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PubMed2006

Transcriptional up-regulation of MMP12 and MMP13 by asbestos occurs via a PKCdelta-dependent pathway in murine lung.

Asbestos is a known inflammatory, carcinogenic, and fibrotic agent, but the mechanisms leading to asbestos-induced lung diseases are unclear. Using a murine inhalation model of fibrogenesis, we show that asbestos causes significant increases in mRNA levels of lung matrix metalloproteinases (MMPs 12 and 13) and tissue inhibitor of metalloproteinases (TIMP1), as well as increased activities of MMP 2, 9, and 12 in bronchoalveolar lavage fluids (BALF). Asbestos-exposed PKCdelta knockout (PKCdelta-/-) mice exhibited decreased expression of lung MMP12 and MMP13 compared with asbestos-exposed wild-type mice. Studies using small molecule inhibitors in murine alveolar epithelial type II cells (C10) and primary lung fibroblasts confirmed that asbestos transcriptionally up-regulates MMPs via an EGFR (or other growth factor receptors)/PI3K/PKCdelta/ERK1/2 pathway. Moreover, use of a broad-spectrum MMP inhibitor showed that MMPs play an important role in further enhancing asbestos-induced signaling events by activating EGFR. These data reveal a potentially important link between asbestos signaling and integrity of the extracellular matrix (ECM) that likely contributes to asbestos-induced lung remodeling and diseases.

Animals↗

PubMed2004

Mitochondrial-derived free radicals mediate asbestos-induced alveolar epithelial cell apoptosis.

Asbestos causes pulmonary toxicity by mechanisms that in part involve reactive oxygen species (ROS). However, the precise source of ROS is unclear. We showed that asbestos induces alveolar epithelial cell (AEC) apoptosis by a mitochondrial-regulated death pathway. To determine whether mitochondrial-derived ROS are necessary for causing asbestos-induced AEC apoptosis, we utilized A549-rho(omicron) cells that lack mitochondrial DNA and a functional electron transport. As expected, antimycin, which induces an oxidative stress by blocking mitochondrial electron transport at complex III, increased dichlorofluoroscein (DCF) fluorescence in A549 cells but not in A549-rho(omicron) cells. Compared with A549 cells, rho(omicron) cells have less asbestos-induced ROS production, as assessed by DCF fluorescence, and reductions in total glutathione levels as well as less caspase-9 activation and apoptosis, as assessed by TdT-mediated dUTP nick end labeling staining and DNA fragmentation. A mitochondrial anion channel inhibitor that prevents ROS release from the mitochondria to the cytoplasm also blocked asbestos-induced A549 cell caspase-9 activation and apoptosis. Finally, a role for nonmitochondrial-derived ROS with exposure to high levels of asbestos (50 microg/cm(2)) was suggested by our findings that an iron chelator (phytic acid or deferoxamine) or a free radical scavenger (sodium benzoate) provided additional protection against asbestos-induced caspase-9 activation and DNA fragmentation in rho(omicron) cells. We conclude that asbestos fibers affect mitochondrial DNA and functional electron transport, resulting in mitochondrial-derived ROS production that in turn mediates AEC apoptosis. Nonmitochondrial-associated ROS may also contribute to AEC apoptosis, particularly with high levels of asbestos exposure.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1994

Contrasting effects of alveolar macrophages and neutrophils on asbestos-induced pulmonary epithelial cell injury.

Pulmonary toxicity from asbestos may be due in part to oxidant-mediated mechanisms. The purpose of this study was to determine whether alveolar macrophages (AM) contribute to asbestos-induced alveolar epithelial cell injury by oxidant-dependent mechanisms similar to that previously described for polymorphonuclear leukocytes (PMN). We assessed 51Cr release from cultured rat alveolar epithelial cells (RAEC) and transformed human pulmonary epithelial-like cell lines (rat L2 and human WI-26: HPEC). Amosite asbestos caused dose-dependent injury to both RAEC and L2 cells after an 18-h incubation period. Rat PMN increased asbestos-induced injury to RAEC (11 vs. 20% 51Cr release). In contrast, rat AM diminished asbestos-induced injury to RAEC and L2 cells by 60-80%. Human monocytes cultured for 72 h also attenuated asbestos-induced HPEC damage. Asbestos stimulated more H2O2 release from PMN than from AM isolated from the same rats (5.3 +/- 0.6 vs. 0.3 +/- 0.1 nmol x 10(6) cells-1 x 2h-1). The protective effect of rat AM, as opposed to PMN, was not due to differences in asbestos-induced toxicity to each cell type, since > 90% of AM and PMN were nonviable after 18 h. Transmission electron microscopy demonstrated comparable uptake of asbestos by AM and PMN after a 2-h incubation period. However, after an 18-h exposure period, the PMN were completely lysed, whereas over 90% of the AM contained fibers, despite morphologic evidence of cytotoxicity. These results demonstrate that AM, unlike PMN, can reduce alveolar epithelial cell injury in this model.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Asbestos exposure increases paracellular transport of fibrin degradation products across human airway epithelium.

