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: Rosmarie A. Faust, Ph.D., Chemical Hazard Evaluation Group in the Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, Oak Ridge National Laboratory*.
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.
2,6-Dinitrotoluene (2,6-DNT; 2-methyl-1,3-dinitrobenzene; CAS Reg. No. 606-20-2) is a pale yellow crystalline solid and one of six possible chemical forms of dinitrotoluene (DNT). Technical grade DNT (t-DNT) is typically composed of 78% 2,4-DNT, 19% 2,6-DNT, and small amounts of 3,4-DNT, 2,3-DNT, and 2,5-DNT (Dunlap 1978). DNT is primarily used as a chemical intermediate in the manufacture of polyurethanes. It is also used as a component of military and commercial explosives, as an intermediate in dye processes (Etnier 1987, Hawley 1981), and as a propellant additive (Sears and Touchette 1982).
The DNTs are absorbed through the gastrointestinal tract, respiratory tract, and skin in most species (EPA 1986). Human data regarding potential health effects of 2,6-DNT are very limited. A significant increase in the death rate due to ischemic heart disease has been associated with occupational exposure to t-DNT (Levine et al. 1986). The evidence for potential reproductive effects (reduction of sperm counts) in male workers exposed to a mixture of DNT isomers is equivocal (Hamill et al. 1982, Ahrenholz 1980).
Oral subchronic toxicity studies with rats, mice, and dogs indicate that the blood, liver, and reproductive system are targets affected by 2,6-DNT in all three species (Lee et al. 1976). These effects were generally observed at doses of 35 mg/kg/day in rats, 51 mg/kg/day in mice, and 20 mg/kg/day in dogs. The primary hematologic effect in all three species was methemoglobinemia with sequelae such as Heinz bodies, reticulocytosis, anemia, and extramedullary hematopoiesis. Also seen in all three species was bile duct hyperplasia, decreased spermatogenesis and testicular atrophy. In addition, dogs exhibited neurotoxic effects (incoordination, weakness, tremors, and paralysis) as well as inflammatory and degenerative kidney changes.
According to EPA (1991a), available data are inadequate for the calculation of a Reference Dose (RfD) or Reference Concentration (RfC) for 2,6-DNT.
In a 1-year carcinogenesis bioassay, 2,6-DNT at oral doses of 7 and 14 mg/kg/day, respectively, produced hepatocellular carcinomas in 85% and 100% of male rats. t-DNT, containing about 76% 2,4-DNT and 19% 2,6-DNT, also yielded a positive hepatocarcinogenic response (Leonard et al. 1987). In another study on the effects of t-DNT, dietary doses of 14 mg/kg/day induced hepatocellular carcinomas in rats (CIIT 1982). Initiating and promoting activities of 2,6-DNT in rat liver have been reported (Popp and Leonard 1982). Although EPA has not evaluated 2,6-DNT for evidence of human carcinogenic potential, the dinitrotoluene mixture (containing 2,4- and 2,6-DNT) has been classified as a B2 carcinogen, probable human carcinogen (EPA 1991a,b). A slope factor of 6.8E-1 (mg/kg/day)-1 was calculated for oral exposure to dinitrotoluene mixture. The drinking water unit risk is 1.9E-5 (µg/L)-1 (EPA 1991b).Retrieve Toxicity Profiles Formal Version
Last Updated 2/13/98