フタル酸ジイソデシル

0.967 at 68 °F (USCG, 1999) - Less dense than water; will float

0.966 g/cu cm at 20 °C

Bulk density: 8 lb/gal

Relative density (water = 1): 0.96

Insoluble (NTP, 1992)

In water, 0.28 mg/L at 25 °C

Soluble in organic solvents

Insoluble in glycerol, glycols and some amines

More soluble in crude sweat than in water and increasing solubility with pH rise

Solubility in water: none

450 °F (NTP, 1992)

275 °C (527 °F) - closed cup

450 °F (232 °C) (Open cup)

229 °C c.c.

This chemical does not meet GHS hazard criteria for 53.8% (157 of 292) of all reports.

Warning

H400 (21.2%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

P273, P391, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 292 reports by companies from 6 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Not Classified

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

Regulation (EC) No 178/2002 (amended)

1,2-Benzenedicarboxylic acid, 1,2-diisodecyl ester is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of 1,2-Benzenedicarboxylic acid, 1,2-diisodecyl 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)

PMN - indicates a commenced PMN (Pre-Manufacture Notices) substance.

Restricted substance: Di-“isodecyl” phthalate (DIDP)

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

This chemical is combustible. (NTP, 1992)

Combustible.

An irritant; [Hawley] Oral LD50 (rat) = 64,000 mg/kg; [ChemIDplus] A skin and eye irritant; May cause liver injury; [ICSC] Like dioctyl phthalate, it may cause CNS depression and mild liver toxicity after ingestion of large amounts; [HSDB] A mild skin and eye irritant; Di-isodecyl phthalate is a complex mixture containing mainly C10-branched isomers, with a mean formula, C28-H46-O4 and a mean molecular weight of 446.68. There are two di-isodecyl phthalate products (DIDP), with two different CAS Nos. (26761-40-0 and 68515-49-1), which contain a number of components. The main chemical structures or chain structures present in DIDP, include trimethylheptyl, dimethyloctyl, methylnonyl and n-decyl. [CHEMINFO] May cause irritation; [MSDSonline] See PHTHALATE ESTERS. See 1,2-Benzenedicarboxylic acid, di-C9-11-branched alkyl esters, C10-rich.

Nat'l Research Council Canada; Phthalate Esters In The Aquatic Environment (1980) NRCC No. 17583

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

Health & Welfare Canada; Phthalic Acid Esters (1980) Report # 80-EDH-62

European Chemicals Bureau; IUCLID Dataset, Di-isodecyl phthate (26762-40-0), 56 pp. (2000 CD-ROM edition).[Available from, as of April 18, 2008: http://esis.jrc.ec.europa.eu/]

DHHS/NTP; CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Diisodecyl Phthalate (DIDP), 247 pp. (2003) NIH Publication No. 03-4485.[Available from, as of April 17, 2008: http://cerhr.niehs.nih.gov/evals/index.html]

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, diisodecyl ester is included on this list. Effective date 10/04/82; Sunset date 10/04/92.

A testing consent order is in effect for diisodecyl phthalate for chemical fate testing. FR citation: 1/9/89.

DIISODECYL PHTHALATE is an ester. Esters react with acids to liberate heat along with alcohols and acids. Strong oxidizing acids may cause a vigorous reaction that is sufficiently exothermic to ignite the reaction products. Heat is also generated by the interaction of esters with caustic solutions. Flammable hydrogen is generated by mixing esters with alkali metals and hydrides. Can generate electrostatic charges. [Handling Chemicals Safely 1980. p. 250].

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Diisodecyl phthalate is produced, as an intermediate or a final product, by process units covered under this subpart.

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

Use water spray, powder, alcohol-resistant foam, carbon dioxide.

Fresh air, rest.

Remove contaminated clothes. Rinse skin with plenty of water or shower.

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

Rinse mouth. Rest.

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.

Extinguish with dry chemical, foam or carbon dioxide. Water may be ineffective on fire.

Alcohol foam. Water or foam may cause frothing.

Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. Wear self contained breathing apparatus for fire fighting if necessary.

ACCIDENTAL RELEASE MEASURES Personal precautions, protective equipment and emergency procedures Use personal protective equipment. Avoid breathing vapours, mist or gas. Ensure adequate ventilation. For personal protection see section Environmental precautions Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up Keep in suitable, closed containers for disposal.

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.

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

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

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.

