to limit the amount of DBP in TEP 2190 oil to no more than 10 ppm (Still et al. 2005). However, the remaining stockpile of DBP-containing TEP 2190 lubricating oil in inventory is being used to supply the fleet for a number of years (MacMahon et al. 1999). Still et al. (2005) indicate that exposure to DBNP may also occur in many submarines because of the mixing of “old” and “new” TEP 2190 oil in submarine turbine systems and storage tanks. Exposures to DBNP are otherwise limited. DBNP was proposed as a miticide for treatment of resistant mite infections in mammals (Vesselinovitch et al. 1961), but there is no indication that it was ever used for this purpose.

Toxicity information on DBNP is limited to animal studies in as much as no case reports, experimental-exposure studies, or epidemiologic studies resulting from human exposure to it are available. The toxicologic database on DBNP primarily includes acute-exposure studies and a few repeated-dose studies. No adequate data from inhalation-toxicity, subchronic toxicity, mutagenicity, carcinogenicity, or reproductive-toxicity studies are available.

After single or repeated oral or intraperitoneal (ip) doses, rats show clinical signs (prostration, rapid breathing, hyperthermia, and rapid induction of rigor mortis after death) that are consistent with inhibition of mitochondrial oxidative metabolism (Alexander et al. 2001; Carpenter et al. 1997). A single oral dose of 40 mg/kg in dimethyl sulfoxide (DMSO) and canola oil is sufficient to induce