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PubMed2004

Occupational exposure to airborne asbestos from coatings, mastics, and adhesives.

Over the past few years, a question has arisen about the degree of exposure to airborne asbestos associated with the application, cleanup, and tear-out of glues and mastics used between 1940 and the present. These liquid products were used either to adhere insulation to pipes and boilers or to cover the insulation so as to protect it. In this study, four asbestos-containing products, a coating, two mastics, and an adhesive, which were representative of the various classes of products that have been used historically, were tested to determine the airborne concentration of asbestos fibers released during five different activities (application, spill cleanup, sanding, removal, and sweep cleaning). Each activity was performed for 30 min (often in triplicate). Personal (n=172) and area (n=280) air samples were collected during the tests, and each was analyzed for total fiber concentrations using phase contrast microscopy (PCM), and for asbestos fiber count using transmission electron microscopy (TEM). A measurable concentration of asbestos fibers was detected in six of the 452 samples collected (0.0017-0.0184 fibers/ml). The observed asbestos fibers counts for each product were similar to background. Only one asbestos fiber was detected in an indoor background sample; no asbestos fibers were identified in any of the outdoor background samples. The (raw) PCM-total fiber concentrations were adjusted based on TEM analyses that reported fraction of asbestos fibers (to derive a PCM-asbestos concentration) and by the fraction of the 8-h workday that a worker spends performing the activity (to derive a calculated TWA). For the coatings, mastics, and adhesives evaluated in the present study, the calculated TWAs using hypothetical work scenarios were well below the current Occupational Safety and Health Administration (OSHA) Permissible Exposure Limit (PEL) of 0.1 fibers/ml. The calculated TWAs ranged from 0.03 to 0.009 fibers/ml. The actual concentration of airborne asbestos due to these products is almost certainly much less than the TWAs, and may be so low as to not be measurable. These results support the historical view that these products, over the past 50 years, did not pose an occupational health hazard under foreseeable uses.

Adhesives↗

PubMedDate not supplied

Asbestos bodies in normal lung of western Mediterranean populations with no occupational exposure to inorganic dust.

The aim of this study was to determine the following: (a) asbestos body count in lung tissue of different western Mediterranean populations; (b) the association, if any, of urban industrial residence with higher lung tissue asbestos exposure posed for lung cancer in our population. Lung-tissue samples were studied in three groups of subjects from the general population: (1) group A comprised 18 patients from Barcelona's urban industrial area (mean age = 62.2 y, standard deviation [SD] = 13.6); (2) group B comprised 16 patients who lived in a rural area of Albacete in the south of Spain (mean age = 62.2 y, SD = 13.7); and (3) group C comprised 8 patients who had been diagnosed with lung cancer, who lived in or near Barcelona, and who had never been exposed occupationally to asbestos (mean age = 62.1 y, SD = 7.4). A wet lung/dry lung weight ratio was determined. In group A, asbestos bodies were observed in 9 of 18 (50%) subjects, and asbestos bodies numbered 52.35 per g dry lung (SD = 101.72) (upper limit of normality [higher value] = 430.12 asbestos bodies per g dry lung). In group B, asbestos bodies were observed in 2 of 16 (12.5%) subjects, and asbestos bodies numbered 5.37 per g dry lung (SD = 8.79) (upper limit normality = 35.15 asbestos bodies per g dry lung). In group C, we observed asbestos bodies in 2 of 8 subjects (25.0%), and asbestos bodies numbered 20.59 per g dry weight (SD = 24.10).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Environmental and occupational health hazards associated with the presence of asbestos in brake linings and pads (1900 to present): a "state-of-the-art" review.

