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PubMed1994

Effect of long-term removal of iron from asbestos by desferrioxamine B on subsequent mobilization by other chelators and induction of DNA single-strand breaks.

The long-term removal of iron from crocidolite or amosite by desferrioxamine B (DF) at pH 7.5 or 5.0 was studied. Crocidolite or amosite (1 mg/ml) was suspended in 50 mM NaCl at pH 7.5 or 5.0 with the addition of 1 mM DF for up to 90 days. Although the rate of iron mobilization decreased with time, iron was continuously mobilized from both forms of asbestos at pH 5.0 or 7.5. The amount of iron mobilized from crocidolite was at least twice that mobilized from amosite at either pH. Iron was mobilized more rapidly from crocidolite at pH 5.0 than at 7.5 for the first 15 days, but at later times the amount being mobilized at pH 7.5 became equal to or slightly greater than that at 5.0. For amosite, the mobilization at pH 5.0 was always greater than that at pH 7.5. Next, the effect of iron removal from asbestos by DF on subsequent iron mobilization by a second chelator (EDTA or citrate) and on induction of DNA single-strand breaks (SSBs) was studied. Asbestos, treated for up to 15 days with DF at pH 7.5, was washed to remove ferrioxamine and excess DF, then incubated with EDTA or citrate (1 mM). The rates of iron mobilization from both forms of asbestos by a second chelator decreased as more and more iron was removed by DF. Induction of DNA SSBs also decreased, reflecting the unavailability of iron to catalyze the damage. The results suggest three things. First, if long-term mobilization of iron from asbestos occurs in vivo as has been observed in vitro, it may play a role in the long-term biological effects of asbestos. Second, more rapid mobilization of iron from asbestos fibers may occur when the fibers are phagocytized by cells and maintained in phagosomes where the pH is 4.0-5.0. Third, treatment of asbestos by iron chelators, such as DF, prior to exposure to cultured cells or whole animals, may reduce the biological effects of asbestos resulting from iron, but may not completely eliminate them.

Asbestos, Amosite↗

PubMed2000

Levels of 8-hydroxy-2'-deoxyguanosine in DNA of white blood cells from workers highly exposed to asbestos in Germany.

Asbestos fibers have genotoxic effects and are a potential carcinogenic hazard to occupationally exposed workers. The ability of inhaled asbestos fibers to induce the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the DNA of white blood cells (WBC) of workers highly exposed at the workplace has been studied. The 8-OHdG adduct level of asbestos-exposed workers was significantly increased (p<0.001) compared to that in the control group in all three years of the study. Asbestos-exposed individuals showed a mean value of 2.61+/-0.91 8-OHdG/10(5) dG (median 2.49, n=496) in 1994-1995, 2.96+/-1.10 8-OHdG/10(5) dG (median 2.76, n=437) in 1995-1996 and 2.55+/-0.56 8-OHdG/10(5) dG (median 2.53, n=447) in 1996-1997. For the control subjects, a mean of 1.52+/-0.39 (median 1.51, n=214) was determined. The results indicate that human DNA samples from exposed individuals contain between 1.7 times and twice the level of oxidative damage relative to that found in control samples in all 3 years of the study. The studies presented here show that asbestos exposure can result in oxidative DNA damage. Our data confirm that oxidative DNA damage occurs in the WBC of workers highly exposed to asbestos fibers, thus supporting the hypothesis that asbestos fibers damage cells through an oxidative mechanism. These in vivo findings underline the importance of oxidative damage in asbestos-induced carcinogenesis and highlight the need for exploring the molecular basis of asbestos-induced diseases, and for more effective diagnosis, prevention and therapy of mesothelioma, lung cancer and pulmonary fibrosis. In addition, preventive and therapeutic approaches using antioxidants may be relevant.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1999

A risk assessment for exposure to grunerite asbestos (amosite) in an iron ore mine.

