Di(2-ethylhexyl) phthalate

H360FD: May damage fertility; May damage the unborn child [Danger Reproductive toxicity]

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

This chemical does not meet GHS hazard criteria for < 0.1% (1 of 1071) of reports.

H360 (94.5%): May damage fertility or the unborn child [Danger Reproductive toxicity]

Aggregated GHS information provided per 1071 reports by companies from 27 notifications to the ECHA C&L Inventory.

Reported as not meeting GHS hazard criteria per 1 of 1071 reports by companies.

There are 26 notifications provided by 1070 of 1071 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.

H320: Causes eye irritation [Warning Serious eye damage/eye irritation]

H335: May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]

H351: Suspected of causing cancer [Warning Carcinogenicity]

H360: May damage fertility or the unborn child [Danger Reproductive toxicity]

H373: May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

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

H411: Toxic to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]

P203, P260, P261, P264+P265, P271, P273, P280, P304+P340, P305+P351+P338, P318, P319, P337+P317, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Not Classified

H316: Causes mild skin irritation [Warning Skin corrosion/irritation]

P203, P260, P264+P265, P280, P305+P351+P338, P318, P319, P332+P317, P337+P317, P405, and P501 (click each P-code to see the statement)

H350: May cause cancer [Danger Carcinogenicity]

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. Give one or two glasses of water to drink.

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. IMMEDIATELY call a hospital or poison control center even if no symptoms (such as redness or irritation) develop. IMMEDIATELY transport the victim to a hospital for treatment after washing the affected areas.

INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. 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.

OTHER: Since this chemical is a known or suspected carcinogen you should contact a physician for advice regarding the possible long term health effects and potential recommendation for medical monitoring. Recommendations from the physician will depend upon the specific compound, its chemical, physical and toxicity properties, the exposure level, length of exposure, and the route of exposure. (NTP, 1992)

(General first aid procedures)

Eye: Irrigate immediately - If this chemical contacts the eyes, immediately wash (irrigate) the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately.

Breathing: Respiratory support

Swallow: Medical attention immediately - If this chemical has been swallowed, get medical attention immediately.

Fire Extinguishing Agents Not to Be Used: Water.

Fire Extinguishing Agents: Carbon dioxide, dry chemical, alcohol foam, or water spray. (USCG, 1999)

Use water spray, foam, powder, carbon dioxide.

Dry powder, carbon dioxide, foam. Water or foam may cause frothing.

Water or foam may cause frothing.

Wear self contained breathing apparatus for fire fighting if necessary.

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

... May give off irritating vapor @ high temperature.

Personal protection: chemical protection suit. Remove all ignition sources. Collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations.

Accident Release Measures. Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U028, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

/Contaminated packaging/ Dispose of as unused product.

/Product/ Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Offer surplus and non-recyclable solutions to a licensed disposal company.

The U.S. Food and Drug Administration (FDA) has issued a Public Health Notification on PVC devices containing di(2-ethylhexyl) phthalate (DEHP), urging health care providers to use DEHP-free devices for certain vulnerable patients. Many hospitals and health systems have successfully transitioned away from use of DEHP, particularly in neonatal intensive care units (NICUs).

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

Avoid contact with skin and eyes. Avoid inhalation of vapor or mist.

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

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.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION. Then, 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 60-70% ethanol followed by washing with a 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 protect this material from exposure to light. Keep it away from oxidizing materials and store it under ambient temperatures. (NTP, 1992)

Separated from strong oxidants, acids, alkalis and nitrates. Cool. Dry. Well closed.

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.

10 [mg/m3]

830 [mg/m3]

5000 [mg/m3]

10 mg/m³

Ca TWA 5 mg/m3 ST 10 mg/m3 See Appendix A

TWA 5 mg/m3 See Appendix G

5000 mg/m3 ; A potential occupational carcinogen. (NIOSH, 2024)

NIOSH considers bis-(2-ethylhexyl)-phthalate to be a potential occupational carcinogen.

5000 mg/m³

Ca [5000 mg/m3]

See: 117817

8 hr Time Weighted Avg (TWA): 5 mg/cu m.

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed three times the TLV-TWA for no more than a total of 30 min during a work day, and under no circumstances should they exceed five times the TLV-TWA, provided that the TLV-TWA is not exceeded.

A3; Confirmed animal carcinogen with unknown relevance to humans.

