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PubMedDate not supplied

Is there transplacental transfer of asbestos? A study of 40 stillborn infants.

An autopsy study was conducted to investigate whether there is transplacental transfer of asbestos in humans. The asbestos burden of lung, liver, skeletal muscle, and placenta digests of 40 stillborn infants was determined using a bleach digestion method. The fibers detected in the tissue digests were characterized as to the type of asbestos, using electron microscopy, energy-dispersive x-ray analysis, and selected-area diffraction analysis. Placental digests of 45 full-term, liveborn infants were similarly processed as controls. Low levels of small, thin, uncoated asbestos fibers were detected in the placentas and organs of 37.5% of the stillborn infants (15 of 40). The fiber sizes ranged from 0.05 to 5.0 microns in length and 0.03 to 0.3 micron in width, with a mean length of 1.15 microns and a mean width of 0.069 micron. Maximum numbers of fibers were found in the lungs (mean 235,400 fibers/g; n = 10), followed by liver (mean 212,833 fibers/g; n = 6), placenta (mean 164,500 fibers/g; n = 4), and skeletal muscle (80,000 fibers/g; n = 1). The fibers were detected at all stages of gestation and showed no association with gestational age. A significant association was found between fiber presence and working mothers, and positive but nonsignificant associations were found with maternal history of drug abuse, previous abortions, and fetal maceration. No association was found between premature rupture of membranes and fiber presence. No fibers were detected in the 45 placentas of the liveborn control infants. There was a highly significant difference in the asbestos fiber counts of the placentas of the stillborn and liveborn infants (P < .001). Our studies demonstrate the presence of short and thin asbestos fibers in stillborn infants and their positive association with working mothers.

Asbestos↗

PubMed1983

Lymphoid and plasma cell malignancies: asbestos-related disorders of long latency.

We have identified 13 asbestos workers with lymphoplasmacytic neoplasms: six with chronic lymphocytic leukemia, four with IgG myeloma, two with IgA myeloma, and one with histiocytic lymphoma. The subjects' occupations were varied, but all had experienced protracted asbestos exposure (ranging from 3-37 years). Tumor latency periods were similar to other known asbestos-related malignancies and ranged from 16-41 years. Stigmata of asbestos-related pulmonary disease were evident in 12 subjects. Malignant pleural mesotheliomas co-existed with IgG myelomas in two individuals, an association which seems unlikely to be fortuitous. It has been speculated previously that asbestos may be a lymphoid system carcinogen. Our findings strongly support this view and indicate that patients presenting de novo with lymphoproliferative neoplasms should be investigated for previous occupational or environmental exposure to asbestos.

Aged↗

PubMed1996

Detection of 8-oxo-2'-deoxyguanosine, a marker of oxidative DNA damage, in culture medium from human mesothelial cells exposed to crocidolite asbestos.

Crocidolite asbestos is associated with the development of mesothelioma. Although chromosomal changes have been documented in mesothelial cells, the mechanisms of interaction of crocidolite with DNA remain obscure. Since human mesothelial cells are exquisitely sensitive to asbestos, oxidative DNA damage was measured in an asbestos-exposed human mesothelial cell line (MET5A) by assaying oxidized guanine bases [8-oxo-2'-deoxyguanosine (oxo8dG), 8-oxoguanine (oxo8G), and 8-oxoguanosine (oxo8Gua)] excreted into the spent culture medium after DNA repair or turnover. At growth inhibitory, but not cytolytic concentrations, asbestos caused significant elevation of all bases in the spent medium over a 48-h period. In contrast, riebeckite, a chemically similar, nonfibrous analog of crocidolite did not cause increased adduct release. Results show that oxidative RNA and DNA bases are produced in response to asbestos in target cells of asbestos-induced cancers.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1997

Patterns of 8-hydroxydeoxyguanosine formation in DNA and indications of oxidative stress in rat and human pleural mesothelial cells after exposure to crocidolite asbestos.

