SEARCH · PubMed Health

Results for “ASBESTOS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources

PubMed1987

Acute injury and regeneration of the mesothelium in response to asbestos fibers.

The mesothelium is a target of the toxic and carcinogenic effects of asbestos fibers. Fibers greater than 8 mu in length and less than 0.25 mu in diameter have been found to be highly tumorigenic in rodents, while shorter asbestos fibers or spherical mineral particles have not been shown to produce mesotheliomas. For investigation of early mesothelial reactions associated with the development of mesotheliomas, C57BL/6 mice were given intraperitoneal injections of 200 micrograms of short or long crocidolite asbestos fibers, toxic silica particles, or nontoxic titanium dioxide particles. At intervals between 3 hours and 21 days after a single injection, the mesothelial surface of the diaphragm was examined by stereomicroscopy, scanning electron microscopy, and autoradiography. Within 6 hours after injection of asbestos fibers, mesothelial cells in the lacunar regions of the diaphragm retracted opening stomata 10.7 +/- 2.3 mu in diameter leading to the submesothelial lymphatic plexus. Short asbestos fibers (90.6% less than or equal to 2 mu in length), silica, or titanium dioxide particles (less than or equal to 5 mu in diameter) were cleared through these stomata without provoking an inflammatory reaction or mesothelial injury. In contrast, long asbestos fibers (60.3% greater than or equal to 2 mu in length) were trapped at the lymphatic stomata in the lacunar regions on the peritoneal surface of the diaphragm. At these sites, an intense inflammatory reaction developed with accumulation of activated macrophages and a 5.5-fold increase in albumin recovered in the peritoneal lavage fluid after 3 days. As early as 12 hours after injection of long asbestos fibers, the adjacent mesothelial cells were unable to exclude trypan blue and lost their surface microvilli, developed blebs, and detached. Recovery of lactate dehydrogenase activity in the peritoneal lavage fluid was increased 5.8-fold after 3 days and returned to normal levels after 14 days. Regenerating mesothelial cells appeared at the periphery of asbestos fiber clusters 3 days after injection. Maximal incorporation of 3H-thymidine by mesothelial cells occurred after 7 days, followed by partial restoration of the mesothelial lining after 14-21 days. As late as 6 months after a single injection of crocidolite asbestos fibers, clusters of fibers remained in the lacunar regions, partially covered by mesothelium but surrounded by macrophages and regenerating mesothelial cells. The anatomic distribution and size of lymphatic stomata on the peritoneal surface of the diaphragm account for the selective accumulation of long asbestos fibers in these regions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2000

Medical examination for asbestos-related disease.

There are millions of workers whose exposure to asbestos dust prior to the implementation of asbestos regulation and improved control measures places them at risk of asbestos-related disease today. In addition, workers are still being exposed to significant amounts of asbestos, when asbestos materials in place are disturbed during renovation, repair, or demolition. Given the continued presence of asbestos-containing materials in industrial, commercial, and residential settings throughout the U.S., a sizeable population remains at risk of asbestos-related disease. This article reviews the health effects associated with exposure to asbestos and delineates the steps necessary for the comprehensive screening and clinical assessment for asbestos-related disease, in order to assist physicians in identifying and preventing illness associated with exposure to asbestos among their patients.

Asbestos↗

PubMed1992

Intensity of exposure to asbestos in metropolitan Kure City as estimated by autopsied cases.

In this study, the intensity of exposure to asbestos was evaluated in the residents of Kure City, the site of the Japanese naval shipyard, Kure. The number of asbestos bodies was counted in 728 autopsied cases from those treated surgically in Kure Kyosai Hospital. Five grams of lung tissue was lysed, and the number of asbestos bodies was counted with the use of light microscopic examination. By this method, the number of asbestos bodies detected in men was significantly higher than that in women. There was a peak between 60 and 70 years of age. The number of asbestos bodies in exposed cadavers in Kure City exceeded greatly that found in other districts of Japan. By this criterion, 58 of 109 patients with lung cancer had asbestos exposure, and 39 had a high exposure to asbestos. All 13 patients with malignant mesothelioma had a high exposure to asbestos. Excess asbestos exposure also was found in a large proportion of patients with gastric cancer, colon cancer, and acute leukemia. The crocidolite type of asbestos was detected frequently in patients of malignant mesothelioma or leukemia, and the chrysotile form was found in those with lung cancer.

