile strength, and fibrous habit which allows it to be spun and woven into textiles. Abundant in nature, it has been mined considerably, and in all continents save Antarctica. The nomenclature concerning asbestos and its related species is complex, owing to the interest held therein by scientific disciplines such as geology, mineralogy and medicine, as well as legal and regulatory authorities. As fibrous silicates, asbestos minerals are broadly classified into the serpentine (chrysotile) and amphibole (crocidolite, amosite, tremolite, anthophyllite, actinolite) groups, both of which may also contain allied but nonfibrous forms of similar or even identical chemical composition, nonpathogenic to humans. Recently, fibrous amphiboles, not historically classified or regulated as asbestos (winchite, richterite), have been implicated in the causation of serious disease due to their profusion as natural contaminants of vermiculite, a commercially useful and nonfibrous silicate mineral. Although generally grouped, classified, and regulated collectively as asbestos, the serpentine and amphibole groups have different geologic occurrences and, more importantly, significant differences in crystalline structures and chemical compositions. These in turn impart differences in fiber structure and dimension, as well as biopersistence, leading to marked differences in relative potency for causing disease in humans for the group of minerals known as asbestos.

Topics: Asbestos; Asbestos, Amosite; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Humans; Mesothelioma; Mineral Fibers

Grunerite asbestos (amosite) has been shown in epidemiological and experimental animal studies to cause lung cancer, mesothelioma and pulmonary fibrosis commonly referred to as asbestosis. An overview of the human and experimental animal studies describing the health hazards of grunerite asbestos (amosite) is presented. Of the many human studies describing the health hazards of asbestos, only three factories using mainly, if not exclusively, grunerite asbestos (amosite) have been studied. The first is a series of reports on a cohort of 820 workers from a plant located in Paterson, NJ. Among this cohort, 18.7% died of lung cancer and 17 mesotheliomas occurred. The Paterson factory closed in 1954 and moved to Tyler, Texas where it operated until 1972. Among the 1130 former workers in the Tyler plant 6 mesotheliomas were reported with 15.8% lung cancer mortality. The third grunerite asbestos (amosite) exposed cohort was an insulation board manufacturing facility in Uxbridge, United Kingdom. Here 17.1% of the workers died of lung cancer and 5 mesotheliomas occurred. The lung content from 48 Uxbridge workers was analyzed by analytical transmission electron microscopy for mineral fibers. The relationship between grunerite asbestos (amosite) concentrations in the lung correlated with grades of fibrosis and asbestos bodies and was lower than the concentration found in the cases with malignant tumors. The lung cancer cases contained more grunerite asbestos (amosite) than mesothelioma cases, and in the cases of non-malignant disease the concentrations were still lower. In both types of malignancies the concentration of grunerite asbestos (amosite) was very high-over a billion fibers per gram of dried lung tissue. Occupational exposure to airborne concentrations of between 14 and 100 fibers of grunerite asbestos (amosite) per milliliter after 20 year latency causes marked increases in lung cancer, mesothelioma and pulmonary fibrosis (asbestosis).

Topics: Air Pollutants, Occupational; Animals; Asbestos, Amosite; Asbestosis; Cohort Studies; Disease Models, Animal; Humans; Lung; Lung Neoplasms; Mesothelioma; New Jersey; Texas; United Kingdom

The authors briefly reviewed the literature concerning the risk factors for primary pleural tumors in humans. The results from the most relevant studies emphasize the fact that the large majority of mesotheliomas are associated with exposure to asbestos or asbestiform fibers. Exposure to asbestos is mainly through industrial use, and mesotheliomas result from occupational, para-occupational, or environmental exposure. Fibers of crocidolite, amosite, and chrysotile appear to be, in descending order, more carcinogenic for pleural tissues. The authors summarize the available data on consumption of asbestos and asbestos-based products in Italy. The chrysotile-asbestos mine in Balangero (Piedmont) stimulated the industrial production of asbestos-cement; asbestos has been largely sprayed among shipyards and user for insulating railroad coaches and carriages. Italy had the greatest consumption of crocidolite in Europe, which was not banned until 1986. The authors discuss the major findings derived from descriptive epidemiological data presented in previous papers dealing with this issue. In addition, standardized mortality rates of primary pleural tumors for European countries are shown. A clearly increasing trend for mortality is observed in Italy, which has also the provinces with the highest mortality rates in Europe. Among Italian provinces, the mortality rates are consistent with the number of asbestosis cases receiving workman's compensation. The authors present the results of both cohort and case-control analytical studies performed in Italy, and provide suggestions for further research.

Topics: Asbestos; Asbestos, Amosite; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Construction Materials; Europe; Female; Humans; Italy; Lung Neoplasms; Male; Mesothelioma; Occupational Diseases; Pleural Neoplasms; Prevalence; Risk Factors

Tissues obtained at autopsy or biopsy from 81 workers and 2 household persons, were chemically digested. The asbestos fibres recovered were characterized by analytical transmission electron microscopy. Among the 83 causes of death were 33 mesotheliomas, 35 lung cancers, 12 asbestosis and 3 from other cancers. Of the three major commercial asbestos fibre types, amosite was found to be the most prevalent fibre, occurring in approximately 76% of the cases, followed by chrysotile in approximately 60% and crocidolite in approximately 24%. Amosite and chrysotile were observed as the single commercial fibre in approximately 22 and approximately 17% of the cases respectively, whereas crocidolite and tremolite were found as the single fibre type in only approximately 2.5% of the cases. Among the fifteen cases where chrysotile and tremolite occurred together, the amount of chrysotile fibre always exceeded tremolite. However, tremolite was also found in ten additional cases where chrysotile was not detected. Amosite was present in four, amosite plus crocidolite in three, and crocidolite alone in one. Amosite was present in all of the insulation workers' lungs studied and was found in the highest concentration in this exposure category. The highest chrysotile concentration was found among workers in general trades. Although most prevalent in shipyard workers lungs, crocidolite concentration is not statistically different among the exposure groups studied. Although crocidolite was found in twenty cases, amosite accompanied it in eighteen of these. Eleven of the 20 cases were from shipyard workers. Of the 8 mesothelioma cases, 7 also contained amosite. Crocidolite alone only occurred in 1 of the 33 mesothelioma cases analysed. We concluded the following: crocidolite exposure occurred among USA insulators and a large percentage of other workers as well; insulation workers are primarily exposed to amosite; mixed fibre exposures are associated with more mesotheliomas than single fibre exposures; chrysotile only exposure is associated with approximately 12% of the mesothelioma cases studied; and if tremolite exposure is associated with chrysotile exposure, the chrysotile amount exceeds that for the associated tremolite.