The potential for health risks to humans exposed to the asbestos minerals continues to be a public health concern. Although the production and use of the commercial amphibole asbestos minerals-grunerite (amosite) and riebeckite (crocidolite)-have been almost completely eliminated from world commerce, special opportunities for potentially significant exposures remain. Commercially viable deposits of grunerite asbestos are very rare, but it can occur as a gangue mineral in a limited part of a mine otherwise thought asbestos-free. This report describes such a situation, in which a very localized seam of grunerite asbestos was identified in an iron ore mine. The geological occurrence of the seam in the ore body is described, as well as the mineralogical character of the grunerite asbestos. The most relevant epidemiological studies of workers exposed to grunerite asbestos are used to gauge the hazards associated with the inhalation of this fibrous mineral. Both analytical transmission electron microscopy and phase-contrast optical microscopy were used to quantify the fibers present in the air during mining in the area with outcroppings of grunerite asbestos. Analytical transmission electron microscopy and continuous-scan x-ray diffraction were used to determine the type of asbestos fiber present. Knowing the level of the miner's exposures, we carried out a risk assessment by using a model developed for the Environmental Protection Agency.

Asbestos, Amosite↗

PubMed1999

Asbestos induces activator protein-1 transactivation in transgenic mice.

Activation of activator protein (AP-1) by crocidolite asbestos was examined in vitro in a JB6 P+ cell line stably transfected with AP-1-luciferase reporter plasmid and in vivo using AP-1-luciferase reporter transgenic mice. In in vitro studies, crocidolite asbestos caused a dose- and time-dependent induction of AP-1 activation in cultured JB6 cells. The elevated AP-1 activity persisted for at least 48 h. Crocidolite asbestos also induced AP-1 transactivation in the pulmonary and bronchial tissues of transgenic mice. AP-1 activation was observed at 2 days after intratracheal instillation of the mice with asbestos. At 3 days postexposure, AP-1 activation was elevated 10-fold in the lung tissue and 22-fold in bronchiolar tissue as compared with their controls. The induction of AP-1 activity by asbestos appeared to be mediated through the activation of mitogen-activated protein kinase family members, including extracellular signal-regulating protein kinase, Erk1 and Erk2. Aspirin inhibited asbestos-induced AP-1 activity in JB6 cells. Pretreatment of the mice with aspirin also inhibited asbestos-induced AP-1 activation in bronchiolar tissue. The data suggest that further investigation of the role of AP-1 activation in asbestos-induced cell proliferation and carcinogenesis is warranted. In addition, investigation of the potential therapeutic benefits of aspirin in the prevention/amelioration of asbestos-induced cancer is justified.

Animals↗

PubMedDate not supplied

Nitric oxide (NO) synthase activity in the lung and NO synthesis in alveolar macrophages of rats increased on exposure to asbestos.

We examined whether the lung of rats induced nitric oxide synthase (NOS) on instillation of Union Internationale Contre le Cancer (UICC) asbestos into the trachea, and whether alveolar macrophages (M phi s) of rats increased synthesis of nitric oxide (NO) on exposure to the asbestos. Instillation of chrysotile asbestos (CH) into rat tracheas increased NOS activity in the lung up to fourfold compared with that of normal control rats. On instillation of amosite asbestos (AM), the activity did not significantly increase. In the culture of alveolar M phi s with CH, NO2-, a stable oxidation product of NO, in the conditioned medium markedly increased while in the culture with AM or crocidolite (CR) asbestos it was comparable to that in the control culture without asbestos. Thus, it was assumed that the lung as well as alveolar M phi s induced NOS on exposure to CH. Viability of M phi s was lower in the culture with CH than in the culture with AM or CR. When alveolar M phi s were cultured in the presence of lipopolysaccharide (LPS), a potent inducer of NOS, NO2- in the medium dramatically increased, indicating a possible induction of NOS, while NO2- was decreased significantly in the presence of both LPS and CH, AM or CR. On the other hand, when M phi s which had previously been stimulated with LPS were cultured in LPS-free medium, NO2- synthesis retained a significantly increased level, irrespective of the presence or absence of asbestos. Thus, the three kinds of asbestos used seemed to interfere with LPS in inducing NOS and to decrease subsequently the synthesis of NO2-, but not to affect the synthesis of NO2- by LPS-induced NOS. Taken altogether, lung or alveolar M phi s of rats induced NOS to increase NO synthesis on exposure to CH.