Adult↗

PubMed2006

Adverse effects of asbestos exposure and smoking on lung function.

BACKGROUND: Exposure to asbestos is a well-recognized cause of both malignant and nonmalignant diseases of lung parenchyma and pleura. This study was conducted to determine the adverse effects of exposure to asbestos and smoking on pulmonary function. METHODS: Four hundred and sixty-eight workers who were occupationally exposed to asbestos for an average of 13 years were selected from an asbestos-product factory in China. Of them, 85 workers were diagnosed with asbestosis. Additionally, 282 workers who had no experience of exposure to industrial dust were included as a control group. A questionnaire was administered during a face-to-face interview and spirometric maneuvers and single-breath CO diffusing capacity (DL(CO)) were performed. RESULTS: Multivariate regression analysis showed that exposure to asbestos was more strongly associated with decreased forced vital capacity (FVC) and DL(CO), and asbestosis more strongly associated with decreased FVC, while smoking was a major contributing factor to reduced FEV1/FVC. The results were confirmed by a further analysis where the subjects were grouped exclusively by smoking, asbestos exposure, and chest radiographic changes. No interaction or joint effect was observed between asbestos exposure and smoking. CONCLUSIONS: This analysis suggested that asbestos and smoking might play independent roles, in which asbestos caused mainly a restrictive impairment, and smoking was a major causal factor for airway obstruction in the workers who were intensively exposed to asbestos.

Adult↗

PubMed1995

Asbestos bodies in lung tissue following exposure to crocidolite.

A series of 206 necropsies in Western Australia (WA) have had routine counts made of asbestos bodies in samples of lung tissue using conventional light microscopy. Thirty-two cases had worked in the asbestos industry at Wittenoom, WA and (log) counts of asbestos bodies in their lung tissue correlated well with estimates of their (log) cumulative airborne exposure to crocidolite fibers (r = 0.60). There was no association between the number of asbestos bodies and time since exposure to asbestos ceased. In subjects without known exposure to asbestos, there was a weak but nonsignificant increase in number of asbestos bodies with increasing age, with 26% of cases having no asbestos bodies present. It is concluded that the relatively simple technique of light microscopy for counting of asbestos bodies in lung tissue provides a reliable indication of the level of past occupational exposure to crocidolite in subjects whose exposure has been only to crocidolite. This could be extremely useful in follow-up studies of cohorts that lack reliable measures of airborne exposure to crocidolite asbestos.

Adult↗

PubMed1993

Asbestos-induced injury to cultured human pulmonary epithelial-like cells: role of neutrophil elastase.

The mechanisms responsible for asbestos-induced pulmonary epithelial cell cytotoxicity, especially oxidant-independent mechanisms, are not established. We determined whether human polymorphonuclear leukocyte (PMN) proteases contribute to asbestos-induced damage to human pulmonary epithelial-like cells (PECs) assessed using an in vitro chromium-51 release assay. Serine antiproteases, phenylmethylsulfonyl fluoride and alpha 1-antitrypsin, each ameliorated PEC injury induced by amosite asbestos and PMNs. A role for a specific proteinase, human neutrophil elastase (HNE), is supported by the facts that (1) asbestos increased HNE release assessed by an enzyme-linked immunosorbent assay technique (1.7 +/- 0.5 vs. 2.8 +/- 0.5 micrograms/ml; P < .025), (2) purified HNE or porcine pancreatic elastase (PPE) each alone caused PEC detachment, (3) asbestos plus either HNE or PPE caused PEC lysis similar to that mediated by asbestos and PMNs, and (4) cationic agents released from PMNs were unlikely to be involved because polyanions did not ameliorate injury resulting from asbestos and PMNs. Compared to elastase, cathepsin G caused less PEC detachment and negligible augmentation in asbestos-induced PEC lysis. Asbestos increased the association of 125I-labeled elastase with PECs nearly 50-fold compared with PPE alone (14.4% vs. 0.3%, respectively; P < .01) and nearly 10-fold compared with another particle, opsonized zymosan. We conclude that PMN-derived proteases, especially elastase, may contribute to asbestos-induced lung damage by augmenting pulmonary epithelial cell injury.

