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PubMedDate not supplied

Dangerous and cancer-causing properties of products and chemicals in the oil refining and petrochemical industry: Part V--Asbestos-caused cancers and exposure of workers in the oil refining industry.

In the oil refining and petrochemical industries exposure to cancer-causing asbestos particles, especially during equipment repair and maintenance, is very high. Up to 90% of workers in the oil refining industry had direct and/or indirect contact with asbestos, and more than half of this contact occurred without the use of any kind of precaution, thus these workers are in high risk of developing lung cancer and mesothelioma, both fatal diseases. The hazards include: inadequate health and safety training for both company personnel and workers, failure to inform about the dangers and diseases (cancers) resulting from exposure to asbestos; excessive use of large numbers of untrained and uninformed contract workers; lack of use of protective equipment; and archaeological approaches and responses to repairing asbestos breaks and replacement of asbestos in oil refining facilities. For a better understanding of practices and policies in the oil refining industry, refer to Rachel Scott's Muscle and Blood, in particular the chapter "Oil" (E.P. Dutton, New York, 1974), as well as to an editorial which appeared in the Oil and Gas Journal, April, 1968.

Asbestos↗

PubMedDate not supplied

Asbestos in Japan.

In 2002 a total ban on asbestos was announced in Japan, following many years of sporadic and variably effective measures intended to control its use in that country. A major factor in instigating the ban was public awareness raised by the publicizing of the experience of asbestos-exposed workers in the U.S. naval base and shipyards at Yokosuka, an inordinate number of whom died of asbestos-related disease. Statistics of asbestos-related disease mortality in Japan are presented. Groups prominent in the effort to establish the ban and make it effective include the Japan Occupational Safety and Health Resource Center (JOSHRC) and the Ban Asbestos Network Japan (BANJAN). Activities of these groups are described.

Asbestos↗

PubMedDate not supplied

Asbestos dispatches.

As the global campaign to ban asbestos gathers momentum, more countries and organizations are restricting the use of chrysotile (white asbestos). Attempting to reverse the fall in global demand, asbestos stakeholders have redoubled marketing efforts in countries such as India where health and safety regulations are not strictly enforced. In the Canadian asbestos heartland, public and media awareness has grown and industry's influence has weakened. In response, chrysotile producers are pressing federal and provincial governments for mandatory increases in consumption, despite new research documenting an asbestos cancer epidemic.

Asbestos↗

PubMedDate not supplied

Asbestos banned in Argentina.

In 1997, Argentina gave priority to asbestos in its National Plan for the Sound Management of Chemicals, and it was the subject of a Technical Task Force on Occupational Cancer. After five years of public hearings in which government, workers, industry advocates, environmentalists, clinicians, scientists, and consumers participated, it was agreed that asbestos exposure is a risk factor for both workers and the general population, and that Argentina should provide to its people the same protections adopted by many developed countries. Pressure from asbestos industry groups initially delayed the inclusion of chrysotile asbestos in the proposed ban, but on January 1, 2003, the mining and import of all forms of asbestos were banned in Argentina.

Argentina↗

PubMedDate not supplied

Chrysotile asbestos as a cause of mesothelioma: application of the Hill causation model.

Chrysotile comprises over 95% of the asbestos used today. Some have contended that the majority of asbestos-related diseases have resulted from exposures to the amphiboles. In fact, chrysotile is being touted as the form of asbestos which can be used safely. Causation is a controversial issue for the epidemiologist. How much proof is needed before causation can be established? This paper examines one proposed model for establishing causation as presented by Sir Austin Bradford Hill in 1965. Many policymakers have relied upon this model in forming public health policy as well as deciding litigation issues. Chrysotile asbestos meets Hill's nine proposed criteria, establishing chrysotile asbestos as a cause of mesothelioma.

Asbestos, Serpentine↗

PubMed1997

Pleural disease during treatment with bromocriptine in patients previously exposed to asbestos.