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

The diisodecyl phthalate metabolite, monocarboxyl isononyl phthalate, was detected in 89.9% of 2548 urine samples at 0.6-672.6 ug/L; samples were collected by the United States National Health and Nutrition Examination Survey (2005-2006)(1). Diisodecyl phthalate metabolites, mono carboxyl isononyl phthalate, mono hydroxyl isodecyl phthalate and mono oxo isodecyl phthalate were detected in urine of 129 US adults with no documented exposure to diisodecyl phthalate at a rate of 98, 96 and 85%, respectively(2). Mono isodecyl phthalate was not detected in any of the samples. Samples were collected in 2005 from a diverse demographic population(2). A survey of chemical substances in the environment of Ibaraki Prefecture, Japan showed that diisodecyl phthalate along with other phthalate esters of higher alcohols were found in humans(3). Workers exposed to phthalate acid esters mainly di(ethylhexyl), diisodecyl, and butylbenzyl phthalate in a polyvinyl chloride processing industry excreted slightly but significantly higher levels of the ester metabolites in their urine(4). The identities of the excreted chemicals were not specified(4). The metabolite of diisodecyl phthalate, monocarboxyl nonyl phthalate, was detected at <0.2-162.8 ug/L in the urine of 623 Norwegian children (294 girls, 329 boys) ages 8.8-12.5 year old; samples were collected Sep 2001 to Dec 2004(5).

Phenols and plasticizers are widely used in the plastic industry, in food packaging and to impart softness and flexibility to normally rigid plastic medical devices and children's toys. The effects on the aryl hydrocarbon receptor (AhR) and the androgen receptor (AR) were assessed using luciferase reporter gene assays of the following compounds: bisphenol A (BPA), 4-n-nonylphenol (nNP), 4-tert-octylphenol (tOP), bis(2-ethylhexyl) phthalate (DEHP), di-isononyl phthalate (DINP), diisodecyl phthalate (DIDP), di-n-octyl phthalate (DNOP), dibutyl phthalate (DBP), benzyl butyl phthalate (BBP), 4-chloro-3-methylphenol (CMP), 2-phenylphenol (2-PP), 2,4-dichlorophenol (DCP), resorcinol and bis(2-ethylhexyl) adipate (DEHA). Furthermore, a mixture of selected compounds was tested at the no-observed-effect concentration (NOEC), the low-observed-effect concentration (LOEC) and the half-maximum-effect/inhibitory concentration (EC50/IC50) of the single chemicals. Both receptors were affected by BPA, nNP, BBP, CMP, DCP and resorcinol whereas DEHP, DIDP and DBP affected only the AhR and tOP and 2-PP antagonised the AR activity. The mixture was composed of 6 compounds, of which one compound weakly induced the AhR but all compounds antagonized the AR activation. Using the concentration addition principle additive effects were observed at the NOEC, LOEC and EC50/IC50 for both receptors. Our in vitro data suggest that the effect of a mixture depends on the concentration, character, potency and composition of the single mixture compounds and that also the combined effects of the compounds should be taken into consideration for risk assessment of human health.

The ability of phthalic acid, phthalic acid anhydride, and various phthalate esters to enhance the mutagenicity of many amino acid pyrolysates was observed with the Ames test (Salmonella typhimurium TA 98), but not the SOS Chromotest. Phthalate enhancement of the mutagenicity of 4-nitroquinoline-1-oxide, 2-nitrofluorene, and benzo[a]pyrene was not observed with either test. The mutagenicity-enhancing ability may be related to the induction of enzymes such as P450IIB, that metabolize amino acid pyrolysates. By quantitative structure activity relationship (QSAR) analysis, a good correlation was observed between the mutagenicity-enhancing activity of phthalates and their octanol-water partition coefficients.

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)

EC50; Species: Pseudokirchneriella subcapitata (Green algae); Conditions: freshwater, static, 22-24 °C, pH 7.6-7.9, hardness 25-50 mg/L CaCO3, alkalinity 25-50 mg/L CaCO3; Concentration: 800 ug/L for 96 hr; Effect: decreased population abundance /> or = 95% purity/

EC50; Species: Americamysis bahia (Opossum shrimp) age < or =24 hr; Conditions: freshwater, static, 20 °C, pH 7.6-7.9, hardness 25-50 mg/L CaCO3, alkalinity 25-50 mg/L CaCO3; Concentration: 80 ug/L for 96 hr; Effect: mortality /> or = 95% purity/