Asbestos↗

PubMed1996

Increased neutrophil adherence to endothelial cells exposed to asbestos.

Inhalation of asbestos may activate the pulmonary endothelium to promote an inflammatory cell phenotype that participates in the development of pulmonary fibrosis. However, little is known about the effects of asbestos on endothelial cell function. Therefore, endothelial cells were exposed to chrysotile and crocidolite asbestos for up to 72 hr to investigate the effects of noncytotoxic concentrations of asbestos on cell function. Noncytolytic concentrations of chrysotile and crocidolite caused localized changes in cell morphology, resulting in activation of endothelial cells to a vacuolated, "spindle-shaped" morphology at sites of fiber deposition. The adherence of neutrophils (PMN) to control and asbestos-treated cultures was examined to determine the functional significance of this altered morphology. Chrysotile asbestos caused a time-dependent, 2- to 4-fold increase in PMN adherence that was localized to spindled endothelial cells in close contact with fibers. Monoclonal antibodies against intercellular adhesion molecule-1 (ICAM-1) inhibited this asbestos-induced PMN adherence. Solution hybridization demonstrated a 2.5-fold increase in steady-state levels of ICAM-1 mRNA in cells exposed to chrysotile asbestos for 8 hr. Exposure to crocidolite asbestos resulted in similar alteration in cell morphology and increase in PMN binding to endothelial cells, while a physically similar nonasbestos fiber, refractory ceramic fiber-1 did not cause morphologic change or increased PMN binding. These data suggest that asbestos fibers can specifically and directly activate endothelial cells, resulting in an activated cell morphology, increased ICAM-1 expression, and enhanced PMN adherence.

Animals↗

PubMed1988

Asbestos-mediated transfection of mammalian cell cultures.

The capacity of asbestos to mediate transfection was tested in a rapid and relatively simple system: picornavirus RNAs and mammalian cells in vitro. Thirteen asbestos samples, including amosite, anthophyllite, chrysotile, and crocidolite, 4 picornaviruses (poliovirus 1 and 2, echovirus 7, and encephalomyocarditis virus), and 4 cell lines (CLI, chimpanzee liver; KB, human carcinoma; eta, monkey kidney; NIH 3T3, mouse embryo) were tested. The results showed that all asbestos samples mediated transfection and that all cell lines were transfectible by viral RNA with asbestos. Transfection was much greater with asbestos added to the viral RNA inoculum than to the cells before or after the RNA. Transfection was directly proportional to asbestos concentration. Initiation of transfection events was rapid, with half becoming irreversible by washing 2 min postinoculation. DNA in the inoculum strongly interfered with asbestos-mediated transfection by the RNA but was ineffective when added, with or without asbestos, to the cells before or after the inoculum. Asbestos compared with six classical "insoluble" facilitators (bentonite, calcium phosphate, chromic oxide, ferric oxide, kaolin, talc) was of intermediate rank in transfection mediation. It is hypothesized that the prominence of asbestos in carcinogenesis is due to a combination of properties, including transfection mediation as well as chromosome mutagenicity, fiber dimensions, biological durability, hydrocarbon transport, and prevalence.

Adsorption↗

PubMed1989

Asbestos: toxicology and risk assessment for the general population in The Netherlands.

