Diisodecyl Phthalate

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

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

H410 (13.7%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

H411 (24.3%): Toxic to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term 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.

Reported as not meeting GHS hazard criteria per 157 of 292 reports by companies.

There are 5 notifications provided by 135 of 292 reports by companies with hazard statement code(s).

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

Not Classified

Reported as not meeting GHS hazard criteria by 1 of 1 companies. For more detailed information, please visit ECHA C&L website.

H413: May cause long lasting harmful effects to aquatic life [Hazardous to the aquatic environment, long-term hazard]

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

H361: 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)

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

H410: Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

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.

SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment.

INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.

INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

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

Fire Extinguishing Agents: Dry chemical, foam, carbon dioxide (USCG, 1999)

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

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.

Collect leaking and spilled liquid in sealable plastic or metal containers as far as possible. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations.

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.

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.

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.

STORAGE PRECAUTIONS: You should store this chemical under refrigerated temperatures and away from oxidizers, mineral acids and bases. (NTP, 1992)

Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage.

carcinogen category: 3

(b) Prohibition on the sale of additional products containing certain phthalates. (1) Interim Prohibition. Beginning on the date that is 180 days after the date of enactment of this Act and until a final rule is promulgated under paragraph (3), it shall be unlawful for any person to manufacture for sale, offer for sale, distribute in commerce, or import into the United States any children's toy that can be placed in a child's mouth or child care article that contains concentrations of more than 0.1 percent of diisononyl phthalate (DINP), diisodecyl phthalate (DIDP), or di-n-octyl phthalate (DnOP).

No indication can be given about the rate at which a harmful concentration of this substance in the air is reached on evaporation at 20 °C.

The substance is irritating to the eyes and skin.

The substance may have effects on the liver.

Goggles or face shield; rubber gloves (USCG, 1999)

Skin protection: Handle with gloves.

Eye/face protection: Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Goggles or face shield; rubber gloves.

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multipurpose combination (US) or type ABEK (EN 14387) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Body Protection: Impervious clothing. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

NO open flames.

Use ventilation, local exhaust or breathing protection.

Protective gloves.

Wear safety goggles.

Do not eat, drink, or smoke during work.

Diisodecyl phthalate appears as colorless liquid. May float or sink in water. (USCG, 1999)

Large Crystals; Other Solid

Clear liquid; [Hawley] Oily viscous liquid; [CHEMINFO]

CLEAR VISCOUS LIQUID.

Clear liquid

Mild odor

482 to 495 °F at 4 mmHg (NTP, 1992)

BP: 253 °C at 4 mm Hg

at 0.5kPa: 250-257 °C

-58 °F (NTP, 1992)

450 °F (NTP, 1992)

275 °C (527 °F) - closed cup

450 °F (232 °C) (Open cup)

229 °C c.c.

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

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

15.4 (NTP, 1992) - Heavier than air; will sink (Relative to Air)

0.00000053 [mmHg]

5.28X10-7 mm Hg at 25 °C

Vapor pressure, Pa at 200 °C: 147

Stable under recommended storage conditions.

755 °F (USCG, 1999)

755 °F (402 °C)

When heated to decomposition it emits acrid smoke and irritating vapors.

108 cP at 20 °C

MAY ATTACK SOME FORMS OF PLASTICS

Index of refraction: 1.483 at 25 °C/D

227.85 Ų [M+H]+

325.43 Ų [2M+Na]+

226.42 Ų [M+Na]+

Will hydrolyze under acidic and basic conditions

Phthalate esters would be expected to have UV maxima in the 230 nm and 270 nm regions. /Phthalate esters/

Insoluble in water.

Esters, Sulfate Esters, Phosphate Esters, Thiophosphate Esters, and Borate Esters

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].

Strong oxidizing agents

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)

No indication of carcinogenicity to humans (not listed by IARC).

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)

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

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

Redness.

Dizziness. Nausea. Vomiting.

Phthalate esters are endocrine disruptors and can cause a number of developmental malformations termed 'phthalate syndrome'. (A2883)

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.

LC (rat) > 130 mg/m3/6h

LD50: >3160 mg/kg (Dermal, Rabbit) (T13)

LD50: 64 000 mg/kg (Oral, Rat) (T13)

LD50 Rabbit dermal >3160 mg/kg

LD50 Rabbit (male) dermal > 10 mL/kg (9,700 mg/kg)

LD50 Rat oral 64 g/kg /64,000 mg/kg/

LD50 Rat oral >6 g/kg />6,000 mg/kg/

For more Non-Human Toxicity Values (Complete) data for DIISODECYL PHTHALATE (6 total), please visit the HSDB record page.

