フタル酸ジ-n-オクチル

Phthalate

Semi-Volatile Organic Compound (SVOC)

log Kow = 8.10

5.22

0.98 at 77 °F (USCG, 1999) - Less dense than water; will float

Specific gravity: 0.978 at 20 °C

0.98

.978 @ 20°C

Clear, oily liquid

Liquid at room temperature

less than 1 mg/mL at 66 °F (NTP, 1992)

In water, 0.022 mg/L at 25 °C

219 °F (NTP, 1992)

420 °F (215 °C) (Open cup)

219 °F

428 °F at 760 mmHg (NTP, 1992)

BP: 220 °C at 2 mm Hg

428 °F

-13 °F (NTP, 1992)

25 °C

-13 °F

25 °C

This chemical does not meet GHS hazard criteria for 57.1% (36 of 63) of all reports.

Warning

H361 (41.3%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

P203, P280, P318, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 63 reports by companies from 7 notifications to the ECHA C&L Inventory.

Not Classified

Chemical: 1,2-Benzenedicarboxylic acid, 1,2-dioctyl ester

Hazard Traits - Developmental Toxicity; Endocrine Toxicity; Immunotoxicity; Reproductive Toxicity; Respiratory Toxicity

Regulation (EC) No 178/2002 (amended)

1,2-Benzenedicarboxylic acid, 1,2-dioctyl ester is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of 1,2-Benzenedicarboxylic acid, 1,2-dioctyl ester are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Restricted substance: Di-n-octyl phthalate (DNOP)

1,2-Benzenedicarboxylic acid, dioctyl ester: Does not have an individual approval but may be used under an appropriate group standard

Di-n-octylphthalate is a colorless, odorless, oily liquid that doesn't evaporate easily. It is a man-made substance used to keep plastics soft or more flexible. This type of plastic can be used for medical tubing and blood storage bags, wire and cables, carpetback coating, floor tile, and adhesives. It is also used in cosmetics and pesticides.

There is confusion in the naming of the dioctyl phthalate (DOP) esters: Di-n-octyl phthalate, Di-sec-octyl phthalate, and Diisooctyl phthalate. [CHEMINFO] A mucous membrane irritant; Like dioctyl phthalate, it may cause CNS depression and mild liver toxicity after ingestion of large amounts; [HSDB] Causes some liver injury in high-dose feeding studies of rats, but no evidence of significant reproductive effects; [ATSDR ToxProfiles] An irritant; [MSDSonline] See PHTHALATE ESTERS.

NTP/CERHR; Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Octyl Phthalate (DnHP), NIH Publication No. 03-4488 (May 2003). DnOP is one of 7 phthalate chemicals evaluated by the NTP CERHR Phthalates Expert Panel. These phthalates were selected for evaluation because of high production volume, extent of human exposures, use in children's products, and/or published evidence of reproductive or developmental toxicity. NTP-CERHR monographs are transmitted to federal and state agencies, interested parties, and the public and are available in electronic PDF format on the CERHR web site and in printed text or CD-ROM from the CERHR.[Available from, as of March 17, 2015: http://ntp.niehs.nih.gov/ntp/ohat/phthalates/dnop/dnop_monograph_final.pdf]

HHS/ATSDR; Toxicological Profile for Di-n-Octylphthalate PB/98/101033/AS (September 1997). The ATSDR toxicological profile succinctly characterizes the toxicologic and adverse health effects information for the hazardous substance described here. Each peer-reviewed profile identifies and reviews the key literature that describes a hazardous substance's toxicologic properties. Other pertinent literature is also presented, but is described in less detail than the key studies.[Available from, as of March 17, 2015: http://www.atsdr.cdc.gov/toxprofiles/index.asp]

Nat'l Research Council Canada; Effects of Phthalate Esters in the Canadian Environ (1976) NRCC No.17583

USEPA; Ambient Water Quality Criteria Doc for: Phthalate Esters (1980) EPA 440/5-80-067

For more Special Reports (Complete) data for DI-N-OCTYL PHTHALATE (8 total), please visit the HSDB record page.

U107; As stipulated in 40 CFR 261.33, when 1,2-benzenedicarboxylic acid, dioctyl ester, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

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. 1,2-Benzenedicarboxylic acid, dioctyl ester is included on this list. Effective date 10/04/82; Sunset date 10/04/92.

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.

Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Water or foam may cause frothing.