Oxidative damage is a proposed mechanism of asbestos-induced carcinogenesis, but the detection of oxidative DNA lesions in target cells of asbestos-induced mesothelioma has not been examined. In studies here, DNA was isolated from both rat pleural mesothelial (RPM) cells and a human mesothelial cell line (MET5A) after exposure in vitro to crocidolite asbestos at various concentrations. DNA was then examined for formation of 8-hydroxydeoxyguanosine (8-OHdG) at 24, 48 and 72 h using HPLC with electrochemical detection. In addition, steady-state mRNA levels of manganese-containing superoxide dismutase (MnSOD) were assessed as an indication of oxidative stress. Whereas RPM cells showed dose-dependent and significant increases in 8-OHdG formation in response to crocidolite asbestos or iron-chelated crocidolite fibers (but not after exposure to glass beads), MET5A cells showed decreases in 8-OHdG. Both cell types exhibited elevations in message levels of MnSOD. In comparison with human MET5A cells, RPM cells exhibited increased cytotoxicity and apoptosis in response to asbestos, as documented by cell viability assays and flow cytometry analysis using propidium iodide. Results in RPM cells indicate that asbestos causes oxidative damage that may result in potentially mutagenic lesions in DNA and/or apoptosis, despite compensatory increases in expression of an antioxidant enzyme.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1977

Cancer in asbestos-mining and other areas of Quebec.

Employing incidence data from the Quebec Tumor Registry, we examined the relative risks of cancer of all sites for the years 1969-73 in the asbestos-mining, rural, and metropolitan counties of Quebec Province, Canada. Generally, rates for males exceeded those for females, and the relative risks in the asbestos-mining counties for 7-10 different sites of cancer, all of low incidence, were from 1.50 to 8.08 times those of other rural counties of the Province for both sexes. Metropolitan counties exhibited equally high risk for many of these sites. We discovered higher risks among males in asbestos-mining counties for cancer of the pleura, peritoneum, lip, tongue, salivary gland, mouth, and small intestine and higher risks among females for cancer of the pleura, lip, kidney, salivary gland, and for melanoma. Because of the likelihood of a long latent period for asbestos-related cancers, the risks we observed were possibly the product of since-altered occupational and environmental conditions existing 20-30 years ago in the asbestos-mining areas. The similarities in risks for most cancers in asbestos-mining and urban areas were noteworthy.

Asbestos↗

PubMed1996

Glutathione S-transferase and N-acetyltransferase genotypes and asbestos-associated pulmonary disorders.

BACKGROUND: Humans vary in their ability to metabolize endogenous and exogenous compounds. Glutathione S-transferases (GSTs) and N-acetyltransferases (NATs) are enzymes involved in the detoxification of hazardous agents. The GSTM1 and GSTT1 genes exhibit null (i.e., deletion) polymorphisms; in specific individuals, homozygous deletion (i.e., both copies lost) of these genes can be detected. Polymorphism of the NAT2 gene results in slow and fast acetylators of potentially toxic substances. The GSTM1-null and the NAT2 slow-acetylator genotypes have been associated with increased risks for the development of environmentally induced cancers. PURPOSE: We assessed whether homozygous GSTM1-null or GSTT1-null genotypes or the NAT2 slow-acetylator genotype were associated with increased risks for the development of malignant and nonmalignant asbestos-related pulmonary disorders in a cohort of Finnish construction workers. METHODS: The study population consisted of 145 asbestos insulators who were classified as having been exposed to high levels of asbestos; 69 of these individuals had no pulmonary disorders (control subjects), and 76 had either malignant mesothelioma (n = 24) or nonmalignant pulmonary disorders, such as asbestosis and/or pleural plaques (n = 52). Lymphocyte DNA and the polymerase chain reaction were used to determine the GSTM1, GSTT1, and NAT2 genotypes of the study subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) estimating the relative risks of disease associated with specific genotypes were calculated from 2 x 2 tables by use of Fisher's exact method. RESULTS: Risks for the development of asbestos-related pulmonary disorders were not affected significantly by homozygous deletion of the GSTM1 or GSTT1 genes. However, the risk of developing both malignant and nonmalignant pulmonary disorders for individuals with a NAT2 slow-acetylator genotype was more than twice that observed for those with a NAT2 fast-acetylator genotype (OR = 2.3; 95% CI = 1.1-4.7); the risk of developing malignant mesothelioma for NAT2 slow acetylators was increased almost fourfold (OR = 3.8; 95% CI = 1.2-14.3). Individuals who lacked the GSTM1 gene and possessed a NAT2 slow-acetylator genotype had a risk of developing malignant and nonmalignant pulmonary disorders that was approximately fivefold greater than that observed for those who had the GSTM1 gene and a NAT2 fast-acetylator genotype (OR = 5.1; 95% CI = 1.6-17.6); these individuals had a fourfold increased risk of developing nonmalignant pulmonary disorders (OR = 4.1; 95% CI = 1.1-17.2) and an eightfold increased risk of developing malignant mesothelioma (OR = 7.8; 95% CI = 1.4-78.7) when compared with the same reference group. CONCLUSIONS: Individuals with homozygous deletion of the GSTM1 gene and a NAT2 slow-acetylator genotype who are exposed to high levels of asbestos appear to have enhanced susceptibility to asbestos-related pulmonary disorders.

