Toxicity Profiles
Condensed Toxicity Summary for BERYLLIUM
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.
April 1992
Prepared by: Mary Lou Daugherty, M.S., Chemical Hazard Evaluation and Communication Group, Biomedical and Environmental Information Analysis Section, Health and Safety Research Division, *, Oak Ridge, Tennessee.
Prepared for OAK RIDGE RESERVATION ENVIRONMENTAL RESTORATION PROGRAM
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.
Beryllium is present in the earth's crust, in emissions from coal combustion, in surface water and soil, and in house dust, food, drinking water, and cigarette smoke (U.S. EPA, 1987a). However, the highest risk for exposure occurs among workers employed in beryllium manufacturing, fabricating, or reclamation industries (ATSDR, 1988). Workers encounter dusts and fumes of many different beryllium compounds; the current occupational standard for worker exposure to beryllium is 2µg/m3 during an 8-hour workshift (OSHA, 1989).
Inhaled beryllium is absorbed slowly and localizes mainly in the lungs, bone, liver and kidneys (Stiefel et al., 1980; Reeves et al., 1967; Reeves and Vorwald, 1967; Zorn et al., 1988; Tepper et al., 1961; Meehan and Smyth, 1967). Ingested beryllium undergoes limited absorption and localizes in liver, kidneys, lungs, stomach, spleen and the large and small intestines (Crowley et al., 1949; Furchner et al., 1973; Watanabe et al., 1985). Significant absorption of beryllium or its compounds through intact skin is unlikely because of its chemical properties (U.S. EPA, 1987b). Beryllium per se is not biotransformed, but soluble salts may be converted to less soluble compounds in the lung (U.S. EPA, 1987b). Most orally administered beryllium passes through the gastrointestinal tract unabsorbed and is excreted in the feces (Reeves, 1965), whereas inhaled water-soluble beryllium salts are excreted mainly by the kidneys (Zorn et al., 1988).
Limited data indicate that the oral toxicity of beryllium is low. No adverse effects were noted in mice given 5 ppm beryllium in the drinking water in a lifetime bioassay (Schroeder and Mitchener, 1975a,b). The dose (converted to 0.54 mg/kg bw/day) was the no-adverse-effect level (NOAEL) used in the calculation of the chronic oral RfD for beryllium of 0.005 mg/kg/day (U.S. EPA, 1991a).
In contrast, the toxicity of inhaled beryllium is well-documented. Humans inhaling "massive" doses of beryllium compounds (such as the water soluble sulfate, fluoride, chloride, and oxide) may develop acute berylliosis (Constantinidis, 1978). ATSDR (1988) estimated that, based on existing data, the disease could develop at levels ranging from approximately 2-1000 µg Be/m3. This disease usually develops shortly after exposure and is characterized by rhinitis, pharyngitis, and/or tracheobronchitis, and may progress to severe pulmonary symptoms. The severity of acute beryllium toxicity correlates with exposure levels, and the disease is now rarely observed in the United States because of improved industrial hygiene (Zorn et al., 1988; Kriebel et al., 1988b).
Humans inhaling beryllium may also develop chronic berylliosis which, in contrast to acute berylliosis, is highly variable in onset, is more likely to be fatal, and can develop a few months to >=20 years after exposure (Constantinidis, 1978; Hall et al., 1959; Kriebel et al., 1988b). Chronic beryllium disease is a systemic disease that primarily affects the lungs and is characterized by the development of non-caseating granulomas. The disease most likely results from a hypersensitivity response to beryllium as evidenced by positive patch tests (Nishimura, 1966) and positive lymphocyte transformation tests (Williams and Williams (1983) in exposed individuals. Granulomas may also appear in the skin, liver, spleen, lymph nodes, myocardium, skeletal muscles, kidney, bone, and salivary glands (Kriebel et al., 1988b; Freiman and Hardy, 1970).
Epidemiologic studies have suggested that beryllium and its compounds could be human carcinogens. In a study that covered 15 regions of the U.S., Berg and Burbank (1972) found a significant correlation between cancers of the breast, bone and uterus and the concentration and detection frequency of beryllium in drinking water. However, imperfect analytical and sampling methods used in the study prompted the U.S. EPA (1986b) to conclude that these results are not proof of cause and effect relationships between cancer and beryllium in drinking water. Studies in workers exposed to beryllium, mostly via inhalation, have shown significant increases in observed over expected lung cancer incidences (Bayliss et al., 1971; Bayliss and Lainhart, 1972; Bayliss and Wagoner, 1977; Wagoner et al., 1980; Mancuso, 1970; 1979; 1980). The U.S. EPA (1986a), in evaluating the total database for the association of lung cancer with occupational exposure to beryllium, noted several limitations, but concluded that the results must be considered to be at least suggestive of a carcinogenic risk to humans. In laboratory studies, beryllium sulfate caused increased incidences of pulmonary tumors in rats and rhesus monkeys (Vorwald, 1953, 1962, 1968; Vorwald et al., 1955, 1966; Schepers et al., 1957; Reeves and Deitch, 1969).
Based on sufficient evidence for animals and inadequate evidence
for humans, beryllium has been placed in the EPA weight-of-evidence classification
B2, probable human carcinogen (U.S. EPA, 1991a). For inhalation exposure,
the unit risk value is 2.4E-3 (µg/m3)-1, and
the slope factor is 8.4 (mg/kg/day)-1 (U.S. EPA, 1991b). For
oral exposure, the unit risk value is 1.2E-4 (µg/L)-1 and
the slope factor is 4.3 (mg/kg/day)-1 (U.S. EPA, 1991a).
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