Topics: Aged; Asbestos; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Autopsy; Biopsy; Female; Humans; Lung; Lung Neoplasms; Male; Microscopy, Electron; Middle Aged; Occupational Exposure; Organ Culture Techniques; United States

The possibility to detect initial "preclinical" pulmonary lesions related to asbestos is under debate. The aim of this study is to report our experience. We have submitted to HRCT 70 shipyard workers with chest X-ray judged "normal" by "outside" readers (mean age 44.5 +/- 6.1 ys) with a similar grade of (low-level) exposure to amosite (mean duration of "direct"/"heavy" exposure was 4.2 +/- 4.9 ys; "environmental"/"light" exposure was 8.4 +/- 5.9 ys). Among the 70 workers, in 34 pleural plaques were shown, in 6 subjects parenchymal abnormalities alone and in 13 parenchymal and pleural abnormalities were found; in the last 17 workers no pathological finding was shown. In six subjects the presence of a combination of parenchymal abnormalities permitted us to diagnose asbestosis. The difference in the duration of exposure to asbestos for the subjects with both pleural and parenchymal involvement compared to all other groups of workers was statistically significant; also the difference in duration of exposure between workers with or without parenchymal involvement resulted significant. In a control group (20 subjects without any known professional exposure to asbestos) HRCT permitted us to identify 5 cases with small pleural plaques while only one case presented parenchymal bands; lesion frequency was significantly lower in comparison with the exposed group. Calcified plaques have been proved to be more common in the workers with heavier exposure, and no one of the reference group had calcified plaques. The CT-determined emphysema score was found to optimally correlate with smoking habit (pack/years). In conclusion our study suggests that pulmonary or pleural involvement can be shown by HRCT before the onset of any clinical symptomatology with high sensitivity and specificity. Furthermore the results seem to indicate that the prevalence of HRCT-shown parenchymal lesions and the severity of lung involvement among asbestos-exposed workers are related to the duration of exposure, as in most of clinically evident asbestos-related lung disorders, in contrast with previous observations.

Topics: Adult; Asbestos, Amosite; Asbestosis; Female; Humans; Lung; Male; Middle Aged; Occupations; Pleura; Ships; Smoking; Time Factors; Tomography, X-Ray Computed

We have conducted a population-based study of pleural mesothelioma patients with occupational histories and measured asbestos lung burdens in occupationally exposed workers and in the general population. The relationship between lung burden and risk, particularly at environmental exposure levels, will enable future mesothelioma rates in people born after 1965 who never installed asbestos to be predicted from their asbestos lung burdens.. Following personal interview asbestos fibres longer than 5 µm were counted by transmission electron microscopy in lung samples obtained from 133 patients with mesothelioma and 262 patients with lung cancer. ORs for mesothelioma were converted to lifetime risks.. Lifetime mesothelioma risk is approximately 0.02% per 1000 amphibole fibres per gram of dry lung tissue over a more than 100-fold range, from 1 to 4 in the most heavily exposed building workers to less than 1 in 500 in most of the population. The asbestos fibres counted were amosite (75%), crocidolite (18%), other amphiboles (5%) and chrysotile (2%).. The approximate linearity of the dose-response together with lung burden measurements in younger people will provide reasonably reliable predictions of future mesothelioma rates in those born since 1965 whose risks cannot yet be seen in national rates. Burdens in those born more recently will indicate the continuing occupational and environmental hazards under current asbestos control regulations. Our results confirm the major contribution of amosite to UK mesothelioma incidence and the substantial contribution of non-occupational exposure, particularly in women.

Topics: Adult; Aged; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Employment; Female; Humans; Lung; Lung Neoplasms; Male; Mesothelioma; Mesothelioma, Malignant; Middle Aged; Mineral Fibers; Occupational Diseases; Occupational Exposure; Pleural Neoplasms; Risk Assessment

The Tyler asbestos plant produced pipe insulation from 1954 to 1972 and exclusively used amosite asbestos. There were 1130 former workers of this plant during the period of operation. A death certificate mortality analysis was published regarding this plant in 1998 for the period through 1993. This study represents an update of the mortality analysis with additional certificates collected for deaths occurring through 2011.Searches of the National Death Index database were conducted in 2004 and again in 2013. At the time of the latter search, only deaths occurring through 2011 were available. In total, 265 distinct additional death certificates were secured and added to 304 available from the original study. After the new certificates were coded (ICD-9), data were analyzed using the Centers for Disease Control and Prevention Life Table Analysis System (LTAS) and standard mortality ratios (SMR) generated with 95% confidence limits (CL). LTAS constructs cause-specific mortality rates by age, gender, race, and person-time at risk, and compares observed rates with a referent population in order to derive SMR. A significant excess number of deaths due to nonmalignant respiratory disease (asbestosis) and from select malignant neoplasms were identified. There were in total 23 mesothelioma deaths (4% of deaths), with 16 pleural and 7 peritoneal. The SMR for malignant neoplasms of the trachea, bronchus, and lung was 244 (with 95% CL 196, 300), suggesting that exposed workers from this cohort were nearly 2.5-fold (244 %) more likely to die from this cause as the general referent population. The analysis also showed that exposures of short duration (<6 mo) produced significantly elevated SMR for all respiratory cancers, lung cancer, and pleural mesothelioma. There was a significant difference in median duration of exposure for mesothelioma types, confirming association of peritoneal mesothelioma with longer duration of exposure. Deaths due to intestinal cancer (predominantly colon; not including rectum) were also found in excess. The mortality experience of the Tyler cohort continues to be followed with great interest, given the exclusivity of exposure to amosite. Data confirm the inherent pathogenicity of this fiber type for nonmalignant disease as well as select cancers, particularly relevant given the importance of this amphibole's use in the United States.

