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PubMed1996

Chrysotile asbestos fibers mediate homologous recombination in Rat2 lambda fibroblasts: implications for carcinogenesis.

Asbestos fibers are widespread environmental carcinogens whose mutagenicity is now established. Nonetheless, the molecular nature of these mutations and the mechanisms by which they accelerate carcinogenesis remain poorly understood. We have assessed the ability of asbestos fibers to promote homologous recombination, a potent mechanism for generating intrachromosomal rearrangements, such as deletions, and mitotic recombination. For this, we have developed a new assay which determines the extent to which a marker gene present in DNA introduced by asbestos can recombine with homologous genes residing in a transfected cell. We have demonstrated that Calidria chrysotile fibers are mutagenic and are able to mediate transfection of molecularly marked mutant lacI genes in a manner that results in their preferential recombination with homologous wild-type genes in the transfected cell. Asbestos induced recombination events may play a significant role in asbestos mutagenesis and carcinogenesis, and promotion of recombination may underlie the well-recognized synergy of asbestos with other carcinogens.

Animals↗

PubMed2000

Asbestos and cigarette smoke cause increased DNA strand breaks and necrosis in bronchiolar epithelial cells in vivo.

Coexposures to asbestos and cigarette smoke cause increased risks of lung cancer in asbestos workers. Although these carcinogens cause DNA damage to epithelial cells in vitro via generation of reactive oxygen species (ROS), it is unclear whether they cause injury to bronchiolar epithelial cells (i.e., the target cells of lung cancers in vivo). We exposed rats to amosite asbestos, cigarette smoke, and the two agents in combination for 1, 2, and 14 d. Numbers of cells exhibiting DNA strand breaks in comparison to sham rats were then evaluated in lungs using the terminal deoxynucleotidyl transferase (TDT)-mediated dUTP-biotin nick end labeling (TUNEL) method and by transmission electron microscopy (TEM). Increases in TUNEL-positive, necrotic epithelial cells occurred after exposure to asbestos alone and in an additive fashion after smoke and asbestos in combination. These results indicate that DNA strand breakage and necrosis are prominent mechanisms of injury by asbestos fibers and cigarette smoke in vivo to epithelial cells of the respiratory tract, thus validating in vitro observations from a number of laboratories.

Animals↗

PubMed2003

Multiple roles of oxidants in the pathogenesis of asbestos-induced diseases.

Exposure to asbestos causes cellular damage, leading to asbestosis, bronchogenic carcinoma, and mesothelioma in humans. The pathogenesis of asbestos-related diseases is complicated and still poorly understood. Studies on animal models and cell cultures have indicated that asbestos fibers generate reactive oxygen and nitrogen species (ROS/RNS) and cause oxidation and/or nitrosylation of proteins and DNA. The ionic state of iron and its ability to be mobilized determine the oxidant-inducing potential of pathogenic iron-containing asbestos types. In addition to their capacity to damage macromolecules, oxidants play important roles in the initiation of numerous signal transduction pathways that are linked to apoptosis, inflammation, and proliferation. There is strong evidence supporting the premise that oxidants contribute to asbestos-induced lung injury; thus, strategies for reducing oxidant stress to pulmonary cells may attenuate the deleterious effects of asbestos.

Animals↗

PubMed2003

Current controversies regarding the role of asbestos exposure in the causation of malignant mesothelioma: the need for an evidence-based approach to develop medicolegal guidelines.

