Toxicity Profiles
Condensed Toxicity Summary for ASBESTOS
NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.
August 1995
Prepared by: Rosmarie A. Faust, Ph.D., Chemical Hazard Evaluation Group, Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, *, Oak Ridge, Tennessee.
Prepared for OAK RIDGE RESERVATION ENVIRONMENTAL RESTORATION PROGRAM.
*Managed by Lockheed Martin Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.
Asbestos (CAS No. 1332-21-4) is the generic name for a variety of naturally formed hydrated silicates containing metal cations such as sodium, magnesium, calcium, or iron. The two major groups of asbestos are serpentine and amphibole based on their physical/chemical properties. Chrysotile (CAS No. 12001-29-5) is the only asbestos in the serpentine group, whereas the amphibole group is represented by actinolite (CAS No. 13768-008), amosite (CAS No. 12172-73-5), anthophyllite (CAS No. 17068-78-9), crocidolite (CAS No. 12001-28-4), and tremolite (CAS No. 14567-73-8) (EPA 1984, ATSDR 1993). Asbestos fibers are chemically inert, or nearly so. They do not evaporate, dissolve, burn, or undergo significant reactions with other chemicals (ATSDR 1993).
Asbestos fibers can enter the body after inhalation or oral exposures. Fibers that are deposited in the lung may be removed from the lung by mucociliary clearance or by macrophages, or they may be retained in the lungs (EPA 1980, 1984). Some ingested asbestos fibers penetrate the gastric mucosa, and a small percentage of the fibers are distributed to other tissues. Ingested fibers are mostly excreted in the feces (Cunningham et al. 1976).
Long-term feeding studies in rats and hamsters indicate that ingestion of high concentrations (1% in the diet or 500-800 mg/kg/day) of chrysotile, amosite, crocidolite, or tremolite does not cause systemic effects (NTP 1985; 1988a, b, c; 1990). Other studies reported some histological and biochemical alterations in cells of the gastrointestinal tract in rats receiving up to 50 mg/kg/day of chrysotile for 14-15 months (Jacobs et al. 1978a, b).
Numerous studies in humans have established that long-term inhalation of asbestos fibers causes chronic, progressive pneumoconiosis (asbestosis). The disease is common among occupational groups directly exposed to asbestos fibers, such as insulation workers, but also extends to those working near the application or removal of asbestos and family contacts of exposed workers (EPA 1980). Asbestosis results from a prolonged inflammatory response stimulated by the presence of fibers in the lungs and is characterized by fibrosis of the lung parenchyma, which usually becomes radiographically discernible 10 years after the first exposure (EPA 1985). The main clinical symptom is shortness of breath, often accompanied by rales and cough. In severe cases, impairment of respiratory function may ultimately result in death (ATSDR 1993). Because asbestos fibers are resistant to breakdown in the lungs, the inflammatory response triggered by the fibers is ongoing, even after exposure has ceased. It has been estimated that cumulative exposures of 17-75 fibers-year/mL would result in fibrotic lung lesions, and cumulative exposures of 3.5-300 fibers-year/mL would cause death in humans (ATSDR 1993).
Smoking has been shown to increase the risk of asbestosis (Schulz 1994). Fibrosis has been produced in laboratory animals following subchronic or chronic inhalation exposure to various forms of asbestos (Wagner 1963, Wagner et al. 1974, Donaldson et al. 1988). Some studies of workers with asbestos-related diseases indicate that the cellular immune system in such patients can be depressed (ATSDR 1993).
Dermal contact with asbestos may result in the formation of warts or corns (Alden and Howell 1944). An oral Reference Dose (RfD) or inhalation Reference Concentration (RfC) for asbestos has not been derived (EPA 1995).
Several epidemiologic studies suggest that high levels of asbestos in drinking water in certain geographic areas may cause gastrointestinal cancer in humans (Cooper et al. 1979, Conforti 1983, Kanarek 1983), whereas other studies failed to find a clear association between ingested asbestos and cancer in humans (Harrington et al. 1978, Polissar et al. 1983). The evidence for carcinogenicity in orally exposed animals is also equivocal. A series of lifetime feeding studies with rats and Syrian golden hamsters with various forms of asbestos have yielded mostly negative results (NTP 1985; 1988a, b, c; 1990). An increased incidence of benign adenomatous polyps of the large intestine was observed in male rats exposed to 1% (500 mg/kg/day) intermediate range chrysotile (65% of fibers >10 µm in length) in the diet (NTP 1985).
Numerous epidemiologic studies have documented an increased incidence of lung cancer and pleural and peritoneal mesothelioma (a tumor involving the lining of the abdomen and chest) as a result of asbestos exposure. All major types of commercial asbestos such as chrysotile, amosite, and crocidolite have been found to produce asbestos-related cancer among workers occupationally exposed in mining and milling, manufacturing, and using materials containing asbestos fibers (EPA 1980). Asbestos-related cancer has also been identified, although less frequently, in individuals who had worked near the application or removal of asbestos material, individuals residing in the vicinity of asbestos plants, and individuals who had lived in the household of an asbestos worker (IARC 1977, 1987).
For lung cancer, the magnitude of the carcinogenic risk appears to be a function of a number of factors, including the level and duration of exposure, the time since exposure occurred, the age at which exposure occurred, the smoking history of the exposed person, and the type and size distribution of asbestos fibers. A substantial latency period (10-30 years) has been observed between exposure to asbestos and the onset of lung cancer (ATSDR 1993). Many reports have documented cases of pleural and peritoneal mesotheliomas resulting from occupational and nonoccupational exposures to various types and mixtures of asbestos. It has been estimated that a third of the mesotheliomas occurring in the U.S. may be due to nonoccupational exposure (IARC 1977, 1987). Asbestos exposure and cigarette smoking act synergistically to produce dramatic increases in lung cancer compared with those from exposure to either agent alone (EPA 1984). The data for possible interactions between smoking and mesothelioma are not certain, but smoking does not appear to increase the risk for this cancer (Schulz 1994).
Reports of excess cancer incidences or mortality from cancers at other sites among workers exposed to asbestos are inconsistent. These cancers include cancers of the gastrointestinal system (esophagus, stomach, colon, bile duct, and rectum), laryngeal cancer, kidney cancer, ovarian cancer, and cancer affecting the lymphopoietic and hematopoietic systems (IARC 1977, Schulz 1994). However, the risk of these cancers appears to be significantly lower than those for lung cancer and mesothelioma in similarly exposed cohorts (Schulz 1994).
Several types of asbestos were shown to induce tumors in rats, including mesotheliomas and lung adenomas/carcinomas following inhalation of 9.7-14.7 mg/m3, 7 hours/day, 5 days/week for up to 24 months (Wagner et al. 1974). Intrapleural administration of asbestos induced mesotheliomas in rats and hamsters, and intraperitoneal administration induced abdominal tumors including mesotheliomas in rats and mice and abdominal tumors in hamsters (IARC 1977, 1987).
Based on EPA guidelines, asbestos was assigned to weight-of-evidence group A, human
carcinogen (EPA 1995). Slope factors for oral or inhalation exposure are not available at this time.
The inhalation unit risk for asbestos is 2.3E-1 [(fibers/mL)-1] (EPA 1995).
Retrieve Toxicity Profiles
Formal Version
Last Updated 8/29/97