Animals↗

PubMed1999

Asbestos exposure in lung carcinoma: a necropsy-based study of 414 cases.

BACKGROUND: The prerequisites necessary for attributing lung carcinoma to asbestos, represent a controversial issue. METHODS: Three parameters (occupational history, pleural plaques, and lung asbestos bodies) were investigated in 414 consecutive cases of lung carcinoma, examined at necropsy at the Hospital of Monfalcone, Italy. Occupational data were obtained from the patients' relatives by personal or telephone interviews. Pleural plaques were classified into three classes (small, moderate, large). Routine lung sections were examined for asbestos bodies in all cases; isolation and counting were performed in 408 cases. RESULTS: The series included 353 men, and 61 women, aged between 38 and 97 years. The male patients had worked in industries in 74% of cases (60% in shipbuilding). Men showed pleural plaques in 82% of cases (moderate or large plaques in 58.7%). Asbestos bodies were observed in routine lung sections in 34.8%, and in 31% exceeded the value of 5,000 bodies per gram of dried tissue. Among women the principal features were: history or domestic exposure to asbestos in 36% of the cases, prevalence of pleural plaques 34% (moderate or large plaques 15%), asbestos bodies in routine lung sections in 3.3% and there was no case with an asbestos body burden over 5,000/g. The fraction of asbestos-related carcinomas among male patients varied between 24.7 and 61%, depending on the criteria used for attribution. CONCLUSIONS: Different criteria indicated about 60% of the present lung carcinomas among men as plausibly attributable to asbestos.

Adult↗

PubMed2004

Asbestos in brakes: exposure and risk of disease.

Asbestos has been incorporated into friction products since the early 1900s. Epidemiological studies have been equivocal in their analysis of the incidence of disease among mechanics servicing brakes. Decomposition of asbestos occurs during the normal usage of the brake due to thermal decomposition into forsterite, although not all asbestos is so converted. Short fibers, below 5 microm in length, are also found in brake products. Several facts are discussed including the toxicity of the remaining asbestos fibers, short asbestos fibers, and the health implications of exposure to forsterite. Control methodologies, when used appropriately, have reduced exposure to asbestos during brake servicing, but have not been able to entirely eliminate exposure to asbestos, thus bring into question the controlled use of asbestos for friction product such as brakes. Even the so called "controlled" use of asbestos containing brakes poses a health risk to workers, users, and their families.

Air Pollutants, Occupational↗

PubMed1987

A rapid and simple method of extracting asbestos bodies from lung tissue by cytocentrifugation.

During analyses of alkali digested lung tissue for asbestos bodies, we observed that the number of asbestos bodies in the discarded waste frequently exceeded the number in the filtered residue, the number reported in the standard diagnostic method. This observation led to the exploration of alternative techniques that would optimize the recovery of asbestos bodies. We describe a new, simple, and rapid method for extracting asbestos bodies from digested lung tissue using a cytocentrifuge, in which the waste extraction and filtration steps are eliminated. Samples of digested lung tissue are ready for light microscopy after 10 minutes of cytocentrifugation directly onto a glass slide. The standard method was compared with the cytocentrifuge technique using lung tissue from four asbestos-exposed workers and four controls with no known history of exposure. The number of asbestos bodies extracted by the centrifuge method was, on average, seven times higher than the number found with the standard method. A detailed quantitative study was made of the case that had the most asbestos bodies (comparison of the number of asbestos bodies counted in both "residue" and "waste", applying the filtration and cytocentrifuge methods). The number of asbestos bodies found in the discarded waste significantly exceeded the number in the "reportable" filtered residue.