Asbestos is a group of fibrous silicate minerals that includes two mineralogic groups: amphiboles and serpentines. While the carcinogenic role of amphiboles (eg, crocidolite and amosite) is well established, medical "experts" that tend to strongly advocate their views currently argue in medicolegal cases multiple specific issues regarding the carcinogenicity of asbestos fibers. For example, it is controversial whether chrysotile causes malignant mesothelioma (MM); what are the specific carcinogenic thresholds for amphiboles and chrysotile; what occupations are truly at risk to develop MM as a result of asbestos exposure; what is the role of chrysotile in the development of peritoneal MM; how to assign causation in individuals exposed to multiple industrial products containing variable concentrations of various asbestos fibers; and, what criteria should be used to accept causation in household exposure cases and others. The causation criteria currently acceptable in U.S. courts are surprisingly flexible and subject to variable interpretation by medical "experts." At a time where thousands of individuals are claiming causation of MM by asbestos exposure, there is a need to develop more specific causation guidelines based on scientific evidence. Evidence-based medicine has been proposed as a new approach to the study, teaching, and the practice of medicine and has been used as a process of systematically reviewing the relevant studies in the literature to assess their scientific validity and development of guidelines. This article summarizes some of the current controversies regarding the role of asbestos exposure in the causation of MM and suggests the need for future evidence-based medicine-type studies to develop causation guidelines that could be used consistently during litigation.

Animals↗

PubMed2000

Kidney cancer and occupational exposure to asbestos: a meta-analysis of occupational cohort studies.

OBJECTIVE: To study the risk of kidney cancer following asbestos exposure. METHODS: We carried out a meta-analysis of the results of cohort studies of workers predominantly exposed to asbestos. We contacted the authors of 70 cohort studies; published results were available from the reports of 10 cohorts; we obtained the relevant information for an additional 27 cohorts. RESULTS: The studies included in the analysis comprised a total of 169 kidney cancer deaths and 69 incident cases. The overall pooled standardized mortality ratio (SMR) of kidney cancer was 1.1, with a 95% confidence interval (95% CI) of 0.9-1.3. The pooled SMR was higher for workers with undefined asbestos exposure (SMR 1.2, 95% CI 0.9-1.6) than for workers with either predominant chrysotile (SMR 0.9, 95% CI 0.7-1.3) or some amphibole (SMR 0.96, 95% CI 0.6-1.5) exposure. Studies with published results had higher SMRs than studies for which information was obtained from the authors. Studies with high asbestos exposure and an elevated SMR of lung cancer tended to show an increased risk of kidney cancer. CONCLUSIONS: It is unlikely that asbestos exposure is responsible for an important increase in kidney cancer risk; however, high asbestos exposure might entail a small increase in risk.

Adult↗

PubMed2000

X-ray evidence of increased asbestos exposure in the US population from NHANES I and NHANES II, 1973-1978. National Health Examination Survey.

OBJECTIVES: Jobs involving heavy asbestos exposure increase risk for lung cancer and mesothelioma substantially, and low-level exposures may carry some risk. At least one indicator of asbestos exposure, mesothelioma, has been increasing in the US for decades. We investigated the prevalence of another indicator, pleural thickening on x-ray, in a defined sample of the US population. METHODS: Certified physicians read 1060 x-rays from the second National Health and Nutrition Examination Survey (1976-1980) for pleural changes consistent with pneumoconiosis, which are a reasonably specific indicator of asbestos exposure. RESULTS: Prevalence estimates, in NHANES II, in the age group 35-74 years, are 6.4% (+/- 0.9%) among males, 1.7% (+/- 0.6%) among females, and 3.9% (+/- 0.6%) overall. These prevalences are approximately twice those estimated from NHANES I data (1971-1975). CONCLUSIONS: X-ray evidence of asbestos exposure was common in the late 1970s and increasing. The increase may be due to occupational asbestos exposure, but it is so large as to suggest some contribution from environmental, non-occupational asbestos exposure.

Adult↗

PubMed1970

Migration of asbestos fibres from subcutaneous injection sites in mice.