Topics: Asbestos, Amosite; Asbestosis; Cohort Studies; Female; Humans; Male; Occupational Diseases; Occupational Exposure; Texas

A diagnosis of asbestosis, lung fibrosis due to asbestos exposure, was proposed in 2003 in a 64-year-old woman on the basis of the history, computed tomography appearances, lung function studies, and biometric data. This diagnosis was confirmed by the pathological examination of a lung lobe resected surgically for bronchial carcinoma in 2010. The diagnosis of asbestosis is now rarely made as a result of a substantial decrease in dust exposure over the past decades and mainly because of the interdiction of asbestos use in western countries. Currently, the most frequent thoracic manifestations of asbestos exposure are benign pleural lesions and mesothelioma. It has also become exceptional to have pathological confirmation of the diagnosis, obtained in this woman thanks to the surgical treatment of another complication of her occupational exposure.

Topics: Antineoplastic Combined Chemotherapy Protocols; Asbestos, Amosite; Asbestosis; Bronchoalveolar Lavage Fluid; Carcinoma, Bronchogenic; Cisplatin; Combined Modality Therapy; Female; Humans; Incidental Findings; Industry; Lung; Lung Neoplasms; Middle Aged; Mineral Fibers; Occupational Exposure; Pleura; Pulmonary Aspergillosis; Respiratory Function Tests; Tomography, X-Ray Computed; Vinblastine; Vinorelbine

Topics: Asbestos, Amosite; Asbestosis; Developing Countries; Global Health; Humans; International Cooperation; Mining

This study focuses on the amosite mining region in South Africa and associated health effects, compared to other mined asbestos fiber types. Historically, dust and fiber levels were high in the amosite mills and mines, and many miners and members of the surrounding communities were exposed to the fibers. Research has shown that amosite produces both benign and malignant disease. Nevertheless, the mesotheliomagenic potential of amosite is several fold lower than crocidolite. The risk of disease associated with amosite exposure is difficult to quantify. Reasons for this include the scarcity of available information, including fiber measurements, and case ascertainment, as well as the juxtaposition of the amosite and crocidolite asbestos seams in South Africa.

Topics: Asbestos, Amosite; Asbestosis; Environmental Exposure; Female; History, 20th Century; Humans; Male; Mesothelioma; Mineral Fibers; Mining; South Africa; Space-Time Clustering

South Africa (SA), a country in which all three commercially important asbestos minerals have been mined and milled, has retained proven cases of mesothelioma linked with environmental exposure to asbestos. This study illustrates the importance of fiber type in the occurrence of environmental mesothelioma. Four studies have reviewed the source of occupational or environmental asbestos exposure in 504 histologically proven cases of mesothelioma in South Africa. One hundred and eighteen cases (23%) were thought to be related to environmental exposure to asbestos. In the vast majority of these cases, exposure was linked to crocidolite mining activities in the Northern Cape Province. Two cases were thought to have occurred in relation to amosite and Transvaal crocidolite exposure in the Limpopo Province. In the balance of cases there was some uncertainty. No cases were reported with exposure to South African chrysotile. Consequently, in the vast majority of cases of mesothelioma, environmental exposure to asbestos occurred in the Northern Cape Province, in proximity to mines, mills and dumps where crocidolite was processed. Crocidolite appears to be far more mesotheliomagenic than amosite, and chrysotile has not been implicated in the disease. This is true for both occupationally and environmentally exposed individuals.

Topics: Asbestos; Asbestos, Amosite; Asbestos, Crocidolite; Asbestosis; Carcinogens; Environmental Exposure; Female; Humans; Male; Mesothelioma; Mineral Fibers; Mining; Occupations; South Africa

Topics: Air Pollutants, Occupational; Asbestos, Amosite; Asbestosis; Environmental Exposure; Humans; Mesothelioma; Mineral Fibers; Mining; New Jersey; South Africa; Texas; United Kingdom

Asbestos causes pulmonary toxicity in part by generating reactive oxygen species that cause DNA damage. We previously showed that the mitochondria-regulated (intrinsic) death pathway mediates alveolar epithelial cell (AEC) DNA damage and apoptosis. Because p53 regulates the DNA damage response in part by inducing intrinsic cell death, we determined whether p53-dependent transcriptional activity mediates asbestos-induced AEC mitochondrial dysfunction and apoptosis. We show that inhibitors of p53-dependent transcriptional activation (pifithrin and type 16-E6 protein) block asbestos-induced AEC mitochondrial membrane potential change (DeltaPsim), caspase 9 activation, and apoptosis. We demonstrate that asbestos activates p53 promoter activity, mRNA levels, protein expression, and Bax and p53 mitochondrial translocation. Further, pifithrin, E6, phytic acid, or rho(0)-A549 cells (cells incapable of mitochondrial reactive oxygen species production) block asbestos-induced p53 activation. Finally, we show that asbestos augments p53 expression in cells at the bronchoalveolar duct junctions of rat lungs and that phytic acid prevents this. These data suggest that p53-dependent transcription pathways mediate asbestos-induced AEC mitochondria-regulated apoptosis. This suggests an important interactive effect between p53 and the mitochondria in the pathogenesis of asbestos-induced pulmonary toxicity that may have broader implications for our understanding of pulmonary fibrosis and lung cancer.

Topics: Animals; Apoptosis; Asbestos, Amosite; Asbestosis; bcl-2-Associated X Protein; Benzothiazoles; Caspase 9; Caspases; Cell Line; Enzyme Activation; Epithelial Cells; Free Radical Scavengers; Humans; Iron Chelating Agents; Lung; Membrane Potentials; Mitochondrial Membranes; Oncogene Proteins, Viral; Phytic Acid; Promoter Regions, Genetic; Protein Transport; Pulmonary Alveoli; Rats; Reactive Oxygen Species; Repressor Proteins; Thiazoles; Toluene; Tumor Suppressor Protein p53

Lung tissue from 15 women who died from mesothelioma was evaluated for tissue burden of ferruginous bodies and uncoated asbestos fibers. The group contained individuals who had occupational exposure to asbestos and others had family members whose work history included vocations where contact with asbestos containing materials occurred.. Tissue samples from tumor free lung were digested and filtered and then investigated for ferruginous bodies by light microscopy and asbestos and non-asbestos fibers by analytical transmission electron microscopy (ATEM). Size and type of fibers were also analyzed.. Asbestos bodies were found in 13 of the 15 samples and asbestos fibers were found in all cases. The most commonly found uncoated asbestos fiber in these individuals was amosite whereas tremolite was the second most commonly found form. The asbestos fiber burden in these females was often of mixed types.. The asbestos body and fiber burden in these cases show variation in tissue burden. Some cases in this study had appreciable burden, which was attributed to secondhand exposure from occupationally exposed family members. Mesothelioma can occur also in individuals with comparatively low tissue burdens of asbestos.