The inflammatory response to asbestos fiber inhalation suggests that the distal respiratory epithelium is an important early target of asbestos-induced injury. We have previously found that asbestos exposure increases the fibrinolytic activity and mannitol permeability of human airway epithelial cell monolayers. Because fibrin degradation products (FDP) are potent inflammatory mediators, we asked whether asbestos fiber exposure would increase the transepithelial flux of FDP into the interstitial space. To stimulate the pericellular environment following fiber deposition, asbestos-exposed epithelial monolayers grown on permeable filters were covered with human plasma containing fluorescein isothiocyanate (FITC)-labeled human fibrinogen. After 24 h, nearly twice as much FITC-FDP appeared in the abluminal chamber of asbestos-exposed monolayers compared with unexposed controls. This did not result solely from increased degradation product production because asbestos-exposed epithelium was more permeable at all apical FDP concentrations. The proteins that crossed asbestos-exposed monolayers included biologically relevant high-molecular-weight FDP, as demonstrated by streptavidin blotting of biotin-labeled FDP. We also found that FDP flux was not vectorial, was not saturable, did not involve proteolytic processing of FDP, and did not require active transport. Thus asbestos exposure increases the paracellular flux of intact FDP across human airway epithelium. This represents a novel mechanism whereby fiber-induced epithelial dysfunction may initiate and sustain inflammation in the distal airspace.

Asbestos↗

PubMed2004

Redistribution of pulmonary EC-SOD after exposure to asbestos.

Inhalation of asbestos fibers leads to interstitial lung disease (asbestosis) characterized by inflammation and fibrosis. The pathogenesis of asbestosis is not fully understood, but reactive oxygen species are thought to play a central role. Extracellular superoxide dismutase (EC-SOD) is an antioxidant enzyme that protects the lung in a bleomycin-induced pulmonary fibrosis model, but its role has not been studied in asbestos-mediated disease. EC-SOD is found in high levels in the extracellular matrix of lung alveoli because of its positively charged heparin-binding domain. Proteolytic removal of this domain results in clearance of EC-SOD from the matrix of tissues. We treated wild-type C57BL/6 mice with 0.1 mg of crocidolite asbestos by intratracheal instillation and euthanized them 24 h later. Compared with saline- or titanium dioxide-treated control mice, bronchoalveolar lavage fluid (BALF) from asbestos-treated mice contained significantly higher total protein levels and increased numbers of inflammatory cells, predominantly neutrophils, indicating acute lung injury in response to asbestos. Decreased EC-SOD protein and activity were found in the lungs of asbestos-treated mice, whereas more EC-SOD was found in the BALF of these mice. The EC-SOD in the BALF was predominantly in the proteolyzed form, which lacks the heparin-binding domain. This redistribution of EC-SOD correlated with development of fibrosis 14 days after asbestos exposure. These data suggest that asbestos injury leads to enhanced proteolysis and clearance of EC-SOD from lung parenchyma into the air spaces. The depletion of EC-SOD from the extracellular matrix may increase susceptibility of the lung to oxidative stress during asbestos-mediated lung injury.

Animals↗

PubMed2004

The duration of nuclear extracellular signal-regulated kinase 1 and 2 signaling during cell cycle reentry distinguishes proliferation from apoptosis in response to asbestos.

