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PubMed1980

Asbestos exposures in Massachusetts public schools.

A Massachusetts legislative commission was established to investigate the potential health hazards associated with the use of sprayed-on asbestos in public school buildings. All schools built, renovated, or added onto from 1946 to 1973 were surveyed. Sprayed-on materials from the public areas of these schools were analyzed for asbestos content. Air samples were collected from 173 schools positively identified for asbestos. Most of the air sampling results were below the predetermined background noise level of 0.04 fibers per cc. It was concluded that it is not possible to quantify public exposures to asbestos because of the limitations of air sampling technology. A rating system was devised which generated a single number known as the Ferris Index which reflected the sprayed-on material's degree of potential health hazard. Data from five predictor variables were incorporated in this index. Although sprayed-on asbestos was present in 12 percent of the surveyed schools, only 3 percent required long-term control recommendations.

Aerosols↗

PubMed1980

Pulmonary fibrosis, carcinoma, and ferruginous body counts in amosite asbestos workers. A study of six cases.

The Tyler Asbestos Workers Program is a continuing study of 1,105 former amosite asbestos workers. This report includes a study of six former workers, five of whom died and had autopsies, and one who underwent a lobectomy. Five of these men were exposed to asbestos for three months or less. Four had lung cancer, and one a rectal carcinoma. All were cigarette smokers. Ferruginous (asbestos) body content of the upper and lower lobes of the lungs was quantitated by a digestion technic. Tissue sections from upper and lower lobes were independently quantitated for fibrosis and ferruginous bodies, and chest roentgenograms were examined for interstitial fibrosis. (Control lung tissue was obtained from consecutive autopsies of 52 adults who did not have a known occupational exposure to asbestos.) Relatively low ferruginous body counts (less than 700/g lung tissue) were associated with mild degrees of fibrosis, and higher counts (greater than 10,000/g) with moderate to severe fibrosis. Mild to moderate pulmonary fibrosis could be identified on tissue sections before interstitial changes were detectable by chest roentgenograms.

Aged↗

PubMed1993

Asbestos induced oxidative injury to DNA.

DNA-damaging effects of asbestos in the presence of organic peroxides and hydroperoxides were investigated. The destabilization of the secondary structure of DNA, damage to deoxyribose sugar and DNA fidelity were measured, respectively, by S-1 nuclease hydrolysis, the formation of thiobarbituric acid (TBA)-reacting species and a melting temperature (Tm) profile using calf thymus DNA. S-1 nuclease hydrolysis and Tm determinations have shown that the presence of benzoylperoxide (BOOB), cumene hydroperoxide (COOH) or tertiary-butyl hydroperoxide (t-BOOH) increased asbestos-mediated DNA damage by a large factor compared either to asbestos alone or to peroxide or hydroperoxide alone. However, no formation of TBA-reacting species could be observed in this system. The quenchers of reactive oxygen species (ROS) afforded protection against DNA damage. These results suggest that asbestos in the presence of organic peroxides and hydroperoxides damage the DNA which is mediated by the generation of oxygen free radicals. The significance of these results in relation to the development of cancer of the respiratory tract among the asbestos exposed population is discussed.

Animals↗

PubMed1994

Airborne concentrations of asbestos in non-occupational environments.

Concentrations of asbestos in air were determined from analysis of samples collected in over 300 buildings involved in litigation. Samples were collected by certified industrial hygienists and analysed in certified laboratories by transmission electron microscopy. Building group mean concentrations of asbestos in building air inhaled by occupants were generally less than 0.0005 f ml-5 > 5 microns (90th percentile). At these concentrations the risk from asbestos exposure would be very low for building occupants. Another data set was obtained from the maintenance logs kept by owners of buildings containing asbestos fireproofing and subject to Operations and Maintenance Programmes to evaluate asbestos inhalation risk to maintenance workers. The logs were kept to document protective measures and maintenance personnel exposures during 1991-1992. Data are presented for one commercial building, which is typical of data for three additional commercial buildings and a medical centre. All samples were evaluated by the NIOSH 1400 protocol for sampling and analysis by phase contrast microscopy. Operations and maintenance precautions to reduce dust emission were modest; they included spraying of ceiling tiles with amended water, HEPA vacuuming tile edges before entry and after tile replacement, respirator usage and careful work. Negative pressure containment was not used. In this building personal exposures in electrical/plumbing work ranged from 0.000 to 0.035 f ml-1 > 5 microns in length (average work time of one job was 118 min); the 8-h TWA was 0.0149 f ml-1 > 5 microns.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants↗

PubMed1994

Carcinogenesis and related cell and tissue responses to asbestos: a review.