5 mg/m³ [1996]

(inhalable fraction): 2 mg/m

Intermediate Oral: 0.1 mg/kg/day (L134)

Chronic Oral: 0.06 mg/kg/day (L134)

(a) Prohibition on the sale of certain products containing phthalates. Beginning on the date that is 180 days after the date of enactment of this Act, 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 or child care article that contains concentrations of more than 0.1 percent of di-(2-ethylhexyl) phthalate (DEHP), dibutyl phthalate (DBP), or benzyl butyl phthalate (BBP).

Evaporation at 20 °C is negligible; a harmful concentration of airborne particles can, however, be reached quickly on spraying.

The substance is irritating to the eyes and respiratory tract.

The substance may have effects on the testes. Animal tests show that this substance possibly causes toxicity to human reproduction or development.

Excerpt from NIOSH Pocket Guide for Di-sec octyl phthalate:

Skin: No recommendation is made specifying the need for personal protective equipment for the body.

Eyes: No recommendation is made specifying the need for eye protection.

Wash skin: No recommendation is made specifying the need for washing the substance from the skin (either immediately or at the end of the work shift).

Remove: No recommendation is made specifying the need for removing clothing that becomes wet or contaminated.

Change: No recommendation is made specifying the need for the worker to change clothing after the workshift. (NIOSH, 2024)

Respirator Recommendations: At concentrations above the NIOSH REL, or where there is no REL, at any detectable concentration.[Table#1087]

Respirator Recommendations: Escape conditions:[Table#1088]

/Skin protection/ Handle with gloves.

/Eye/face protection/ Safety glasses with side-shields conforming to EN166 Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

For more Personal Protective Equipment (PPE) (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (6 total), please visit the HSDB record page.

At concentrations above the NIOSH REL, or where there is no REL, at any detectable concentration:

(APF = 10,000) Any self-contained breathing apparatus that has a full facepiece and is operated in a pressure-demand or other positive-pressure mode

(APF = 10,000) Any supplied-air respirator that has a full facepiece and is operated in a pressure-demand or other positive-pressure mode in combination with an auxiliary self-contained positive-pressure breathing apparatus

(APF = 50) Any air-purifying, full-facepiece respirator with an N100, R100, or P100 filter.

Click here for information on selection of N, R, or P filters. 

Any appropriate escape-type, self-contained breathing apparatus

Important additional information about respirator selection

NO open flames.

Di(2-ethylhexyl) phthalate is a colorless to pale yellow oily liquid. Nearly odorless. (USCG, 1999)

Other Solid; Large Crystals; Liquid; Liquid

COLOURLESS-TO-LIGHT COLOURED VISCOUS LIQUID WITH CHARACTERISTIC ODOUR.

Colorless, oily liquid with a slight odor.

Colorless, oily liquid

Slight odor

723 °F at 760 mmHg (NTP, 1992)

BP: 231 °C at 5 mm Hg

384 °C @760 [mm Hg]

-58 °F (NTP, 1992)

405 °F (NTP, 1992)

420 °F (215 °C) (Open cup)

215 °C o.c.

420 °F (open cup)

(oc) 420 °F

less than 0.1 mg/mL at 72 °F (NTP, 1992)

In water, 2.70X10-1 mg/L at 25 °C

LESS THAN 0.01% IN WATER @ 25 °C

Soluble in blood and fluids containing lipoproteins

MISCIBLE WITH MINERAL OIL & HEXANE

Slightly soluble in carbon tetrachloride

Solubility in water: none

(75 °F): 0.00003%

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

0.981 g/cu cm at 25 °C

Relative density (water = 1): 0.986

0.981 @25 °C

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

16.0 (Air = 1)

Relative vapor density (air = 1): 13.45

1.32 mmHg at 392 °F (NTP, 1992)

Vapor pressure = 9.75X10-6 mm Hg at 25 °C

1.42X10-7 mm Hg at 25 °C

Vapor pressure, kPa at 20 °C: 0.001

1.32 mmHg at 392 °F

<0.01 mmHg

log Kow = 7.60

735 °F (NTP, 1992)

735 °F (390 °C)

When heated to decomp it emits acrid smoke.

Insoluble in water.

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

DI(2-ETHYLHEXYL) PHTHALATE reacts 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 with alkali metals and hydrides. Incompatible with nitrates (NTP, 1992).