Asbestos exposure causes activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in lung epithelial cells, the targets of asbestos-associated lung carcinomas. The functional significance of ERK1/2 activation in pulmonary epithelial and mesothelial cells is unclear. Using serum-stimulated mouse alveolar type II epithelial cells as a model for cell cycle reentry, we show that the duration of phospho-ERK1/2 in the nucleus determines cell fate in response to crocidolite asbestos. In response to 10% serum, a proliferative stimulus, phosphorylated ERK1/2 initially accumulated in the nucleus, and reduction of nuclear phospho-ERK1/2 after 2 to 4 hours was followed by expression of cyclin D1 and S-phase entry. Low levels of asbestos (<0.5 microg/cm2) promoted S-phase entry in low (2%) serum through an epidermal growth factor receptor-dependent pathway but did not promote cell cycle progression or induce apoptosis in the presence of high (10%) serum-containing medium. Higher levels of asbestos (1.0 to 5.0 microg/cm2) prolonged the localization of phospho-ERK1/2 in the nucleus in the presence of high serum, impeded S-phase entry, and induced apoptosis in a dose-dependent manner. Immunofluorescence microscopy indicated that the duration of signaling by phospho-ERK1/2 in the nucleus was predictive of cell fate at any concentration of asbestos. After 8 hours of exposure, cells with nuclear phospho-ERK1/2 also were positive for nuclear localization of apoptosis-inducing factor (AIF), an early event in apoptosis. In contrast, asbestos-exposed cells that displayed cytoplasmic phospho-ERK1/2 at 8 hours expressed cyclin D1 and proceeded to S phase. Our studies show that prolonged localization of phospho-ERK1/2 in the nucleus is incompatible with expression of cyclin D1 and is predictive of asbestos-associated cell death by AIF, thereby providing an approach for determining cell fate in asbestos-induced tumorigenesis.

Animals↗

PubMed1993

Distribution of asbestos bodies in the human lung as determined by bronchoalveolar lavage.

Asbestos-related lung diseases tend to have distinct local distributions, for example, asbestosis first appears and tends to be more severe in the peripheral parts of the lower lung zones. The risk for asbestosis is related to the total asbestos burden of the lung. This suggests that the lower lobes in asbestos-exposed individuals may contain more asbestos than the other lobes. To test whether such topographic differences exist, we compared the number of retrieved asbestos bodies (AB) per ml BAL fluid in three groups of occupationally asbestos-exposed subjects who underwent BAL at different sampling sites. In Group 1 (n = 24) we performed BAL at three sites, namely in a segment of the right upper, right middle, and right lower lobe, to evaluate differences in asbestos body burden from lung apex to basis. There was a distinct increase in BAL asbestos body concentrations from the upper (21.2 +/- 9.1 AB/ml BAL fluid) to the middle (30.4 +/- 12.8 AB/ml BAL fluid) and to the lower lobe (56.0 +/- 20.2 AB/ml BAL fluid), all differences being significant (p < 0.01). In Group 2 (n = 40), we found good interlobar correlations for asbestos body counts between the right middle lobe (21.0 +/- 5.8 AB/ml BAL fluid) and the lingula (22.4 +/- 5.9 AB/ml BAL fluid) (r = 0.941, p < 0.001) and, in Group 3 (n = 15), between the ventral basal segment of the right (41.2 +/- 13.6 AB/ml BAL fluid) and left lung (39.0 +/- 13.6 AB/ml BAL fluid) (r = 0.966, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestos↗

PubMed1986

Asbestos exposure--quantitative assessment of risk.

Methods for deriving quantitative estimates of asbestos-associated health risks are reviewed and their numerous assumptions and uncertainties described. These methods involve extrapolation of risks observed at past relatively high asbestos concentration levels down to usually much lower concentration levels of interest today--in some cases, orders of magnitude lower. These models are used to calculate estimates of the potential risk to workers manufacturing asbestos products and to students enrolled in schools containing asbestos products. The potential risk to workers exposed for 40 yr to 0.5 fibers per milliliter (f/ml) of mixed asbestos fiber type (a permissible workplace exposure limit under consideration by the Occupational Safety and Health Administration (OSHA) ) are estimated as 82 lifetime excess cancers per 10,000 exposed. The risk to students exposed to an average asbestos concentration of 0.001 f/ml of mixed asbestos fiber types for an average enrollment period of 6 school years is estimated as 5 lifetime excess cancers per one million exposed. If the school exposure is to chrysotile asbestos only, then the estimated risk is 1.5 lifetime excess cancers per million. Risks from other causes are presented for comparison; e.g., annual rates (per million) of 10 deaths from high school football, 14 from bicycling (10-14 yr of age), 5 to 20 for whooping cough vaccination. Decisions concerning asbestos products require participation of all parties involved and should only be made after a scientifically defensible estimate of the associated risk has been obtained. In many cases to date, such decisions have been made without adequate consideration of the level of risk or the cost-effectiveness of attempts to lower the potential risk.

Asbestos↗

PubMed1994

Asbestos exposure stimulates pleural mesothelial cells to secrete the fibroblast chemoattractant, fibronectin.