EC50; Species: Daphnia magna (Water flea) age < or =24 hr; Conditions: freshwater, static, 20 °C, pH 7.6-7.9, hardness 25-50 mg/L CaCO3, alkalinity 25-50 mg/L CaCO3; Concentration: 20 ug/L for 48 hr; Effect: intoxication, immobilization /> or = 95% purity/

LC50; Species: Cyprinodon variegatus (Sheepshead minnow) juvenile, length 6-17 mm; Conditions: freshwater, static, 22 °C, pH 7.6-7.9, hardness 25-50 mg/L CaCO3, alkalinity 25-50 mg/L CaCO3; Concentration: 470 ug/L for 96 hr /> or = 95% purity/

For more Ecotoxicity Values (Complete) data for DIISODECYL PHTHALATE (8 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), estimated log Koc values of 5.46-6.04(2-3), indicate that diisodecyl phthalate is expected to be immobile in soil(SRC). Volatilization of diisodecyl phthalate from moist soil surfaces is expected(SRC) given an estimated Henry's Law constant of 1.1X10-6 atm-cu m/mole(SRC), based upon its vapor pressure, 5.28X10-7 mm Hg(4), and water solubility, 0.28 mg/L(5). However, adsorption to soil is expected to attenuate volatilization(SRC). Diisodecyl phthalate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). Biodegradation of >99% and 56% of theoretical CO2 evolution after 28 days using an acclimated soil and sewage inoculum and the shake flask CO2 evolution test(6) suggests that biodegradation may be an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), an average Koc value of 2.86X10+5 determined in sediment(2), indicates that diisodecyl phthalate is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 1.1X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 5.28X10-7 mm Hg(4), and water solubility, 0.28 mg/L(5). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 70 days and 1.4 years, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond is 2000 years if adsorption is considered(6). Diisodecyl phthalate is not expected to undergo hydrolysis based on estimated hydrolysis half-lives of 3.4 years and 125 days at pHs 7 and 8, respectively(7). According to a classification scheme(8), BCFs of <14.4 in carp(9) suggest bioconcentration in aquatic organisms is low(SRC). Diisodecyl phthalate at a concentration of 100 ppm, was degraded 14% to 30% after three days cultivation in river water inoculum(10), suggesting that biodegradation may be an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), diisodecyl phthalate, which has a vapor pressure of 5.28X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase diisodecyl 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 15 hours(SRC), calculated from its rate constant of 2.6X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase diisodecyl phthalate may be removed from the air by wet and dry deposition(SRC). Diisodecyl phthalate contains chromophores that absorb at wavelengths >290 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Diisodecyl phthalate was not detected (detection limit 0.01 mg/kg) in 74 samples of composite fatty foods (meat, meat products, offal, poultry, eggs, fish, fats and oils, milk and milk products) from the UK(1). Diisodecyl phthalate was not detected in 59 samples of 15 different brands of infant formula analyzed at a typical detection limit of 0.01 mg/kg wet weight. In a follow-up survey, diisodecyl phthalate was not detected in 39 infant formula samples from the UK(1).

The substance can be absorbed into the body by inhalation of its vapour.

Oral (L1903) ; inhalation (L1903) ; dermal (L1903)

ENVIRONMENTAL: Diisodecyl phthalate was not detected (detection limit 0.01 mg/kg) in milk and milk products from the UK(1). Diisodecyl phthalate was not detected in 59 samples of 15 different brands of infant formula analyzed at a typical detection limit of 0.01 mg/kg wet weight. In a follow-up survey, diisodecyl phthalate was not detected in 39 infant formula samples from the UK(1).