Strong oxidizing agents

Nitrates; strong oxidizers, acids & alkalis.

Nitrates; strong oxidizers, acids & alkalis

CDC-ATSDR Toxicological Profile

IDENTIFICATION AND USE: Di(2-ethylhexyl)phthalate (DEHP) is a colorless, oily liquid. Plastics may contain from 1 to 40% DEHP by weight and are used in consumer products such as imitation leather, rainwear, footwear, upholstery, flooring, wire and cable, tablecloths, shower curtains, food packaging materials and children's toys. DEHP is also used as a hydraulic fluid and as a dielectric fluid (a non-conductor of electric current) in electrical capacitors, a detector for leaks in respirators. DEHP is not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses. HUMAN EXPOSURE AND TOXICITY: DEHP has been found in various types of food, such as fish, shellfish, eggs and cheese. Blood transfusions and other medical treatment using plastic devices may lead to involuntary human exposure to DEHP. Available data on oral administration indicate that DEHP is hydrolyzed in the gut by pancreatic lipase. The metabolites formed, i.e., mono(2-ethylhexyl)phthalate and 2-ethyl hexanol, are rapidly absorbed. Mono-2-ethylhexyl phthalate was detected in human teeth. When administered orally, DEHP is extensively hydrolyzed in the gut in certain animals, e.g., rats, and is mainly distributed as monoethylhexyl phthalate. However, hydrolysis occurs to a much lesser extent in primates and humans. Several further metabolites have been identified, omega- and omega-1-oxidation being the major metabolic pathways. DEHP metabolism shows considerable species differences, e.g., the omega-oxidation pathway is less extensive in humans than in rats. Bile and urine are the major excretory pathways. DEHP metabolites do not produce peroxisome proliferation in cultured human hepatocytes. Only very limited information is available on the effects of DEHP on humans. Mild gastric disturbances, but no other deleterious effects, were reported for two subjects. Adolescents exposed to significant quantities of DEHP as neonates showed no significant adverse effects on their physical growth and pubertal maturity. Thyroid, liver, renal, and male and female gonadal functions tested were within normal range for age and sex distribution. ANIMAL STUDIES: Hepatomegaly and increased relative kidney weights have been observed in treated animals in long term studies, also hypertrophic cells in the anterior pituitary. Several studies have shown testicular atrophy. Younger rats seem to be more susceptible than older ones, and rats and mice seem to be more sensitive than marmosets and hamsters. Reversibility of the atrophy has been observed. DEHP, as well as monoethylhexyl phthalate, shows teratogenic properties. Tests for mutagenicity and related end points have been negative in most studies. DEHP may induce cellular transformation, and it has been shown to be carcinogenic in rats and in mice. There was a dose-related increase in hepatocellular tumors in both sexes of both species. The induction of hepatic peroxisome proliferation and cell replication is strongly associated with the liver carcinogenic effects of certain non-genotoxic carcinogens including DEHP. However, marked differences have been observed among animal species with respect to DEHP-induced peroxisome proliferation. ECOTOXICITY STUDIES: Although few relevant studies have been reported, the acute toxicity of DEHP to algae, plants, and birds appears to be low.

Monoethylhexylphthalate (MEHP), one of the major metabolites of DEHP, induces peroxisome proliferation by activating peroxisome proliferator activated receptors. This is believed to increase production of hydrogen peroxide by peroxisomes and enhance cell proliferation, leading to hepatotoxic and carcinogenic effects. MEHP is also believed to exhibit testicular toxicity by targeting and damaging the Sertoli cells. DEHP may act as an antiandrogen during a critical stage of reproductive tract differentiation by reducing testosterone in fetal males, hindering development. (L181, A106)

Di (2-ethylhexyl)phthalate (DEHP)

2 x 10 ^-2 mg/kg-day

bis(2-Ethylhexyl) phthalate

Semi-Volatile Organic Compound (SVOC)

Listed as Di (2-ethylhexyl)phthalate (DEHP)

Smith, C.D. and Nowell, L.H., 2024. Health-Based Screening Levels for evaluating water-quality data (3rd ed.). DOI:10.5066/F71C1TWP

Classification of carcinogenicity: There is inadequate evidence in humans for the carcinogenicity of di(2-ethylhexyl) phthalate. There is sufficient evidence in experimental animals for the carcinogenicity of di(2-ethylhexyl) phthalate. Overall evaluation: Di(2-ethylhexyl) phthalate is not classifiable as to its carcinogenicity to humans (Group 3).

bis(2-Ethylhexyl) Phthalate: reasonably anticipated to be a human carcinogen.