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.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Esters and related compounds/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilation if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Esters and related compounds/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Esters and related compounds/

/HUMAN EXPOSURE STUDIES/ There was no evidence of clinical sensitization or dermal irritation in human volunteers participating in a 21-day repeated insult patch test. In 144 subjects with suspected dermatoses to plastic or glue allergens, two subjects (1.4% of the group) experienced irritation after patch testing with 5.0% DIDP. None of the patients had allergic reactions.

/HUMAN EXPOSURE STUDIES/ Primary irritation potential of 0.2 mL of undiluted DIDP was evaluated during a single 24-hour application (occluded patch) on 14 female subjects and 1 male subject. Examinations at 30 minutes and 24 hours after patch removal did not reveal any sign of irritation ... .

/HUMAN EXPOSURE STUDIES/ A repeated insult patch test (modified Draize procedure) ... has been performed on 128 volunteers, 104 completed the study. All exposures were by 24 + or - 1 hour contact under occluded patches with undiluted DIDP. Induction applications were made three times per week for three successive weeks. Following a 10 to 17-day rest period, a challenge application of the test article was made to a naive site located away from the original application site. Simultaneous application to a pre-exposed site (ie the original site used for induction application) was made concurrently with the challenge at a naive site. Reactions were scored 48 or 72 hours after each induction application (24 or 48 hours after patch removal) and 48 and 96 hours after challenge (24 and 72 hours after patch removal). In induction and challenge phases, no responses were observed to the test article throughout the pilot and main phase of the study. Under the conditions of the study, no evidence of clinical sensitisation or irritation was observed in any of the 104 subjects completing the pilot and the main phase of the study.

/SIGNS AND SYMPTOMS/ Exposure to phthalic acid esters, mainly di-(2-ethylhexyl), diisodecyl and butylbenzyl phthalates, workers in a polyvinyl chloride processing industry ranged from 0.02 to 2 mg/cu m in different job categories. The workers excreted slightly but significantly higher levels of phthalic acid ester metabolites in urine than controls. In 54 workers studied clinically, there were no indications of peripheral nerve or respiratory system effects. Some biochemical tests were abnormal.

For more Human Toxicity Excerpts (Complete) data for DIISODECYL PHTHALATE (7 total), please visit the HSDB record page.

/LABORATORY ANIMALS: Acute Exposure/ 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.

/LABORATORY ANIMALS: Acute Exposure/ In a rabbit occlusive study ... two groups of 2 males and 2 females were exposed cutaneously for 24 hours to 200 and 3,160 mg/kg. During the observation period of 14 days, no death occurred, no systemic toxicity was noted, skin changes at 24 hours were characterized by a well-defined erythema and slight desquamation at 7 and 14 days. Necropsy examination did not reveal any gross pathologic alterations except for the local skin changes previously described. ...

/LABORATORY ANIMALS: Acute Exposure/ In a 24-hour exposure dermal study ... in rabbits (4 animals, sex not specified), a dose of 3,160 mg/kg was applied on abraded skin and remained in contact with the skin by means of a non-absorbent binding. There was no mortality during the 14-day test period ... . Clinical observations reported slight to marked anorexia and slight to moderate depression in all animals; at termination all four rabbits appeared normal. Very slight to well-defined erythema was noted in all rabbits at 24 hours, only two exhibited very slight erythema at day 3. Gross pathology findings noted on day 14 included dark red lungs in 3 rabbits and raised areas on all lobes of the lungs in the fourth rabbit.

/LABORATORY ANIMALS: Acute Exposure/ Six male rabbits were exposed to 0.5 mL of the /DIDP/ ... during 4 hours, the patch held in contact with the skin by means of a semi-occlusive dressing. Only very slight erythema in one animal was noted at 60 minutes after removal of the patch, no other irritating signs at 24, 48 and 72 hours were observed.

For more Non-Human Toxicity Excerpts (Complete) data for DIISODECYL PHTHALATE (54 total), please visit the HSDB record page.

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=26761-40-0]

The ability of diisodecyl phthalate to induce morphological transformation in the BALB/c-3T3 mouse cell line (Cell Transformation Assay) was evaluated. The test material was relatively nontoxic at treatment doses below and above the solubility limit in culture medium (1000 to 5000 nL/mL). Diisodecyl phthalate at concentrations of 200 to 20,000 nL/mL did not induce statistically significant increases in transforming activity, and 51 to 74% survival was observed in simultaneous colony survival assays.