Wear self contained breathing apparatus for fire fighting if necessary.

Environmental precautions: Do not let product enter drains.

/ACCIDENTAL RELEASE MEASURES/ Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapours, mist or gas. Ensure adequate ventilation.

Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U107, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

The following wastewater treatment technologies have been investigated for di-n-octyl phthalate: Biological treatment, solvent extraction.

A good candidate for liquid injection incineration at a temperature range of 650 to 1,600 °C and a residence time of 0.1 to 2 seconds. A good candidate for fluidized bed incineration at a temperature range of 450 to 980 °C and residence times of seconds for liquids and gases, and longer for solids. A good candidate for rotary kiln incineration at a temperature range of 820 to 1,600 °C and residence times of seconds for liquids and gases, and hours for solids.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contaminated packaging: Dispose of as unused product.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid inhalation of vapour or mist. Normal measures for preventive fire protection.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of work day.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

5.0 [mg/m3]

1600 [mg/m3]

9300 [mg/m3]

Di-n-octyl phthalate was detected in human adipose tissue collected throughout the US during the 1982 National Human Adipose Tissue Survey(1). Di-n-octyl phthalate was found in the serum of 1 of 41 young (17-47 months) Puerto Rican girls with premature breast development at a concentration of 438 ug/L(2). The degradation product di-n-octyl phthalate, mono-n-octyl phthalate was detected in the serum of 12 of 501 female and 15 of 502 male seniors from Uppsala, Sweden at a maximum of 5.55 and 10.7 mg/mL, respectively(3).

Male rats, initiated with a single intraperitoneal dose of the carcinogen diethylnitrosamine and then partially hepatectomized, did not experience any liver weight gain after 10 weeks of dietary exposure to 500 mg/kg/day of di-n-octylphthalate ... When exposure was extended to 26 weeks, small increases in absolute liver weight that were not significant (p < 0.05) were observed at di-n-octylphthalate doses of 250 mg/kg/day (2% increase) and 500 mg/kg/day (8% increase). However, when combined with diminished body weight gains, relative liver weight gains were increased by 5-16% when compared with control values.

Male Sprague-Dawley rats were subjected to two-thirds partial hepatectomy which was followed 18 hr later by an intraperitoneal injection of diethylnitrosamine (DEN) at a dose of 30 mg/kg. Di(2-ethylhexyl)phthalate (DEHP) was added to the diet at 0.5%. Mono(2-ethylhexyl)phthalate (MEHP) and 2-ethylhexanol (2-EH) were added at equimolar levels with di(2-ethylhexyl)phthalate. Di-n-octyl-phthalate (DOP) was added to 1%. The development of gamma-glutamyl-transpeptidase positive (GGT+) foci was strongly induced by di-n-octyl-phthalate in the livers of rats that had received a subcarcinogenic dose of diethylnitrosamine. None of the other compounds showed any tumor promoting activity. The development of gamma-glutamyl-transpeptidase positive preneoplastic foci in livers of rats was neither enhanced nor suppressed when rats were fed a dose equimolar to 0.5% di(2-ethylhexyl)phthalate. An elevated carnitine acetyltransferase (CAT) level was found following treatment with mono(2-ethylhexyl)phthalate or di(2-ethylhexyl)phthalate. Mono(2-ethylhexyl)phthalate significantly decreased liver gamma-glutamyl-transpeptiase activity. In addition mono(2-ethylhexyl) phthalate lowered the mean number of foci/square centimeter below that of the 2-ethylhexanol treated group. /It was found/ that di-n-octyl-phthalate can act as a tumor promoter, and this activity seems to be unrelated to liver peroxisome proliferation (as measure by carnitine acetyltransferase).

An in vivo assay using Salmonella typhimurium TA 98 showed that di-n-octylphthalate enhanced the mutagenicity of two tryptophan pyrolysis products, which is suggestive of increased mutagenic activity in high-temperature cooking if di-n-octylphthalate is present ... .