Crocidolite asbestos fibres, suspended in physiological saline, were injected subcutaneously into one or both flanks of 95 CBA/Lac female mice; 75 control mice received injections of saline only. Most animals were killed at chosen intervals of between 2 and 42 days after injection but some were left for longer periods of up to 623 days. At autopsy, many lymphoid and non-lymphoid structures were removed and examined for the presence of asbestos by the following techniques: haematoxylin and eosin staining followed by conventional and polarized light microscopy; Perl's stain; microincineration followed by phase-contrast microscopy; maceration with KOH followed by phase-contrast microscopy; and electron microscopy.A combination of haematoxylin and eosin staining and microincineration was found to be the most convenient and reliable method for demonstrating asbestos fibres in the tissues. Electron microscopy was essential for detecting very small fibres and for locating them to specific intracellular structures.The morphological findings indicate that some migration of asbestos fibres away from the initial site of injection takes place. Dissemination is usually along lymphatic pathways and fibres tend to accumulate in the lymphoid tissues, particularly in the regional (axillary) lymph nodes; smaller amounts were found in inguinal, mediastinal and lumbar nodes. The fibres were usually intracellular, lying inside the phagosomes of macrophages, but larger fibres weresometimes encountered lying free. Small numbers of fibres were seen in the spleen and also in non-lymphoid organs such as the liver, kidneys and brain-suggesting that some asbestos may enter the blood stream. There was no evidence of massive or selective spread to subserosal tissues in the thorax or abdomen, though trapping of asbestos fibres was observed in pleural "milky spots" in long-term survivors. The possible role of milky spots in the development of pleural plaques and mesotheliomata is discussed.

Animals↗

PubMed2003

beta1-integrin mediates asbestos-induced phosphorylation of AKT and ERK1/2 in a rat pleural mesothelial cell line.

Integrin-mediated signalling has been implicated in asbestos-induced carcinogenesis. In studies here, we examined signal transduction events associated with integrin-directed cell reactions triggered by crocidolite asbestos in the pleural mesothelial cell line 4/4 RM-4. Crocidolite fibres induced a significant time- and dose-dependent activation of the extracellular-signal-regulated kinases ERK1 and ERK2. ERK activation was specifically inhibited by integrin-blocking agents, that are integrin-binding peptides containing the sequence arginine-glycine-aspartic acid (RGD), and monoclonal antibodies against the integrin beta1-chain. Integrin-dependent activation of ERK1/2 in response to asbestos appeared to be independent of focal adhesion kinase pp125FAK (FAK) since FAK autophosphorylation remained unaffected in crocidolite-exposed mesothelial cells. Instead, we observed striking similarities in the kinetics of asbestos-induced ERK1/2 responses and phosphorylation of protein kinase B (AKT) at serine 473, a possible target residue for integrin-linked kinase. As with ERK activation, asbestos-induced AKT stimulation was significantly blocked by both the RGD-peptide and the beta1-integrin antibodies. These studies are the first to establish that in mesothelial cells ERK1/2 and AKT are simultaneously phosphorylated upon asbestos exposure in a beta1-integrin-dependent manner.

Animals↗

PubMed2004

Determination of environmental exposure to asbestos (tremolite) and mesothelioma risks in the southeastern region of Turkey.

In this study, the authors examined the concentrations and mineralogical analyses of asbestos, and investigated mesothelioma risk in southeastern Anatolia, Turkey. They used a gravimetric dust sampler to collect samples from 2 villages and 2 asbestos mines (1 active). Samples were then evaluated by an X-ray diffractometer and an electron microscope. The authors found high concentrations of asbestos in an active mine (4.9 fibers[f]/cm3) and at a house that was plastered with asbestos (1.24 f/cm3) and had a very active population. They found a low concentration (0.0042 f/cm3) in indoor measurements taken in Armutova village, and an even lower concentration (0.000081 f/cm3) in the inactive mine environment. Outdoor measurements included a low concentration of 0.007 f/cm3 in the village environment, and a high concentration of 1.17 f/cm3 on the mine road during the passing of a sheep herd. The people in the region are continuously exposed to asbestos during normal activities. This cumulative exposure to asbestos carries sufficient risks for mesothelioma development.

Asbestos↗

PubMed2005

Expression of heme oxygenase-1 in the lungs of rats exposed to crocidolite asbestos.