Throughout the history of automobile development, chrysotile asbestos has been an essential component of vehicle brake linings and pads. Acceptable alternatives were not fully developed until the 1980s, and these were installed in vehicles produced over the past decade. This article presents a "state-of-the-art" analysis of what was known over time about the potential environmental and occupational health hazards associated with the presence of chrysotile asbestos in brake linings and pads. As part of this analysis, the evolution of automobile brakes and brake friction materials, beginning with the early 1900s, is described. Initial concerns regarding exposures to asbestos among workers involved in the manufacture of friction products were raised as early as 1930. Between 1930 and 1959, eight studies were conducted for which friction product manufacturing workers were part of the population assessed. These studies provided evidence of asbestosis among highly exposed workers, but provided little information on the magnitude of exposure. The U.S. Public Health Service proposed the first occupational guideline for asbestos exposure in 1938. The causal relationship between asbestos exposure and lung cancer was confirmed in 1955 in asbestos textile workers in the United Kingdom, and later, in 1960, in South Africa, mesothelioma was attributed to asbestos exposure to even relatively low airborne concentrations of crocidolite. Between 1960 and 1974, five epidemiology studies of friction product manufacturing workers were conducted. During this same time period, the initial studies of brake lining wear (dust or debris) emissions were conducted showing that automobile braking was not a substantial contributor of asbestos fibers greater than 5 microm in length to ambient air. The first exposure surveys, as well as preliminary health effects studies, for brake mechanics were also conducted during this period. In 1971, the Occupational Safety and Health Administration promulgated the first national standards for workplace exposure to asbestos. During the post-1974 time period, most of the information on exposure of brake mechanics to airborne asbestos during brake repair was gathered, primarily from a series of sampling surveys conducted by the National Institute of Occupational Safety and Health in the United States. These surveys indicated that the time-weighted average asbestos

Air Pollutants, Occupational↗

PubMed1988

Binding of deferoxamine to asbestos fibers in vitro and in vivo.

We studied the binding of tritium-labeled deferoxamine, a strong iron chelator, to crocidolite asbestos fibers in vitro and in vivo. In aqueous suspension of asbestos, deferoxamine binding was rapid and strong, suggesting specific binding to iron. For the in vivo experiments, diffusion chambers containing native asbestos fibers or deferoxamine-washed asbestos were implanted in the peritoneal cavities of mice. Five days after parenteral injection of tritiated deferoxamine chambers were removed and the asbestos counted. More than twice as much label (2206 +/- 348 c.p.m./100 mg asbestos) was bound to the native asbestos as compared to the deferoxamine-washed asbestos (1080 +/- 201 c.p.m./100 mg asbestos), suggesting specific binding in vivo. Since deferoxamine can inhibit asbestos toxicity in vitro, these experiments suggest the feasibility of testing whether deferoxamine can prevent asbestos-related disease in vivo.

Animals↗

PubMed1994

A meta-analysis of colorectal cancer and asbestos exposure.

A meta-analysis of the relation between asbestos exposure and colorectal cancer mortality was conducted, using published reports of 20 asbestos-exposed cohorts. Summary standardized mortality ratios (SMRs) for colorectal cancer were examined in relation to asbestos type and estimates of dust exposure (as direct estimators of asbestos exposure) and in relation to lung cancer SMR and the proportion of all deaths due to mesothelioma (as proxy estimators of asbestos exposure). An elevated summary SMR was observed in cohorts exposed to amphibole asbestos (summary SMR = 1.47; 95% confidence interval (CI) 1.09-2.00), but not in cohorts exposed to serpentine asbestos (summary SMR = 1.04; 95% CI 0.81-1.33) or in cohorts exposed to both serpentine and amphibole asbestos (summary SMR = 1.03; 95% CI 0.74-1.42). Cohorts having a lung cancer SMR greater than 2.00 had a summary SMR of 1.51 (95% CI 1.29-1.76), and cohorts in which more than 1% of all deaths were attributed to mesothelioma had a summary SMR of 1.24 (95% CI 0.94-1.64). After stratifying the cohorts based on mortality due to all cancers excluding those known or suspected to be associated with asbestos exposure, lung cancer mortality was not clearly associated with colorectal cancer mortality, suggesting that the crude association between these factors may be due to misdiagnosis of lung cancer as other types of cancer in the reported causes of death. These results suggest that exposure to amphibole asbestos may be associated with colorectal cancer, but these findings may reflect an artifact of miscertification of cause of death. The results also suggest that serpentine asbestos is not associated with colorectal cancer.

Asbestos↗

PubMed2003

Benign asbestos pleural diseases.