Phthalate esters are endocrine disruptors. Animal studies have shown that they disrupt reproductive development and can cause a number of malformations in affected young, such as reduced anogenital distance (AGD), cryptorchidism, hypospadias, and reduced fertility. The combination of effects associated with phthalates is called 'phthalate syndrome’. (A2883)

LC50; Species: Micropterus salmoides (Large mouth bass); Concentration: 32,900 ug/L for 7-8 days /Conditions of bioassay not specified/ /From table/

LC50; Species: Ictalurus punctatus (Channel catfish); Concentration: 690 ug/L for 7 days /Conditions of bioassay not specified/ /From table/

LC50; Species: Phasianus colchicus (ring-necked pheasant) age 10 days; oral >5000 ppm for 5 days

LC50; Species: Eisenia fetida (earthworm) adult, weight 300-500 mg; dermal 3140 (2270-4330) ug/sq cm for 48 hr

LC50; Species: Americamysis bahia (Opossum shrimp); Conditions: saltwater, flow through, 24.8 °C, pH 7.9-8.1, salinity 20-22 ppt, dissolved oxygen 6.6-7.0 mg/L; Concentration: 125000 ug/L for 28 days /98% purity/

TERRESTRIAL FATE: Based on a classification scheme(1), log Koc values of 4.38-6.3(2-3), indicate that di-n-octyl phthalate is expected to be immobile in soil(SRC). Volatilization of di-n-octyl phthalate from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.6X10-6 atm-cu m/mole(SRC), based upon its vapor pressure, 1.0X10-7 mm Hg(3), and water solubility, 0.022 mg/L(4). However, adsorption to soil is expected to attenuate volatilization(SRC). Di-n-octyl phthalate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). Di-n-octyl phthalate, present at 100 mg/L, reached 67% of its theoretical BOD in 4 weeks using an activated sludge inoculum at 30 mg/L in the Japanese MITI test(5). In a model terrestrial-aquatic ecosystem, di-n-octyl phthalate was rapidly degraded by organisms in the system, having a half-life of 5 days(6). Respirometric measurements of soil amended with di-n-octyl phthalate shows that when acclimated, there is some microbial utilization, although this is marginal at 4 and 10 °C(7).

AQUATIC FATE: Based on a classification scheme(1), log Koc values of 4.38-6.3(2-3), indicate that di-n-octyl phthalate is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(4) based upon an estimated Henry's Law constant of 2.6X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 1.0X10-7 mm Hg(3), and water solubility, 0.022 mg/L(5). Using this Henry's Law constant and an estimation method(4), volatilization half-lives for a model river and model lake are 31 and 230 days, respectively(SRC). Hydrolysis half-lives of 7.7 years and 280 days at pH values of 7 and 8, respectively, were estimated(6). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column(SRC). Volatilization of di-n-octyl phthalate from model waste stabilization ponds was not observed(7). According to a classification scheme(8), BCFs of 1.16-9400 in mosquito fish(9), suggest the potential for bioconcentration in aquatic organisms is low to very high(SRC), this range may indicate the ability of aquatic organisms to readily metabolize this class of compounds(3). Di-n-octyl phthalate was biodegraded 85% after 10 days incubation in Rhine river water at 20 °C; at 4 °C, biodegradation was negligible(10).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), di-n-octyl phthalate, which has a vapor pressure of 1.0X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase di-n-octyl phthalate 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 19 hours(SRC), calculated from its rate constant of 2.1X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase di-n-octyl phthalate may be removed from the air by wet and dry deposition(SRC). Di-n-octyl phthalate has a strong UV absorption band at 274.5 nm which extends beyond 290 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Di-n-octyl phthalate was detected in one sample of 80 proof vodka at a concentration of 131 ppb and one sample of 100 proof vodka at 57 ppb(1). It was also detected in two samples of flavored 80 proof vodka at 75 and 123 ppb(1). Di-n-octyl phthalate was not detected (detection limit 20 ng/g dry weight) in food samples collected over four days from a university restaurant, Paris, France; food samples tested were fish terrine, mixed salad, corn salad, radishes, lasagne, roast beef, chicken leg, mixed steak, basmati rice, fried vegetables, fried potatoes, plain yogurt, Gruyere cheese, Camembert cheese, granny apple, black grapes, stewed apples and fruit salad(2).

