2,6-Di-tert-butylphenol

Fire Extinguishing Agents Not to Be Used: Water may be ineffective.

Use water spray, foam, powder, carbon dioxide.

Fresh air, rest.

Remove contaminated clothes. Rinse and then wash skin with water and soap.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Give one or two glasses of water to drink. Refer for medical attention .

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Personal protection: filter respirator for organic gases and vapours adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered plastic containers. Carefully collect remainder. Then store and dispose of according to local regulations.

TERRESTRIAL FATE: According to a recommended classification scheme(1), a measured Koc of 3600 determined for 2,6-di-tert-butylphenol in river sediment(2), indicates that this compound should have only slight mobility in soil(SRC). Volatilization of 2,6-di-tert-butylphenol may be important from moist soil surfaces(SRC) given an estimated Henry's Law constant of 3.15X10-6 atm-cu m/mole(3,SRC). Photooxidation may be an important fate process on the soil surface; 29.5% of this compound was photomineralized over a period of 17 hours(4). Based on limited data, it seems likely that 2,6-di-tert-butylphenol will biodegrade(SRC). Conversion of 1.1% (a further 44.9% was metabolized, but not to completion)(5), 3.5%(6), and 7.7%(7) of the parent compound to CO2 by an activated sludge inoculum was reported over a 5 day time period.

AQUATIC FATE: Adsorption, volatilization, bioconcentration, and biodegradation are expected to be important fate processes for this compound in water(SRC). Following 5 days incubation with sludge, 7.7% of the initial 2,6-di-tert-butylphenol had volatilized, 46% had biodegraded, and 31.9% was adsorbed to the sludge(1). According to a recommended classification scheme(2), a measured Koc of 3600(3) determined in river sediment, indicates that 2,6-di-tert-butylphenol will adsorb to suspended solids and sediment(SRC) in the water. Mineralization of 1.1%(4), 3.5%(5), and 7.7%(6) by an activated sludge inoculum was reported over a 5 day time period; a further 44.9% was metabolized, but not to completion(4). Oxidation of this compound in the water column occurs readily, resulting in the formation of 2,6-di-tert-butylbenzoquinone(7). 2,6-Di-tert-butylphenol may volatilize from water surfaces based on an estimated Henry's Law constant of 3.15X10-6 atm-cu m/mole(SRC), developed using a fragment constant estimation method(8). Estimated half-lives for a model river and model lake are 17 and 130 days, respectively(9,SRC). BCF values of 800(10) and 660(1), measured in chlorella and fish, respectively, indicate that 2,6-di-tert-butylphenol does bioconcentrate in aquatic organisms, according to a suggested classification scheme(11).

ATMOSPHERIC FATE: According to a suggested classification scheme(1), an estimated vapor pressure of 7.3X10-3 mm Hg at 25 °C(2,SRC) indicates that 2,6-di-tert-butylphenol will mainly exist in the vapor phase in the ambient atmosphere. Vapor-phase 2,6-di-tert-butylphenol is degraded in the atmosphere by reaction with photochemically produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be about 7.8 hours(3,SRC).

Cough. Sore throat.

Redness. Pain.

Redness. Pain.

Sore throat. Burning sensation in the throat and chest.

A Koc of 3600 was measured in river sediment(1). The Koc of 2,6-di-tert-butylphenol is estimated as approximately 11,000(SRC), using an experimental log Kow of 4.92(2) and a regression-derived equation(3,SRC). According to a recommended classification scheme(4), these Koc values suggest that 2,6-di-tert-butylphenol will have slight to no mobility in soil(SRC). Following 5 days incubation, 31.9% of the initial concentration of 2,6-di-tert-butylphenol was present in the non-extractable residue fraction in sludge(5).

2,6-di-t-butylphenol (CAS # 128-39-2) was evaluated for subchronic oral toxicity. The test substance was administered by oral gavage to 6 female rats/CFE for 6 days at a dosage level of 309 mg/kg body weight. Toxic effects included an increase in liver weight and hepatic enzymes. No further information was reported.

2,6-di-t-butylphenol (CAS # 128-39-2) was evaluated for subchronic dietary toxicity. The test substance was administered orally to 9 female CD-1 mice for 12 days at a concentration of 8.7 mg/kg diet. Toxic effects included an increase in liver to body weight ratios and phase I and II liver enzyme activities. No further information was reported.

2,6-di-t-butylphenol (CAS # 128-39-2) was evaluated for subchronic oral toxicity. The test substance was administered by oral gavage to 6 female rats/CFE for 6 days at a dosage level of 309 mg/kg body weight. Toxic effects included an increase in liver weight and hepatic enzymes. No further information was reported.

2,6-di-t-butylphenol (CAS # 128-39-2) was evaluated for subchronic dietary toxicity in 9 female CD-1 mice for 12 days at a concentration of 8.7 mg/kg diet. Toxic effects included an increase in liver to body weight ratios and phase I and II liver enzyme activities. No further information was reported.