Adult↗

PubMed1979

Milky spots (Taches laiteuses) as structures which trap asbestos in mesothelial layers and their significance in the pathogenesis of mesothelial neoplasia.

The UICC standard sample of asbestos, crocidolite, was injected subcutaneously into the flanks of CBA/lac mice. Asbestos fibres were found in milky spots in the serosal cavities more than 442 days after the injection, in the form of either naked fibres or asbestos bodies. Milky spots were the only structure in which asbestos fibres were observed in the mesothelial layer. The fact that asbestos fibres were found in the liver, spleen, kidney, brain, etc., in addition to milky spots, suggested that they were transported by the blood stream throughout the body. This assumption was confirmed by the similar distribution of asbestos after intravenous administration. The vascular and cellular structure of milky spots is such that they are particularly likely to trap blood-borne asbestos fibres. Hyperplastic changes were observed in milky spots after both subcutaneous and intravenous administration of asbestos in mice. The possible involvement of milky spots in the genesis of tumors of the mesothelium following exposure of animals to asbestos is discussed.

Animals↗

PubMed2001

Inhibition of asbestos-induced transformation of rat pleural mesothelial cells in co-culture with rat macrophages.

The aim of this work was to investigate the influence of macrophages on the process of rat pleural mesothelium cells (RPMC) transformation in vitro. For this purpose prolonged many-passage co-cultivation of rat pleural mesothelial cells and rat peritoneal macrophages was performed both in the presence (to study macrophage influence on asbestos-induced morphologic transformation) and in the absence (to study spontaneous transformation) of asbestos. It was shown that spontaneous transformation of RPMC slightly accelerated in the co-cultures, whereas asbestos-induced transformation was strongly inhibited. For instance, RPMC acquired the ability to form multilayer cell growth foci and colonies in semisolid agar at 22-24 passages in the absence and at 14-16 passages in the presence of asbestos, while in co-culture with macrophages these signs of transformation appeared at 17-19 passages without asbestos treatment and were not observed at the 40th passage under exposure to asbestos. It was shown that the observed inhibition of transformation was caused by preferential depletion of transformed cells in co-cultures of mesothelium and macrophages in the presence of asbestos: when equal concentrations of macrophages and asbestos were taken, the viability of early-passage RPMC was greater as compared with late passages, and the viability of late-passage RPMC was greater than that of mesothelioma cells. The amount of late-passage RPMC and mesothelioma cells able to form colonies in semisolid media was also drastically decreased in these conditions. These findings suggest that though macrophages can influence the process of asbestos-induced mesothelium transformation by different ways, as a whole the inhibitory action appears to be the strongest.

Animals↗

PubMed1986

Suppression of the in vitro humoral immune response by chrysotile asbestos.

The direct addition of UICC chrysotile B asbestos to spleen cell cultures produced a dose-dependent suppression of the antibody-forming cell (AFC) response to the T-dependent antigen, sheep erythrocytes. Concentrations of 0.1, 1, 10, and 100 micrograms/ml, which had no effect on either cell number or viability, suppressed the in vitro response by 12, 43, 71, and 95%, respectively. By separating spleen cells into nonadherent and plastic-adherent populations, the effects of asbestos on each cell type were studied utilizing reconstituted cultures. Treatment of adherent cells for 1 hr with asbestos and reconstitution with untreated nonadherent cells resulted in a dose-dependent suppression of the AFC response similar to that observed when asbestos was added to whole spleen cultures. Reconstitution studies were also conducted with spleen cell populations from animals administered asbestos in vivo. In cultures reconstituted with adherent cells from asbestos-treated mice and nonadherent cells from saline-treated animals, the AFC response was significantly suppressed. The T-dependent AFC response with reconstitution of adherent cells from saline-treated mice and nonadherent cells from asbestos-exposed animals was no different from reconstituted saline controls. Both adherent alveolar and pleural cells were capable of reconstituting the T-dependent AFC response with nonadherent spleen cells and demonstrated reduced immunological capability when exposed to asbestos fibers. The results of this investigation have identified the adherent spleen cell (macrophage) as the target cell type responsible for asbestos-induced immunosuppression of the in vitro T-dependent antibody-forming cell response.