Cancer Classification: Group B2 Probable Human Carcinogen

CLASSIFICATION: B2; probable human carcinogen. BASIS FOR CLASSIFICATION: Orally administered DEHP produced significant dose-related increases in liver tumor responses in rats and mice of both sexes. HUMAN CARCINOGENICITY DATA: Inadequate. ANIMAL CARCINOGENICITY DATA: Sufficient. /based on former classification system/

A3; Confirmed animal carcinogen with unknown relevance to humans.

Di(2-ethylhexyl)phthalate

Group 2B: Possibly carcinogenic to humans

Volume Sup 7: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, 1987; 440 pages; ISBN 92-832-1411-0 (out of print)

Volume 77: (2000) Some Industrial Chemicals

Volume 101: (2012) Some Chemicals Present in Industrial and Consumer Products, Food and Drinking-water

Di(2-ethylhexyl) phthalate

TR-601: Toxicology and Carcinogenesis Studies of Di(2-ethylhexyl) Phthalate (CASRN 117-81-7) Administered in Feed to Sprague Dawley (Hsd:Sprague Dawley SD) Rats (2021 )

04/02/21

Clear Evidence

During the perinatal period, lower maternal mean body weight, maternal mean body weight gain, and feed consumption were observed in F0 dams exposed to 10,000 ppm DEHP relative to control animals. Also in that exposure group, litter size and pup weights on PND 1 were significantly decreased compared to the control group. Male and female pup mean body weight gains were significantly decreased in the 10,000 ppm group during lactation and resulted in significantly decreased pup body weights at weaning when compared to the control group. Pup survival was not affected following gestational and lactational DEHP exposure.

Following perinatal and 2 years of postweaning DEHP exposure, survival of exposed male and female rats to study termination was similar to that of control groups; however, there were decreases in mean body weight in the 10,000 ppm group compared to the control group.

Significant increases in the incidences of hepatocellular adenoma, hepatocellular adenoma or carcinoma (combined), pancreatic acinar adenoma, and pancreatic acinar adenoma or carcinoma (combined) were observed in the 3,000 and 10,000 ppm male rats relative to the control group. Higher incidences of hepatocellular carcinomas (10,000 ppm males) and pancreatic acinar carcinomas (3,000 ppm males) were also observed. In female rats, significant increases in the incidences of liver neoplasms occurred in the 3,000 ppm (hepatocellular adenoma and hepatocellular adenoma or carcinoma [combined]) and 10,000 ppm (hepatocellular carcinoma and hepatocellular adenoma or carcinoma [combined]) groups. Occurrences of pancreatic acinar adenomas were observed in the 3,000 and 10,000 ppm female groups, and a trend of higher incidence of uterine adenocarcinomas with increasing exposure was observed given the incidence in the 10,000 ppm group. Nonneoplastic lesions were observed in the liver (male and female), pancreas (female), testis, epididymis, kidney (male and female), heart (male only), bone marrow (male only), and pituitary gland (male only).

Back to TopPostweaning-only Study in Rats (Study 2)Following 2 years of postweaning DEHP exposure, survival of male and female rats was commensurate with or greater than that of control animals, and lower body weights were observed in the 10,000 ppm group. Notably, the magnitude of decreased weight was smaller in the control animals in Study 2 than in the control animals in Study 1. Significant increases in the incidences of hepatocellular adenoma, carcinoma, and adenoma or carcinoma (combined) were observed in male and female rats exposed to 10,000 ppm DEHP relative to the respective control group. In male rats, significantly increased incidences of pancreatic acinar neoplasms were observed in the 3,000 (adenoma) and 10,000 ppm (adenoma and carcinomas) groups. A trend of increasing incidence of testicular interstitial cell adenoma with increasing exposure was observed in male rats given the incidence observed in the 10,000 ppm DEHP group. In female rats, significantly increased incidences of uterine adenocarcinoma and uterine adenoma, adenocarcinoma, squamous cell carcinoma, or squamous cell papilloma (combined) were observed in the 10,000 ppm group compared to the control group. Occurrences of uterine squamous cell papilloma (including multiple) were observed in the 10,000 ppm group. Nonneoplastic lesions were observed in the liver (male and female), pancreas (male and female), testis, epididymis, uterus, heart (male only), bone marrow (male), and pituitary gland (male only).