The global incidence of asbestos-related lung diseases is expected to continue to rise. Although much attention is devoted to malignant diseases induced by asbestos, benign asbestos pleural diseases (pleural plaques, benign asbestos-related pleural effusion, diffuse pleural thickening, and rounded atelectasis) are common in clinical practice and often produce diagnostic difficulties. The authors describe the clinical features of benign asbestos-related pleural disease, before focusing on recent advances in radiology and on controversies surrounding the pathogenesis of asbestos-induced pleural injury. Advances in computed tomography have assisted the understanding and diagnosis of these diseases, and increasing evidence suggests radiologic appearances on computed tomography can predict impairment in pulmonary function tests. The pathogenesis of asbestos-induced pleural diseases has also been subject to extensive investigation. Asbestos fibers can provoke pleural inflammation from direct toxicity to mesothelial cells. Inhaled asbestos fibers can also elicit pleural injury indirectly via the release of growth factors and inflammatory cytokines from within the lung. Although progress has been made in the understanding of the mechanisms of asbestos pleural injury, many important questions remain unanswered. The role of genetic factors and possible environmental cofactors (eg, simian virus 40) in the pathogenesis of benign asbestos pleural diseases requires further research.

Asbestos↗

PubMed1975

Prevalence of asbestos bodies in a necropsy series in East London: association with disease, occupation, and domiciliary address.

The prevalence of asbestos bodies was measured in lung sections in a necropsy series carried out at the London Hospital (1965-66) after exclusion of all known asbestos factory workers and cases of asbestosis and of mesothelioma. Associations were sought between the presence and number of asbestos bodies with the patients' sex, domiciliary address, occupation, industry, and diseases recorded at necropsy. Asbestos bodies were present in 42% of the 216 men in the series and in 30% of the 178 women. The number of bodies in the positive cases was small in comparison with the numbers seen typically in asbestosis; thus there were less than 6 asbestos bodies per 6-75 mm-3 lung tissue in 107 of the total 145 positive cases in contrast to 1 000 or more in asbestosis. In comparison with the overall series, an increased number of asbestos body positives was present in males with carcinoma of stomach and females with carcinoma of breast. In view of this finding lung sections were counted in further post-mortem examples of these carcinomas making a total of 50 males with carcinoma stomach and 82 females with carcinoma breast. Thirty-five positive cases were found in the carcinoma stomach group as against 22-7 expected and 38 in the carcinoma breast group against 26-35 expected. There was no excess of observed over expected asbestos body positives in 51 males with carcinoma of bronchus. There was an excess of asbestos body positives (60-9%) in heavy manual workers and in both heavy and light manual male workers in the shipping (61%), electrical and engineering (56%), and transport (54%) industries. The incidence in male clerical workers was 12-8%. The incidence of asbestos body positives according to home address was highest (53% in males, 45% in females) in patients living in the industrial and cockland area due east of the hospital. The incidence fell in the less industrial areas north-east of the hospital. Consideration of possible environmental sources of the inhaled asbestos suggests that in this survey occupation, industry, and comiciliary area all play a part. The comparatively minor intensity of asbestos pollution in our positive cases showed a positive association with carcinoma of stomach and breast, possibly playing a direct pathogenic role in carcinoma of stomach. No positive association was identified with any other neoplastic disease including carcinoma of bronchus.

Adolescent↗

PubMed1988

Exposure to asbestos and the risk of gastrointestinal cancer: a reassessment.

In 1964 it was first reported that asbestos workers had a higher risk of gastrointestinal cancer. This notion has persisted despite several studies that have found no increased risk. The risks of gastrointestinal cancer to workers exposed to asbestos were reassessed, based on the results of published studies on 32 independent cohorts of asbestos workers. Not all studies provided risk estimates (SMRs) for all gastrointestinal sites (ICD codes 150-159). No consistent evidence was found to indicate that exposure to asbestos increases the risk of gastrointestinal cancer. Generally, the higher SMRs came from studies conducted in the United States or Canada and might reflect factors not related to exposure to asbestos. In studies in which asbestos exposed and non-asbestos exposed workers were evaluated the SMRs were not consistently higher for the group exposed to asbestos. There was no apparent dose response relation between accumulated asbestos dose and the risk of gastrointestinal cancer. It is concluded that there is no dose response relation between exposure to asbestos and risk of gastrointestinal cancer, and asbestos workers are not at an increased risk of gastrointestinal cancer.

Asbestos↗

PubMed2001

Relation between exposure to asbestos and smoking jointly and the risk of lung cancer.