Animals↗

PubMed2005

Short, thin asbestos fibers contribute to the development of human malignant mesothelioma: pathological evidence.

Based on animal studies, long and thin asbestos fibers (> or =8 microm in length and < or = 0.25 microm in width) have been postulated to be strongly carcinogenic inducing pleural malignant mesothelioma, while shorter, thicker fibers have been postulated to pose a lesser risk (Stanton hypothesis). The objective of this study is to test the validity of the Stanton hypothesis through direct pathologic analysis of human mesothelioma tissue. Digested bulk tissue samples, or ashed 25 microm thick sections, or both, were prepared from lung and mesothelial tissues taken from 168 cases of human malignant mesothelioma. In these tissues, 10,575 asbestos fibers (4820 in the lung and 5755 in mesothelial tissues (1259 in fibrotic serosa and 4496 in mesotheliomatous tissue)) were identified by high-resolution analytical electron microscopy. Dimensions of these asbestos fibers were measured in printed electron micrographs. Results were as follows: (1) long, thin asbestos fibers consistent with the Stanton hypothesis comprised only 2.3% of total fibers (247 / 10,575) in these tissues; (2) the majority (89.4%) of the fibers in the tissues examined were shorter than or equal to 5 microm in length (9454 of 10,575), and generally (92.7%) smaller than or equal to 0.25 microm in width (9808 of 10,575). (3) Among asbestos types detected in the lung and mesothelial tissues, chrysotile was the most common asbestos type to be categorized as short, thin asbestos fibers. (4) Compared with digestion technique of the bulk tissue, ashing technique of the tissue section was more effective to detect short, thin fibers. We conclude that contrary to the Stanton hypothesis, short, thin, asbestos fibers appear to contribute to the causation of human malignant mesothelioma. Such fibers were the predominant fiber type detected in lung and mesothelial tissues from human mesothelioma patients. These findings suggest that it is not prudent to take the position that short asbestos fibers convey little risk of disease.

Animals↗

PubMed2005

Asbestos problem in India.

Primary exposure to asbestos in India can be encountered in the form of asbestos mining, asbestos cement industries, asbestos processing unit and during renovation and demolition of old asbestos cemented roof or other structures as well as modern electrical as well as mechanical appliances in which asbestos is still found. Ultimately construction workers, electricians, vehicle mechanics and other workers in the building trades who are exposed to asbestos inhale hundreds and thousands of amphiboles, which causes lung damage. It is being mined in India at places such as Andhra Pradesh (Pulivendla), Jharkand (Roro), Rajasthan (Ajmer, Bhilwara, Udaipur, Rajsamand) and the common problem faced by the locals are asbestosis through air and fluorosis through drinking water. The problem continues to be in India as well as other developing countries. Also, India import and re-export asbestos to other countries and workers at shipyard, transport of the hazardous material on road and roadside residents all are vulnerable to this uncommon disease. The signs and symptoms generally found with the workers are shortness of breath, persistent and productive cough due to pulmonary fibrosis can show up many years after the asbestos exposure.

Asbestos↗

PubMed1989

Lung asbestos burden in shipyard and construction workers with mesothelioma: comparison with burdens in subjects with asbestosis or lung cancer.