Parietal pleural plaques and visceral pleural fibrosis are well-recognized stigmata of occupational asbestos exposure. However, their pathogenesis is poorly understood. Conceivably, phagocytosis of asbestos fibers by pleural mesothelial cells may stimulate the recruitment of fibroblasts to sites of asbestos-induced pleural injury. To test this hypothesis, rat parietal pleural mesothelial cells were cultured for 6 to 96 h with or without crocidolite or chrysotile asbestos fibers (concentration range, 2 to 100 micrograms/cm2). Asbestos fibers were actively phagocytosed by pleural mesothelial cells and were incorporated within phagosomes. Conditioned medium was assayed for chemotactic activity toward RL-87 rat lung fibroblasts and for fibronectin immunoreactivity. The effects of asbestos were compared with those of alpha-cristobalite (which is strongly fibrogenic), alpha-quartz (a less fibrogenic particulate), and carbonyl iron (a nonfibrogenic agent). Both types of asbestos stimulated the secretion of fibroblast chemoattractant activity by pleural mesothelial cells in a time-dependent manner. This effect peaked at 96 h in cultures containing 4 micrograms/cm2 of asbestos (P < 0.001). alpha-Cristobalite also enhanced the secretion of the mesothelial cell-derived chemoattractant, an effect that was maximal at a concentration of 20 micrograms/cm2 (P < 0.001). Furthermore, crocidolite, chrysotile, and alpha-cristobalite stimulated pleural mesothelial cell fibronectin synthesis. In contrast, alpha-quartz and carbonyl iron particles had no noticeable effect on either immunoreactive fibronectin secretion or chemoattractant release by pleural mesothelial cells. The ability of asbestos fibers and alpha-cristobalite particles to stimulate the secretion of the fibroblast chemoattractant, fibronectin, by pleural mesothelial cells may have relevance to the induction of pleural injury by fibrogenic particulates.

Animals↗

PubMed1994

Hydroxyl radicals are formed in the rat lung after asbestos instillation in vivo.

The hydroxyl radical (.OH) has been implicated as a cause of lung injury following asbestos exposure. However, despite in vitro evidence associating asbestos with .OH production, there has been no demonstration of such generation in vivo. We tested the hypothesis that .OH is formed in the lungs of rats exposed to asbestos in vivo by using salicylate as a free radical trap. Asbestos was instilled intratracheally, and control rats were sham-exposed. Six to seven days after exposure, the rats were given salicylate, the lungs were isolated, and salicylate hydroxylation products (2,3- and 2,5-dihydroxybenzoic acid), reflecting .OH production, were measured. There was significantly more 2,3-dihydroxybenzoic acid in asbestos-exposed lungs compared with control lungs (2.32 +/- 0.360 nmol/lung versus 0.292 +/- 0.125, respectively, P < 0.001) and 2,5-dihydroxybenzoic acid (9.69 +/- 1.65 nmol/lung versus 2.63 +/- 0.274, respectively, P < 0.001). To demonstrate that the dihydroxybenzoic acid was actually formed in the lungs, the lungs from asbestos-exposed and control rats were isolated and perfused with either salicylate or 2,3-dihydroxybenzoic acid. In the lungs perfused with salicylate, 2,3- and 2,5-dihydroxybenzoic acids were detectable only in asbestos-exposed lungs. In the isolated lungs perfused with 2,3-dihydroxybenzoic acid, there was no significant difference in 2,3-dihydroxybenzoic acid between asbestos-exposed and control lungs. We conclude that asbestos stimulates .OH production in lungs in vivo.

Animals↗

PubMedDate not supplied

Airborne fiber concentrations during splitting open and boxing bags of asbestos.