IDENTIFICATION AND USE: Di-n-octylphthalate (DNOP) is a clear, oily liquid. It is used as a plasticizer; DNOP can represent 5-60% of the total weight of the plastics and resins. It is found in cosmetics and colorants. DNOP also serves as a carrier for catalysts or initiators and as a substitute for electrical capacitor fluid. HUMAN EXPOSURE AND TOXICITY: In 173 subjects with suspected dermatoses to plastic or glue allergens, two subjects (1.2% of the group) experienced irritation after patch testing with 2.0% DNOP. None of the patients had allergic reactions. There is a case study of a worker with continuous exposure to DNOP during the manufacture of imitation leather, who developed an asthmatic reaction to the substance. Women with endometriosis showed significantly higher concentrations of DNOP in their blood in a study of 49 infertile women with endometriosis (study group), and 38 age-matched women without endometriosis (control group I) but with infertility related to tubal defects, fibroids, polycystic ovaries, idiopathic infertility and pelvic inflammatory diseases diagnosed by laparoscopy and a further group of 21 age-matched women (control group II). An increase in toxic polyneuritis has been reported in workers exposed primarily to dibutyl phthalates. Lesser levels of exposure to dioctyl, diisooctyl, benzylbutyl phthalates, and tricresyl phosphate were also noted. ANIMAL STUDIES: DNOP was reported to be a slight skin irritant when applied to the depilated skin of guinea pigs. However, DNOP was not a skin sensitizer in guinea pigs. Ocular administration of DNOP resulted in slight conjunctival irritation and no corneal damage. The results of several acute- and intermediate-duration oral studies in rodents indicate that the potential of DNOP to cause adverse reproductive and developmental effects is low. Unlike other phthalate esters such as DEHP, DNOP does not appear to affect testicular function or morphology. Observed hepatic effects in intermediate duration studies consisted of a statistically significant increase in hepatic ethoxyresorufin-0-deethylase activity and histological changes in hepatic architecture. Thyroid toxicity was also noted at this concentration. Rats treated with 100, 300, or 600 mg/kg DNOP by ip injection for up to 90 day were evaluated for immunological responses. The high dose resulted in early loss of distinction between the cortex and medulla of the thyroid, reduced numbers of follicles in the lymph nodes, and loss of morphology in the adrenal glands. However, there was no effect on immune response. Results of studies in Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 (with and without S-9 metabolic activation systems) indicated that DNOP is not mutagenic. ECOTOXICITY STUDIES: The toxicity of DNOP was assessed by measuring the effect of exposure to these compounds on the fecundity of Daphnia magna and on the hatching and survival of the early life stages of the fathead minnow Pimephales promelas. For Daphnia magna, exposure to 1.0 mg/L DNOP caused a significant reduction in reproduction. Exposure to DNOP did not affect survival of either early embryos or larvae of the fathead minnow at doses up to 10 mg/L (the highest dose tested). Hatching of the embryos was significantly decreased at 10 mg/L, but not at 3.2 mg/L DNOP.

Phthalate esters are endocrine disruptors. They decrease foetal testis testosterone production and reduce the expression of steroidogenic genes by decreasing mRNA expression. Some phthalates have also been shown to reduce the expression of insulin-like peptide 3 (insl3), an important hormone secreted by the Leydig cell necessary for development of the gubernacular ligament. Animal studies have shown that these effects disrupt reproductive development and can cause a number of malformations in affected young. (A2883)

U107; As stipulated in 40 CFR 261.33, when 1,2-benzenedicarboxylic acid, dioctyl ester, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

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. 1,2-Benzenedicarboxylic acid, dioctyl ester is included on this list. Effective date 10/04/82; Sunset date 10/04/92.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 5000 lb or 2270 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

... Di-n-octyl phthalate (DnOP) is metabolized to its hydrolytic monoester, mono-n-octyl phthalate (MnOP), and other oxidative products. The urinary levels of one of these oxidative metabolites, mono-(3-carboxypropyl) phthalate (MCPP), were about 560-fold higher than MnOP in Sprague-Dawley rats dosed with DnOP by gavage. Furthermore, MCPP was also found in the urine of rats dosed with di-isooctyl phthalate (DiOP), di-isononyl phthalate (DiNP), di-isodecyl phthalate (DiDP), di-(2-ethylhexyl) phthalate, and di-n-butyl phthalate (DBP), although at concentrations considerably lower than in rats given similar concentrations of DnOP. The comparatively much higher urinary concentrations of MCPP than of the hydrolytic monoesters of the high-molecular-weight phthalates DiOP, DiNP, and DiDP in the exposed rats suggest that these monoesters may be poor biomarkers of exposure to their precursor phthalates and may explain the relatively low frequency of detection of these monoester metabolites in human populations. MCPP and MnOP were also measured in 267 human urine samples. The frequent detection and higher urinary concentrations of MCPP than MnOP suggest that exposure to DnOP might be higher than previously thought based on the measurements of MnOP alone. However, because MCPP is also a minor metabolite of DBP and other phthalates in rats, and the metabolism of phthalates in rodents and humans may differ, additional data on the absorption, distribution, metabolism, and elimination of MCPP are needed to completely understand the extent of human exposure to DnOP from the urinary concentrations of MCPP.