Effects on the liver and liver lipids were evaluated in groups of male and female Fischer 344 rats (5/sex/dose level) fed nominal concentrations of 0, 0.3, 1.2, 2.5% diisodecyl phthalate in the diet for 21 days. Toxicity was evident by statistical differences between dosed groups and controls for: mean body weights (males at 2.5% remained lighter, 1.2% lighter on day 17, females at 2.5% were lighter), absolute and relative liver weights (increased, both sexes at 2.5 and 1.2%, males at 0.3%), absolute kidney weights (increased for males at 0.3 and 1.2%, decreased for both sexes at 2.5%), relative kidney weights (increased for all groups except females at 0.3%), absolute and relative weights of testes (decreased and increased, respectively, for males at 2.5%). There was a statistically significant decrease in serum triglycerides for males at 1.2 and 2.5% levels and a decrease in cholesterol for females at 0.33 and males at 1.2%. Also observed was a significant increase in hepatic palmitoyl CoA oxidation in both sexes at 1.2 and 2.5% levels, an increase in 12-hydroxylation of lauric acid at all dose levels for males and at 2.5% for females, an increase in 11-hydroxylation of lauric acid at all doses in the males but it did not reach significance in the females, and an increase in hepatic protein concentrations of both sexes at 1.2 and 2.5% levels. There was a marked increase in peroxisome proliferation in the high dose groups of both sexes. There was a reduction of neutral lipids in all treated groups but no obvious dose relationship was observed.

The ability of diisodecyl phthalate to induce specific locus mutations at the TK locus in cultured L5178Y mouse lymphoma cells (Mouse Lymphoma Mutagenicity Test) was evaluated in the presence and absence of rat liver S9 metabolic activation. The test material was incompletely soluble in the test medium at all concentrations tested. Under nonactivation conditions, concentrations of 2000, 4000, 5000, 6000, 8000, and 10,000 nL/mL induced moderate to high toxicities (33.3% to 7.3% relative growths) but mutant frequency indicated the test material was not mutagenic in this assay. Under activation conditions, concentrations of 250, 500, 1000, and 2000 nL/mL induced low to moderate toxicities (88.6% to 10.3% relative growths) but mutant frequency indicated the test material again was not mutagenic in this assay.

The ability of T1678 (which is diisodecyl phthalate (DIP)) to induce morphological transformation was evaluated in the Balb/3T3 mouse cell line (Cell Transformation Assay). Based on preliminary toxicity determinations (exposure time = 24 hrs), DIP was tested at concentrations of 0, 0.01, 0.1 and 1.0 ug/ml, with survival ranging from 91.3-81.6%. DIP produced significantly greater transformation frequencies at 1.0 ug/ml (p < 0.01, modified Poisson distribution).

For more TSCA Test Submissions (Complete) data for DIISODECYL PHTHALATE (6 total), please visit the HSDB record page.

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: 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.

/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.

Diisodecyl phthalate's production and use as a plasticizer may result in its release to the environment through various waste streams. Congress has banned (on an interim basis) three types of phthalates, which includes diisodecyl phthalate, in any amount greater than 0.1 percent in a children's toy that can be placed in a child's mouth, and in child care articles. If released to air, a vapor pressure of 5.28X10-7 mm Hg at 25 °C indicates diisodecyl phthalate will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase diisodecyl phthalate will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 15 hours. Particulate-phase diisodecyl phthalate will be removed from the atmosphere by wet and dry deposition. Diisodecyl phthalate contains chromophores that absorb at wavelengths >290 nm and, therefore, may be susceptible to direct photolysis by sunlight. If released to soil, diisodecyl phthalate is expected to have no mobility based upon estimated log Koc values of 5.46-6.04. Volatilization from moist soil surfaces is expected based upon an estimated Henry's Law constant of 1.1X10-6 atm-cu m/mole. However, adsorption to soil is expected to attenuate volatilization. Diisodecyl phthalate is not expected to volatilize from dry soil surfaces based upon its vapor pressure. 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 suggests that biodegradation may be an important environmental fate process in soil. If released into water, diisodecyl phthalate is expected to adsorb to suspended solids and sediment based upon the average Koc value of 2.86X10+5 determined in sediment. Diisodecyl phthalate at a concentration of 100 ppm, was degraded 14% to 30% after three days cultivation in river water inoculum, suggesting that biodegradation may be an important environmental fate process in water. Volatilization from water surfaces is expected based upon this compound's estimated Henry's Law constant. Estimated volatilization half-lives for a model river and model lake are 70 days and 1.4 years, respectively. 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. BCFs of <14.4 measured in carp suggest bioconcentration in aquatic organisms is low. Hydrolysis is not expected to be an important environmental based on estimated hydrolysis half-lives of 3.4 years and 125 days at pHs 7 and 8, respectively. Occupational exposure to diisodecyl phthalate may occur through inhalation and dermal contact with this compound at workplaces where diisodecyl phthalate is produced or used. Monitoring and use data indicate that the general population may be exposed to diisodecyl phthalate via inhalation and dermal contact with consumer products containing diisodecyl phthalate. (SRC)