Topics: Aged; Aged, 80 and over; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Crocidolite; Asbestosis; Body Burden; Environmental Exposure; Female; Humans; Lung; Lung Neoplasms; Mesothelioma; Microscopy, Electron; Middle Aged; Mineral Fibers; Occupational Exposure; Reproducibility of Results

Asbestos bodies (ABs) form as asbestos fibers become coated by a cellular iron- and protein-rich matrix. ABs have been reported in lymph nodes and a few extrapulmonary sites, but no data exist as to their formation outside of the lung. It is not clear whether the AB found in these extrapulmonary areas have been transported as mature structures from the lung or formed at the extrapulmonary site. This study was designed to determine if ABs are produced in extrapulmonary sites. The guinea pig efficiently forms ferruginous bodies in the lung and so it was chosen as a model to test the coating efficiency of amosite asbestos fibers in lung, liver and spleen.. Sized amosite asbestos (5 mg) was administered either endotracheally into lung (n = 2) or directly into liver (n = 4) and spleen (n = 4) of healthy 10-week-old male guinea pigs. The lung, liver and splenic tissues were removed at 40 and 180 days post inoculation and were examined histologically for the presence of AB via light microscopy. Uncoated fibers isolated from the tissues were characterized by electron microscopy. The coating efficiency was calculated as a ratio of uncoated/coated fibers per organ.. The coating efficiency ratios of fibers that were collected at 40 days post-injection from the individual sites were: lung - 350:1, liver - 4200:1, and spleen - 220,000:1. At 6 months post-injection the ratios for the individual sites consisted of: lung - 176:1, liver - 11,000:1, and spleen - 1000:1.. This study indicates that AB can be formed in extrapulmonary sites and that the coating efficiency in the lung is much greater than that within the liver or spleen.

Topics: Animals; Asbestos, Amosite; Asbestosis; Disease Models, Animal; Ferritins; Foreign Bodies; Guinea Pigs; Liver; Lung; Male; Mineral Fibers; Spleen

Recent studies have shown that iron is an important factor in the chemical activity of asbestos and may play a key role in its biological effects. The most carcinogenic forms of asbestos, crocidolite and amosite, contain up to 27% iron by weight as part of their crystal structure. These minerals can acquire more iron after being inhaled, thereby forming asbestos bodies. Reported here is a method for depositing iron on asbestos fibers in vitro which produced iron deposits of the same form as observed on asbestos bodies removed from human lungs. Crocidolite and amosite were incubated in either FeCl(2) or FeCl(3) solutions for 2 h. To assess the effect of longer-term binding, crocidolite was incubated in FeCl(2) or FeCl(3) and amosite in FeCl(3) for 14 days. The amount of iron bound by the fibers was determined by measuring the amount remaining in the incubation solution using an iron assay with the chelator ferrozine. After iron loading had been carried out, the fibers were also examined for the presence of an increased amount of surface iron using X-ray photoelectron spectroscopy (XPS). XPS analysis showed an increased amount of surface iron on both Fe(II)- and Fe(III)-loaded crocidolite and only on Fe(III)-loaded amosite. In addition, atomic force microscopy revealed that the topography of amosite, incubated in 1 mM FeCl(3) solutions for 2 h, was very rough compared with that of the untreated fibers, further evidence of Fe(III) accumulation on the fiber surfaces. Analysis of long-term Fe(III)-loaded crocidolite and amosite using X-ray diffraction (XRD) suggested that ferrihydrite, a poorly crystallized hydrous ferric iron oxide, had formed. XRD also showed that ferrihydrite was present in amosite-core asbestos bodies taken from human lung. Auger electron spectroscopy (AES) confirmed that Fe and O were the only constituent elements present on the surface of the asbestos bodies, although H cannot be detected by AES and is presumably also present. Taken together for all samples, the data reported here suggest that Fe(II) binding may result from ion exchange, possibly with Na, on the fiber surfaces, whereas Fe(III) binding forms ferrihydrite on the fibers under the conditions used in this study. Therefore, fibers carefully loaded with Fe(III) in vitro may be a particularly appropriate and useful model for the study of chemical characteristics associated with asbestos bodies and their potential for interactions in a biosystem.

Topics: Adenocarcinoma; Aged; Asbestos, Amosite; Asbestos, Crocidolite; Asbestosis; Chlorides; Ferric Compounds; Ferrous Compounds; Humans; In Vitro Techniques; Lung; Lung Neoplasms; Male; Microscopy, Atomic Force; Microscopy, Electron, Scanning; Models, Biological; Spectrometry, X-Ray Emission

To examine the causes of death among 1130 former workers of a plant in Tyler, Texas dedicated to the manufacture of asbestos pipe insulation materials. This cohort is important and unusual because it used amosite as the only asbestiform mineral in the production process. High level exposure of such a specific type was documented through industrial hygiene surveys in the plant.. Deaths were ascertained through various sources including data tapes from the Texas Department of Health and the national death index files. As many death certificates as possible were secured (304/315) and cause of death assigned. After select exclusions, 222 death certificates were used in the analysis. Causes of death were compared with age, race, and sex specific mortalities for the United States population with a commercial software package (OCMAP Version 2.0).. There was an excess of deaths from respiratory cancer including the bronchus, trachea, and lung (standardised mortality ratio (SMR) 277 with 95% confidence interval (95% CI) 193 to 385). Four pleural mesotheliomas and two peritoneal mesotheliomas were identified. The analysis also showed an increasing risk of respiratory malignancy with increased duration of exposure including a significant excess of total deaths from respiratory cancer with less than six months of work at the plant (SMR 268 with 95% CI 172 to 399).. The importance of the cohort lies with the pure amosite exposure which took place in the plant and the extended period of latency which has followed. The death certificate analysis indicates the pathogenicity of amosite, the predominant commercial amphibole used in the United States. These data confirm a link between amosite asbestos and respiratory malignancy as well as mesothelioma.