Bromocriptine, which is used in the treatment of Parkinson's disease, can cause adverse pleuropulmonary reactions. Exposure to asbestos can result in similar lesions. Fifteen patients with former exposure to asbestos, who developed pleural fibrosis after treatment with bromocriptine, were observed independently in Sweden (11 patients) and Australia (four patients). The patients complained of malaise, often associated with weight loss, dyspnoea, and a disturbing cough. Laboratory values included increased erythrocyte sedimentation rate and a low haemoglobin level. Lung function tests showed a restrictive lung function defect. Chest radiographs showed bilateral pleural fibrosis, with small amounts of fluid in some cases. Soon after bromocriptine was withdrawn, the patients improved clinically, and the laboratory values returned to normal. However, in most cases, pleural fibrosis and a restrictive lung function defect persisted to some extent. In conclusion, in patients who develop pleuropulmonary fibrosis whilst being treated with bromocriptine, former exposure to asbestos should be investigated. Conversely, when pleural changes develop in a patient on bromocriptine and with prior exposure to asbestos, the possible causative role of the drug should be discussed. Special follow-up may be indicated when bromocriptine is planned in a patient with previous asbestos exposure, and if symptoms or signs of pleural fibrosis develop, bromocriptine withdrawal should be considered.

Adolescent↗

PubMed2006

The economic costs of health service treatments for asbestos-related mesothelioma deaths.

This article explores the complex and neglected picture of occupational and environmental disease healthcare costs specifically relating to asbestos. Diagnosed mesothelioma cases in Scotland in one calendar year were used to investigate the subject in greater depth. Data from UK sources on asbestos disease types recorded in 2000 and their disease treatment costs were obtained. Acute care economic costs of these diseases are estimated. One hundred and twenty diagnosed, recorded, and treated cases of asbestos-related diseases occurred in 2000 in Scotland. Mesothelioma accounted for 100 cases and directly cost Scottish National Health Service hospitals an estimated 942,038 pounds. The estimated UK figure in 2000 was at least 16,014,646 pounds because official figures for diagnosed and recorded deaths from mesothelioma are running at over 1700 a year with rises predicted for 2010 of 2000 deaths. By 2003, 50,000 people in the UK had died from diagnosed and recorded mesothelioma since records began. Earlier disease treatment costs would have been significantly lower than those in 2000 but, at 2000 prices, cost to the UK was roughly 471,019,000 pounds in acute hospital expenditure. Figures for primary care costs, including caregiver costs, are incomplete or unknown. These disease costs are substantial and have some international generalizability. Treatment patterns and costs vary greatly. Many lung cancer cases due to asbestos exposure occur globally for each mesothelioma case. Hence figures provided in this article are certain to be gross underestimates of the total health service and personal economic costs of asbestos illness and treatment in Scotland.

Asbestos↗

PubMed2001

An unusual case of mixed-dust exposure involving a "noncommercial" asbestos.

Our health center evaluated an individual for suspected pneumoconiosis, which had resulted from exposures in a foundry/metal reclamation facility. Appropriate consent forms were obtained for the procedures. Historically, individuals who work in foundries have been exposed to various types of dusts. The clinical findings in this case were consistent with silicosis with a suspicion of asbestos-induced changes as well. A sample from this individual, analyzed by electron microscopy, showed both classical and atypical ferruginous bodies. The uncoated fiber burden in this individual indicated an appreciable number of anthophyllite asbestos fibers. This finding, coupled with analysis of cores from ferruginous bodies and the presence of ferruginous bodies in areas of interstitial fibrosis, pathologically supported the diagnosis of asbestos-related disease. The unique factor associated with this case is that unlike in some settings in Finland where anthophyllite was mined and used commercially, this mineral fiber is not commonly found in commercially used asbestos products in the United States. Although the actual source of the asbestos exposure in this case is still being sought, it should be recognized that anthophyllite is a contaminant of many other minerals used in workplace environments, including foundries. The fiber burden indicates a unique type of exposure, differing from that usually construed as typical in occupational settings in the United States.

