Isopropylphenyl diphenyl phosphate

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, use absorbent paper to pick up all liquid spill material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with alcohol followed by washing with a strong soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

TERRESTRIAL FATE: Based on a measured log Kow of 5.31(1), an estimated Koc value of 18400 can be calculated using a regression-derived equation(2) suggesting isopropylphenyl diphenyl phosphate is immobile in soil(3). Based on a low estimated vapor pressure and Henry's Law constant, isopropylphenyl diphenyl phosphate is not expected to evaporate from dry or moist soil surfaces(SRC). Biodegradation tests with activated sludge and river water(1) suggests that biodegradation of isopropylphenyl diphenyl phosphate in soil may be important(SRC).

AQUATIC FATE: Primary biodegradation tests with activated sludge and river water(1), suggest that isopropylphenyl diphenyl phosphate primary biodegradation in water will be important (50% primary degradation in 3 days). Isopropylphenyl diphenyl phosphate biodegrades slowly in aerobic and anaerobic freshwater sediment (1-8% 14-CO2 evolution in 4 weeks)(2), indicating that isopropylphenyl diphenyl phosphate biodegradation in sediment may not be an important fate process. The Henry's Law constant for isopropylphenyl diphenyl phosphate can be estimated to be 7.744X10-8 atm-cu m/mole using a structure estimation method(3,SRC). This value of Henry's Law constant indicates slow volatilization of isopropylphenyl diphenyl phosphate from water(4). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep flowing 1 m/sec with a wind velocity of 3 m/sec) can be estimated to be about 907 days(4,SRC). Based on a measured log Kow of 5.31(5), an estimated Koc of 18400(4) and BCF of 6390(4) can be calculated, which indicate that isopropylphenyl diphenyl phosphate adsorption to suspended solids and sediment and bioconcentration in aquatic organisms should be important fate processes(3,SRC).

ATMOSPHERIC FATE: Based on an estimated vapor pressure of 3.515X10-7 mm Hg at 25 °C(SRC), isopropylphenyl diphenyl phosphate is expected to exist in both the vapor and particulate phases in the ambient atmosphere(1). Vapor-phase isopropylphenyl diphenyl phosphate is degraded rapidly in the ambient atmosphere by reaction with photochemically formed hydroxyl radicals. The half-life for this reaction in typical air can be estimated to be about 0.85 day(2,SRC). Particulate phase isopropylphenyl diphenyl phosphate may be removed from the atmosphere through dry deposition(SRC).

Isopropylphenyl diphenyl phosphate was detected at a concn less than 1.0 ppm in vegetation samples taken from sources nearby Bethlehem Steel Company, Bethlehem, PA(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 5.0 ppm in vegetation samples taken from sources nearby U.S. Steel Company, Fairless Hills, PA(1). Isopropylphenyl diphenyl phosphate was detected at a concn less than 1.0 ppm in vegetation samples taken from sources nearby FMC Corporation, Nitro, WV(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 2.5 ppm in vegetation samples taken from sources nearby Hooker Chemical Company, Burlington, NJ(1). Isopropylphenyl diphenyl phosphate was qualitatively detected in vegetation samples taken from sources nearby Stauffer Chemical Company, Delaware City, DE(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 1.0 ppm in vegetation samples taken from sources nearby Bethlehem Steel Company, Sparrows Point, MD(1).

Based upon a measured log Kow value of 5.31(1), the Koc for isopropylphenyl diphenyl phosphate can be estimated to be about 18400 from a regression-derived equation(2,SRC). According to a suggested classification scheme(3), this estimated Koc suggests that isopropylphenyl diphenyl phosphate is immobile in soil(SRC).

SOURCE DOMINATED: Isopropylphenyl diphenyl phosphate was detected in a concn range of 0.001 to 0.005 ng/cu m on high volume air filter pads and at a concn less than or equal to 0.001 ng/cu m in activated charcoal canisters taken from sources nearby the grounds of Bethlehem Steel Company, Bethlehem, PA(1). Isopropylphenyl diphenyl phosphate was detected in a concn range of 0.005 to 0.04 ng/cu m on high volume air filter pads and in a concn range of 0.001 to 0.004 ng/cu m in activated charcoal canisters taken from sources nearby the grounds of U.S. Steel Company, Fairless Hills, PA(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 0.05 ng/cu m on high volume air filter pads and in a concn range of 0.002 to 0.004 ng/cu m in activated charcoal canisters taken from sources nearby the grounds of FMC Corporation, Nitro, W. Va(1).