Oxidative stress is thought to be the pathogenesis of pulmonary fibrosis induced by asbestos, and heme oxygenase-1 (HO-1) protects lung tissue against oxidative stress. We hypothesized that HO-1 is associated with oxidative lung injury caused by exposure to asbestos. This study was conducted to investigate the time course of HO-1 expression of lungs exposed to crocidolite asbestos in vivo. Male Wistar rats were administered 1 mg or 2 mg crocidolite asbestos suspended in saline by a single intratracheal instillation and were sacrificed at 3 d, 1 wk, 1 mo, 3 mo, and 6 mo of recovery time. The expression of HO-1 was observed by Western blot analysis and immunostaining. Protein levels of HO-1 increased at from 3 d to 6 mo following intratracheal instillation of 2 mg crocidolite asbestos. The levels of HO-1 increased at 1 wk and 1 mo following intratracheal instillation of 1 mg crocidolite asbestos. Many HO-1-positive cells were found, particularly in the alveolar macrophages, during immunostaining. These findings suggest that HO-1 may be related to lung disorder induced by dust and therefore can act as a biomarker of lung injury due to dust exposure.

Animals↗

PubMed2006

A review of the federal government's health activities in response to asbestos-contaminated ore found in Libby, Montana.

Vermiculite ore is a naturally occurring fibrous mineral widely used in various consumer products, such as attic insulation, lawn and garden products, and fireproofing material. While most vermiculite ore and products do not pose a health hazard, the vermiculite mined from Libby, MT was contaminated with naturally occurring asbestos. The federal Agency for Toxic Substances and Disease Registry (ATSDR) has documented a significant number of asbestos-related deaths among Libby residents. Additionally, as part of the ongoing investigation, ATSDR has learned that this contaminated ore was shipped to hundreds of locations around the United States for processing. While the Libby mine is now closed, studies from ATSDR and elsewhere show that people who worked in the Libby mine or vermiculite processing facilities may have been exposed to hazardous levels of asbestos while the facilities were in operation. People who lived or worked near these sites also may have been exposed to asbestos if they came into contact with contaminated vermiculite. Prolonged exposure to asbestos can cause serious and life-threatening health conditions, including asbestosis, lung cancer, and mesothelioma. In response, ATSDR has initiated 10 different activities to help evaluate the potential health effects among Libby residents and populations throughout the United States who might have been exposed to the asbestos-contaminated ore found in Montana. Some of these activities include conducting environmental exposure evaluations, health statistics reviews, community screenings, and disease-specific surveillance. This article presents the various follow-up activities that have been conducted to date by ATSDR and partnering state health departments.

Aluminum Silicates↗

PubMed2000

Exposures to asbestos arising from bandsawing gasket material.

A simulation of bandsawing sheet asbestos gasket material was performed as part of a retrospective exposure evaluation undertaken to assist in determining causation of a case of mesothelioma. The work was performed by bandsawing a chrysotile asbestos (80%)/neoprene gasket sheet with a conventional 16-inch woodworking bandsaw inside a chamber. Measurements of airborne asbestos were made using conventional area and personal sampling methods, with analysis of collected samples by transmission electron microscopy (TEM) and phase contrast microscopy (PCM). These were supplemented by qualitative scanning electron microscopy (SEM) examinations of some of the airborne particles collected on the filters. In contrast with findings from studies examining manual handling (installation and removal) of gaskets, airborne asbestos concentrations from this operation were found to be well above current Occupational Safety and Health Administration (OSHA) permissible exposure limit (PEL) (eight-hour time-weighted average [TWA]) and excursion limit (30-minute) standards. Although some "encapsulation" effect of the neoprene matrix was seen on the particles in the airborne dust, unencapsulated individual fiber bundles were also seen. Suggestions for the implications of the work are given. In summary, the airborne asbestos concentrations arising from this work were quite high, and point to the need for careful observation of common sense precautions when manipulation of asbestos-containing materials (even those believed to have limited emissions potential) may involved machining operations.