Asbestos↗

PubMed1994

One-year follow-up of the phagocytic activity of leukocytes after exposure of rats to asbestos and basalt fibers.

The phagocytic activity of leukocytes in peripheral blood was investigated after 2, 24, and 48 hr; 1, 2, 4, and 8 weeks; and 6 and 12 months following intraperitoneal administration of asbestos and basalt fibers to Wistar rats. Asbestos and basalt fibers differed in their effects on the parameters studied. Both granulocyte count and phagocytic activity of leukocytes during the 1-year dynamic follow-up in both dust-exposed groups of animals changed in two phases, characterized by the initial stimulation of the acute phase I, followed by the suppression of the parameters in the chronic phase II. Exposure to asbestos and basalt fibers led, in phase II, to impairment of the phagocytic activity of granulocytes. Asbestos fibers also significantly decreased phagocytic activity of monocytes. Exposure to basalt fibers did not affect the phagocytic activity of monocytes in phase II. Results suggest that the monocytic component of leukocytes plays an important role in the development of diseases caused by exposure to fibrous dusts, but basalt fibers have lesser biological effects than asbestos fibers.

Animals↗

PubMed1974

The ingestion of asbestos fibers.

Feeding of baboons with crocidolite showed small numbers of asbestos needles 0.5-1 mum in ashed tissue of the gut wall, which probably came from iron-containing macrophages. It is suggested that pleural plaques and hyaline nodules in the peritoneum represent a hypersensitivity reaction to ferritin protein coating on asbestos fibers. In South Africa only a few peritoneal mesotheliomas come from the asbestos areas, and the incidence of gastrointestinal carcinomas is no greater than normal. Intrapleural and intraperitoneal injection produces unrealistic situations. Calcium salts are deposited on asbestos cement pipes from hard water and organic material from soft water. It is difficult to envisage asbestos contamination of the water so reticulated.

Animals↗

PubMed1980

Clinical observations following asbestos exposure.

There is a spectrum of clinical entities following occupational exposure to asbestos. Methods of evaluation for these problems are reviewed. Nonmalignant clinical conditions include asbestos warts, asbestos bodies, parenchymal fibrosis (asbestosis), pleural fibrosis and calcification, and benign asbestotic pleural effusion. Asbestosis, though a benign process, is a significant cause of death. Malignant conditions associated with asbestos exposure include lung cancer, accounting for about 20% of all deaths among insulation workers and significantly related to cigarette smoking. The lung cancers tend to occur more frequently in the lower lobes and are more peripheral. Pleural and peritoneal mesothelioma and some excesses in gastrointestinal cancers are found with asbestos exposure, although these are not related to cigarette smoking. Increased rates of malignancy first become significant after 20 years from onset of exposure and are also related to duration of exposure. Difficulties with the use of death certificate data are reviewed.

Asbestos↗

PubMed1983

Epidemiologic basis for the asbestos standard.

The current standard for occupational exposure to asbestos is 2 fibers/cm3 averaged over an 8-hr day. A NIOSH/OSHA committee has recently concluded that the 2 fiber/cm3 standard is grossly inadequate to protect workers from asbestos-related disease, and that all levels of asbestos exposure studied thus far have demonstrated asbestos-related disease. The committee recommends that a 0.1 fiber/cm3 limit replace the current 2 fiber/cm3 standard on the grounds that this is the lowest level detectable with currently available analytical techniques. Thus a 0.1 fiber/cm3 limit is not based on epidemiological data but on the presumption that any level of exposure is disease producing. This paper addresses the question of whether it would be possible to detect health effects of exposure below the current 2 fiber/cm3 standard. Five studies are reviewed which provide evidence on the strength of the relationship between asbestos fiber exposure and lung cancer. Calculation of sample sizes needed to be 95% certain of detecting the kind of excess probably associated with exposure to 2 fibers/cm3 suggests that epidemiology is not likely to be useful in detecting lung cancer below the current standard. Some outcome measures other than lung cancer or clinical asbestosis will be needed if observations on humans are to be used as evidence for a lowering of the present standard.