Within the scope of the preparation of Integrated Criteria Documents for priority compounds in The Netherlands, the possible health effects of oral and inhalatory exposure to asbestos for the general population were evaluated. It was concluded from the results of experiments in animals that exposure to asbestos by the oral route is not carcinogenic and is not expected to present a health risk to the general population. Inhaled asbestos, however, is distinctly carcinogenic to man, giving rise to lung tumours, and mesotheliomas of the pleura and peritoneum. Chrysotile asbestos appears to be less potent in inducing mesotheliomas than the amphiboles, but all types of asbestos appear to have a similar potency for inducing lung cancer. The risk of mesothelioma is not expected to be influenced by smoking, whereas the risk of lung cancer is expected to be ten times higher in smokers than in non-smokers exposed to the same asbestos concentrations. Risk-assessment models for the inhalatory route, for the general population, are based on linear non-threshold extrapolation of occupational exposure to much lower environmental concentrations. These models give only a rough approximation of the risk of environmental exposure to asbestos. In accordance with the Air Quality Guidelines of the World Health Organization (World Health Organization, 1987), it was estimated that an extra risk of lung cancer of one in 10(6) (in the general population, with 30% smokers) may be presented by lifetime exposure to asbestos fibres longer than 5 microns, measured by electron microscopy, at concentrations of 100-1000/m3. It was further estimated that an extra risk of mesothelioma of one in 10(6) may be presented by lifetime exposure to 10-100 amphibole fibres/m3 or to a range of 100-10000 chrysotile fibres/m3 (fibres longer than 5 microns). From the current asbestos concentrations, the risk of mesothelioma for the general population in The Netherlands appears to be negligible; the extra risk of lung cancer is expected to be higher than 1 in 10(6) near asbestos sources, whereas it appears to be negligible in background areas and in most large cities and industrial areas. However, it must be borne in mind that the validity of the risk figures given is difficult to judge.

Asbestos↗

PubMed2006

Toxicity evaluation for the broad area of the asbestos mine of northern Greece.

The existing data regarding the quality of the environment in the asbestos mine of northern Greece (MABE) region related to the presence of asbestos are insufficient to determine the current pollution problem. In the present work, a first approach to this problem has been taken through a toxicity risk assessment. The environmental quality of an open air asbestos mine was evaluated over a long period of time by measuring and monitoring the concentration of asbestos fibres in air, soil and water. Air measurements were made to determine the concentration of asbestos fibres in the atmospheric air of the mine, the depositions and the nearby villages. The asbestos fibre concentration was also specified inside the building facilities of MABE. Analyses of soil, dust and water samples were carried out showing the presence of enormous quantities of chrysotile asbestos. The concentration of asbestos fibres in the atmospheric air was compared to older measurements that were taken at the same sampling points during the operation of the mine. The results of this work, in conjunction with individual researches that have been carried out in the past and with the evaluation of international standards of scientific and experience-based findings, provide a reliable framework with which to estimate the threat of MABE to its surrounding environment, and help to determine a basic criterion for the remediation and rehabilitation of the region. In addition, mathematical models based on human and animal studies were used to estimate the probability of a person developing cancer from breathing air containing asbestos fibres in the wider vicinity of the mine in order to define appropriate procedures for evaluating asbestos-related risk.

Air↗

PubMed2003

Respiratory impairment due to asbestos exposure in brake-lining workers.

There is extensive evidence that exposure to asbestos causes pulmonary parenchymal fibrosis, pleural disease, and malignant neoplasm in asbestos-exposed workers. However, few data concerning brake-lining workers are available in the literature. In this study, we aimed to assess the long-term effects of chrysotile asbestos exposure on lung function and the risk of asbestos-related diseases in brake-lining workers. Seventy-four asbestos-exposed workers who processed brake-lining products and 12 unexposed office workers were offered pulmonary function tests (spirometry and transfer factor) in 1992 and 1999. In 1999, the mean duration of asbestos exposure was 10.00+/-4.07 and 11.02+/-4.81 years (7-31 years) in nonsmoking and smoking asbestos workers, respectively. Transfer factor (T(L), CO) and transfer coefficient (K(CO)) decline were significant in the 7-year follow-up in both smoking and nonsmoking asbestos workers. However, lung function indices of the control group, whom were all current smokers; were also found to be decreased, including FEF(75), T(L), CO and K(CO). We found minimal reticular changes in 10 asbestos workers who were all current smokers, they underwent high-resolution computed tomography scans of the chest and we found that they had peribronchial thickening resulting from smoking. As a conclusion, even in the absence of radiographic asbestosis, T(L), CO and K(CO) may decrease after a mean 10-year duration of exposure to asbestos in brake-lining workers and this is more noticeable with cigarette burden.

