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.
Prepared by: Dennis M. Opresko, Ph.D., 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.
Vanadium is a metallic element that occurs in six oxidation states and numerous inorganic compounds. Some of the more important compounds are vanadium pentoxide (V2O5), sodium metavanadate (NaVO3), sodium orthovanadate (Na3VO4), vanadyl sulfate (VOSO4), and ammonium vanadate (NH4VO3). Vanadium is used primarily as an alloying agent in steels and non-ferrous metals (ATSDR, 1990). Vanadium compounds are also used as catalysts and in chemical, ceramic or specialty applications.
Vanadium compounds are poorly absorbed through the gastrointestinal system (0.5-2% of dietary amount) (NRCC, 1980; ICRP, 1960; Byrne and Kosta, 1978), but slightly more readily absorbed through the lungs (20-25%) (ICRP, 1960; Davies and Bennett, 1983). Absorbed vanadium is widely distributed in the body, but short-term localization occurs primarily in bone, kidneys, and liver (Vouk, 1979; Roshchin et al., 1980; Parker et al., 1980; Sharma et al., 1980; Wiegmann et al., 1982). In the body, vanadium can undergo changes in oxidation state (interconversion of vanadyl (+4) and vanadate (+5) forms) and it can also bind with blood protein (transferin) (Harris et al., 1984). Vanadium is excreted primarily in the feces following oral exposures and primarily in the urine following inhalation exposures (Tipton et al., 1969; ATSDR, 1990).
The toxicity of vanadium depends on its physico-chemical state; particularly on its valence state and solubility. Based on acute toxicity, pentavalent NH4VO3 has been reported to be more than twice as toxic as trivalent VCl3 and more than 6 times as toxic as divalent VI2. Pentavalent V2O5 has been reported to be more than 5 times as toxic as trivalent V2O3 (Roschin, 1967). In animals, acutely toxic oral doses cause vasoconstriction, diffuse desquamative enteritis, congestion and fatty degeneration of the liver, congestion and focal hemorrhages in the lungs and adrenal cortex (Gosselin et al., 1984). Minimal effects seen after subchronic oral exposures to animals include diarrhea, altered renal function, and decreases in erythrocyte counts, hemogloblin, and hematocrit (Domingo et al., 1985; Zaporowska and Wasilewski, 1990). In humans, intestinal cramps and diarrhea may occur following subchronic oral exposures. These studies indicate that for subchronic and chronic oral exposures the primary targets are the digestive system, kidneys, and blood.
Reference Doses (RfD) for chronic oral exposures are: 0.007 mg/kg/day for vanadium; 0.009 mg/kg/day for vanadium pentoxide; 0.02 mg/kg/day for vanadyl sulfate; and 0.001 mg/kg/day for sodium metavanadate (U.S. EPA, 1987, 1991a,b). The subchronic RfDs for these compounds are the same as the chronic RfDs, except for sodium metavanadate, which is 0.01 mg/kg/day (U.S. EPA, 1987, 1991a,b).
Inhalation exposures to vanadium and vanadium compounds result primarily in adverse effects to the respiratory system (Sax, 1984; ATSDR, 1990). In laboratory studies, minimal effects (throat irritation and coughing) occurred after an 8-hr exposure to 0.1 mg V/m3 (Zenz and Berg, 1967). In studies on workers occupationally exposed to vanadium, the most common reported symptoms were: irritation of the respiratory tract, conjunctivitis, dermatitis, cough, bronchospasm, pulmonary congestion, and bronchitis (Symanski, 1939; Sjoberg, 1950, 1951, 1955, 1956; Vintinner et al., 1955; Lewis 1959; Tebrock and Machle, 1968; Roshchin, 1968; Kiviluoto et al., 1981b). Quantitative data are; however, insufficient to derive a subchronic or chronic inhalation Reference Concentration (RfC) for vanadium or vanadium compounds.
There is little evidence that vanadium or vanadium compounds are reproductive toxins or teratogens. There is also no evidence that any vanadium compound is carcinogenic; however, very few adequate studies are available for evaluation. Vanadium has not been classified as to carcinogenicity by the U.S. EPA (1991a).Retrieve Toxicity Profiles Formal Version
Last Updated 2/13/98