Asbestos↗

PubMed2001

Morphological characteristics of asbestos fibers released during grinding and drilling of friction products.

There has been considerable interest during the past 30 years regarding the potential for exposure to asbestos fibers generated during asbestos-containing automobile and light-duty truck brake replacement and repair operations. Less attention has been directed to asbestos fiber exposures resulting from servicing of brakes on heavy-duty trucks and other machinery. Potential for the generation of respirable fibers as a result of using a rotary bench grinder and the drilling of asbestos-containing friction pads was investigated to assess the characteristics of the fibers generated from these procedures. The data from the grinding process revealed that this material was either resin matrix or fibers bound to the resin matrix. Fibers generated from the drilling procedure revealed morphology consistent with chrysotile asbestos. In each case, nonfibrous materials remained bound to the fibers released from these processes. These fibers had resin deposits attached. This investigation offers evidence that drilling and grinding of brake pads generates fibers that, for the most part, remain bound to the underlying matrix, suggesting that grinding and drilling may not pose an important source of exposure to respirable asbestos fibers.

Asbestos↗

PubMed2002

Fiber release during the removal of asbestos-containing gaskets: a work practice simulation.

Work practice studies were conducted involving the removal of asbestos-containing sheet gaskets from steam flanges. These studies were performed to determine potential exposure levels to individuals who have worked with these types of materials in the past and may still work with these products today. The work practices were conducted inside an exposure characterization laboratory (ECL) and were performed by scraping and wire brushing, chrysotile-containing (65% to 85%) sheet gaskets from a number of used steam flanges. Airborne asbestos levels were measured by phase contrast microscopy (PCM) and transmission electron microscopy (TEM) for the personnel and area air samples collected during the study. These workplace simulations showed substantial asbestos fiber release using scraping, hand wire brushing, and power wire brushing techniques during the gasket removal process. The range of concentration was 2.1 to 31.0 fibers/cc greater than 5 micrometers when measured by PCM. These results contrasted with the few reported results in the published literature where lower airborne asbestos levels were reported. In these studies the airborne asbestos fiber levels measured in many of the samples exceeded all current and historical Occupational Safety and Health Administration (OSHA) excursion limits (15-30 minutes) and some previous permissible exposure limits (PEL) based on eight-hour time-weighted average (TWA) standards. Also, individuals who performed this type of work in the past may have had exposures higher than previously suspected. The results demonstrated that employees who remove dry asbestos-containing gaskets with no localized ventilation should wear a full face supplied air respirator with a HEPA escape canister and the work area should be designated a regulated area.

Air Pollution, Indoor↗

PubMed2003

An evaluation of the historical exposures of mechanics to asbestos in brake dust.

This article presents a historical analysis of published data regarding the exposure of brake mechanics to asbestos as a result of doing brake work. Concerns about this possible hazard were first raised in the late 1960s. This analysis focuses on 30 years of data collected during the brake repair event (e.g., a brake job) and 8-hour time-weighted average (TWA) personal samples. A brake job TWA represents the average concentration a mechanic experienced during brake servicing, rather than throughout the workday, and an 8-hour TWA represents the average airborne concentration of asbestos for the entire workday (which would involve brake work and other activities). Nearly 200 brake job and 8-hour TWA airborne asbestos samples were analyzed to assess how asbestos concentrations varied by type of vehicle serviced, country in which mechanics worked, time period, and brake-cleaning method. To facilitate comparisons, brake job TWAs were converted to estimated 8-hour TWAs using the durations and number of brake jobs performed per mechanic each day. Estimated and measured 8-hour TWAs for mechanics servicing automobiles and light trucks ranged from <0.002 to 0.68 f/cc, with a mean of 0.04 f/cc. In contrast, the 8-hour TWAs for mechanics servicing heavy trucks and buses ranged from 0.002 to 1.75 f/cc, with a mean of 0.2 f/cc, suggesting that these mechanics experienced higher daily asbestos exposures than automobile and light truck mechanics. Brake job and 8-hour TWAs for brake mechanics worldwide were found to be similar during the same time periods, and they were consistently below contemporaneous occupational health standards in the United States. The increased use of brake-dust control measures in some garages resulted in at least a 10-fold decrease in the TWA airborne concentrations of asbestos from the 1970s to the late 1980s.