Adult↗

PubMed1990

Airborne asbestos in public buildings.

The U.S. Environmental Protection Agency sampled air in 49 government-owned buildings (six buildings with no asbestos-containing material, six buildings with asbestos-containing material in generally good condition, and 37 buildings with damaged asbestos-containing material). This is the most comprehensive study to date of airborne asbestos levels in U.S. public buildings during normal building activities. The air outside each building was also sampled. Air samples were analyzed by transmission electron microscopy using a direct transfer preparation technique. The results show an increasing trend in average airborne asbestos levels; outdoor levels are lowest and levels in buildings with damaged asbestos-containing material are highest. However, the measured levels and the differences between indoors and outdoors and between building categories are small in absolute magnitude. Comparable studies from Canada and the UK, although differing in their estimated concentrations, also conclude that while airborne asbestos levels may be elevated in buildings that contain asbestos, levels are generally low. This conclusion does not eliminate the possibility of higher airborne asbestos levels during maintenance or renovation that disturbs the asbestos-containing material.

Air Pollutants↗

PubMed1999

Oxidant and antioxidant mechanisms of lung disease caused by asbestos fibres.

The pathogenesis of asbestos-related lung diseases is complicated and still poorly understood. Studies on animal models and cell cultures have indicated that asbestos fibres generate reactive oxygen and nitrogen species and cause oxidation and/or nitrosylation of proteins and deoxyribonucleic acid as a marker of cell injury. These effects are potentiated by the inflammation caused by the fibres. Recent studies have shown that individual variability in the antioxidant and/or detoxifying mechanisms probably has an important role in the development of asbestos-related lung diseases. Asbestos fibres cause both cell proliferation and apoptosis by multiple mechanisms, one of them being activation of signal transduction pathways by reactive oxygen and nitrogen species. Asbestos activates transcription factors such as nuclear factor kappa B, which has been shown to lead to the upregulation of antioxidant enzymes, most importantly manganese superoxide dismutase. This enzyme is also overexpressed in asbestos-related human malignant mesothelioma, whereas the induction of other antioxidant enzymes (copper-zinc superoxide dismutase, catalase, glutathione peroxidase) by asbestos fibres appears to be marginal. The significance of antioxidant enzymes in asbestos related diseases has, however, remained unclear. Furthermore, previous studies have not been able to offer successful therapies to the patients with asbestos-associated diseases. Only an improved understanding of the pathogenetic mechanisms in the human lung provides a basis for future therapies for asbestos-related diseases.

Animals↗

PubMed2004

Src-dependent ERK5 and Src/EGFR-dependent ERK1/2 activation is required for cell proliferation by asbestos.

Crocidolite asbestos elicits oxidative stress and cell proliferation, but the signaling cascades linked to these outcomes are unclear. To determine the role of mitogen-activated protein kinases (MAPK) in asbestos-induced cell signaling, we evaluated the effects of crocidolite asbestos, EGF and H2O2, on MAPK activation in murine lung epithelial cells (C10 line). In contrast to rapid and transient activation of extracellular signal-regulated kinase 5 (ERK5) by EGF or H2O2, asbestos caused protracted oxidant-dependent ERK5 activation that was inhibited by an Src kinase inhibitor (PP2), but not by an inhibitor of epidermal growth factor receptor (EGFR) phosphorylation (AG1478). ERK1/2 activation by asbestos was inhibited by either PP2 or AG1478. To confirm the involvement of Src in ERK1/2 and ERK5 activation, a dominant-negative Src construct was used. These experiments showed that Src was essential for ERK1/2 and also ERK5 phosphorylation by asbestos. Time frame studies indicated immediate activation of Src by asbestos fibers, whereas EGFR phosphorylation occurred subsequently. Data suggest that asbestos causes activation of ERK5 through an EGFR-independent pathway, whereas ERK1/2 activation is dependent on Src through a mechanism involving phosphorylation of the EGFR. Furthermore, Src, ERK1/2 and ERK5 activation are essential for cell proliferation by asbestos. The use of a dominant-negative ERK5 construct caused selective downregulation of c-jun expression, whereas inhibition of Src by PP2 or MEK1 by PD98059 caused decreases in c-fos, fra-1 and c-jun expression in asbestos-exposed C10 cells. These observations may have broad relevance to cell proliferation by carcinogenic mineral fibers and oxidants.