Acetylation↗

PubMed2004

Rounded atelectasis in an asbestos exposed worker.

The case history is presented of a 51-year-old electrical power worker with a history of asbestos exposure presenting with rounded atelectasis. No other radiological markers of asbestos exposure were present. A documented history of asbestos exposure and exclusion of other causes of rounded atelectasis led to the diagnosis of asbestos related rounded atelectasis. It is important to understand that rounded atelectasis can be an isolated finding due to asbestos exposure. This facilitates investigation of lung masses of unknown etiology and initiation of appropriate follow up of patients at risk for future development of more debilitating asbestos related pathology.

Asbestos↗

PubMed1976

Cancer mortality and asbestos deposits.

Asbestos deposits are found in many parts of the United States. In this paper the question is asked: Is there an increase in risk from cancer associated with naturally-occurring asbestos? In an attempt to control for the urban effect, geographic gradient and socioeconomic class, each county in the United States with asbestos deposits was matched for percent of area that was urban and for median years in school with two nearby counties that did not have known asbestos deposits. The study of cancer mortality rates in these matched counties provides no evidence that naturally-occurring asbestos is a great hazard to the general population of counties with asbestos depostis.

Age Factors↗

PubMed1981

Asbestos fibers in human lung: forensic significance.

Asbestos is a fibrous mineral which, because of its unique properties, has innumerable applications in many industries and is used in a large variety of consumer products. It has become ubiquitous and is woven, literally and figuratively, into the fabric of our present-day civilization. However, its presence is sometimes unknown and unsuspected by those who are exposed to asbestos by virtue of occupation or environment and inhale its fibers. Exposed workers and even urban dwellers may have a variable lung burden of asbestos fibers. There is indisputable clinical, pathological, experimental and epidemiological proof that, after varying periods of latency, asbestos may cause benign and malignant disease often leading to disability or death. Forensic investigation of suspected asbestos-related deaths includes a life-time occupational history, a complete autopsy, and identification of the asbestos fiber tissue burden. The latter usually requires special procedures.

Asbestos↗

PubMed1982

Asbestos-related diseases. Algorithm for forensic pathological diagnosis.

The pathological diagnosis and proof of asbestos causation in environmental-occupational diseases is based on a spectrum of increasingly sophisticated determinations with greater confidence in detection of asbestos bodies and fibers. These include the following: pathology (histology) and/or thick smears of lung, microincineration, bulk chemical digestion, and electron beam instruments. The requisites of medical and forensic asbestos causation differ, and do not always require the full range of these analytical techniques. The need and significance of some of these determinations, as expressed in number of asbestos bodies and fibers, may be related in many cases to the evidence of asbestosis; to the gross and microscopic pathological findings (asbestosis, lung carcinoma, mesothelioma); the exposure history (type, duration, intensity, and period of latency); and nature of the asbestos mineral. An algorithm for the forensic pathological diagnosis of asbestosis and of asbestos-related diseases is proposed.

Asbestos↗

PubMed2002

Incidence of digestive cancers and occupational exposure to asbestos.

While the role of exposure to asbestos in the development of several cancers such as mesotheliomas and bronchopulmonary cancers is now well established, the possible relationship between digestive cancers, other than peritoneal mesotheliomas, and occupational exposure to asbestos is still controversial. The great majority of the studies are based on mortality data. The aim of the study was to analyse the relationship between digestive cancer incidence and occupational exposure to asbestos in a population of subjects for whom precise occupational exposure data and precise incidence data were available. The population consisted of salaried and retired workers from a company using asbestos to manufacture fireproof textiles and friction materials. There were 1454 men (79.9%) and 366 women (20.1%). A cumulative exposure index and a mean exposure concentration in fibres/ml for each subject were calculated with the aid of an in-house job-exposure matrix. The number of cases of digestive cancer observed was compared with the expected and Standardized Incidence Ratio (SIR) was estimated. Precise occupational exposure data allowed us to study the dose-response relationship between asbestos exposure and risk of digestive cancer using Cox model. Fifty-six digestive cancers occurred in the study population over the 18-year follow-up period for 48.4 expected (SIR = 1.16 [0.87-1.50]). Comparing with incidence in the county, SIR was not significant for any of the digestive localization, but for peritoneum. However, even after taking into account the potential confounders via the Cox model, there was a significant dose-response relationship between the occurrence of digestive cancers and the mean exposure concentration, even after exclusion of peritoneum cancers. Our study provides initial evidence suggesting a relationship between occupational exposure to asbestos and the risk of digestive cancer: first, it is a study of incidence although the risk evidenced is not significant; secondly, a dose-effect relationship is demonstrated in the whole population. However, these preliminary results require confirmation by more powerful studies focusing on larger series.