Asbestos↗

PubMed1983

Review of published studies on gut penetration by ingested asbestos fibers.

During the 1970s, potential health risks associated with exposure to asbestos in drinking water became a national concern. One of the key questions that arose from debate over whether ingestion of mineral fibers could result in increased gastrointestinal cancer risk was whether fibers can penetrate the gastrointestinal mucosa and thus have some chance of residing in tissue. It is likely that such movement of a large number of fibers is a necessary precursor for carcinogenesis following ingestion of asbestos. Studies of the potential for fiber accumulation in tissues and body fluids following introduction of asbestos to the alimentary canal have provided seemingly contradictory observations. This review, which places particular emphasis on the impact of experimental and analytical limitations on the evidential strengths of each study, indicates the likelihood that a very small fraction of ingested microscopic asbestos fibers penetrates the gastrointestinal mucosa. A reliable estimate of the magnitude of long-term fiber retention in tissues as a consequence of chronic human ingestion of asbestos cannot be made at this time.

Animals↗

PubMed1983

Critical review of epidemiologic studies related to ingested asbestos.

Thirteen epidemiologic studies of ingested asbestos conducted in five areas of the United States and Canada were reviewed and evaluated for the definitiveness and applicability regarding the development of ambient water quality standards. One or more studies found male or female associations between asbestos in water supplies and cancer mortality (or incidence) due to neoplasms of the esophagus, stomach, small intestine, colon, rectum, gallbladder, pancreas, peritoneum, lungs, pleura, prostate, kidneys, brain, and thyroid, and also due to leukemia. Several methodologic weaknesses and limitations were found in each study, leading to the determination that no individual study or aggregation of studies exist that would establish risk levels from ingested asbestos. A binomial probability analysis of the eight independent studies suggested that, while the level of male-female agreement was generally low, the number of observed positive associations in males and females for neoplasms of the esophagus, stomach, pancreas, and prostate was unlikely to have been generated by chance factors alone, and thus, may have a biological basis related to ingested asbestos. Cancers of the small intestine and leukemia were implicated to a lesser degree in this analysis. The patterns of integrated findings for most gastrointestinal cancers were somewhat consistent with patterns observed among asbestos-exposed occupational groups, whereas the patterns found for pancreatic cancer, kidney cancer, and leukemia were not consistent.(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestos↗

PubMed1989

Mechanisms of asbestos-induced squamous metaplasia in tracheobronchial epithelial cells.

Within 1 to 4 weeks after exposure to asbestos, differentiated rodent and human tracheobronchial epithelial cells in organ culture undergo squamous metaplasia, a putative preneoplastic lesion characterized by conversion of mucociliary cell types to keratinizing cells. The exogenous addition of retinal acetate (RA) to culture medium of hamster tracheal organ cultures reverses preestablished, asbestos-induced squamous metaplasia, although data suggest that the effectiveness of RA decreases as the length of time between exposure to asbestos and initial application of RA increases. alpha-Difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase (ODC), inhibits squamous metaplasia caused by asbestos or vitamin A deficiency, whereas addition of methylglyoxal bis(guanylhydrazone) (MGBG), a structural analog of spermidine and inhibitor of S-adenosylmethionine decarboxylase, causes an enhancement of metaplasia under both circumstances. Basal cell hyperplasia and increased incorporation of 3H-thymidine by tracheal epithelial cells also are seen after addition of the polyamines, putrescine or spermidine, to tracheal organ cultures, an observation supporting the importance of polyamines in the development of this lesion. The use of retinoids and inhibitors of ODC could be promising as preventive and/or therapeutic approaches for individuals at high risk for development of asbestos-associated diseases.

