Toxicity Profiles
Condensed Toxicity Summary for THALLIUM
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.
DECEMBER 1994
Prepared by: Tim Borges and Mary Lou Daugherty, Chemical Hazard Evaluation Group, Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, Oak Ridge National Laboratory*, 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.
This report is an update of the Toxicity Summary for Thallium (CAS Registry No. 7440-28-0). The original summary for this chemical was submitted in 1991. The update was performed by incorporating any new human health toxicity data published since the original submittal of the report. Pertinent pharmacokinetic, toxicologic, carcinogenic, and epidemiologic data were obtained through on-line searches of the TOXLINE database from 1991 through 1994. In addition, any changes to EPA-approved toxicity values (reference doses, reference concentrations, or cancer slope factors) from the Integrated Risk Information System (IRIS) (current as of December 1994) and/or the Health Effects Assessment Summary Tables, Annual FY-94 and July Supplement No. 1, for this chemical were incorporated in this update.
Thallium, a naturally occurring elemental metal, is commonly found in minerals and as thallium salts. It can also be released into the environment from industrial sources. Atmospheric thallium contaminates surface soils by deposition allowing for the exposure of humans by oral, dermal, or inhalation routes. The most common nonoccupational sources of thallium exposure are contaminated food crops and tobacco. Although normally present in the urine of humans, elevated urine thallium concentrations have been associated with adverse health effects.
The primary targets of thallium toxicity are the nervous, integumentary, and reproductive systems. In humans, acute exposures produce paresthesia, retrobulbar neuritis, ataxia, delirium, tremors, and hallucinations. This implies central, peripheral, and autonomic nervous system involvement (Stokinger, 1981; de Groot and Van Heijst, 1988; Kazantzis, 1986). Human and animal chronic exposures result in alterations of the brain, spinal cord, and peripheral nerves (Stokinger, 1981; Manzo et al., 1983b). In both humans and animals, alopecia is the most common indicator of long-term thallium poisoning (Stokinger, 1981; Manzo et al., 1983b).
An increased incidence of congenital malformations was found in children of parents exposed to thallium through the consumption of home-grown fruits and vegetables. However, a causal relationship between these effects and thallium exposure could not be confirmed (Dolgner et al., 1983). In animal studies, thallium compounds produced testicular effects in male rats and slight fetotoxicity and significant impairment of learning ability in the offspring of treated female rats (Formigli et al., 1986; Roll and Matthiaschk, 1981; Bornhausen and Hagen, 1984).
Reference doses (RfDs) have been calculated for subchronic and chronic oral exposure to several thallium compounds. The values, derived from a single study where thallium treatment increased AST and LDH activities in rats, are based on NOAELs ranging from 0.23 to 0.28 mg/kg/day (EPA, 1986). The subchronic RfDs are 8.00E-04 (thallium sulfate, chloride, and carbonate) or 9.00E-04 mg/kg/day (thallium nitrate and acetate) (EPA, 1994a), and the chronic RfDs are 8.00E-05 (thallium sulfate, chloride, and carbonate) or 9.00E-05 mg/kg/day (thallium nitrate and acetate) (EPA, 1994b-f).
Data suitable for evaluating the carcinogenicity of thallium to humans or animals by ingestion, inhalation, or other routes of exposure were not found. Thallium sulfate, selenite, nitrate, chloride, carbonate, and acetate have been placed in EPA's weight-of evidence Group D, not classifiable as to human carcinogenicity based on inadequate human and animal data (EPA, 1994b-g).
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