OBJECTIVES: To review evidence about the joint relation of exposure to asbestos and smoking on the risk of lung cancer to answer three questions: (1) does asbestos increase risk in non-smokers; (2) are the data consistent with an additive model; and (3) are the data consistent with a multiplicative model? METHODS: Analysis of 23 studies reporting epidemiological evidence on the joint relation. Comparison of risk of lung cancer in subjects unexposed to asbestos or smoking, exposed to asbestos only, to smoking only, or to both. Estimation of the relative risk associated with asbestos exposure in non-smokers and of statistics testing for additivity and multiplicativity of risk. RESULTS: Eight of the 23 studies provided insufficient data on the risk of lung cancer in non-smokers to test for possible effects of asbestos. Asbestos exposure was associated with a significantly (p<0.05) increased risk in non-smokers in six of the remaining studies and with a moderately increased, but not significant, increase in a further six. In two of the three studies that found no increase, asbestos exposure was insufficient to increase risks in smokers. In 30 of 31 data sets analysed, risk in the combined exposure group was greater than predicted by the additive model. There was no overall departure from the multiplicative model, the proportional increase in risk of lung cancer with exposure to asbestos being estimated as 0.90 (95% confidence interval (95% CI) 0.67 to 1.20) times higher in smokers than non-smokers. For two studies significant (p<0.05) departures from a multiplicative relation were found in some, but not all, analyses. Reasons are presented why these may not indicate true model discrepancies. CONCLUSIONS: Asbestos exposure multiplies risk of lung cancer by a similar factor in non-smokers and smokers. The extent to which it multiplies risk varies between studies, no doubt depending on the type of asbestos involved, and the nature, extent, and duration of exposure.

Asbestos↗

PubMed1977

The significance of asbestos exposure in the diagnosis of mesothelioma: a 28-year experience from a major urban hospital.

A continued increase in the incidence of diffuse mesothelioma has been attributed to greater industrial use of asbestos but is also due in part to wider acceptance of this tumor by pathologists. In this retrospective study, the epidemiology, clinical presentation, and pathology of asbestos and non-asbestos-related mesothelioma from a major urban hospital were reviewed. Of the 36 cases of mesothelioma on file, 19 were not associated with exposure to asbestos. Although a retrospective study raises the possibility of inadequate occupational histories, the lack of history of asbestos exposure correlated with postmortem histology by light microscopy. When postmortem material was reviewed, evidence of asbestos exposure was present in all cases of mesothelioma with history of exposure to asbestos, and in no cases in which the patient denied history of asbestos exposure. Using strict histologic and histochemical criteria, the diagnosis of mesothelioma was confirmed in 8 of 9 patients with asbestos-related mesothelioma but in only 4 of 13 cases of non-asbestos-related mesothelioma. The diagnosis of diffuse methelioma is often difficult to make even wtih complete autopsy examinations. It should be entertained only with adherence to strict clinical and pathologic criteria, especially in women with no history to exposure to asbestos dust.

Adult↗

PubMed2003

The mitochondria-regulated death pathway mediates asbestos-induced alveolar epithelial cell apoptosis.

The mechanisms underlying asbestos-induced pulmonary toxicity are not fully understood. Alveolar epithelial cell (AEC) apoptosis by iron-derived reactive oxygen species (ROS) is one important mechanism implicated. The two major pathways regulating apoptosis include (i) the mitochondrial death (intrinsic) pathway caused by DNA damage, and (ii) the plasma-membrane death receptor (extrinsic) pathway. However, it is unknown whether asbestos activates either death pathway in AEC. We determined whether asbestos triggers AEC mitochondrial dysfunction by exposing cells (A549 and rat alveolar type II) to amosite asbestos and assessing mitochondrial membrane potential changes (deltapsi(m)) using a fluorometric technique involving tetremethylrhodamine ethyl ester (TMRE) and mitotracker green. Unlike inert particulates (titanium dioxide and glass beads), amosite asbestos caused dose- and time-dependent reductions in deltapsi(m). Asbestos-induced deltapsi(m) was associated with the release of cytochrome c from the mitochondria to the cytoplasm as well as activation of caspase 9, a mitochondrial-activated caspase. In contrast, a lower level of caspase 8, the death receptor-activated caspase, was detected in asbestos-exposed AEC. An iron chelator (phytic acid or deferoxamine) or a hydroxyl radical scavenger (sodium benzoate) each blocked asbestos-induced reductions in deltapsi(m) and caspase 9 activation, suggesting a role for iron-derived ROS. Finally, Bcl-X(L), a mitochondrial antiapoptotic protein that prevents cell death by preserving the outer mitochondrial membrane integrity, blocked asbestos-induced decreases in A549 cell deltapsi(m) and reduced apoptosis as assessed by DNA fragmentation. We conclude that asbestos-induced AEC apoptosis results from mitochondrial dysfunction, in part due to iron-derived ROS, which is followed by the release of cytochrome c and caspase 9 activation. Our findings suggest an important role for the mitochondria-regulated death pathway in the pathogenesis of asbestos-associated pulmonary toxicity.