Animals↗

PubMed1990

The relationship between fibrosis and cancer in experimental animals exposed to asbestos and other fibers.

The association between occupational asbestos exposure and the development of both pulmonary fibrosis or asbestosis and pulmonary carcinomas is well documented. It has been suggested that the two pathological conditions are associated with asbestos-related carcinomas developing from areas of asbestosis and not occurring when exposure has been too low to produce this type of pulmonary scarring. Experimental inhalation studies so far published have not been designed to examine this association specifically, but many publications have reported that asbestos samples producing high levels of fibrosis is experimental animals are also very carcinogenic. Samples of asbestos or man-made fibers that produce little fibrosis also produce few tumors. These works are reviewed. In order to examine the association between fibrosis and tumor production in more detail, groups of animals with and without pulmonary tumors and with individual fibrosis measurements were assembled from a number of inhalation studies undertaken over a period of years at this Institute. It was found that animals with pulmonary tumors had almost double the amount of pulmonary fibrosis as animals of similar age that did not. In a few of the animals where tumors were found at an early stage of development, their origin from fibrotic areas could be confirmed, although in most cases where tumor deposits were widespread this was not possible. Experimental confirmation of the site of origin of most pulmonary tumors in asbestos-treated rats would require new studies with rats examined specifically at an age when early tumors would be expected.

Animals↗

PubMed2006

Nested case-control study of autoimmune disease in an asbestos-exposed population.

OBJECTIVE: To explore the potential association between asbestos exposure and risk of autoimmune disease, we conducted a case-control study among a cohort of 7,307 current and former residents of Libby, Montana, a community with historical occupational and environmental exposure to asbestos-contaminated vermiculite. METHODS: Cases were defined as those who reported having one of three systemic autoimmune diseases (SAIDs): systemic lupus erythematosus, scleroderma, or rheumatoid arthritis (RA). Controls were randomly selected at a 3:1 ratio from among the remaining 6,813 screening participants using frequency-matched age and sex groupings. RESULTS: The odds ratios (ORs) and 95% confidence intervals (CIs) for SAIDs among those >or=65 years of age who had worked for the vermiculite mining company were 2.14 (95% CI, 0.90-5.10) for all SAIDs and 3.23 (95% CI, 1.31-7.96) for RA. In this age group, exposure to asbestos while in the military was also an independent risk factor, resulting in a tripling in risk. Other measures of occupational exposure to vermiculite indicated 54% and 65% increased risk for SAIDs and RA, respectively. Those who had reported frequent contact with vermiculite through various exposure pathways also demonstrated elevated risk for SAIDs and RA. We found increasing risk estimates for SAIDs with increasing numbers of reported vermiculite exposure pathways (p<0.001). CONCLUSION: These preliminary findings support the hypothesis that asbestos exposure is associated with autoimmune disease. Refined measurements of asbestos exposure and SAID status among this cohort will help to further clarify the relationship between these variables.

Adolescent↗

PubMed1994

Cellular and molecular mechanisms of asbestos carcinogenicity: implications for biopersistence.

Carcinogenic agents can influence the carcinogenic process either by mutating critical target genes or by increasing the number of cells at risk for mutations. Cytogenetic and molecular studies of asbestos-related cancers indicate that inactivation or loss of multiple tumor suppressor genes occurs during lung cancer development. Aneuploidy and other chromosomal changes induced by asbestos fibers may be involved in genetic alterations in asbestos-related cancers. Furthermore, asbestos fibers may influence the carcinogenic process by inducing cell proliferation, free radicals, or other promotional mechanisms. Therefore, asbestos fibers may act at multiple stages of the carcinogenic process by both genetic and epigenetic mechanisms. Biopersistence is undoubtedly important in fiber carcinogenicity. However, the time required for a fiber to remain in the lung to exert a cancer-related effect is difficult to specify.

Asbestos↗