A review of the literature reveals that chrysotile asbestos has a mulitiplicity of effects on cells and tissues which can provide a framework for assessment of its role(s) in initiation, promotion, or as a co-carcinogen which acts in concert with chemical carcinogens found in cigarette smoke in the development of lung cancer. Several caveats important in the interpretation of these data include the general lack of dose-response protocols both for in vivo and for in vitro studies as well as the absence, in many studies, of minerals which are appropriate positive or negative controls based on epidemiological data in man. Other factors which may account for disparities in results between studies include the use of different preparations of chrysotile fibres with distinct chemical and physical compositions and different cell types and species. Whether chrysotile is an initiator of lung cancer or mesothelioma in human cells is unclear, as evidence of chromosomal aberrations in human bronchial epithelial cells are for the most part negative (Kodoma et al., 1993; see Mossman, B., this Workshop): only one study employing pleural mesothelial cells from four individuals, two of whom exhibited chromosomal abnormalities before exposure to asbestos, has documented chromosomal changes with chrysotile, crocidolite and amosite asbestos, and this study did not use a non-pathogenic dust as a negative control. Studies using human lymphocytes show chromosomal changes after exposure to latex beads or chrysotile at equal weight concentrations (Korkina et al., 1992; see Mossman, B., this Workshop). Lastly, although both chrysotile and crocidolite asbestos demonstrated dose-dependent increase in aberrant anaphases in an SV40 T antigen-transformed human mesothelial cell line (Pelin et al., 1992, see Mossman, B., this Workshop), erionite, a potent mesotheliomagenic fibre in rodents and humans, caused no aberrations in this bioassay. Several studies have been performed to determine the interactions of chrysotile with rodent cells or isolated bacterial DNA. Results in a number of bioassays have been positive, but chrysotile is less potent on a fibre number comparative basis than crocidolite and no-observed-effect-levels (NOELs) have been observed in several systems. Cell proliferation by asbestos may be a more relevant phenomenon to tumour development and promotion, and the ability of chrysotile to stimulate cell proliferation, using a number of biomarkers, has been demonstrated both in vitro and after inhalation by rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2004

The interaction of asbestos and smoking in lung cancer: a modified measure of effect.

OBJECTIVES: The ratio of the relative risk of lung cancer due to asbestos exposure in non-smokers to that in smokers has been termed the relative asbestos effect (RAE). In a review, Liddell [Liddell FDK (2001) Ann Occup Hyg; 45: 341-56] estimated that the RAE was approximately 2. This measure is satisfactory when there is an appreciable relative risk due to asbestos but does not generalize to lower levels of exposure. A modified measure is proposed to overcome this difficulty. The modified measure, RAEm, is defined as the ratio of the excess relative risk (RR - 1) in non-smokers to that in smokers. METHODS: The cohort studies combined in Liddell's 2001 analysis have been used to give a combined estimate of the modified measure. RESULTS: The combined value of RAEm is 3.19 with 95% confidence interval 1.67-6.13. CONCLUSION: The excess relative risk of lung cancer from asbestos exposure is about three times higher in non-smokers than in smokers. The modified measure has been placed within a more versatile model of interaction. If interaction is present the relative risk from asbestos exposure changes only slightly between light and heavy smokers, but is higher in very light smokers and non-smokers. The relative risk estimated from epidemiological studies of a mixed population of non-smokers and smokers applies to smokers.

Asbestos↗

PubMed2000

mRNA expression patterns in different stages of asbestos-induced carcinogenesis in rats.