Although mesothelioma is generally considered to be caused by asbestos, epidemiologic studies indicate that some cases have another cause. In order to determine whether pulmonary asbestos burden can be used to define asbestos-related mesotheliomas, asbestos burden was quantified in 27 shipyard or construction workers with diffuse malignant mesothelioma of the pleura or peritoneum and a history of asbestos exposure. Their burden was significantly greater than the burden found in 19 unexposed men (P less than 0.001). The burdens were also compared to those of previously reported subjects with asbestosis or lung cancer. The median concentration for total amphibole fibers (2.7 million/g dry lung) in subjects with mesothelioma did not differ significantly from our previously reported median values for 14 subjects with asbestosis (1.3 million/g dry lung) or for 60 asbestos workers with lung cancer (1.3 million/g dry lung). Fiber size distribution for amosite, the most prevalent fiber type, was similar in all three subject groups. Fifteen of 25 (60%) subjects with mesothelioma had mild asbestosis. Asbestos body (AB) concentrations were greater than or equal to 1900/g dry lung, and total amphibole fiber concentrations were greater than or equal to 390,000/g dry lung. Counts of ABs greater than or equal to 0.5/cm2 in histologic sections always signified both of these concentrations in extracts. Thus, histologic sections showing greater than or equal to 0.5 ABs/cm2 or extracts containing asbestos body or amphibole fiber concentrations of at least 1900 or 390,000/g dry lung, respectively, will confirm an asbestos-related mesothelioma.

Aged↗

PubMed1998

Mechanisms of asbestos-induced nitric oxide production by rat alveolar macrophages in inhalation and in vitro models.

To evaluate the contribution of reactive nitrogen species to inflammation by asbestos, Fischer 344 rats were exposed to crocidolite or chrysotile asbestos by inhalation to determine whether increases occurred in nitric oxide (NO.) metabolites from alveolar macrophages (AMs). AMs from animals inhaling asbestos showed significant elevations (p < .05) in nitrite/nitrate levels which were ameliorated by NG-monomethyl-L-arginine (NMMA), an inhibitor of inducible nitric oxide synthase (iNOS) activity. Temporal patterns of NO. generation from AMs correlated with neutrophil influx in bronchoalveolar lavage samples after asbestos inhalation or bleomycin instillation, another model of pulmonary fibrosis. To determine the molecular mechanisms and specificity of iNOS promoter activation by asbestos, RAW 264.7 cells, a murine macrophage-like line, and AMs isolated from control rats were exposed to crocidolite asbestos in vitro. These cells showed increases in steady-state levels of iNOS mRNA in response to asbestos and more dramatic increases in both iNOS mRNA and immunoreactive protein after addition of lipopolysaccharide (LPS). After transfection of an iNOS promoter/luciferase reporter construct, RAW 264.7 cells exposed to LPS, crocidolite asbestos and its nonfibrous analog, riebeckite, revealed increases in luciferase activity whereas cristobalite silica had no effects. Studies suggest that NO. generation may be important in cell injury and inflammation by asbestos.

Administration, Inhalation↗

PubMed2001

Asbestos causes apoptosis in alveolar epithelial cells: role of iron-induced free radicals.

Asbestos causes asbestosis and malignancies by mechanisms that are not fully understood. Alveolar epithelial cell (AEC) injury by iron-induced reactive oxygen species (ROS) is one important mechanism. To determine whether asbestos causes apoptosis in AECs, we exposed WI-26 (human type I-like cells), A549 (human type II-like cells), and rat alveolar type II cells to amosite asbestos and assessed apoptosis by terminal deoxynucleotidyl transferase-mediated deoxyuridine-5'-triphosphate-biotin nick end labeling (TUNEL) staining, nuclear morphology, annexin V staining, DNA nucleosome formation, and caspase 3 activation. In contrast to control medium and TiO2, amosite asbestos and H2O2 each caused AEC apoptosis. A role for iron-catalyzed ROS was suggested by the finding that asbestos-induced AEC apoptosis and caspase 3 activation were each attenuated by either an iron chelator (phytic acid and deferoxamine) or a.OH scavenger (dimethyl-thiourea, salicylate, and sodium benzoate) but not by iron-loaded phytic acid. To determine whether asbestos causes apoptosis in vivo, rats received a single intratracheal instillation of amosite (5 mg) or normal saline solution, and apoptosis in epithelial cells in the bronchoalveolar duct regions was assessed by TUNEL staining. One week after exposure, amosite asbestos caused a 3-fold increase in the percentage of apoptotic cells in the bronchoalveolar duct regions as compared with control (control, 2.1% +/- 0.35%; asbestos, 7.61% +/- 0.15%; n = 3). However, by 4 weeks the number of apoptotic cells was similar to control. We conclude that asbestos-induced pulmonary toxicity may partly be caused by apoptosis in the lung epithelium that is mediated by iron-catalyzed ROS and caspase 3 activation.