The metabolism of di-n-octyl phthalate (DnOP) results in the hydrolysis of one ester linkage to produce mono-n-octyl phthalate (MnOP), which subsequently metabolizes to form oxidative metabolites. ... The toxicokinetics of DnOP in adult female Sprague-Dawley rats /was investigated/ by monitoring the excretion of DnOP metabolites in urine after oral administration of DnOP (300 mg/kg). By using authentic standards, the presence of urinary phthalic acid (PA), MnOP, and the major DnOP metabolite, mono-(3-carboxypropyl) phthalate (MCPP) was clearly established. Furthermore, ... five additional urinary DnOP oxidative metabolites /were identified/ based on their chromatographic behavior and mass spectrometric fragmentation pattern. These DnOP oxidative metabolites, are postulated to be mono-carboxymethyl phthalate (MCMP), mono-(5-carboxy-n-pentyl) phthalate (MCPeP), mono-(7-carboxy-n-heptyl) phthalate (MCHpP), and isomers of mono-hydroxy-n-octyl phthalate (MHOP) (e.g., mono-(7-hydroxy-n-octyl) phthalate) and of mono-oxo-n-octyl phthalate (MOOP) (e.g., mono-(7-oxo-n-octyl) phthalate). The urinary excretion of DnOP metabolites followed a biphasic excretion pattern. The metabolite levels decreased significantly after the first day of DnOP administration although MCPP, MCHpP, MHOP, and MOOP were detectable after 4 days. We also studied the in vitro metabolism of DnOP and MnOP by rat liver microsomes. DnOP produced MnOP, MHOP, and PA in vitro whereas, MnOP produced MHOP and PA in vitro at detectable levels.

Hepatic prepn from rat, baboon & ferret hydrolyzed the phthalate diester of di-n-octyl to corresponding monoester derivatives. /in addition,/ intestinal prepn from the 3 animal species & from man also catalyzed the monohydrolysis of phthalate diesters.

n-Octanol is a metabolite of DnOP. Octanol is oxidized to the fatty acid and metabolized by the fatty acid oxidation pathway.

For more Metabolism/Metabolites (Complete) data for DI-N-OCTYL PHTHALATE (6 total), please visit the HSDB record page.

Phthalate esters are first hydrolyzed to their monoester derivative. Once formed, the monoester derivative can be further hydrolyzed in vivo to phthalic acid or conjugated to glucuronide, both of which can then be excreted. The terminal or next-to-last carbon atom in the monoester can also be oxidized to an alcohol, which can be excreted as is or first oxidized to an aldehyde, ketone, or carboxylic acid. The monoester and oxidative metabolites are excreted in the urine and faeces. (A2884)

Di-n-octyl phthalate (DnOP) is found as a component of mixed C6-C10 linear-chain phthalates used as plasticizers in various polyvinyl chloride applications, including flooring and carpet tiles. Following exposure and absorption, DnOP is metabolized to its hydrolytic monoester, mono-n-octyl phthalate (MnOP), and other oxidative products. The urinary levels of one of these oxidative metabolites, mono-(3-carboxypropyl) phthalate (MCPP), were about 560-fold higher than MnOP in Sprague-Dawley rats dosed with DnOP by gavage. Furthermore, MCPP was also found in the urine of rats dosed with di-isooctyl phthalate (DiOP), di-isononyl phthalate (DiNP), di-isodecyl phthalate (DiDP), di-(2-ethylhexyl) phthalate, and di-n-butyl phthalate (DBP), although at concentrations considerably lower than in rats given similar concentrations of DnOP. The comparatively much higher urinary concentrations of MCPP than of the hydrolytic monoesters of the high-molecular-weight phthalates DiOP, DiNP, and DiDP in the exposed rats suggest that these monoesters may be poor biomarkers of exposure to their precursor phthalates and may explain the relatively low frequency of detection of these monoester metabolites in human populations. MCPP and MnOP were also measured in 267 human urine samples. The frequent detection and higher urinary concentrations of MCPP than MnOP suggest that exposure to DnOP might be higher than previously thought based on the measurements of MnOP alone. However, because MCPP is also a minor metabolite of DBP and other phthalates in rats, and the metabolism of phthalates in rodents and humans may differ, additional data on the absorption, distribution, metabolism, and elimination of MCPP are needed to completely understand the extent of human exposure to DnOP from the urinary concentrations of MCPP.