Back to TopComparative Carcinogenic Benchmark Dose AnalysesBenchmark dose (BMD) levels corresponding to a 10% increased risk of carcinogenic response (BMD10) were estimated for exposure-related carcinogenic responses that were observed in both studies. Generally, the BMDs between studies were within threefold of each other. The lowest estimated BMD10 (30.99 mg DEHP/kg body weight/day) corresponded to pancreatic acinar adenoma or carcinoma (combined) in males in the postweaning-only study (Study 2).

Back to TopGenetic ToxicologyDEHP was tested in a variety of genotoxicity assays in vitro and in vivo; most results were negative. In vitro, negative results were obtained in the following assays: six independent bacterial mutation assays in Salmonella typhimurium bacterial strains (TA100, TA1535, TA1537, TA97, and TA98) with and without exogenous metabolic activation systems (S9 mix; induced hamster, rat, and mouse liver S9), a single mouse lymphoma gene mutation assay (with and without induced rat liver S9 mix), and three independent chromosomal aberration assays conducted in Chinese hamster ovary (CHO) cells (with and without rat liver S9). In nine in vitro sister chromatid exchange tests conducted in CHO cells with and without S9, DEHP produced positive responses in four tests, equivocal results in three, and negative results in two.

In vivo, no increases in chromosomal aberrations were observed in bone marrow cells of female B6C3F1 mice following exposure to DEHP in dosed feed for 14 days. DEHP produced mixed results in three independent erythrocyte micronucleus assays: equivocal in female B6C3F1 mice exposed to DEHP in dosed feed for 14 days, equivocal in male TgAC (FVB/N) mice and positive in female TgAC (FVB/N) mice following exposure via dosed feed for 26 weeks, and negative in male and female TgAC (FVB/N) mice following a 26-week dermal exposure. DEHP produced negative results in two independent studies that tested for induction of sex-linked recessive lethal mutations in Drosophila melanogaster.

Back to TopConclusionsUnder the conditions of the perinatal and postweaning feed study (Study 1), there was clear evidence of carcinogenic activity of di(2-ethylhexyl) phthalate (DEHP) in male Hsd:Sprague Dawley SD rats based on the increased incidences of hepatocellular adenoma or carcinoma (combined) and acinar adenoma or carcinoma (combined) neoplasms (predominately adenomas) of the pancreas. There was clear evidence of carcinogenic activity of DEHP in female Hsd:Sprague Dawley SD rats based on the increased incidence of hepatocellular adenoma or carcinoma (combined). The occurrence of pancreatic acinar adenoma or carcinoma (combined) was considered to be related to exposure. The occurrence of uterine (including cervix) adenoma, adenocarcinoma, squamous cell carcinoma, or squamous cell papilloma (combined) in female rats may have been related to exposure.

Under the conditions of the postweaning-only feed study (Study 2), there was clear evidence of carcinogenic activity of DEHP in male Hsd:Sprague Dawley SD rats based on the increased incidences of hepatocellular adenoma or carcinoma (combined) and acinar adenoma or carcinoma (combined) neoplasms (predominately adenomas) of the pancreas. The occurrence of testicular interstitial cell adenoma in male rats may have been related to exposure. There was clear evidence of carcinogenic activity of DEHP in female Hsd:Sprague Dawley SD rats based on the increased incidences of hepatocellular adenoma or carcinoma (combined) and uterine (including cervix) adenoma, adenocarcinoma, squamous cell carcinoma, or squamous cell papilloma (combined). The occurrence of pancreatic acinar adenoma or carcinoma (combined) in female rats was considered to be related to exposure.

The BMD analysis shows there was no consistent pattern indicating that perinatal and postweaning exposure was more sensitive compared to postweaning-only exposure and modeled responses were within threefold of each other. However, there was a stronger carcinogenic response in the reproductive organs (uterus and testis) in the postweaning-only exposure study compared to the perinatal and postweaning exposure study.

Perinatal and postweaning exposure to DEHP (Study 1) resulted in increased incidence of nonneoplastic lesions in the liver, kidney, heart (male), pancreas (female), pituitary gland (male), bone marrow (male), testis, and epididymis. In addition, exposure increased gross lesions within the reproductive tract of males and females.