Measured airborne concentrations of asbestos are often unavailable to assess different epidemiologic estimates of past personal exposure levels or concentrations near specific operations involving handling asbestos. The purpose of this study was to assess the potential use of a laboratory study in estimating exposure to asbestos in operations that ceased for many years. The asbestos transfer operations were simulated by splitting and boxing 4.5-kg paper bags of chrysotile asbestos in an enclosed chamber ventilated at 28.2 air changes per hour (ACH). Two recirculation fans achieved chamber air mixing. The airborne concentration of asbestos fibers was determined by sampling air through membrane filters at a rate of 10 l/min and by analysing fibers by phase contrast optical microscopy to determine 15-min average airborne concentrations. Samplers were located at four equidistant locations from the operation. Opening a maximum of seven bags in 15 min was associated with an asbestos-in-air concentration of less than 2 x 10(-6) fibers/m3 (f/m3) in splitting open and boxing and less than 0.85 x 10(-6) f/m3 in boxing of pre-split bags. The measured airborne asbestos concentration exhibited a linear trend with the number of bags opened per 15 min. The empirical results were utilised to model fiber concentrations for various ventilation rates. It was concluded that the distribution of the operation within the workday and the ventilation rate are the two most important variables in the determination of the estimated time-weighted average concentration. Splitting open and boxing 32 bags of asbestos over an 8-h period at a rate of 4 bags/h over an 8-h period results in a calculated time-weighted average exposure of about 1 x 10(-6) f/m3 in a work space with 20 ACH and approximately 7 x 10(-6) f/m3 in a work space with 2 ACH. Splitting open and boxing at a rate of 12 bags/h for 2 h and 45 min yielded calculated concentrations less than one-half of the above mentioned values. These results should serve as a useful benchmark for epidemiologists concerned with the magnitude of exposure in historically dusty industrial tasks.

Air Pollution↗

PubMed1994

Increased incidence of DNA double-strand breaks and anti-ds DNA antibodies in blood of workers occupationally exposed to asbestos.

Asbestos, proven to be carcinogenic in humans and animals, is reported to have no genotoxic effect. Asbestos workers have an increased risk of lung cancer, mesothelioma, and other tumours. Earlier findings showed that crocidolite can induce DNA strand breaks in cultured rat embryo cells as assessed by nick translation. We investigated DNA double-strand breaks in white blood cells (WBC) of ten workers occupationally exposed to asbestos. According to our results, obtained with neutral filter elution, individuals who had been exposed to asbestos fibres showed two to four times more DNA double-strand breaks (dsb) in white blood cells than ten non-exposed persons. The induced DNA fragments are of about 250 kb (compared to chromosomal DNA of Saccharomyces cerevisiae standard marker). Using additionally the chromosomal DNA protective method of agarose-plugs, DNA fragments in the range of 200 to 1000 kb have been found in the white blood cells of the same ten workers occupationally exposed to asbestos. In the white blood cells of non-exposed subjects no DNA fragments could be detected with this method. Compared to 51 non-exposed persons, elevated anti-ds DNA antibody concentrations were found in ten workers occupationally exposed to asbestos. The fact that workers occupationally exposed to asbestos have distinctly more double-strand breaks and anti-ds DNA antibodies could mean that an increased incidence of DNA-fragments may be an important indicator in the chronic effect of asbestos-associated carcinogenesis. Apparently, the chronic effects of asbestos observed here do not seem to be identical with that of previously reported acute in vitro effects.

Adult↗

PubMedDate not supplied

Asbestos-related morbidity in India.

In India, locally mined asbestos is not enough for its current needs, hence a great deal of asbestos is imported from Canada. Asbestos products manufacturers have prevailed upon the government to reduce tariffs on imported material. The efforts of the health and safety professionals who joined with nongovernmental organizations to form the Ban Asbestos Network of India (BANI) are being consistently sabotaged by the industry, using its influence and false propaganda that chrysotile asbestos can be safely used in a controlled manner. Weak legislation and lack of data are being exploited by the industry to convince policymakers that asbestos use in India has caused no major health problems. Despite this, the ban-asbestos movement has gained momentum and was able to persuade government to consider banning asbestos use. With the growing strength of the movement it is expected that asbestos manufacturers may find it increasingly difficult to manipulate the government in the future.

Asbestos↗

PubMedDate not supplied

Globalization and the transfer of hazardous industry: asbestos in Mexico, 1979-2000.

This study quantified asbestos use in Mexico in the past decade and evaluated available data on mortality due to malignant mesothelioma in Mexico between 1979 and 2000. Mortality data were analyzed from secondary databases of the Mexican Social Security System and the Ministry of Health. Data on the import and export of asbestos in Mexico were obtained from the Ministry of Trade and Industrial Development of Mexico. Deaths due to pleural mesothelioma significantly increased in this period. Although the import of asbestos declined, the number of Mexican products that contain asbestos tripled. Export of Mexican asbestos-containing products to Central America grew rapidly in the last ten years of the study. Mexico continues the appreciable use of asbestos and has experienced a significant increase in the occurrence of the sentinel asbestos-related disease, malignant mesothelioma. Given the many limitations to the control of hazardous work exposures in Mexico, a ban on asbestos is advocated as the most feasible means of limiting an epidemic of asbestos-related disease.