Sprague-Dawley rats were administered ... 5,000 parts per million (ppm) di-n-octyl phthalate (DNOP) in their diet for 13 weeks. Similar control groups received either 4% corn oil or 5000 ppm of di(2-ethylhexyl) phthalate (DEHP). ... Trace quantities (3-5 ppm) of DEHP and DNOP were detected in the liver, and 15-31 ppm were found in adipose tissue ... .

... Male CD rats /were dosed/ by gavage with 0.2 mL DnOP and collected urine for analysis of metabolites. They recovered 31% of the dose in the urine by 48 hours. The monoester and some free phthalic acid were detected, but no parent DnOP was observed. Blood levels of the monoester, mono-octylphthalate, were measured in rats following administration of 2,000 mg/kg of DnOP by gavage. The biological halflife in the blood was 3.3 hours with an area under the curve (AUC) of 1,066 ug/hr/mL. Peak blood levels were observed at 3 hours following administration.

Following an oral dose of 2,000 mg/kg DnOP to rats, mono-octylphthalate was found in blood and testes in 3-6 hours.

Used as a plasticizer and dye carrier for film, wire, cables, and adhesives; [HSDB] Used as a plasticizer in carpet backing, packaging films, medical tubing, blood storage bags, floor tile, wire, cables, and adhesives; Also used in cosmetics and pesticides; [ATSDR ToxProfiles]

Working with Glues and Adhesives [Category: Other]

There are no known commercial uses for pure DnOP. However, DnOP constitutes approximately 20% of C6-10 phthalate substance. ... C6-10 phthalate substance is used in PVC utilized in the manufacture of flooring and carpet tile, canvas tarps, swimming pool liners, notebook covers, traffic cones, toys, vinyl gloves, garden hoses, weather stripping, flea collars, and shoes. DnOP-containing phthalate substances are also used in PVC intended for food applications such as seam cements, bottle cap liners, and conveyor belts.

Di-n-octylphthalate is principally used as a plasticizer in the production of plastics and PVC resins. When used as a plasticizer, di-n-octylphthalate can represent 5-60% of the total weight of the plastics and resins. It increases flexibility and enhances or alters the properties of the material. It is also used for cellulose ester and polystyrene resins, as a dye carrier in plastic production (primarily PVC), and as a chemical intermediate in the manufacture of adhesives, plastisols, and nitrocellulose lacquer coatings. ... Di-n-octylphthalate also serves as a carrier for catalysts or initiators and as a substitute for electrical capacitor fluid.

Monomeric plasticizer for vinyl and cellulosic resins.

PLASTICIZER FOR POLYSTYRENE RESINS

2023: <75,000 lb

(1978) GREATER THAN 2.27X10+6 G

(1982) GREATER THAN 2.27X10+6 G

(1985) 2.75X10+8 lb /DIOCTYL PHTHALATE/

(1986) 2.90X10+8 LB /DIOCTYL PHTHALATE/

For more U.S. Production (Complete) data for DI-N-OCTYL PHTHALATE (10 total), please visit the HSDB record page.

Di-n-octylphthalate is produced commercially as a component of mixed phthalate esters, including straight- chain C6, C8, and Cl0 phthalates. Di-n-octylphthalate is produced at atmospheric pressure or in a vacuum by heating an excess of n-octanol with phthalic anhydride in the presence of an esterification catalyst such as sulfuric acid or p-toluenesulfonic acid. The process may be either continuous or discontinuous. Di-n-octylphthalate can also be produced by the reaction of n-octylbromide with phthalic anhydride.

n-Dioctyl phthalate is formed via the esterification of n-octanol with phthalic anhydride in the presence of a catalyst (sulfuric acid or p-toluenesulfonic acid) or noncatalytically at high temperature.

Adhesive Manufacturing

1,2-Benzenedicarboxylic acid, 1,2-dioctyl ester: ACTIVE

Di-n-octyl phthalate is sometimes mistakenly reported as its isomer, bis(2-ethyl-hexyl) phthalate, in the literature.