Adult↗

PubMed1987

Co-carcinogenic effect of asbestos and benzo(a)pyrene in the lung of hamster.

Epidemiological reports indicate that occupational asbestos exposure and smoking habit make increase the incidence of lung carcinomas greatly. To elucidate the synergetic effect of smoking and asbestos exposure, hamsters were injected intratracheally with asbestos and benzo(a)pyrene(Bap), which is contained in cigarette smoke, singly or in combination. Tumor was not induced in the hamsters injected with asbestos or Bap alone except epithelial hyperplasia. On the other hand, 7 tumors out of 34 animals were found in groups injected with both asbestos and Bap from 12 months to 19 months after injection. Two of them were carcinomas. This result seemed to indicate synergetic effect of asbestos and Bap in causing carcinoma of the lung.

Animals↗

PubMed1991

Human health risks associated with asbestos abatement.

Upperbound lifetime excess cancer risks were calculated for activities associated with asbestos abatement using a risk assessment framework developed for EPA's Superfund program. It was found that removals were associated with cancer risks to workers which were often greater than the commonly accepted cancer risk of 1 x 10(-6), although lower than occupational exposure limits associated with risks of 1 x 10(-3). Removals had little effect in reducing risk to school populations. Risks to teachers and students in school buildings containing asbestos were approximately the same as risks associated with exposure to ambient asbestos by the general public and were below the levels typically of concern to regulatory agencies. During abatement, however, there were increased risks to both workers and nearby individuals. Careless, everyday building maintenance generated the greatest risk to workers followed by removals and encapsulation. If asbestos abatement was judged by the risk criteria applied to EPA's Superfund program, the no-action alternative would likely be selected in preference to removal in a majority of cases. These conclusions should only be interpreted within the context of an overall asbestos risk management program, which includes consideration of specific fiber types and sizes, sampling and analytical limitations, physical condition of asbestos-containing material, episodic peak exposures, and the number of people potentially exposed.

Air Pollutants↗

PubMed1991

The Veterans Administration's Asbestos Abatement Program.

1. The Veterans Administration has developed a program of asbestos abatement for its more than 1000 buildings, where health care personnel from 173 hospitals and 238 ambulatory care clinics are likely to encounter respirable asbestos. 2. This is a costly program, which has averaged about $25 million annually for the past ten years. 3. The VA has banned the use of new asbestos products containing more than 1% of asbestos in building construction or renovation projects. 4. Industrial hygiene engineering programs have been ordered instituted at all VA medical centers to monitor dust levels in compliance with OSHA and EPA requirements. 5. Health surveillance programs, managed by an environmental health physician at each medical center, have been instituted for all personnel who have been identified to have breathed asbestos fibers in excess of OSHA-EPA threshold limit values. 6. The health care program focuses on the identification of asbestosis and asbestos-related cancer through periodic X-ray films, lung function tests, and electrocardiographic and physical examination screening. 7. The program also stresses cessation of smoking.

Air Pollution, Indoor↗

PubMed1973

Death and lysis of leptospirae when cultured in asbestos-filtered growth media.

Death and lysis of leptospirae, when cultured in asbestos-filtered bovine albumin polysorbate 80 media, was quantitated. The pathogens (virulent and avirulent) required 2 x 10(6) cells/ml to initiate growth in such media, whereas inocula of 2 to 20 cells/ml grew in control medium. Saprophytic leptospirae initiated growth from 2 cells/ml in asbestos-filtered medium as well as control medium. The adverse action of asbestos-filtered medium was not removed by storage of medium for 2 years at 25 C and was not diminished when such medium was frozen at -80 C. Washing with water, HCl and NaHCO(3)-NaCl, citric acid, and medium components did not remove the lytic activity associated with asbestos-filtered culture medium. Continuous subculture in asbestos-filtered medium was possible from large inocula; however, upon subsequent dilution and reinoculation into asbestos-filtered media, there was no evidence of acquired resistance, and all pathogens failed to grow.