IDENTIFICATION AND USE: Diisodecyl phthalate (DIDP) is a clear liquid with mild odor. It is used as a general purpose plasticizer for polyvinyl chloride; preferred plasticizer for PVC in wire and cable applications. DIDP in the PVC end-use includes: calendering (film, sheet and coated products, flooring, roofing, wall covering), extrusion (hose and profile, wire and cable, clear, medical, film), injection moulding (footwear and miscellaneous), plastisol spread coating, other plastisol applications (car undercoating and sealants, slush/rotational moulding). Non-PVC applications are in other vinyl resins than PVC /acrylic plastic resins, which are basically polymethyl methacrylate/, cellulose ester plastics and other polymer containing products, such as pressure sensitive adhesives and printing inks. Otherwise DIDP is applied in non-polymer applications, such as anti-corrosion and anti-fouling paints. HUMAN EXPOSURE AND TOXICITY: There was no evidence of clinical sensitization or dermal irritation in human volunteers participating in a 21-day repeated insult patch test. In an epidemiology study, current asthma in children was associated with the highest quartiles of metabolites of two high molecular weight phthalates, diisononyl phthalate and diisodecyl phthalate. All plastisol workers had post shift values of DIDP metabolites that were approx. 20-times higher, and pre-shift values that were approx. 5-10 times higher than those of the general background exposure. ANIMAL STUDIES: In acute inhalation studies, rats, mice and guinea pigs were exposed to a nominal concentration of 0.13 mg/L for 6 hr. There was no mortality, no evidence of systemic effects, and no apparent respiratory irritation. In one 90-day subchronic toxicity study in rats, DIDP was given in the feed at levels of 0.05, 0.3, and 1% (approximately 30, 200, and 650 mg/kg/day). The predominant effect was an increase in liver weight in animals treated with the highest dose. There were no effects noted in the mid-dose animals (approximately 200 mg/kg/day). Other studies ranging from 3 wk to 90 day have confirmed the liver as the target organ. In one of these studies, significant effects on liver weight and liver enzyme induction were noted in animals treated with approximately 350 mg/kg/day. In other studies, the lowest effect levels were higher. Treatment for three weeks at levels up to 2.5% DIDP in the diet (approximately 2600 mg/kg/day) did not result in significantly decreased testicular weight or histological changes in male rats. At concentrations up to 1X10-3 M, DIDP was inactive in a recombinant yeast screen for estrogenic activity. In developmental studies DIDP showed fetal effects of borderline significance at 1000 mg/kg/day. DIDP shows no evidence of mutagenic potential. It was inactive in Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 at concentrations up to 10 mg/plate (with and without metabolic activation). DIDP was non-carcinogenic in rats due to its limited potential for peroxisomal proliferating activity. It did produce hepatocellular adenomas in the male rasH2 mice receiving 1% DIDP, compared with the findings in the liver of control rasH2 mice or wild-type mice. ECOTOXICITY STUDIES: DIDP had no effect on reproduction of Daphnia. Environmental studies demonstrate pattern of observed toxicity with the lower-molecular-weight phthalate esters and not the higher-molecular-weight phthalate esters in acute toxicity studies for several aquatic species. In laboratory experiments performed to determine the antioxidant responses to nine phthalates in the liver of the goldfish Carassius auratus the toxicity order was as follows: dibutyl phthalate (DBP)>diethyl phthalate (DEP)>diisodecyl phthalate (DIDP)>diphenyl phthalate (DPP)>butyl benzyl phthalate (BBP)>diallyl phthalate (DAP)>dicyclohexyl phthalate (DCHP)>dimethyl phthalate (DMP)>di(2-ethylhexyl) phthalate (DEHP).

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)

The average daily intake of diisodecyl phthalate was estimated as 30-40 ng/kg body weight/day in studies of foods and beverages purchased from Norwegian grocery stores(1). In infants, toddlers and children 55-82, 40 and 16% of the average daily intake of diisodecyl phthalate is due to mouthing plastic, ingestion of dust and inhalation of indoor air, respectively(2). In teenagers and adults 55-70, >10, 9-13, 5-7 and 5-7% is due to ingestion of food, ingestion of dust, inhalation of indoor air, gloves and spray paint fumes, respectively(2). An analysis of indirect exposure models and urinary biomonitoring data of various population segments indicate an average daily intake of <1 ug/kg/day of diisodecyl phthalate(3).

/AQUATIC SPECIES/ Daphnia magna were exposed to diisodecyl phthalate (DIDP) at nominal concentrations up to 100 ug/L over 21 days. DIDP had no effect on reproduction and the parent Daphnia showed bioconcentration factor of 116 DIDP as determined by (14)C analysis.

/AQUATIC SPECIES/ Mussels (Mytilus edulis) were exposed to diisodecyl phthalate (DIDP) over 28 days. The bioconcentration factor (BCF), as measured by (14)C analysis, reached estimated plateau levels corresponding to mean bioconcentration factor values. The mussels were then held in clean seawater for 14 days ... . During the entire 42 days of the experiment, general observations on the health of the animals showed no adverse effects.