Conversion of 1.1% of the initial concentration of 2,6-di-tert-butylphenol (50 ug) (a further 44.9% was metabolized, but not to completion)(1), 3.5%(2), and 7.7%(3) of the parent compound to CO2 by an activated sludge inoculum was reported over a 5 day time period.

2,6-Di-tert-butylphenol was detected in sediment cores taken downstream from a chemical manufacturing plant in Rhode Island(1). Two cores taken from near the plant had concentrations of this compound from 0.5 to 180 ppm. Two cores taken 1 km downstream had concentrations ranging from 4-760 ppm(1).

Chlorella, a green algae, had a measured bioaccumulation factor of 800 after exposure to 50 ug/L 2,6-di-tert-butylphenol for 24 hours(1). In fish (Golden Orfe), a bioaccumulation factor of 660 was measured following exposure to 37 ug/L 2,6-di-tert-butylphenol for 3 days(2). An estimated BCF value of 3230 was calculated for 2,6-di-tert-butylphenol(SRC), using an experimental log Kow of 4.92(3) and a recommended regression-derived equation(4). According to a recommended classification scheme(5), these BCF values indicate that bioconcentration in aquatic organisms is an important fate process(SRC).

The Henry's Law constant for 2,6-di-tert-butylphenol is estimated as 3.15X10-6 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This value indicates that 2,6-di-tert-butylphenol will volatilize from water surfaces(2,SRC). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec) is estimated as approximately 17 hours(2,SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind volocity of 0.5 m/sec) is estimated as approximately 130 days(2,SRC). Following 5 days incubation with sludge, 7.7% of the initial 2,6-di-tert-butylphenol had volatilized(3). 2,6-Di-tert-butylphenol's Henry's Law constant(1,SRC) indicates that volatilization from moist soil may occur slowly(SRC).

2,6-DI-TERT-BUTYLPHENOL WAS EXAMINED FOR ITS ABILITY TO INDUCE IN VIVO CHANGES IN MOUSE HEPATIC MONO-OXYGENASE & DETOXICATION ENZYME ACTIVITIES, & TO ACT AS MONO-OXYGENASE INHIBITOR WHEN ADDED IN VITRO. IT PRODUCED A 2-FOLD INDUCTION IN CYTOCHROME P450 LEVELS, & CAUSED MICROSOMES TO SHOW SUBSTANTIAL INCR IN ANILINE HYDROXYLASE & PEROXIDASE ACTIVITIES. THESE MICROSOMES SHOWED SUBSTANTIAL REDUCTION IN DNA BINDING OF BENZO(A)PYRENE (BAP) METABOLITES RELATIVE TO METABOLISM. GLUTATHIONE S-TRANSFERASE & EPOXIDE HYDRATASE WERE READILY INDUCED. IN VITRO ABILITY TO INHIBIT BAP METABOLISM & DNA-BINDING ABILITY WAS APPROX EQUAL TO BUTYLATED HYDROXANISOLE (BHA). ABILITY IN VITRO TO DISCHARGE ACTIVATED OXYGEN COMPLEX OF CYTOCHROME P450 WAS APPROX EQUAL TO 2-T-BUTYLPHENOL WHICH WAS GREATER THAN BHA. RESULTS ARE CONSISTENT WITH THEORY THAT INHIBITION OF NEOPLASIA IS RELATED TO INDUCIBILITY OF DETOXICATION ENZYMES, THOUGH ALTERATIONS IN CYTOCHROME P450 COULD PLAY SIGNIFICANT ROLE IN SOME CASES.

LD50 OF 2,6-DI-TERT-BUTYLPHENOL WAS 2995 MG/KG FOR MICE FOLLOWING ORAL ADMIN. IT MARKEDLY INCR ACTIVITIES OF CHOLINESTERASE IN BLOOD OF RATS AS WELL AS MICE. MICE TREATED WITH 1/3 THE LD50 DOSE SHOWED 24.4% INCR IN BLOOD CHOLINESTERASE ACTIVITIES AFTER 1 HR. AT 1/5 THE LD50 DOSE IT INCR THE METABOLISM OF TOLUENE BY LIVER MITOCHONDRIA OF MICE & LIVER CYTOCHROME P450 WAS ALSO INCREASED, INDICATING AN ENZYME-INDUCING EFFECT.

PROSTAGLANDIN E FORMATION BY RABBIT KIDNEY SLICES WAS INHIBITED BY 2,6-DI-TERT-BUTYLPHENOL, SUGGESTING A REQUIREMENT FOR LIPID PEROXIDASE IN ACTIVITY OF PROSTAGLANDIN CYCLOOXYGENASE.

Section 8(a) of TSCA requires manufacturers of this chemical substance to report preliminary assessment information concerned with production, use, and exposure to EPA as cited in the preamble in 51 FR 41329.

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. 2,6-Di-tert-butylphenol is included on this list.