Topics: Adult; Aged; Asbestos, Amosite; Asbestosis; Cohort Studies; Humans; Male; Mesothelioma; Middle Aged; Occupational Exposure; Respiratory Tract Neoplasms; Retrospective Studies; Texas; Time Factors

To investigate effects of asbestos on the process of cancer development, the capacity of asbestos which increases cellular uptake of external carcinogens was tested for asbestos-mediated viral RNA transfection in cultured cells. For the transfection, crocidolite, amosite, anthophyllite and chrysotile were placed onto Vero-E6 cells with poliovirus RNA inoculum, respectively. All asbestos samples mediated viral RNA transfection compared with the background including only viral RNA. The transfection was much greater with combined exposure to asbestos and kaolin than with exposure to asbestos alone.

Topics: Animals; Asbestos; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Chlorocebus aethiops; Kaolin; Neoplasms; Poliovirus; RNA, Viral; Transfection; Vero Cells

To analyze the correlation between asbestos lung burden and lung cancer, lungs of 211 female cases with and without lung cancer were examined. Phase-contrast microscopic (PCM) counting of ferruginous (FBs) and uncoated fibers (UFs), which had length longer than 5 microns and aspect ratios greater than 3:1, revealed a significantly higher level of FBs plus UFs in urban lung cancer cases than urban non-lung cancer cases (1380.5 vs. 550.3; p < 0.001). No difference was noted between rural lung cancer and non-lung cancer cases. Analytical electron microscopic studies identified various kinds of mineral fibers with an aspect ratio greater than 3:1 in the lung tissue including chrysotile, actinolite/tremolite, amosite/crocidolite, fibrous talc, mica, silica, iron, wollastonite, chlorite, kaoline, and others. The most frequently detected fibers were thin, short chrysotile fibers, most of which could not be found by PCM, followed by relatively thick, long actinolite/tremolite fibers, fibrous talc, and in a smaller number, amosite/crocidolite of intermediate length and width. Amosite/crocidolite and fibrous talc counts in urban lung cancer cases were greater than those of urban non-lung cancer cases, rural lung cancer, and rural non-lung cancer cases; these findings were consistent with PCM analysis. Therefore, it is suggested that fibers detected in PCM observation may be mainly amosite/crocidolite with some parts fibrous talc and that fibrous talc in urban environments may be another candidate for carcinogenic or cocarcinogenic factors of female lung cancer.

Topics: Adult; Aged; Asbestos, Amosite; Asbestos, Crocidolite; Asbestosis; Carcinogens; Case-Control Studies; Female; Humans; Japan; Lung Neoplasms; Microscopy, Electron, Scanning Transmission; Microscopy, Phase-Contrast; Middle Aged; Rural Health; Talc; Urban Health

In order to investigate how endogenous iron can be deposited in vivo on inhaled mineral fibers during early stages of formation of asbestos bodies, in vitro experiments were performed on the adsorption of ferritin onto amosite asbestos. The mineral dust was found to adsorb the protein from an aqueous solution containing 0.3 mg/ml horse spleen ferritin. In order to simulate physiological conditions the aqueous solution was adjusted with 150 mM saline. Polyacrylamide-SDS gel electrophoresis of the desorbed protein showed subunits of approximately 13 and 15 kD, aside from the 20-kD subunit present in the native protein. This suggests that as a result of interactions between ferritin molecules and the solid surface of the mineral fibers, the protein iron core may be released or partially exposed. Data indicate these interactions may have implications in the observed mineral fiber toxicities.

Topics: Adsorption; Animals; Asbestos, Amosite; Asbestosis; Electrophoresis, Polyacrylamide Gel; Ferritins; Horses; Microscopy, Electron, Scanning; Mineral Fibers; Molecular Weight; Solutions; Spleen; Surface Properties

About 8% of our cases of mesothelioma occur in women, with a median age of 59 years. Our percentage is lower than other series reported in the literature because of the large number of occupationally exposed men referred to our laboratory. Tumor arose in the pleura in 86% of the women in our study, and the majority were epithelial. Pleural plaques were found in half of the women for which this information was available, and asbestosis was found in only 16%. A history of exposure to asbestos was identified in three quarters of the women, more than half of whom were household contacts of asbestos workers. Occupational exposure to asbestos was identified in only 19% of patients. An elevated tissue asbestos burden was noted in 70% of women from whom lung tissue was available for analysis. The main fiber type identified was amosite, followed by tremolite and chrysotile. These findings and those from other countries suggest a need for reassessment of the background rate of mesothelioma in industrialized nations.

Topics: Adult; Aged; Aged, 80 and over; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Serpentine; Asbestosis; Female; Humans; Male; Mesothelioma; Middle Aged; Mineral Fibers; Peritoneal Neoplasms; Peritoneum; Pleura; Pleural Neoplasms

The Cape Boards Plant at Uxbridge produced insulation board containing amosite asbestos between 1947 and 1973 with only small amounts of chrysotile. After 1973 only amosite was used. In this study we examined lung samples from 48 workers who had been employed at the plant and who had come to autopsy. The study investigated the fiber levels against the lung pathology including amount of interstitial fibrosis and numbers of ferruginous bodies. The degree of interstitial fibrosis and number of asbestos bodies were graded and the tissues were analyzed by transmission electron microscopy and energy dispersive X-ray analysis and the fibers counted and typed. The 48 cases included 5 mesotheliomas and 14 lung cancers. The mineral analysis results were dominated by the amosite fiber levels. The amounts of chrysotile were relatively small. There were higher levels in lung cancer cases than mesotheliomas and higher levels in mesothelioma cases than those who had died from nonasbestos related diseases. Analysis of the lung tissues showed a consistent pattern of high amosite levels, which confirms the impression that amosite was the predominant form of asbestos used and also indicates that the factory had been a very dusty one.