/AQUATIC SPECIES/ Chronic toxicity studies were performed with commercial phthalate esters and Daphnia magna (14 phthalates) and rainbow trout (Oncorhynchus mykiss) (six phthalates). For the lower-molecular-weight phthalate esters - dimethyl phthalate (DMP), diethyl phthalate (DEP), di-n-butyl phthalate (DBP), and butylbenzyl phthalate (BBP) - the results of the studies indicated a general trend in which toxicity for both species increased as water solubility decreased. The geometric mean maximum acceptable toxicant concentration (GM-MATC) for D. magna ranged from 0.63 to 34.7 mg/L. For the higher-molecular-weight phthalate esters - dihexyl phthalate (DHP), butyl 2-ethylhexyl phthalate (BOP), di-(n-hexyl, n-octyl, n-decyl) phthalate (610P), di-(2-ethylhexyl) phthalate (DEHP), diisooctyl phthalate (DIOP), diisononyl phthalate (DINP), di-(heptyl, nonyl, undecyl) phthalate (711P), diisodecyl phthalate (DIDP), diundecyl phthalate (DUP), and ditridecyl phthalate (DTDP) - the GM-MATC values ranged from 0.042 to 0.15 mg/L. Survival was equally sensitive and sometimes more sensitive than reproduction. The observed toxicity to daphnids with most of the higher-molecular-weight phthalate esters appeared to be due to surface entrapment or a mode of toxicity that is not due to exposure to dissolved aqueous-phase chemical. Early life-stage toxicity studies with rainbow trout indicated that survival (DMP) and growth (DBP) were affected at 24 and 0.19 mg/L, respectively. This pattern of observed toxicity with the lower-molecular-weight phthalate esters and not the higher-molecular-weight phthalate esters is consistent with previously reported acute toxicity studies for several aquatic species.

/AQUATIC SPECIES/ A two-generation feeding study has been carried out though with Oryzias latipes ... . DIDP was added to dry flake food at 20 mg/kg. DIDP, control (no treatment and acetone control) were divided into five replicate tanks (N=50) per treatment. In the F0 generation 14 days old fish were fed at 5% body weight per day. The F0 adults were terminated at day 123. There were no statistically significant changes in mortality or fecundity between the treatment groups. There was no reduced egg production. Evaluation of F1 and F2 embryos showed normal development except for a transient decrease in red blood cell pigmentation. This effect was observed in both the DIDP treatment and the acetone control group. The only histopathological change observed in the F0 adults was a minor alteration in hepatocellular staining around the central vein. The male to female ratios (3:1) in all groups were similar. Phenotypic gender classification of male and female fish were histopathologically confirmed to be 100% correct. Ale somatic gonadal index and liver somatic index were not significantly different in any group.

For more Ecotoxicity Excerpts (Complete) data for DIISODECYL PHTHALATE (8 total), please visit the HSDB record page.

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, diisodecyl ester is included on this list. Effective date 10/04/82; Sunset date 10/04/92.

A testing consent order is in effect for diisodecyl phthalate for chemical fate testing. FR citation: 1/9/89.

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Diisodecyl phthalate is produced, as an intermediate or a final product, by process units covered under this subpart.

Diisodecyl phthalate (DiDP) is an isomeric mixture of phthalates with predominantly 10-carbon branched-dialkyl chains, widely used as a plasticizer for polyvinyl chloride. The extent of human exposure to DiDP is unknown in part because adequate biomarkers of exposure to DiDP are not available. We identified several major metabolites of DiDP in urine of adult female Sprague-Dawley rats after a single oral administration of DiDP (300 mg/kg). These metabolites can potentially be used as biomarkers of exposure to DiDP. The metabolites extracted from urine were chromatographically resolved and identified by their chromatographic behavior and full scan negative ion electrospray ionization mass spectrum. The identity of metabolites with similar molecular weights was further examined in accurate mass mode. For some metabolites, unequivocal identification was done using authentic standards. Among these were the hydrolytic monoester of DiDP, monoisodecyl phthalate (MiDP), detected as a minor metabolite, and one omega oxidation product of MiDP, mono(carboxy-isononyl) phthalate (MCiNP), which was the most abundant urinary metabolite. We also tentatively identified other secondary metabolites of MiDP, mono(hydroxy-isodecyl) phthalate, mono(oxo-isodecyl) phthalate, mono(carboxy-isoheptyl) phthalate, mono(carboxy-isohexyl) phthalate, mono(carboxy-isopentyl) phthalate, mono(carboxy-isobutyl) phthalate, and mono(carboxy-ethyl) phthalate. Oxidative metabolites of diisoundecyl phthalate (DiUdP) and diisononyl phthalate(DiNP) were also detected suggesting the presence of DiUdP and DiNP in the DiDP formulation. The urinary concentrations of all these metabolites gradually decreased in the 4 days following the administration of DiDP. MCiNP and other DiDP secondary metabolites are more abundant in urine than MiDP, suggesting that these oxidative products are better biomarkers for DiDP exposure assessment than MiDP. Additional research on the toxicokinetics of these metabolites is needed to understand the extent of human exposure to DiDP from the urinary concentrations of MCiNP and other DiDP secondary metabolites.