Animals↗

PubMed2003

Synchronous diffuse malignant mesothelioma and carcinomas in asbestos-exposed individuals.

AIMS: The development of synchronous diffuse malignant mesothelioma and carcinoma in individuals exposed to asbestos is rare. We report nine cases and discuss the medico-legal implications. METHODS AND RESULTS: Five hundred patients seeking compensation for asbestos-related diffuse malignant mesothelioma were reviewed with access to post-mortem data. The study group comprised cases in which a second (non-mesothelial) neoplasm was identified. The study group comprised eight males, one female, mean age 68 years (range 60-75). All individuals gave a history of asbestos exposure. Synchronous malignant mesothelioma with carcinoma was identified in 9/500 (1.8%). Eight malignant mesotheliomas were pleural, one was primary peritoneal in origin. By morphological subtyping there were four epithelioid, three biphasic and two sarcomatoid mesotheliomas. In 6/9 (67%) the second tumour was a primary bronchogenic carcinoma (three adenocarcinomas, two squamous cell carcinomas and one small-cell carcinoma). In 3/9 (33%) the second tumour was a non-bronchogenic carcinoma (colonic, pancreatic and breast ductal adenocarcinoma). No other neoplasms were identified in the cohort of malignant mesotheliomas studied. Five persons had pathological evidence of asbestosis (four had bronchogenic carcinomas, one colorectal adenocarcinoma). Two persons with non-bronchogenic carcinomas had identifiable asbestos bodies but no interstitial fibrosis. In two cases the second neoplasms (primary bronchogenic squamous cell and small-cell carcinomas) were associated with diffuse interstitial fibrosis but no asbestos bodies were seen on light microscopy. In each case transmission electron microscopic mineral analysis revealed an asbestos fibre burden within the background population range for control subjects and well below that seen in cases of established asbestosis. These cases were considered to represent cryptogenic fibrosing alveolitis in subjects with a history of asbestos exposure. CONCLUSIONS: Synchronous malignant mesothelioma with carcinomas in asbestos-exposed workers is rare and identified in 1.8% of 500 malignant mesotheliomas in this series. In most cases the carcinoma represents a primary bronchogenic neoplasm. Primary lung carcinomas are recognized to be asbestos related only when occurring in association with asbestosis. In this series this combination (bronchogenic carcinoma and asbestosis) was seen in four (0.8%) cases. In post-mortem cases for possible malignant mesothelioma it is important to identify any other neoplasia and determine whether it is related to asbestos. Their presence impact upon anticipated life expectancy and in the presence of malignant mesothelioma will affect the compensation settlement.

Adenocarcinoma↗

PubMedDate not supplied

Asbestos fiber analysis in seven asbestosis cases.

Asbestos bodies and fibers deposited in the lungs of seven asbestosis cases were counted after tissue digestion. The types and sizes of 100 asbestos fibers for each case were also analyzed. Asbestos bodies were counted with an optical microscope at 100x magnification, and asbestos fibers were counted with a transmission electron microscope (TEM) at 2000x magnification. Most asbestos fibers detected with TEM were longer than 3 microns (92.5%) and thicker than 0.1 microns (92.3%). Short fibers less than 2 microns--both chrysotile and amphiboles, as well as long, thin fibers less than 0.06 microns--would be missed at 2000x (TEM). An average of 1.37 (0.081-5.5) x 10(6) asbestos bodies and 164.8 (0.55-610) x 10(6) asbestos fibers per 5 g wet (0.88 g dry) lung tissue were found, and these values are higher than what was reported in mesothelioma cases without asbestosis that were reported previously. More than 13 (average = 266.2) asbestos bodies were found in a 4-micron-thick tissue section (average area = 3.24 cm2). One asbestos body in a section equaled approximately 5,000 per 5 g wet lung tissue. The intensity of fibrosis was minimal in one case, mild in four, moderate and severe in one each, and the intensity was correlated with the number of asbestos bodies and fibers. The fibrosis in the severe case may have been intensified by repeated infection. Crocidolite fibers were found most frequently (84.7%), were thin, and had a high aspect ratio by our counting rules. Crocidolite with a high aspect ratio may be most fibrogenic in the lung.