Human malignant mesotheliomas are induced almost exclusively by fibrous dusts. The nature of interactions between fibers and target cells, and the molecular mechanisms leading to tumorigenesis, are not yet understood. Here, the mRNA expression patterns at different stages of asbestos-induced carcinogenesis in rats were monitored by suppression subtractive hybridization (SSH) and array assay. Several genes were upregulated in pretumorous tissues from asbestos-treated rats, in asbestos-induced tumors and in cells treated with asbestos in vitro. The upregulation of the proto-oncogene c-myc, fra-1 and egfr in fiber-induced carcinogenesis was demonstrated at different stages of carcinogenesis. A possible role of Fra-1 as one of the dimeric proteins generating the AP-1 transcription factor was substantiated by its dose-dependent expression in mesothelial cells treated with asbestos in vitro. The upregulation of osteopontin (an extracellular matrix protein) and of zyxin and integrin-linked kinase (intracellular proteins associated with the focal adhesion contact), indicate that fibers may affect integrin-linked signal transduction and extracellular matrix proteins.

Animals↗

PubMed1985

Induction by asbestos fibers of anaphase abnormalities: mechanism for aneuploidy induction and possibly carcinogenesis.

Syrian hamster embryo cells were treated with crocidolite asbestos at a dose (1 microgram/cm2) which was shown in previous studies to induce cell transformation and aneuploidy in these cells. Treatment of cells with asbestos induced a greater than 20-fold increase in the incidence of cells in anaphase with abnormalities, including lagging chromosomes, bridges, and sticky chromosomes. Asbestos fibers were observed in mitotic cells and appeared, in some cases, to be interacting directly with the chromosomes. From these studies, we propose that the physical interaction of the asbestos fibers with the chromosomes or structural proteins of the spindle apparatus causes missegregation of chromosomes during mitosis resulting in aneuploidy. These findings provide a mechanism, at the chromosomal level, by which asbestos and other mineral fibers might induce cell transformation and cancer.

Anaphase↗

PubMed1993

Retrospective assessment of asbestos exposure--II. At the job level: complementarity of job-specific questionnaire and job exposure matrices.

Retrospective assessment of asbestos exposure--II. At the job level: Complementarity of job-specific questionnaire and job exposure matrices. International Journal of Epidemiology 1993; 22 (Suppl. 2): S96-S105. The assessments of asbestos exposure by two a priori job exposure matrices (JEM) and by a job-specific questionnaire (SQ) are compared at job level. The data used for the comparison were generated by an ongoing case-control study on lung cancer in a region of northern Germany with a relatively high past prevalence of asbestos exposure. Among job periods assessed as unexposed by either JEM, 96% are recognized as such by the SQ. Discrepancies between the SQ and JEM were observed in jobs rated potentially exposed by the JEM. Despite varying estimates, the JEM and SQ were consistent as regards the relative classification of job periods by probability of exposure. The concordance of the methods, estimated by Kappa statistics, was stronger for the two JEM than for either of the JEM and the SQ. The identification of specific occupation/industry combinations in which discrepancies were most frequent and the comparison with expert ratings in some jobs yield insights into the sources of the disagreement between the methods. The misclassification of exposure by the JEM usually results in an overestimation of exposure. This is essentially related to loss of information due to the use of job codes as surrogates for job task descriptions and to the insufficiency of published data on asbestos exposure in different industries. As regards the SQ, two main sources of potential loss of sensitivity were identified: 1) possible omission of indirect sources of exposure by this method, 2) possible incompleteness of the SQ. The present comparison of methods of asbestos exposure assessment does not allow any one approach to be considered superior to another. Indeed, as proposed by Ahrens et al. in Part I of the study, both should be used to ensure optimal epidemiological performance.

Asbestos↗

PubMed2000

DNA breakage in asbestos-treated normal and transformed (TSV40) rat pleural mesothelial cells.