Topics: Asbestos, Amosite; Asbestosis; Humans; Lung Diseases; Lung Neoplasms; Mesothelioma; Occupational Diseases; Pulmonary Fibrosis

Experimental inhalation in a number of studies has demonstrated that chrysotile asbestos can cause pulmonary fibrosis and both benign and malignant pulmonary tumours, two lesions which are associated in that the studies reporting high tumour rates also found high levels of asbestosis. One comparison reported that animals with malignant tumours had approximately twice the amount of fibrosis in the lung parenchyma as those of similar age without tumours. Many studies have examined the pathogenicity of asbestos administered by ingestion and most of these included chrysotile asbestos: the results have been universally negative apart from one study with amosite that contained no control animals and is best discarded. Only one inhalation study has reported an examination of the larynxes of animals: this found no pathological changes. In many studies, tumours other than the lung had been listed, but significant numbers of kidney tumours have never been recorded. Injection studies inducing mesothelioma have indicated that fibre geometry is important with long thin fibres (> 8 microns in length and < 0.25 microns in diameter) being the most carcinogenic. This has been difficult to confirm for inhaled fibres although fibres less than 5 microns in length appear to cause neither fibrosis nor pulmonary tumours. Similar results have been found with amosite for fibres up to 10-15 microns although longer fibres do produce these conditions. It is suggested that to produce pulmonary fibrosis and neoplasia fibres may need to be longer than 20 microns. Chrysotile has been shown in many studies to be removed from lung tissue much more rapidly than amphibole fibres.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Administration, Inhalation; Animals; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Serpentine; Asbestosis; Cricetinae; Dust; Injections; Laryngeal Neoplasms; Lung Neoplasms; Mesothelioma; Pleural Neoplasms; Pulmonary Fibrosis; Rats

The different pulmonary macrophage (airway macrophages, alveolar macrophages, interstitial macrophages, intravascular macrophages, pleural macrophages) are an important part of the lungs' defences against non-fibrous and fibrous particles deposited by inhalation. The first line of defence is airway macrophages and alveolar macrophages (AM) which initially interact with deposited chrysotile fibres and subsequently release a number of mediators including growth regulatory and chemotactic proteins, arachidonic acid metabolites, proteases, NO and active oxygen species, all of which can affect--also adversely--specific target cells in the lung. Mechanical clearance via the mucociliary escalator and dissolution of phagocytized fibres in the acidic milieu of the phagolysosome in pulmonary macrophages are further important functions of AM. Chrysotile appears to be more toxic or at least has the same toxicity to AM as amphibole fibres when doses of a similar mass are administered. However, on a fibre number basis chrysotile appears to be less toxic to AM. The importance of the appropriate dose parameter--i.e. fibre mass, number or surface area--needs to be considered in in vitro as well as in in vivo studies. Short chrysotile fibres are cleared from rat lungs very rapidly whereas longer ones are cleared at a much slower rate. This is due to efficient phagocytosis of short fibres by AM accompanied by dissolution in the acidic milieu of the phagolysosome. Prediction of chrysotile clearance in primate lung based on results from rat studies result in an overall retention half-time of approximately 105 days, based on which no long-term accumulation of chrysotile in the primate lung is to be expected. Long-term inhalation studies in baboons exposed to chrysotile confirm the very fast build up of a low steady-state lung burden, consistent with a pulmonary retention half-time for chrysotile of approximately 90 days. Despite the fast clearance and low pulmonary accumulation of chrysotile, the resulting effects, such as asbestosis, were found to be of the same severity in rats as those induced by amphibole exposure. In the amphibole-exposed rats, the fibre lung burden continued to increase with exposure time. The potential contamination of chrysotile with tremolite cannot explain these results since there was no increased pulmonary accumulation of fibres in the chrysotile-exposed rats. Effects due to lung particle overload are not to be expected in long-term chrysotile inha

Topics: Animals; Asbestos, Amosite; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Coal Mining; Cytokines; Dogs; Dust; Humans; Lung; Lymph; Macrophages, Alveolar; Papio; Pneumoconiosis; Quartz; Rats; Silicosis; Time Factors

Studies of human lungs indicate that, for virtually all types of exposure, the relative proportion of amphibole asbestos retained in the lung far exceeds the proportion in the original dust and, conversely, the relative proportion of chrysotile is far less than that in the original dust. Although amphiboles appear to accumulate in lung in proportion to exposure and chrysotile does not, failure of chrysotile deposition is probably not the reason for the disproportionate retention of amphibole fibres. The available data suggest that chrysotile is deposited in the parenchyma but is cleared extremely rapidly, with the vast bulk of fibres removed from human lungs within weeks to months after inhalation; by comparison, amphibole clearance half-lives are of the order of years to decades. The mechanisms of preferential chrysotile clearance remain uncertain, but fragmentation of chrysotile into short fibres, possibly accompanied by extremely rapid dissolution of such fibres, appears to be important in this process. Chrysotile fibres do penetrate to the periphery of the lung, so that differences in mesothelial pathogenicity of chrysotile and amphiboles in regard to mesothelioma are not caused by failure of chrysotile to reach the pleura. The theory that the tremolite contaminant rather than the chrysotile itself is the cause of 'chrysotile-induced' disease (especially mesothelioma) is consistent with the available human data, but the contrary ideas that disease is caused either by the total transient burden of inhaled chrysotile fibres or by a small, sequestered, long-retained fraction of chrysotile fibres still need to be excluded.