... Radiolabeled DIDP (carboxyl-(14)C) was administered /to Sprague Dawley rats (200 g body weight)/ in corn oil by gavage at doses of 0.1-11.2 and 1,000 mg/kg. Feces were collected over 24-hour periods. Urine was collected over 12-hour periods. ... In urine, phthalic acid and the oxidized monoester derivative were detected but not monoisodecyl phthalate (MIDP) or DIDP at any of the doses. The percentage of radioactivity associated with the monoester derivative group increased with increasing dose from 52% after 0.1 mg/kg to 72% after 1,000 mg/kg. Concurrently, the proportion of radioactivity associated with phthalic acid was observed to decrease from 38 to 18% after 0.1 and 1,000 mg/kg doses, respectively. In feces, the monoester oxidative derivative, MIDP and DIDP were detected. Because of potential bacterial degradation of DIDP or its metabolites in feces, quantification of the data is difficult. It was readily apparent, however, that with increasing dose the percentage of parent compound recovered in feces increased: 30%, 55% and 60% after 0.1, 11 and 1,000 mg/kg, respectively. The percentage of oxidative derivatives of the monoester and of MIDP were respectively 25 and 30%, 14 and 26%, 13 and 13% after 0.1, 11 and 1,000 mg/kg, respectively. When bile samples were taken from 0-24 hours following dosing or when liver and kidneys samples were taken 72 hours following dosing, DIDP was not detected in extracts. The data based on end products suggest a metabolic scheme comparable to the one reported for DEHP: de-esterification to monoester form and an alcohol moiety by apparent non-specific pancreatic lipase and intestinal mucosa esterases prior to absorption; the high content of MIDP in feces is consistent with this proposed mechanism. Further metabolism of the monoester by omega or omega-1 oxidation probably occurred in the liver. With increasing dose, the percentage of fecal radioactivity associated with the parent compound was increased by a factor of two comparing 0.1 to 1,000 mg/kg doses. Therefore it is probable that esterases capacity has been partially saturated. The parent compound is recoverable from feces even at the lowest dose, which is not the case for DEHP, for which an absorption threshold of 200 mg/kg in a single intake was reported. Below this value, the parent DEHP was not detected. In contrast, even at extremely low doses, DIDP may be less susceptible to the hydrolysis step prerequisite to absorption. Phthalic acid and apparent oxidative products of MIDP were identified in urine. In bile, it is indicated that only monoester metabolites were detected accounting in part for the content in feces. With increasing dose the metabolite composition in bile was not altered, suggesting that metabolic capacity by that route was not compensated. In urine the percentage of radioactivity associated with phthalic acid decreased with dose while an increase was observed in the oxidative derivatives of the monoester. The percentage of phthalic acid ranged from 38% at 0.1 mg/kg to 18% at 1,000 mg/kg, far exceeding the value of 3% phthalic acid associated with DEHP exposures. The markedly higher production of phthalic acid suggests that DIDP derivatives may be more susceptible to de-esterification within the body perhaps due to destabilisation of the ester bond resulting from the highly branched nature of the ester groups. However, the decrease in phthalic acid content with increasing DIDP dose may suggest partial saturation of metabolite capacity. ...

High molecular-weight phthalates, such as diisononyl phthalate (DINP), and diisodecyl phthalate (DIDP), are widely used as plasticizers in the manufacturing of polymers and consumer products. Human biological monitoring studies have employed the metabolites of DINP and DIDP as biomarkers to assess human exposure. In this review, we summarize and analyze publicly available scientific data on chemistry, metabolism, and excretion kinetics, of DINP and DIDP, to identify specific and sensitive metabolites. Human biological monitoring data on DINP and DIDP are scrutinised to assess the suitability of these metabolites as biomarkers of exposure. Results from studies carried out in animals and humans indicate that phthalates are metabolised rapidly and do not bioaccmulate. During Phase-I metabolism, ester hydrolysis of DINP and DIDP leads to the formation of hydrolytic monoesters. These primary metabolites undergo further oxidation reactions to produce secondary metabolites. Hence, the levels of secondary metabolites of DINP and DIDP in urine are found to be always higher than the primary metabolites. Results from human biological monitoring studies have shown that the secondary metabolites of DINP and DIDP in urine were detected in almost all tested samples, while the primary metabolites were detected in only about 10% of the samples. This indicates that the secondary metabolites are very sensitive biomarkers of DINP/DIDP exposure while primary metabolites are not. The NHANES data indicate that the median concentrations of MCIOP and MCINP (secondary metabolites of DINP and DIDP, resp.) at a population level are about 5.1 ug/L and 2.7 ug/L, respectively. Moreover, the available biological monitoring data suggest that infants/children are exposed to higher levels of phthalates than adults.