Asbestos has been shown to induce cell cycle arrest, DNA repair and some abnormalities consistent with DNA damage but not DNA breakage. The purpose of the study was to investigate DNA breakage in asbestos-exposed rat pleural mesothelial cells (RPMC). RPMC were compared with their transformed counterparts, RPMC-TSV40 (i.e. p53-inactivated by infection with a retroviral recombinant encoding the SV40 large T antigen), as in the latter cells the cell cycle does not arrest and DNA repair is deficient due to ineffective p53-dependent cell cycle control. RPMC and RPMC-TSV40 were exposed to chrysotile and crocidolite asbestos and also to camptothecin for comparison. The presence of DNA breakage was determined using the single cell gel (Comet) assay with alkaline electrophoresis and quantified by measuring comet tail length (TL) and the percentage of total DNA in the tail and calculating tail moment (TM). We found that comets were generated by both types of asbestos in RPMC and in RPMC-TSV40 as well as by camptothecin in RPMC. On a per weight basis, chrysotile induced more abnormalities in comet parameters than did crocidolite. The comet TL and TM increased with fibre concentration, although less so with crocidolite than with chrysotile. When exposed to chrysotile at similar concentrations, RPMC consistently showed more abnormal comet parameters than did RPMC-TSV40. We concluded that asbestos causes DNA breakage and suggest that some of the DNA breakage measured was due to repair mechanisms in the normal RPMC.

Animals↗

PubMed2006

Effectiveness of smoking cessation advice for asbestos workers.

AIM: To assess effectiveness of smoking cessation advice to asbestos workers at statutory medical examinations. METHODS: Workers are required to be examined every 2 years while continuing potential exposure to asbestos, including cessation advice if smokers. Records of 170 workers seen between 1986 and 2004 in Kent and Canterbury Hospital were reviewed. Respiratory symptoms, signs, lung function, radiological findings and smoking status were analysed. RESULTS: At initial visit 109 (64%) were smokers. Thirty-four of these attended twice. Despite verbal advice, including emphasis on respiratory abnormalities detected in 62%, only three (9%) had ceased smoking by self-reporting at the second visit. CONCLUSION: Despite appropriate counselling regarding the potential risks of asbestos exposure and smoking, the cessation rate among asbestos workers was disappointingly low. Further measures to encourage asbestos workers to enter smoking cessation programmes should be considered.

Adolescent↗

PubMed1978

An investigation of the use of asbestos cement pipe for public water supply and the incidence of gastrointestinal cancer in Connecticut, 1935-1973.

The age adjusted sex specific incidence data for stomach, colon, and rectal cancer for Connecticut townships for the period 1935 to 1973 were used to investigate whether asbestos cement pipe usage for domestic drinking water is associated with gastrointestinal cancer. The townships were grouped according to the Assessment of Exposure (AOE) and Risk Factor (RF) for asbestos. These are composite indices of asbestos exposure including factors relating to the age of the pipe, the ability of water to leach asbestos from the pipe, and the length of pipes used by the population. No association was noted between these asbestos risk scores and gastrointestinal tumor incidence.

Asbestos↗

PubMed1999

Lessons learnt from a factory fire with asbestos-containing fallout.

BACKGROUND: Fallout containing asbestos from a factory fire at Tranmere, Wirral, England, landed on a highly populated urban area with an estimated 16000 people living in the area worst affected, which included a shipbuilding community. There was considerable public concern over the health impact of the acute environmental incident, and great media interest. METHODS: A descriptive study was carried out of the acute environmental incident and its management, and the difficulties encountered. RESULTS: Practical lessons learnt include need for: increased fire-fighter awareness of potential adverse health effects from asbestos in the structure of buildings; early involvement of both Local Authority environmental health and National Health Service public health departments; creation of a systematic local database of potential environmental health hazards in the structure of buildings as well as their contents; 24 hour on-call arrangements with laboratories expert in analyses of fire fallout; rapid quantitative analyses of multiple environmental samples; district written policy on handling asbestos incidents; systematic assessment of fright and media factors in public impact of an incident; dedicated public help-lines open long hours; consistent evidence-based public messages from all those communicating with the public; measurement of asbestos levels in the street and homes for public reassurance; local and health authorities' subscription to an environmental incident support service; formation of an acute environmental incident team to jointly manage and publicly report on airborne acute environmental incidents; clear government definition of responsibilities of different agencies. CONCLUSIONS: This paper provides a description of important lessons learnt during an acute environmental incident with asbestos-containing fallout. It will be helpful to those involved in the practical planning for and management of future incidents.