Topics: Animals; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Guinea Pigs; Humans; Lung; Mesothelioma; Mining; Occupational Exposure; Pleura; Pleural Neoplasms; Textile Industry; Time Factors

Topics: Asbestos; Asbestos, Amosite; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Humans; Mesothelioma; Pleural Neoplasms; Risk Factors

Topics: Asbestos; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Humans; Mesothelioma; Pleural Neoplasms; Risk Factors

To attempt to determine the mineralogic factors that relate to the appearance of specific types of asbestos-related disease in workers with heavy mixed exposure to amphiboles and chrysotile, we analyzed the pulmonary asbestos fiber burden in a series of 144 shipyard workers and insulators from the Pacific Northwest. Amosite was found in all lungs, and tremolite and chrysotile in most lungs, but the vast majority of fibers were amosite. Tremolite and chrysotile concentrations were significantly correlated, indicating that the tremolite originated from chrysotile products, but no correlation was found between tremolite or chrysotile concentration and amosite concentration. Time since last exposure was correlated with decreasing amosite concentration and the calculated clearance half time was about 20 yr. In a multiple regression analysis that accounted for the presence of more than one disease in many subjects, a high concentration of amosite fibers was correlated with the presence of airway fibrosis and asbestosis, whereas subjects with mesothelioma, lung cancer, pleural plaques, or no asbestos-related disease had about the same, much lower, amosite concentration. No relationship was found between the concentration of chrysotile or tremolite and any disease. Analysis of fiber size measures (length, width, aspect ratio, surface, mass) showed that pleural plaques were strongly associated with high aspect ratio amosite fibers and suggested that mesotheliomas were associated with low aspect ratio amosite fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Aged, 80 and over; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Serpentine; Asbestosis; British Columbia; Construction Materials; Female; Humans; Lung; Male; Middle Aged; Northwestern United States; Occupational Exposure; Regression Analysis; Ships; Time Factors

Chest radiographs were read from a sub-cohort of 386 factory workers with short term exposure to amosite asbestos (median exposure six months) and long follow up (median 25 years). Prevalence of abnormality was determined independently by two readers from the first film available after 20 years from first employment. Serial films were obtainable for 238 men (median interval from first to last film: nine years). Progression was classified with a direct progression scoring scale. Individual dust exposure estimates were derived from dust counts from two similar plants. With as little as one month or less of employment, about 20% of the films showed parenchymal abnormality and about a third showed pleural abnormality. Those in the lowest cumulative exposure stratum (less than 5 fibre-years/ml) were similarly found to have high rates of abnormality. Dose-response relations were present in the data of both readers. Smokers had higher rates of parenchymal abnormality. On multivariate analysis, cumulative exposure was the exposure variable most closely related to parenchymal abnormality, and time from first employment was the variable most closely related to pleural abnormality. Progression (including first attacks) 20 or more years after ceasing employment occurred and was more common for pleural than for parenchymal abnormality. It is concluded that with exposure to high concentrations to amosite such as existed in this factory and with follow up for at least 20 years, (1) exposure for as little as a month was sufficient to produce radiological signs of parenchymal and pleural fibrosis, (2) no cumulative exposure threshold for parenchymal and pleural fibrosis was detectable, and (3) parenchymal and pleural progression were still detectable >/= 20 years after the end of exposure.

Topics: Asbestos; Asbestos, Amosite; Asbestosis; Cohort Studies; Follow-Up Studies; Humans; Lung; Lung Diseases; Male; Middle Aged; Multivariate Analysis; Occupational Exposure; Pleura; Radiography; Smoking

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.

Topics: Animals; Asbestos; Asbestos, Amosite; Asbestosis; Cell Count; Female; Guinea Pigs; Lung; Macrophages; Microscopy, Electron; Smoking; Time Factors

The concentration of airborne fibers longer than 5 microns, thinner than 3 microns, and with an aspect ratio exceeding 3 as counted by phase contrast optical microscopy is the most widely used fiber exposure index. Recently, more adequate, specific exposure indices for asbestosis, lung cancer, and mesothelioma risk have been suggested by Lippmann (1988, Environ. Res., 46, 86-106). The consequences of using these indices are examined on the basis of calculations for a broad range of theoretical and published size distributions. Optical microscopy appears to be a good predictor of the exposure indices for asbestosis and for lung cancer after scaling. Only fibers longer than about 3 microns need to be counted in a transmission electron microscope. The lung cancer index still cannot explain the large differences of risk among chrysotile exposures. Both the mesothelioma exposure index and the ratio mesothelioma to lung cancer index ranks in order of increasing risk: wollastonite, glass and mineral wool, amosite, glass microfibers, chrysotile, and crocidolite. Amosite is thus not ranked according to epidemiological evidence. Detailed size information should be made available so that the size criteria can be adjusted. It may still prove necessary to use fiber type specific concentration limits.

Topics: Asbestos; Asbestos, Amosite; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Environmental Exposure; Environmental Monitoring; Humans; Lung Neoplasms; Mesothelioma; Microscopy, Electron; Microscopy, Phase-Contrast; Minerals; Risk Factors

We have previously shown that in the lungs of a group of chrysotile miners and millers, grade of interstitial fibrosis (asbestosis) is directly proportional to tremolite fiber or chrysotile fiber concentration but is inversely proportional to mean fiber length and length-related parameters. To compare the effects of the commercial amphibole asbestos amosite on parenchymal fibrosis, we histologically graded fibrosis in four different sites in the lungs of 20 shipyard and insulation workers with heavy amosite exposure and measured by analytic electron microscopy fiber concentration and size in corresponding portions of lung tissue. Fibrosis grade was found to be strongly positively correlated with amosite concentration and negatively correlated with mean fiber size parameters, including fiber length, width, surface area, and mass. A comparison of our present results with our data on the chrysotile miners and millers showed that the regression lines of fibrosis grade versus concentration for amosite, chrysotile, and tremolite were statistically different. These findings indicate that amosite concentration, like chrysotile and tremolite concentration, is closely and directly related to fibrosis at the local lung level. Furthermore, these observations again raise the possibility that short fibers may be more important than is commonly believed in the genesis of fibrosis in man. Last, the concentration comparison data indicate that, fiber for fiber, amosite is more fibrogenic than is chrysotile or tremolite, and indirectly suggest that tremolite is more fibrogenic than is chrysotile.

Topics: Aged; Asbestos; Asbestos, Amosite; Asbestosis; Electron Probe Microanalysis; Humans; Lung

A case of clinically and radiologically typical asbestosis manifesting in a 55 year old man occurred 36 years after a brief exposure period of less than one year. A transbronchial lung biopsy was performed but the samples were considered non-diagnostic. The diagnosis was supported by the use of bronchoalveolar lavage to obtain alveolar samples and scanning electron microscopy-energy dispersive x ray analysis of fibres found in the bronchoalveolar lavage fluid which showed a predominance of amosite.

