TABLE 4-1 Physical and Chemical Properties of 2,6-Di-tert-butyl-4-nitrophenol

Synonyms

2,6-Di-t-butyl-4-nitrophenol; dibutyl-4-nitrophenol; di-tert-butyl-4-nitrophenol; di-tertiary-butyl-4-nitrophenol; dibutyl-p-nitrophenol; dibutyl-p-nitrophenol; di-t-butyl-p-nitrophenol

CAS registry number

728-40-5

Molecular formula

C14H21NO3

Molecular weight

251

Boiling point

NA

Melting point

157.0°C

Flash point

NA

Explosive limits

NA

Specific gravity

NA

Vapor pressure

NA

Solubility

NA

Conversion factors

1 ppm = 10.27 mg/m3; 1 mg/m3 = 0.09741 ppm

Abbreviations: NA, not available or not applicable.

Source: Data on molecular weight and melting point from Alexander et al. 2001.

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.

SUMMARY OF TOXICITY

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



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