Di-isodecyl phthalate (DiDP), primarily used as a plasticiser, is a mixture of isomers with predominantly ten-carbon branched side chains. Assessment of DiDP exposure has not been conducted before because adequate biomarkers were lacking. In 129 adult volunteers with no known exposure to DiDP, the urinary concentrations of three oxidative metabolites of DiDP: monocarboxyisononyl phthalate (MCiNP), monooxoisodecyl phthalate (MOiDP) and monohydroxyisodecyl phthalate (MHiDP), previously identified in DiDP-dosed rats, were estimated by solid-phase extraction coupled to high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) using the respective oxidative metabolites of di(2-ethylhexyl)phthalate since authentic standards of the DiDP oxidative metabolites were unavailable. Interestingly, the hydrolytic monoester of DiDP, monoisodecyl phthalate (MiDP), was not detected in any of the samples, while MCiNP, MHiDP and MOiDP were detected in 98%, 96% and 85%, respectively, of the samples tested. MCiNP was excreted predominantly in its free form, whereas MOiDP was excreted as its glucuronide. MCiNP, MHiDP and MOiDP eluted as clusters of multiple peaks from the HPLC column probably due to the presence of numerous structurally similar isomers present in commercial DiDP formulations. The urinary concentrations of these oxidative metabolites correlated significantly (p < 0.0001) with each other, thus confirming a common precursor. The urinary concentrations of these DiDP oxidative metabolites also correlated significantly (p < 0.0001) with oxidative metabolites of di-isononyl phthalate (DiNP) suggesting the potential presence of DiNP isomers in commercial DiDP or simultaneous use of DiDP and DiNP in consumer products. The concentrations presented are semiquantitative estimates and should be interpreted cautiously. Nevertheless, the higher frequency of detection and higher urinary concentrations of MCiNP, MHiDP and MOiDP than of MiDP suggest that these oxidative metabolites are better biomarkers for DiDP exposure assessment than MiDP. These data also suggest that unless oxidative metabolites are measured, the prevalence of exposure to DiDP will probably be underestimated.

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)

This study examined the extent of dermal absorption of a series of phthalate diesters in the rat. Those tested were dimethyl, diethyl, dibutyl, diisobutyl, dihexyl, di(2-ethylhexyl), diisodecyl, and benzyl butyl phthalate. Hair from a skin area (1.3 cm in diameter) on the back of male F344 rats was clipped, the 14(C)phthalate diester was applied in a dose of 157 mumol/kg, and the area of application was covered with a perforated cap. The rat was restrained and housed for 7 days in a metabolic cage that allowed separate collection of urine and feces. Urine and feces were collected every 24 hr, and the amount of (14)C excreted was taken as an index of the percutaneous absorption. At 24 hr, diethyl phthalate showed the greatest excretion (26%). As the length of the alkyl side chain increased, the amount of (14)C excreted in the first 24 hr decreased signficantly. The cumulative percentage dose excreted in 7 days was greatest for diethyl, dibutyl, and diisobutyl phthalate, about 50-60% of the applied (14)C; and intermediate (20-40%) for dimethyl, benzyl butyl, and dihexyl phthalate. Urine was the major route of excretion of all phthalate diesters except for diisodecyl phthalate. This compound was poorly absorbed and showed almost no urinary excretion. After 7 days, the percentage dose for each phthalate that remained in the body was minimal showed no specific tissue distribution. Most of the unexcreted dose remained in the area of application. These data show that the structure of the phthalate diester determines the degree of dermal absorption. Absorption maximized with diethyl phthalate and then decreased significantly as the alkyl side chain length increased.

In rats, 80% of dermally applied (14)C-DIDP (ring-label) was recovered at the site of application 7 days after the application. Only 2% of the applied dose was recovered in other tissues or excreta with a total recovery of only 82% reported. In another study in rats in which total recoveries were better (94% or greater), similar results were obtained.