Animals↗

PubMedDate not supplied

Phytic acid, an iron chelator, attenuates pulmonary inflammation and fibrosis in rats after intratracheal instillation of asbestos.

Reactive oxygen species, especially iron-catalyzed hydroxyl radicals (.OH) are implicated in the pathogenesis of asbestos-induced pulmonary toxicity. We previously demonstrated that phytic acid, an iron chelator, reduces amosite asbestos-induced .OH generation, DNA strand break formation, and injury to cultured pulmonary epithelial cells (268[1995, Am. J. Physiol.(Lung Cell. Mol. Physiol.) 12:L471-480]). To determine whether phytic acid diminishes pulmonary inflammation and fibrosis in rats after a single intratracheal (it) instillation of amosite asbestos, Sprague-Dawley rats were given either saline (1 ml), amosite asbestos (5 mg; 1 ml saline), or amosite treated with phytic acid (500 microM) for 24 hr and then instilled. At various times after asbestos exposure, the rats were euthanized and the lungs were lavaged and examined histologically. A fibrosis score was determined from trichrome-stained specimens. As compared to controls, asbestos elicited a significant pulmonary inflammatory response, as evidence by an increase (approximately 2-fold) in bronchoalveolar lavage (BAL) cell counts at 1 wk and the percentage of BAL neutrophils (PMNs) and giant cells at 2 wk (0.1 vs 6.5% and 1.3 vs 6.1%, respectively; p < 0.05). Asbestos significantly increased the fibrosis score at 2 wk (0 +/- 0 vs 5 +/- 1; p < 0.05). The inflammatory and fibrotic changes were, as expected, observed in the respiratory bronchioles and terminal alveolar duct bifurcations. The increased percentage of BAl PMNs and giant cells persisted at 4 wk, as did the fibrotic changes. Compared to asbestos alone, phytic acid-treated asbestos elicited significantly less BAL PMNs (6.5 vs 1.0%; p < 0.05) and giant cells (6.1 vs 0.2%; p < 0.05) and caused significantly less fibrosis (5 vs 0.8; p < 0.05) 2 wk after exposure. We conclude that asbestos causes pulmonary inflammation and fibrosis in rats after it instillation and that phytic acid reduces these effects. These data support the role of iron-catalyzed free radicals in causing pulmonary toxicity from asbestos in vivo.

Animals↗

PubMed1999

Asbestos and cancer: An overview of current trends in Europe.

This review assesses the contribution of occupational asbestos exposure to the occurrence of mesothelioma and lung cancer in Europe. Available information on national asbestos consumption, proportions of the population exposed, and exposure levels is summarized. Population-based studies from various European regions on occupational asbestos exposure, mesothelioma, and lung cancer are reviewed. Asbestos consumption in 1994 ranged, per capita, between 0. 004 kg in northern Europe and 2.4 kg in the former Soviet Union. Population surveys from northern Europe indicate that 15 to 30% of the male (and a few percent of the female) population has ever had occupational exposure to asbestos, mainly in construction (75% in Finland) or in shipyards. Studies on mesothelioma combining occupational history with biologic exposure indices indicate occupational asbestos exposure in 62 to 85% of the cases. Population attributable risks for lung cancer among males range between 2 and 50% for definite asbestos exposure. After exclusion of the most extreme values because of methodologic aspects, most of the remaining estimates are within the range of 10 to 20%. Estimates of women are lower. Extrapolation of the results to national figures would decrease the estimates. Norwegian estimates indicate that one-third of expected asbestos-related lung cancers might be avoided if former asbestos workers quit smoking. The combination of a current high asbestos consumption per capita, high exposure levels, and high underlying lung cancer rates in Central Europe and the former Soviet Union suggests that the lung cancers will arise from the smoking-asbestos interaction should be a major concern.

Asbestos↗

PubMed1999

The hazards of chrysotile asbestos: a critical review.