SOURCE DOMINATED: Isopropylphenyl diphenyl phosphate was detected at a concn less than 0.01 ng/cu m in activated charcoal canisters taken from sources nearby the grounds of Stauffer Chemical Company, Gallipolis Ferry, W. Va(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 0.1 ng/cu m on high volume air filter pads and qualitatively identified in activated charcoal canisters taken from sources nearby the grounds of E.F. Houghton, Philadelphia, PA(1).

Organophosphorus cmpd can produce dermal irritation but most are weak sensitizers. /Organophosphate cmpd/

A women at 34 to 35 weeks' gestation presented in acute respiratory distress with cyanosis and tachypnea and bilateral rhonchi and crepitation. Her heart rate was 78 beats per minute and her blood pressure 120/80 mm Hg, with a fetal heart rate of 140 beats per minute. The mother was salivating markedly and her pupils were reduced to "pinpoint size." An uncorrected metabolic acidosis was diagnosed. Serum and erythrocyte acetylcholinesterase determinations were near zero. Cholinesterase inhibitor poisoning was felt to be the likely cause of disorders. Administration of atropine 2.4 mg intravenous bolus with infusion of 0.02 mg/kg/hr lead to unacceptable fetal tachycardia. The woman had shown increased cooperativeness and secretion control until the atropine had to be stopped. A cesarean section was performed for delivery of a hypotonic infant with a 1-minute Apgar score of 3. The baby was mechanically ventilated for 2 days and required atropine therapy at 0.1 mg/kg/hr for 8 days. The mother required 8 days of mechanical ventilation and 11 days of atropine therapy. In this case, the infant appeared relatively less poisoned than the mother by a presumed organophosphate exposure. /Organophosphate poisoning/

Primary biodegradation data from semicontinuous activated sludge studies at a chemical addition rate of 3 ppm per 24 hour cycle, indicated 49% biodegradation of isopropylphenyl diphenyl phosphate(1). Ultimate biodegradation of isopropylphenyl diphenyl phosphate in activated sewage sludge under static aerobic conditions was 9.4, 48.8, and 61.8% of added C-14 labelled compound evolved as 14-CO2 in 7, 28, and 48 days, respectively(1). A river-die away study indicated 55, 50, 60, 75, 75, 80, 77.5% biodegradation after 2, 3, 6, 10, 15, 21, and 28 days, respectively(1).

Three biodegradation studies spiked with either 0.0156 ppm or 0.585 ppm of C-14 diphenyl and C-14 isopropyl labelled isopropylphenyl diphenyl phosphate in freshwater sediment under aerobic conditions were undertaken(1). After 4 weeks aerobic incubation at 22 °C, 7.1% of the 0.0156 ppm concn C-14 diphenyl labelled isopropylphenyl diphenyl phosphate sample, 8.4% of the 0.585 ppm concn C-14 diphenyl labelled isopropylphenyl diphenyl phosphate sample, and 2.0% of the 0.0156 ppm concn C-14 isopropyl labelled isopropylphenyl diphenyl phosphate sample degraded to 14-CO2(1). Two biodegradation studies spiked with 0.0156 ppm concns of C-14 diphenyl and C-14 isopropyl labelled isopropylphenyl diphenyl phosphate in freshwater sediment under anaerobic conditions were also undertaken(1). After 4 weeks of anaerobic incubation at 22 °C, 7.3% of the 0.0156 ppm concn C-14 diphenyl labelled isopropylphenyl diphenyl phosphate sample and 1.1% of the 0.0156 ppm concn C-14 diphenyl labelled isopropylphenyl diphenyl phosphate sample degraded to 14-CO2(1).

Isopropylphenyl diphenyl phosphate was detected in a concn range of 0.3 to 5.0 ppm in sediment samples and at a concn less than 0.1 ppm in soil samples taken from sources nearby Bethlehem Steel Company, Bethlehem, PA(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 8.0 ppm in sediment samples and at a concn of 0.1 ppm in soil samples taken from sources nearby FMC Corporation, Nitro, WV(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 0.1 ppm in sediment samples taken from sources nearby Firestone Tire and Rubber Company, Pottstown, PA(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 2.0 ppm in sediment samples and at a concn less than 1.0 ppm in soil samples taken from sources nearby Hooker Chemical Company, Burlington, NJ(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 400 ppm in soil samples taken from E.F. Houghton, Philadelphia, PA(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 0.1 ppm in soil samples taken from Firestone Tire and Rubber Company, Perryville, MD(1). Isopropylphenyl diphenyl phosphate was detected at a concn of 1.0 ppm in soil samples taken from Bethlehem Steel Company, Sparrows Point, MD(1).

Based on a measured log Kow of 5.31(1), an estimated BCF of 6390(2) can be calculated, which indicates that bioconcentration of isopropylphenyl diphenyl phosphate in aquatic organisms should be important fate process(3,SRC).