Air Pollutants↗

PubMed1981

Pleural plaques and cigarette smoking in asbestos workers.

In a survey of 45 men aged 40 or over who had worked five years or more in an asbestos manufacturing plant, the prevalence of pleural plaques was studied with respect to age, duration of asbestos exposure, estimated cumulative asbestos dose, and smoking habit. Plaques were found in 38 to 53% of the men, depending on the interpretation of the chest film reader. Cigarette habit appeared to be the most important factor; the prevalence was lowest in non-smokers, intermediate in current smokers, and particularly high in exsmokers. There was some confounding of this relationship by estimated cumulative asbestos dose but such confounding did not seem to be sufficient to explain fully the relationship between the prevalence of plaques and smoking habit. Both factors must be considered in studies of the risk of pleural plaques in asbestos workers.

Adult↗

PubMed1985

Asbestos and tuberculosis in Trieste, Italy.

The distribution of counts of asbestos bodies in lung specimens from 25 persons dying of fibrocaseous tuberculosis was essentially identical to that in age- and sex-matched control subjects. Although tuberculosis mortality has been elevated in the past in cohorts of asbestos workers, asbestos exposure at environmental levels found in a region with a history of heavy asbestos use appears to be unassociated with risk of tuberculosis. Potentiation of the risk of death from tuberculosis may require both a high risk of tuberculosis in the general community and intense personal exposure to asbestos.

Adult↗

PubMed1986

Asbestos and airflow limitation.

To assess the effect of asbestos on the airways, researchers studied 45 shipyard workers who were lifelong nonsmokers and had asbestos-related abnormalities seen on their chest roentgenograms. Patients with interstitial lung disease, bronchial asthma prior to asbestos exposure, recurrent pneumonias, or significant cardiovascular disease were excluded from the study. In addition to chest films, they had spirometry performed before and after bronchodilator inhalation, lung volumes, diffusing capacity, and arterial blood gases. Forced vital capacity and forced expired volume in one second were normal in all patients. Maximum midexpiratory flow rates (MMFR) were abnormal (MMFR less than 75% of predicted) in 13 patients (29%). Therefore, 29% of lifetime nonsmokers with asbestos exposure exhibited evidence of small airways dysfunction. An abnormal MMFR in these workers may be due, in part, to asbestos exposure and could conceivably indicate a population at risk for pulmonary fibrosis and/or obstructive airways disease.

Asbestos↗

PubMed2001

Asbestos exposure assessment by mineralogical analysis of bronchoalveolar lavage fluid.

Mineralogical analysis of bronchoalveolar lavage fluid (BALF) by electron microscopy can represent the most suitable method for assessing asbestos exposure. However, it has been claimed that no standardized or systematic approach to the subject of mineralogical analysis exists. This study aimed to evaluate BALF mineralogical analysis by transmission electron microscopy as biomarker of asbestos fiber load. BALF was examined in 108 exposed workers and 57 patients who underwent diagnostic fiberoptic bronchoscopy for various clinical purposes. Asbestos bodies in BALF were counted with a phase-contrast microscope. Fibers were counted and analyzed by transmission electron microscopy, which showed a significant difference between the two populations and positive results for all exposed subjects. Only 82.2% of the exposed population tested positive for asbestos bodies. Subjects with long-term exposure had higher concentrations of fibers than did those with more recent exposure, probably because of the higher workplace exposure levels in the past. The results of the study confirm that fiber concentration in BALF can be considered as a reliable biomarker of past asbestos exposure, even many years after the end of exposure.

Adult↗

PubMed2000

Environmental asbestos exposure and mesothelioma.

Epidemiologic studies of mesothelioma have focused primarily on occupational exposures to asbestos. Nonoccupational exposure to asbestos can be grouped into three main categories: paraoccupational (familial), neighborhood, and true environmental exposures. Elevated mesothelioma rates not attributable to occupational exposures have been observed in asbestos mining and manufacturing areas. Asbestos is one of the most dangerous environmental carcinogens because of the small dose known to cause mesothelioma and the rapid lethality of the disease once it develops. Further research is needed to characterize the contribution and risk profile for environmental asbestos and mesothelioma, and for the development of public health policy.

Asbestos↗