(14)C-DIDP was applied to the skin and the dose site was occluded. At 1, 3, and 7 days, 96, 92, and 93% of the doses, respectively, were still at the application site. Only trace amounts of radioactivity were found in other tissues and excreta. The total absorbed dose was approximately 4% of the administered dose.

Six male Sprague Dawley rats were exposed for 6 hours by inhalation (head only) to 91 mg/cu m of (14)C-DIDP. Excreta were collected over a 72-hour period and 3 animals were analyzed for radioactivity immediately after the exposure and at 72 hours after the exposure. Assuming a minute volume of 200 mL for the rats, the estimated total amount of DIDP inhaled would be approximately 14.4 umoles. The initial body burden was 8.3 umoles, indicating that approximately 58% of what was inhaled was retained in the body. Twelve percent of the initial body burden was in the gut and 85% was in the lung. 73% of the dose to the lung was cleared during the first 72 hours, indicating that absorption of DIDP or its metabolites from the lung into the rest of the body was about 73%.

For more Absorption, Distribution and Excretion (Complete) data for DIISODECYL PHTHALATE (9 total), please visit the HSDB record page.

Used as plasticizer for polyvinyl chloride in calendered film, coated fabrics, building wire jackets, wire and cable extrusion, and other applications; [HSDB]

Plastic Composites Manufacturing [Category: Industry]

Congress has also banned (on an interim basis) three additional types of phthalates (DINP, DIDP, DnOP) in any amount greater than 0.1 percent (computed for each phthalate individually) in (1) a children's toy that can be placed in a child's mouth, and (2) child care articles. Please note that the interim ban on DINP, DIDP, and DnOP only applies to children's toys that can be placed in a child's mouth. A toy that can be placed in a child's mouth is defined as any part of a toy that actually can be brought to the child's mouth and kept there so that it can be sucked or chewed on. If a toy or a part of the toy is smaller than 5 centimeters, it can be placed in the mouth. /Diisononyl phthalate (DINP), diisodecyl phthalate (DIDP), or di-n-octyl phthalate (DnOP)/

PLASTICIZER FOR POLYVINYL CHLORIDE FOR CALENDERED FILM, SHEET, COATED FABRICS, BUILDING WIRE JACKETS, & IN WIRE & CABLE EXTRUSION

Wire cable, and auto vinyl upholstery.

General purpose plasticizer for polyvinyl chloride; preferred plasticizer for PVC in wire and cable applications.

(1972) NEGLIGIBLE

(1975) 8.17X10+7 GRAMS (PRINCPL CUSTMS DISTS)

2023: 250,000 - <400,000 lb

(1972) 6.96X10+10 GRAMS

(1975) 4.8X10+10 GRAMS

(1984) 6.62X10+10 g

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. [Table#2468]

For more U.S. Production (Complete) data for DIISODECYL PHTHALATE (7 total), please visit the HSDB record page.

DIDP is prepared from propylene and butenes through an oligomerisation process forming hydrocarbons with 8 to 15 carbon atoms. After distillation (in view of obtaining nonene), oxonation forms aldehydes with one more carbon atom ("isodecanal"). The latter are hydrogenated and distilled to form monohydric alcohols (mainly C10). These are reacted with phthalic anhydride (PA). The first reaction step, alcoholysis of PA to give the monoester, is rapid and goes to completion. By charging in excess alcohol and by removing the water which is formed, the equilibrium can be shifted almost completely towards the products side. The reaction rate is accelerated by using a catalyst and high temperature. ...

DIDP is manufactured by reaction of phthalic anhydride with isodecanol in the presence of an acid catalyst.

Grade: Technical.

Stabilized and unstabilized grades/available from badische, stabilizer unknown/

Commercial names: Jayflex DIDP; Palatinol Z; Vestinol DZ; Emkarate 1020.

Palatinol Z stab. (DIDP + 0.5-1% bisphenol A)

Cosmetics product ingredient: Di-isodecyl phthalate (DIDP)

Information on 7 consumer products that contain Diisodecyl phthalate in the following categories is provided:

Transportation Equipment Manufacturing

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

1,2-Benzenedicarboxylic acid, 4,4'-carbonylbis-, 1,1',2,2'-tetraisodecyl ester: INACTIVE

Commercially, diisodecyl phthalate is not a pure compound, but refers to a mixture of materials with an average side chain length of 10.

In the "oxo" Industry, the term "iso" is used for designating a mixture and does not refer to the IUPAC definition.