Topics: Asbestos; Asbestos, Amosite; Asbestosis; Bronchoalveolar Lavage Fluid; Electron Probe Microanalysis; Humans; Male; Middle Aged; Time Factors

The lungs from 36 former workers at an East London asbestos factory dying of asbestos-related disease were compared with lung tissue from 56 matched control patients operated on in East London for carcinoma of the lung. The severity of asbestosis and the presence of pulmonary carcinoma or mesothelioma of the pleura or peritoneum were correlated with an asbestos exposure index and with the type and amount of mineral fibre of the lungs. Asbestosis was associated with far heavier fibre burdens than mesothelioma. Moderate or severe asbestosis was more common among those with carcinoma of the lung than in those with mesothelial tumours. Crocidolite and amosite asbestos were strongly associated with asbestosis, carcinoma of the lung and mesothelial tumours, whereas no such correlation was evident with chrysotile or mullite. It is suggested that greater emphasis should be placed on the biological differences between amphibole and serpentine asbestos fibre.

Topics: Aluminum Silicates; Asbestos; Asbestos, Amosite; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Female; Humans; London; Lung; Lung Diseases; Lung Neoplasms; Male; Mesothelioma; Middle Aged; Occupational Diseases; Pleural Neoplasms

Topics: Air Pollutants; Air Pollutants, Occupational; Asbestos; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Humans; Neoplasms; Risk

To determine whether asbestos dust produces pathologic changes in the small airways, and to determine where the anatomic lesions of asbestosis commence, the authors examined lungs from guinea pigs exposed to 10 or 30 mg of amosite asbestos by intratracheal instillation and sacrificed 6 months later. Measurement of airway wall thickness revealed that membranous and respiratory bronchioles of all sizes in exposed animals were significantly thicker than those of controls. Amosite fibers were found embedded in the walls of bronchi and in membranous and respiratory bronchioles; where these fibers penetrated the airway walls, an interstitial inflammatory and fibrotic reaction (asbestosis) occurred. It is concluded that 1) amosite asbestos produces diffuse abnormalities throughout the noncartilagenous airways and possibly the cartilagenous airways as well; 2) this effect is independent of interstitial fibrosis of the parenchyma (classical asbestosis); 3) asbestosis, at least that induced by amosite, commences at any site in the parenchyma to which the asbestos fibers can gain access, either by deposition in alveoli and alveolar ducts or by direct passage of fibers through the walls of all types and sizes of small airways.

Topics: Animals; Asbestos; Asbestos, Amosite; Asbestosis; Bronchi; Disease Models, Animal; Guinea Pigs; Pulmonary Fibrosis

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.

Topics: Acute Disease; Animals; Asbestos; Asbestos, Amosite; Asbestosis; Bronchi; Disease Models, Animal; Female; Guinea Pigs; Leukocytes; Lung; Male; Microscopy, Electron, Scanning; Phagocytosis; Pulmonary Alveoli; Sodium Chloride; Time Factors

Topics: Asbestos; Asbestos, Amosite; Asbestos, Crocidolite; Asbestosis; Disease Susceptibility; Humans; Male; Mining; Risk; South Africa

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.

Topics: Acute Disease; Animals; Asbestos; Asbestos, Amosite; Asbestosis; Guinea Pigs; Histocytochemistry; Iron; Lung; Macrophages; Phagocytosis

This report describes the second in a series of three parallel cohort studies of asbestos factories in South Carolina, Pennsylvania, and Connecticut to assess the effects of mineral fibre type and industrial process on mortality from malignant mesothelioma, respiratory cancer, and asbestosis. In the present plant (in Pennsylvania) mainly chrysotile, with some amosite and a small amount of crocidolite, were used primarily in textile manufacture. Of a cohort of 4137 men comprising all those employed 1938-59 for at least a month, 97% were traced. By the end of 1974, 1400 (35%) had died, 74 from asbestosis and 70 from lung cancer. Mesothelioma was mentioned on the certificate in 14 deaths mostly coded to other causes. All these deaths occurred after 1959, and there were indications that additional cases of mesothelioma may have gone unrecognised, especially before that date. The exposure for each man was estimated in terms of duration and dust concentration in millions of dust particles per cubic foot (mpcf) from available measurements. Analyses were made both by life table and case referent methods. The standardised mortality ratio for respiratory cancer for the whole cohort was 105.0, but the risk rose linearly from 66.9 for men with less than 10 mpcf.y to 416.1 for those with 80 mpcf.y or more. Lines fitted to relative risks derived from SMRs in this and the textile plant studied in South Carolina were almost identical in slope. This was confirmed by case referent analysis. These findings support the conclusion from the South Carolina study that the risk of lung cancer in textile processing is very much greater than in chrysotile production and probably than in the friction products industry. The much greater risk of mesothelioma from exposure to processes in which even quite small quantities of amphiboles were used was also confirmed.

Topics: Adult; Aged; Asbestos; Asbestos, Amosite; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Dust; Humans; Lung Neoplasms; Male; Mesothelioma; Middle Aged; Occupational Diseases; Textile Industry

Incubation of chrysotile and amphibole asbestos fibers with normal human peripheral blood polymorphonuclear leukocytes (PMN) resulted in a significant stimulation of PMN metabolic activity and generation of toxic oxygen by-products as measured by chemiluminescence (CL). Although all asbestos fibers tested were cytotoxic to PMN, cytotoxicity and CL varied disproportionately with fiber type. Anthophyllite asbestos produced the greatest PMN cytotoxicity. It also depressed PMN phagocytosis of latex beads the most and induced the greatest PMN CL response of the fiber types examined. We postulate that asbestos-induced release of toxic oxygen by-products from PMN which have infiltrated into the pulmonary alveoli may contribute to disease pathogenesis in asbestosis.

Topics: Asbestos; Asbestos, Amosite; Asbestos, Amphibole; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Cell Survival; Humans; Luminescent Measurements; Neutrophils; Phagocytosis; Silicon Dioxide

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.

Topics: Antibody Formation; Antibody-Producing Cells; Asbestos; Asbestos, Amosite; Asbestosis; B-Lymphocytes; Cell Separation; Herpesvirus 4, Human; Humans; Lymphocyte Activation; Monocytes; Pokeweed Mitogens

Topics: Adult; Asbestos; Asbestos, Amosite; Asbestosis; Humans; Middle Aged; Radiography; Respiration Disorders; Respiratory Function Tests; Smoking; Texas; Time Factors