Agglutination Tests↗

PubMed2005

The effect of asbestosis on lung cancer risk beyond the dose related effect of asbestos alone.

AIMS: To determine if the presence of asbestosis is a prerequisite for lung cancer in subjects with known exposure to blue asbestos (crocidolite). METHODS: Former workers and residents of Wittenoom with known amounts of asbestos exposure (duration, intensity, and time since first exposure), current chest x ray and smoking information, participating in a cancer prevention programme (n = 1988) were studied. The first plain chest radiograph taken at the time of recruitment into the cancer prevention programme was examined for radiographic evidence of asbestosis according to the UICC (ILO) classification. Cox proportional hazards modelling was used to relate asbestosis, asbestos exposure, and lung cancer. RESULTS: Between 1990 and 2002 there were 58 cases of lung cancer. Thirty six per cent of cases had radiographic evidence of asbestosis compared to 12% of study participants. Smoking status was the strongest predictor of lung cancer, with current smokers (OR = 26.5, 95% CI 3.5 to 198) having the greatest risk. Radiographic asbestosis (OR = 1.94, 95% CI 1.09 to 3.46) and asbestos exposure (OR = 1.21 per f/ml-year, 95% CI 1.02 to 1.42) were significantly associated with an increased risk of lung cancer. There was an increased risk of lung cancer with increasing exposure in those without asbestosis. CONCLUSION: In this cohort of former workers and residents of Wittenoom, asbestosis is not a mandatory precursor for asbestos related lung cancer. These findings support the hypothesis that it is the asbestos fibres per se that cause lung cancer, which can develop with or without the presence of asbestosis.

Aged↗

PubMed2006

Occupational exposure to asbestos and man-made vitreous fibres and risk of lung cancer: a multicentre case-control study in Europe.

OBJECTIVES: To investigate the contribution of occupational exposure to asbestos and man-made vitreous fibres (MMVF) to lung cancer in high-risk populations in Europe. METHODS: A multicentre case-control study was conducted in six Central and Eastern European countries and the UK, during the period 1998-2002. Comprehensive occupational and sociodemographic information was collected from 2205 newly diagnosed male lung cancer cases and 2305 frequency matched controls. Odds ratios (OR) of lung cancer were calculated after adjusting for other relevant occupational exposures and tobacco smoking. RESULTS: The OR for asbestos exposure was 0.92 (95% CI 0.73 to 1.15) in Central and Eastern Europe and 1.85 (95% CI 1.07 to 3.21) in the UK. Similar ORs were found for exposure to amphibole asbestos. The OR for MMVF exposure was 1.23 (95% CI 0.88 to 1.71) with no evidence of heterogeneity by country. No synergistic effect either between asbestos and MMVF or between any of them and smoking was found. CONCLUSION: In this large community-based study occupational exposure to asbestos and MMVF does not appear to contribute to the lung cancer burden in men in Central and Eastern Europe. In contrast, in the UK the authors found an increased risk of lung cancer following exposure to asbestos. Differences in fibre type and circumstances of exposure may explain these results.

Asbestos↗

PubMed1976

Thirty-two cases of mesothelioma in Victoria, Australia: a retrospective survey related to occupational asbestos exposure.

Mesotheliomas have been reported in four states in Australia. Crocidolite has been mined and milled at Wittenoom in West Australia where five cases of mesothelioma were reported after exposure of high intensity. The 32 cases of mesothelioma reported in this paper occurred during a period of 11 years in Victoria; 29 were pleural and three peritoneal. There were 22 autopsies. End occupations were misleading in 66% of cases. Two of the three subjects with peritoneal mesothelioma were siblings, and there was no evidence of occupational or other exposure to asbestos in either. There was a significant prevalence of pulmonary asbestos bodies in the tumour series as compared with an unselected consecutive series of 200 routine autopsies (0.01 greater than P greater than 0.001). The occupational history was as effective a method of assessing 'true' asbestos exposure as the pulmonary asbestos body count. Five cases had had a duration of exposure of one year or less, but they had had heavy exposure. The latent interval before tumour development was 25 years or longer in each case. There was no known exposure to asbestos in five cases (16%). The rare association of mesothelioma with types of asbestos other than crocikolite may not exist and could be explicable on the basis of the proportion (16%) of these tumours arising randomly in the population.

Adult↗