Air Pollutants, Occupational↗

PubMed1999

Asbestos fiber release from the brake pads of overhead industrial cranes.

The purpose of this evaluation was to determine the actual contribution of airborne asbestos fibers to the work environment from the operation of overhead cranes and hoists that use asbestos composition brake pads. The evaluation was conducted in a working manufacturing facility. Other potential sources of asbestos were accounted for by visual inspection and background air monitoring. An overhead crane assembly comprised of a trolley and two hoists was employed for this study. The crane was operated for two consecutive eight-hour shifts representative of a heavy-duty cycle. Forty-four personal and area air samples were collected during the assessment. Asbestos fibers were analyzed for by phase contrast (NIOSH 7400), and transmission electron (NIOSH 7402) microscopy methods. Eight-hour time-weighted average (TWA) asbestos fiber concentrations ranged from < 0.005 to 0.011 fibers/cc (PCM), and < 0.0026 to < 0.0094 f/cc (TEM). There were no asbestos fibers detected by the TEM method from air samples collected during the operation of the cranes.

Air Pollutants, Occupational↗

PubMed2004

Airborne asbestos levels in school buildings in Italy.

This article provides a summary of environmental investigations carried out from 1992 to 2002 by the National Institute for Occupational Prevention and Safety on airborne asbestos fiber concentrations in Italian schools. The monitoring was performed to evaluate the risk from asbestos exposure to students and school staff. Fifty-nine schools located in several Italian regions were studied. A detailed visual examination assisted with locating asbestos-containing materials in different school areas. Asbestos was mainly present in the vinyl floor coverings and in the asbestos-cement products (roofs, facades, and heating ducts). After the identification of the potential sources of exposure, several bulk and air samplings were performed in the areas where the contamination was suspected. All air samplings were collected on membrane filters and analyzed by phase contrast optical microscopy and scanning electron microscopy. During the course of the samplings, the schools were in operation and normal student activities took place. Most of the results provided no significant evidence of airborne asbestos fibers, although some dispersion was found in a few school buildings where, during the past years, monitoring and safety programs had not been implemented.

Air Pollution, Indoor↗

PubMed2005

Occupational exposure to airborne asbestos from phenolic molding material (Bakelite) during sanding, drilling, and related activities.

In this study, a historical phenolic (Bakelite) molding material, BMMA-5353, was tested to determine the airborne concentrations of asbestos fibers released during four different activities (sawing, sanding, drilling, and cleanup of dust generated from these activities). Each activity was performed for 30 min, often in triplicate. The primary objective for testing BMMA-5353 was to quantitatively determine the airborne concentration of asbestos fibers, if any, in the breathing zone of workers. Uses of this product typically did not include sawing or sanding, but it may have been drilled occasionally. For this reason, only small quantities were sawed, sanded, and drilled in this simulation study. Personal (n = 40), area (n = 80), and background/clearance (n = 88) air samples were collected during each activity and analyzed for total fiber concentrations using phase contrast microscopy (PCM) and, for asbestos fiber counts, transmission electron microscopy (TEM). The raw PCM-total fiber concentrations were adjusted based on TEM analyses that reported the fraction of asbestos fibers, to derive a PCM-asbestos concentration that would enable calculation of an 8-hour time-weighted average (TWA). The estimated 8-hour TWAs ranged from 0.006 to 0.08 fibers per cubic centimeter using a variety of worker exposure scenarios. Therefore, assuming an exposure scenario in which a worker uses power tools to cut and sand products molded from BMMA-5353 and similar products in the manner evaluated in this study, airborne asbestos concentrations should not exceed current or historical occupational exposure limits.

Asbestos↗