Chrysotile, or "white", asbestos is the dominant form of asbestos in international commerce today. It accounts for 99% of current world asbestos production of 2 million tonnes. Chrysotile is an extremely hazardous material. Clinical and epidemiologic studies have established incontrovertibly that chrysotile causes cancer of the lung, malignant mesothelioma of the pleura and peritoneum, cancer of the larynx and certain gastrointestinal cancers. Chrysotile also causes asbestosis, a progressive fibrous disease of the lungs. Risk of these diseases increases with cumulative lifetime exposure to chrysotile and rises also with increasing time interval (latency) since first exposure. Comparative analyses have established that chrysotile is 2 to 4 times less potent than crocidolite asbestos in its ability to cause malignant mesothelioma, but of equal potency of causation of lung cancer. The International Agency for Research on Cancer of the World Health Organization has declared chrysotile asbestos a proven human carcinogen. Sales of chrysotile asbestos have virtually ended in Western Europe and North America, because of widespread recognition of its health hazards. However, asbestos sales remain strong in Japan, across Asia and in developing nations worldwide. The claim has been made that chrysotile asbestos can be used "safely" under "certain conditions" in those nations. That claim is not accurate. The Collegium Ramazzini, an international learned society in environmental and occupational medicine, has called for an immediate worldwide ban on all sales and uses of all forms of asbestos, including chrysotile. The rationale for this ban is threefold: (1) that safer substitute materials are readily available, (2) that "controlled" use of asbestos is not possible, and (3) that the health risks of asbestos are not acceptable in either the industrialized or the newly industrializing nations.

Asbestos↗

PubMed2001

Asbestos tissue burden study on human malignant mesothelioma.

Asbestos fibers in the lung and mesothelial tissues (mesotheliomatous tissue and hyaline plaque) taken from 151 human malignant mesothelioma cases were identified and characterized by high resolution analytical electron microscopy. Asbestos fibers were present in almost all of the lung tissue as well as in the mesothelial tissue. The most common asbestos types seen in the lung were an admixture of chrysotile with amphiboles followed by amphiboles alone and chrysotile alone. The majority of asbestos types seen in the mesothelial tissues were chrysotile alone, followed by chrysotile plus amphibole and amphibole alone. A disproportion of asbestos types between the lung and mesothelial tissues was frequently observed. The most common pattern of the disproportion was chrysotile plus amphibole(s) in the lung and chrysotile only in the mesothelial tissues, followed by amphibole(s) in the lung and chrysotile only in the mesothelial tissues. Such a disproportion was considered to have been caused by chrysotile fiber's strong capacity to translocate from the lung to mesothelial tissues. The number of asbestos fibers in the lung was 456.4 x 10(6) fibers/dry gram in maximum, 0.08 x 106 fibers/dry gram in minimum and 105 x 10(6) fibers/dry gram on average; in the mesothelial tissues it was 240.0 x 106 fibers/dry gram in maximum, 0.03 x 106 fibers/dry gram in minimum and 49.84 x 106 fibers/dry gram on average. These numbers were greater than those seen in the general population. The majority of asbestos fibers detected in the lung and mesothelial tissues were shorter than 5 microm in length. Asbestos fibers fit to Stanton's hypothetical dimensions (> or =8.0 microm in length and < or =0.25 microm in diameter) were only 4.0%, since the majority of these fibers were shorter (<8 microm) and thinner (<0.25 microm) fibers. We concluded that such short, thin asbestos fibers should not be excluded from those contributing to the induction of human malignant mesothelioma. The present study supports that chrysotile asbestos can induce human malignant mesothelioma, since, in some of the mesothelioma cases, asbestos fibers detected in both the lung and mesothelial tissues, or lung tissue alone or mesothelial tissues alone were exclusively chrysotile fibers.

Asbestos↗

PubMedDate not supplied

Human alveolar macrophage cytokine release in response to in vitro and in vivo asbestos exposure.