Diisodecyl phthalate's production and use as a plasticizer(1) may result in its release to the environment through various waste streams(SRC). Congress has banned (on an interim basis) three types of phthalates, which includes diisodecyl phthalate, in any amount greater than 0.1 percent in a children's toy that can be placed in a child's mouth, and in child care articles(2).

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).

AEROBIC: In a semi-continuous activated sludge test (Soap and Detergent Association biodegradation test method), the mean degradation for diisodecyl phthalate was 68% in 24 hr(1). In a die-away phase of the testing, it took 9 days to achieve 90% degradation(1). Diisodecyl phthalate is confirmed to be degradable in the screening procedure of the Japanese Ministry of Trade and Industry (MITI) which uses a mixed inoculum derived from soil, fresh water and sewage(2). In an acclimated shake flask CO2 evolution test, loss of parent compound (primary degradation) as well as CO2 evolution (ultimate degradation) was measured using an inoculum prepared from soil and sewage, >99% of diisodecyl phthalate was lost and 56% of theoretical CO2 was evolved after 28 days(3). The biodegradation half-life was 9.6 days with a 4.9 day lag(3). Diisodecyl phthalate, present at 100 mg/L, reached 2% of its theoretical BOD in 2 weeks using an activated sludge inoculum at 30 mg/L in the Japanese MITI test(4). Diisodecyl phthalate, present at a concentration of 100 ppm, was degraded 14 and 30% after three days cultivation in water from the Mino River and Akashi Beach, Japan, respectively(5). Diisodecyl biodegraded 67% from an initial concentration of 48 ppm and 100 ppm in 28 days in activated sludge at 22 and 25 °C, respectively(6). Diisodecyl phthalate degraded 42% in 21 days at 25 °C from a starting concentration of 100 ppm(6). An aerobic aquatic half-life of 23 days was given for diisodecyl phthalate(7).

The rate constant for the vapor-phase reaction of diisodecyl phthalate with photochemically-produced hydroxyl radicals has been estimated as 2.6X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 15 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). A base-catalyzed second-order hydrolysis rate constant of 0.064 L/mole-sec(SRC) was estimated using a structure estimation method(1); this corresponds to half-lives of 3.4 years and 130 days at pH values of 7 and 8, respectively(1). Diisodecyl phthalate contains chromophores that absorb at wavelengths >290 nm(2) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

BCFs of <3.6 and <14.4 were measured for diisodecyl phthalate at chemical concentrations of 1 and 0.1 mg/L, respectively, using carp (Cyprinus carpio) which were exposed over an 8-week period(1). According to a classification scheme(2), these BCFs suggest that bioconcentration in aquatic organisms is low(SRC). The mean log BCF of diisodecyl phthalate in Daphnia magna as determined in a 21 day test using ring-labeled chemical was 2.06(3), corresponding to a BCF of 115(SRC). The mean log BCF in mussels (Mytilus edulis) was 3.54 between 14 and 28 days also using ring-labeled ester(4), corresponding to a BCF of 3467(SRC). However depuration was rapid in mussels, the half-life being 3.5 days(4).

Using a structure estimation method based on molecular connectivity indices(1), the log Koc of diisodecyl phthalate can be estimated to be 6.04(SRC). Other estimated log Koc values reported were 5.46 and 5.78(2). According to a classification scheme(3), these estimated log Koc values suggest that diisodecyl phthalate is expected to be immobile in soil. The average Koc of (14)C-diisodecyl phthalate using three standard USEPA sediments (supplied and characterized by the EPA) was measured at 2.86X10+5(4).