Asbestos↗

PubMedDate not supplied

Justice for asbestos victims and the politics of compensation: the French experience.

This paper presents the history of asbestos mining and manufacture in France, the strategies of the multinational asbestos firms to become major international participants, the failures of occupational health and safety that allowed an epidemic of asbestos-related diseases to occur, and the important social movement of the victims of asbestos exposure. The asbestos industry thrived in France until the health effects of asbestos exposure were made public. At that time, the industry had already moved its mining and manufacture to developing countries, where they were able to take advantage of limited regulation and enforcement of occupational and environmental laws. The author analyzes the compensation systems that were approached with varying degrees of success by the victims of asbestos exposure. France banned all manufacture and use of asbestos in 1997, and in the years that have followed, it has enjoyed many successes in achieving compensation for asbestos victims.

Asbestos↗

PubMedDate not supplied

Collaborative research, participatory solutions: research on asbestos in Kuruman, South Africa.

The 1998 South African National Asbestos Summit proposed a post-apartheid asbestos policy for the country. In the areas of environmental rehabilitation, health care, and compensation, it envisioned connecting asbestos mitigation to participatory development. In 2001, the Asbestos Collaborative, an international and interdisciplinary team, conducted follow-up research on the recommendations of the 1998 Summit, researching environmental, health, and compensation issues through consultation of documents and interviews with officials in urban areas and with people in Kuruman, a former crocidolite-mining site with high rates of asbestos-related disease. In Kuruman, local opinion supported the recommendations of the Asbestos Summit, insisting that policies to mitigate the problem of asbestos must also address poverty. In the wake of the 2001 research, a new organization, the Asbestos Interest Group (AIG), has been founded to facilitate grassroots participation in asbestos issues. One success of the AIG has been the settlement of a lawsuit by former workers against the former mining company in Kuruman.

Asbestos↗

PubMed2006

Asbestos ban in India: challenges ahead.

Rapidly industrializing India is described by the International Monetary Fund as a young, disciplined, and vibrant economy with a projected growth of 6.7% for 2005. The total workforce of 397 million has only 7% of workers employed in the organized sector with construction, where asbestos exposure is prevalent, employing 4.4%. The domestic production of asbestos declined from 20,111 tons in 1998-1999 to 14,340 tons in 2002-2003. The imports from Russia and Canada increased from 61,474 tons in 1997-1998 to 97,884 tons in 2001-2002. The production of asbestos cement products went up from 0.68 million tons in 1993-1994 to 1.38 million tons in 2002-2003. The asbestos industry has been delicensed since March 2003. The number of asbestos-based units stood at 32, with the western state of Maharashtra having the largest number. According to official figures, the industry employs 8000 workers. The occupational exposure standard is still 2 fibers/mL, worse still, mesothelioma is not recognized as an occupational disease. The latest cancer registry data have no information on mesothelioma. The health and safety legislation does not cover 93% of workers in the unorganized sector where asbestos exposures are extremely high. Workers remain uninformed and untrained in dealing with asbestos exposure. Enforcement agencies are not fully conscious of the risks of asbestos exposure. Industrial hygiene assessment is seldom carried out and pathologists do not receive training in identifying mesothelioma histopathologically. The lack of political will and powerful influence of the asbestos industry are pushing India toward a disaster of unimaginable proportion.

Asbestos↗

PubMed1997

Mechanism of asbestos-mediated DNA damage: role of heme and heme proteins.

Several observations, including studies from this laboratory, demonstrate that asbestos generates free radicals in the biological system that may play a role in the manifestation of asbestos-related cytotoxicity and carcinogenicity. It has also been demonstrated that iron associated with asbestos plays an important role in the asbestos-mediated generation of reactive oxygen species. Exposure to asbestos leads to degradation of heme proteins such as cytochrome P450-releasing heme in cytosol. Our simulation experiments in the presence of heme show that such asbestos-released heme may increase lipid peroxidation and can cause DNA damage. Further, heme and horseradish peroxidase (HRP) can cause extensive DNA damage in the presence of asbestos and hydrogen peroxide/organic peroxide/hydroperoxides. HRP catalyzes oxidation reactions in a manner similar to that of prostaglandin H synthetase. Iron released from asbestos is only partially responsible for DNA damage. However, our studies indicate that DNA damage mediated by asbestos in vivo may be caused by a combination of effects such as the release and participation of iron, heme, and heme moiety of prostaglandin H synthetase in free radical generation from peroxides and hydroperoxides.

Animals↗