Fathead minnows (Pimephales promelas) accumulated isopropyl phenyl diphenyl phosphate to levels 495 times that of the surrounding medium (exposure concn= 2.5 ug/l) in 28 days.

The Henry's Law constant for isopropylphenyl diphenyl phosphate can be estimated to be 7.744X10-8 atm-cu m/mole using a structure estimation method(1,SRC). This value of Henry's Law constant indicates slow volatilization of isopropylphenyl diphenyl phosphate from water(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep flowing 1 m/sec with a wind velocity of 3 m/sec) can be estimated to be about 907 days(2,SRC). Based on this Henry's Law constant and a measured water solubility of 2.2 ppm at 25 °C(3), an estimated vapor pressure of 3.515X10-7 mm Hg at 25 °C can be calculated for isopropylphenyl diphenyl phosphate(SRC). From this value of the vapor pressure, isopropylphenyl diphenyl phosphate can be expected to evaporate slowly from dry soil surfaces(SRC).

Triphenyl phosphate /was found/ as an apparent product of isopropyl phenyl diphenyl phosphate degradation in sediment /water microcosms, suggesting that microbial attack on alkyl substituents of tryaryl phosphates may procede hydrolysis.

The signs of poisoning due to organophosphorus cmpd are those due to accumulation of acetylcholine & hence overstimulation of parasympathetic nervous system. It is usual to divide them under 3 headings: muscarinic, nicotinic & central. Muscarinic signs ... consist of hypersalivation, lacrimation, sweating & nasal discharge. Miosis, dyspnea, vomiting, diarrhea & frequency of urination ... Nicotinic effects consist of fasciculation of muscles, weakness & paralysis. Central nervous system effects include nervousness, apprehension, ataxia, convulsions & coma. Death is due to resp failure, or sometimes cardiac arrest. There is little difference between signs produced by different organophosphorus compounds, but route of absorption may influence one system more than another. /Organophosphorus cmpd/

The potential of isopropyl triphenyl phosphate to produce delayed neurotoxicity in hens was examined using several techniques. Isopropyl triphenyl phosphate contained O,O,O-triphenyl phosphate (24%), O-O-isopropylphenyl O,O-diphenyl phosphate (25%), O,O-diisopropyl-phenyl O-phenyl phosphate (20%), O-O, p-diisopropylphenyl O,O-diphenyl phosphate (18%) and O-p-isopropylphenyl O,O-diphenyl phosphate (6%). Hens treated twice, 3 wk apart, with doses of isopropyl triphenyl phosphate as high as 11.7 g/kg showed no clinical signs of delayed neurotoxicity and only mild signs of general toxicity. Furthermore, none showed even subtle neurohistologic changes suggestive of delayed neurotoxicity. Isopropyl triphenyl phosphate produced dose-dependent inhibition of hen plasma cholinesterase and brain neurotoxic esterase. The study was continued because neurotoxic esterase inhibition has been shown to be a reliable predictor of organophosphates that produce delayed neurotoxicity. Isopropyl triphenyl phosphate was administered prior to tri-o-tolyl phosphate challenge in order to determine if it altered development of tri-o-tolyl phosphate delayed neurotoxicity. Isopropyl triphenyl phosphate neither enhanced nor reduced the onset or severity of neurotoxicity produced by tri-o-tolyl phosphate. The time-course for brain and spinal cord neurotoxic esterase inhibition by isopropyl triphenyl phosphate and tri-o-tolyl phosphate were compared and found to be different. The maximum brain neurotoxic esterase inhibition produced by isopropyl triphenyl phosphate (dose up to 11.7 g/kg) was never complete (always less than 90%), and spinal cord neurotoxic esterase inhibition was significantly less than that produced in the brain. In contrast, brain and spinal cord inhibition produced by 500 mg/kg tri-o-tolyl phosphate were equal and greater than 90%. This testing regimen showed that isopropyl triphenyl phosphate produced an effect on neurotoxic esterase at the biochemical level without producing clinical or neurohistologic abnormalities in treated hens. Furthermore, this biochemical effect was qualitatively different than that produced by the delayed neurotoxicant tri-o-tolyl phosphate. /Isopropyl triphenyl phosphate/

The rate constant for the vapor-phase reaction of isopropylphenyl diphenyl phosphate with photochemically produced hydroxyl radicals has been estimated to be 1.888X10-11 cu cm/molecule-sec at 25 °C(1) which corresponds to an atmospheric half-life of about 0.85 day at an atmospheric concn of 5X10+5 hydroxyl radicals per cu cm(1).

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. Phosphoric acid, (1-methylethyl)phenyl diphenyl ester is included on this list.