The Henry's Law constant for diisodecyl phthalate is estimated as 1.1X10-6 atm-cu m/mole(SRC) derived from its vapor pressure, 5.28X10-7 mm Hg(1), and water solubility, 0.28 mg/L(2). This Henry's Law constant indicates that diisodecyl phthalate is expected to volatilize from water surfaces(3). 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)(3) is estimated as 70 days(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(3) is estimated as 1.4 years(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(4). Diisodecyl phthalate's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). Diisodecyl phthalate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

SURFACE WATER: 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 the waters of the Tone and Kido Rivers and Kasumiga Ura Lake(1). Diisodecyl phthalate was found in 55% of 375 water samples at an average concentration of 0.94 ppb, samples were collected 1974 to 1976, along the Pacific coast of Japan including Tokyo Bay, Ise Bay, Osaka Bay, Seto Inland Sea and 2 or 3 industrial zones along the coast(2).

An effluent sample from a New Jersey publicly owned treatment work contained diisodecyl phthalate at an estimated concentration of 3 ppb(1). Diisodecyl phthalate was detected at a maximum of 17 ug/L in urban run-off samples from Sweden(2).

SEDIMENT: 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 the environment(1). Coastal sediments were high in phthalate esters, probably as a result of inland discharge and rainwater from populated areas(1). Diisodecyl phthalate was found in 44% of 370 sediment samples at an average concentration of 0.08 ppm, 1974-1976, along the Pacific coast of Japan including Tokyo Bay, Ise Bay, Osaka Bay, Seto Inland Sea and 2 or 3 industrial zones along the coast(2). Diisodecyl phthalate was detected at a maximum of 66 ug/g dry weight in sediment from 3 urban run-off catchment basins in Sweden(3).

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).

Diisodecyl phthalate was found in aquatic organisms June to Sept 1999 from False Harbor, Vancouver, British Columbia. Concentrations in green algae (Enteromorpha intestinalis) were 3.44 ng/g lipid and in brown algae (Nereocysitis luetkeana, Fucus gardneri), 2.46 ng/g lipid(1).

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 fish(1). Anit fish from coastal waters were high in phthalate esters, probably as a result of inland discharge and rainwater from populated areas(1). Diisodecyl phthalate was found in 37% of 332 fish samples at an average concentration of 0.13 ppm, 1974-1976, along the Pacific coast of Japan including Tokyo Bay, Ise Bay, Osaka Bay, Seto Inland Sea and 2 or 3 industrial zones along the coast(2).

Aquatic organisms collected June to Sept 1999 from False Harbor, Vancouver, British Columbia, Canada were analyzed for concentrations of diisodecyl phthalate(1).[Table#2466]

Diisodecyl phthalate concentrations in surf scoters (Melanitta perspicillata) sampled from June to Sept 1999 in False Harbor, Vancouver, British Columbia was 3.15 ng/g lipid(1). Concentrations in plankton (composite of phytoplankton, zooplankton and other pelagic invertebrates) sampled was 3.87 ng/g lipid(1).

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).

Diisodecyl phthalate was detected in dust samples collected from homes in Canada(1). Diisodecyl phthalate was detected in 3 of 14 gasket seals used in the food industry at 37-41%(2). Food packaging items were acquired from Brazilian retail markets; diisodecyl phthalate was detected at 10-11% wet weight in films and closure seals(3). In a Dutch survey of teething rings and toy animals, diisodecyl phthalate levels were 1.4-15%(4). Surveys conducted by the UK government found diisodecyl phthalate in 6 of 18 toys in 1990, 4 of 27 toys in 1991, 0 of 16 toys in 1992 and 0 of 29 toys in 1996(4). Diisodecyl phthalate was detected in 3 of 4 teethers and 1 of 3 dolls tested at 0.7 to 10.1%(4). The Consumer Product Safety Commission (US) did not detect diisodecyl phthalate in 35 toys that contained poly vinyl chloride(4).

According to the 2012 TSCA Inventory Update Reporting data, 4 reporting facilities estimate the number of persons reasonably likely to be exposed in the manufacturing, processing, or use of diisodecyl phthalate in the United States may be as low as <10 workers per plant; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 80,441 workers (31,734 of these are female) were potentially exposed to diisodecyl phthalate in the US(1). Occupational exposure to diisodecyl phthalate may occur through inhalation and dermal contact with this compound at workplaces where diisodecyl phthalate is produced or used(SRC). Workers were exposed to phthalic acid esters mainly di(ethylhexyl), diisodecyl, and butylbenzyl phthalate in air in a polyvinyl chloride processing industry whose mean ranged from 0.02 to 2.0 mg/cu m in 6 different job categories(2). Monitoring and use data indicate that the general population may be exposed to diisodecyl phthalate via inhalation and dermal contact with consumer products containing diisodecyl phthalate(SRC).

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).

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).

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.