Adult↗

PubMed1991

Radiological abnormalities and asbestos exposure among custodians of the New York City Board of Education.

Six hundred sixty custodians employed by the New York City Board of Education underwent examination from 1985 through 1987 for asbestos-related disease and other general medical conditions by the clinical staff of the Division of Environmental and Occupational Medicine of the Mount Sinai School of Medicine of the City University of New York. Two-thirds of the men (no women were examined) were 20 or more years from onset of any custodial work, with 44% having had at least 20 years of employment as custodial workers in New York City Board of Education schools. Twenty-four percent had begun custodial work in buildings 30 or more years earlier. Findings among them were of particular interest since asbestos-related disease might forecast what might be expected among school custodians with less seniority. Since the Board of Education, in selecting custodians for examination, had chosen only custodians currently employed, the study group comprised men still working in the school system. These, then, represented a "survivor population" (4% had retired between the time of enrollment in the study and the date of examination, and only one of the seventeen retirees had left work owing to disability). Although a considerable amount of clinical information was obtained, abnormalities on chest X-ray consistent with asbestos-induced scarring were used as the key index of disease resulting from exposure to asbestos. Since scarring of the lung tissue or lining of the lung or chest wall (pleura) may be present but undetectable on standard chest radiographs (a relatively insensitive diagnostic technique), the prevalence of abnormality on X-ray film represents a conservative estimate of the actual burden of scarring lung disease in the group. Such changes are indicative of previous asbestos exposure, however, and provide evidence of an increased risk of later asbestos-related malignancy. Overall, abnormalities on chest X-ray consistent with asbestos-related scarring were found in 28% of the men examined. The expected relationship of increasing prevalence of radiographic changes with increasing time since onset of exposure in buildings was demonstrated; among those with 35 or more years since beginning custodial work, 39% had abnormal films. This is evidence that custodial workers as a group have had asbestos exposure in the past, as reflected also in the work histories obtained at the time of examination. Eighty-four percent reported that they themselves removed asbestos-containing materials in the course of their work. Eighty-nine percent had been present in the work area during asbestos abatement projects in the schools in more recent years.(ABSTRACT TRUNCATED AT 400 WORDS)

Air Pollution, Indoor↗

PubMed2002

Asbestos fibers contributing to the induction of human malignant mesothelioma.

UNLABELLED: To elucidate the features of the asbestos fibers contributing to the induction of human malignant mesothelioma, we used high-resolution analytical electron microscopy to determine the type, number, and dimensions of asbestos fibers in lung and mesothelial tissues in 168 cases of mesothelioma. RESULTS: 1. Asbestos fibers were present in almost all of the lung and mesothelial tissues from the mesothelioma cases. 2. The most common types of asbestos fibers in lung were either an admixture of chrysotile with amphiboles, amphibole alone, and occasionally chrysotile alone. In mesothelial tissues, most asbestos fibers were chrysotile. 3. In lung, amosite fibers were greatest in number followed by chrysotile, crocidolite, tremolite/actinolite, and anthophyllite. In mesothelial tissues, chrysotile fibers were 30.3 times more common than amphiboles. 4. In some mesothelioma cases, the only asbestos fibers detected in either lung or mesothelial tissue were chrysotile fibers. 5. The average number of asbestos fibers in both lung and mesothelial tissues was two orders of magnitude greater than the number found in the general population. 6. The majority of asbestos fibers in lung and mesothelial tissues were shorter than 5 micro m in length. CONCLUSIONS: 1) Fiber analysis of both lung and mesothelial tissues must be done to determine the types of asbestos fibers associated with the induction of human malignant mesothelioma; 2) short, thin asbestos fibers should be included in the list of fiber types contributing to the induction of human malignant mesothelioma; 3) RESULTS support the induction of human malignant mesothelioma by chrysotile.

Asbestos↗