The lung macrophage is proposed to be involved in the development of asbestos-induced pulmonary fibrosis. Knowledge of the effects of long-term asbestos exposure on lung macrophage cytokine release should better define the role of the macrophage in fibrogenesis. This study examines the effects of acute in vitro asbestos exposure and chronic in vivo asbestos exposure on human alveolar macrophage cytokine release. As indicators of asbestos-induced macrophage activation, the cellular release of IL-1 beta, TNF-alpha, IL-6, GM-CSF, and PGE2 was measured during a 24-h in vitro culture. Alveolar macrophages from normal volunteers were cultured in vitro with chrysotile asbestos. Of the factors measured, only TNF-alpha was elevated in response to asbestos exposure. Alveolar macrophages from asbestos-exposed individuals were placed into one of two groups based on their exposure history. These two groups were matched for age, smoking history, and diagnosis; none met the criteria for asbestosis. Cells isolated from subjects that had been exposed to asbestos for more than 10 years secreted enhanced basal amounts of IL-1 beta, TNF-alpha, IL-6, and PGE2, while those who had been exposed for less than 10 years did not. The results indicate that while asbestos had minimal acute effects on cytokine production by the human alveolar macrophage, intense, chronic exposure to asbestos leads to the enhanced basal release of significant amounts of several cytokines that have activity for the fibroblast, even in the absence of overt fibrosis.

Aged↗

PubMed1999

Multi-parameter observation of environmental asbestos pollution at the Institut de Physique du Globe de Paris (Jussieu Campus, France).

An original multi-parameter system has been used to study the nature of dust in the ambient air, particularly the total fibers and asbestos fibers, in eight areas of the Institut de Physique de Globe de Paris (France). These analyses provide a detailed case study of environmental pollution by asbestos fibers at low levels. The levels of total fibers with a length greater than 3 microns, measured with a real time fiber analyser monitor (FAM), give a baseline of 2.5 fibers per l., throughout the duration of sampling. The same levels, calculated during periods of effective presence of staff, are smaller than 10 fb per l. During these periods, the instantaneous value can show high peaks, reaching a maximum of 60 fb per l., but more often of about 5 to 10 fb per l. A direct cause and effect relationship exists between fiber concentrations and the presence of people, and indirectly with the variation of the other environmental parameters (temperature, humidity, air velocity). The baseline concentration of asbestos fibers, determined by analytical transmission electron microscopy (ATEM), is about 10(-1) fb per l., with a mean value during the presence of people always less than 1.5 fb per l. The low levels of asbestos fibers do not allow us to establish a precise correlation between the concentration of total fibers and the asbestos concentration, but a rough estimate suggests that asbestos could represent 10-20% of the airborne fibers monitored with the FAM. The statistical study of fiber sizes shows that 70 and 55% of analyzed chrysotile and amosite fibers respectively are smaller than 5 microns. These numbers are 40 and 35% for fibers smaller than 3 microns, which are undetected by the FAM. Amosite, which characterizes most of the asbestos-containing materials (ACM) in the analyzed areas, is detected in the ambient air in quantities ten times less important than chrysotile. The low asbestos levels and the difference between the nature of building asbestos and airborne fibers, show that the mean measured asbestos contents in the ambient air represent the geochemical background of chrysotile asbestos fibers in the Parisian air.

Air Pollution↗

PubMedDate not supplied

Involvement of hydrogen peroxide in asbestos-induced NFAT activation.

The present study investigated the role of reactive oxygen species (ROS) in activation of nuclear factor of activated T cells (NFAT), a pivotal transcription factor responsible for regulation of cytokines, by asbestos in mouse embryo fibroblast PW cells. Exposure of cells to asbestos led to the transactivation of NFAT in a time- and dose-dependent manner. Scavenging of asbestos-induced H2O2 with N-acety-L-cyteine (NAC, a general antioxidant) or catalase (a specific H2O2 inhibitor) resulted in inhibition of NFAT activation. In contrast, an increase in H2O2 generation by the addition of superoxide dismutase (SOD) slightly enhanced asbestos-induced NFAT activation. In addition, pretreatment of cells with sodium formate did not exhibit any inhibition of NFAT activity induced by asbestos. These results demonstrated that H2O2 appeared to play an important role in asbestos-induced NFAT transactivation. Furthermore, it was observed that incubation of cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) not only resulted in NFAT activation by itself, but also enhanced asbestos-induced NFAT induction. Pretreatment of cells with cyclosporin A (CSA), a pharmacological inhibitor of the phosphatase calcineurin, blocked both asbestos- and TPA plus asbestos-induced NFAT activation. These data suggest that asbestos is able to induce NFAT activation through H2O2-dependent and CSA-sensitive pathways, which may be involved in asbestos-induced carcinogenesis.

Acetylcysteine↗