Animals↗

PubMed2006

An exposure study of bystanders and workers during the installation and removal of asbestos gaskets and packing.

From 1982 until 1991, a series of studies was performed to evaluate the airborne concentration of chrysotile asbestos associated with replacing gaskets and packing materials. These studies were conducted by the senior author in response to concerns raised by a report from the Navy in 1978 on asbestos exposures associated with gasket work. A series of studies was conducted because results of those who worked with gaskets within the Navy study did not address the background concentrations of asbestos in the work areas, which may have been significant due to the presence of asbestos insulation in the ships and shipyards. The intent of the studies performed from 1982 through 1991 was to re-create the Navy's work practices in a contaminant-free environment during an 8-hour workday (so the data could be compared with the OSHA permissible exposure limit [PEL]). Samples were collected to characterize personal and area airborne asbestos concentrations associated with the formation, removal, and storage of gaskets, as well as the scraping of flanges and the replacement of valve packing. The results indicate that the 8-hour time-weighted average (TWA) exposures of pipefitters and other tradesmen who performed these activities were below the current PEL and all previous PELs. Specifically, the highest average 8-hour TWA concentration measured for workers manipulating asbestos gaskets during this study was 0.030 f/cc (during gasket removal and flange face scraping onboard a naval ship). Likewise, the 8-hour TWA breathing zone concentrations of a worker removing and replacing asbestos valve packing did not exceed 0.016 f/cc. In most cases, the concentrations were not distinguishable from ambient levels of asbestos in the ships or the general environment. These results are not surprising given that asbestos fibers in gasket materials are encapsulated within a binder.

Air Pollutants↗

PubMed1992

Asbestos and colon cancer: lack of association in a large case-control study.

Previous studies linking exposure to asbestos with human colon cancer have used mortality rather than incidence as their endpoint and have neither assessed nor controlled for confounding by diet, genetic factors, or other risk factors for colon cancer. A case-control study of 746 histologically confirmed cases of colon cancer and 746 matched neighborhood controls was conducted in Los Angeles County, California. In univariate analyses of the 419 male pairs, a weak association was found between asbestos exposure and colon cancer (odds ratio (OR) = 1.16, 95% confidence interval (CI) 0.80-1.69). When confounding by family history of large bowel cancer, diet, body weight, and physical activity was controlled, there was no association between colon cancer and exposure to asbestos among males (OR = 0.99, 95% CI 0.66-1.50). When asbestos exposure was restricted to occurrences preceding diagnosis by more than 15 years, there was no clear association between such exposure and colon cancer, either before (OR = 1.14, 95% CI 0.76-1.70) or after confounding was controlled (OR = 0.93, 95% CI 0.60-1.44). Further analyses by frequency and duration of exposure failed to show any association between asbestos and risk of colon cancer, but did show a consistent pattern of confounding by nonoccupational factors that, when controlled, invariably produced a weak protective effect of asbestos exposure. Among the 327 female pairs, only 6 cases and 11 controls reported asbestos exposure (OR = 0.55, 95% CI 0.20-1.48), and there was no evidence of risk increasing as the frequency or duration of exposure increased. This study suggests not only that occupational exposure to asbestos is not a risk factor for colon cancer in the general population of Los Angeles, but also that observed associations between asbestos and colon cancer should not be interpreted as causal unless confounding by nonoccupational factors has been evaluated and controlled.

Aged↗