Postweaning exposure to DEHP (Study 2) resulted in increased incidence of nonneoplastic lesions in the liver, pancreas, heart (male), pituitary gland (male), bone marrow (male), testis, epididymis, and uterus.

Synonyms: Bis(2-ethylhexyl)phthalate; dioctyl phthalate; phthalic acid di(2-ethylhexyl) ester; bis(2-ethylhexyl) 1,2-benzenedicarboxylate; 1,2-benzenedicarboxylic acid bis(2-ethylhexyl) ester

Trade names: Platinol DOP; Octoil; Silicol 150; Bisoflex 81; Eviplast 80

Summary of the Two-year Carcinogenesis and Genetic Toxicology Studies of Di(2-ethylhexyl) Phthalate Perinatal and Postweaning Study (Study 1) Postweaning-only Study (Study 2) Male Sprague Dawley Rats Female Sprague Dawley Rats Male Sprague Dawley Rats Female Sprague Dawley Rats Concentrations in feed 0, 300, 1,000, 3,000, or 10,000 ppm 0, 300, 1,000, 3,000, or 10,000 ppm 0, 300, 1,000, 3,000, or 10,000 ppm 0, 300, 1,000, 3,000, or 10,000 ppm Survival rates 25/50, 33/49, 40/50, 35/50, 29/50 31/50, 32/50, 34/50, 34/50, 27/50 32/50, 35/50, 39/50, 35/50, 42/50 33/50, 34/50, 33/50, 34/50, 32/50 Body weights 10,000 ppm group 29.7% less than the control group 3,000 ppm group 9.9% less than the control group; 10,000 ppm group 31.7% less than the control group 10,000 ppm group 15.6% less than the control group 10,000 ppm group 21.9% less than the control group Gross lesions Testis: small (2/49, 2/49, 4/50, 2/50, 45/49); enlarged (or swelling) (0/49, 0/49, 0/50, 0/50, 1/49); fluid or blood filled (0/49, 1/49, 1/50, 1/50, 1/49); right or left, abdominal, undescended (1/49, 0/49, 0/50, 0/50, 19/49); right or left, inguinal, undescended (0/49, 1/49, 1/50, 0/50, 4/49); right or left, abdominal or inguinal, undescended (1/49, 1/49, 1/50, 0/50, 23/49); right, not present (0/49, 0/49, 0/49, 0/50, 1/49); cranial suspensory ligament (0/49, 0/49, 0/50, 0/50, 5/49)Epididymis: small (0/49, 0/49, 2/50, 0/50, 14/49); right, cauda, agenesis (0/49, 0/49, 0/49, 0/50, 2/49); right or left, caput, agenesis (0/49, 0/49, 0/50, 0/50, 4/49); right or left, cauda, agenesis (0/49, 0/49, 0/50, 0/50, 2/49); right or left, corpus, agenesis (0/49, 0/49, 0/50, 0/50, 3/49)Levator ani/bulbocavernosus muscle: small (0/50, 0/49, 0/50, 0/50, 2/48)Cowper’s glands: left, small (0/50, 0/49, 0/50, 0/50, 1/47); right, small (0/50, 0/49, 0/50, 0/50, 1/47)Prostate glands: small (0/50, 0/49, 0/50, 0/50, 1/47)Seminal vesicles/ coagulating glands: small (1/50, 0/49, 1/50, 1/50, 8/47)Phallus: small (0/50, 0/49, 0/49, 0/50, 3/49); cleft (0/50, 0/49, 0/49, 0/50, 3/49)Prepuce: cleft (0/50, 0/49, 0/50, 0/50, 1/49); incomplete preputial separation (0/50, 0/49, 0/50, 0/50, 7/49)Gubernaculum: right or left, not present (0/47, 0/49, 0/49, 0/50, 18/41); ↑ right length Vagina: not patent (0/50, 0/50, 0/50, 0/50, 5/48)Phallus: cleft (0/50, 0/50, 0/50, 2/50, 1/48) None None Nonneoplastic effects Liver: hepatocyte, cytoplasmic alteration (0/50, 0/49, 1/50, 28/50, 37/49); hepatocyte, hypertrophy (0/50, 0/49, 0/50, 3/50, 17/49); pigment (0/50, 1/49, 5/50, 40/50, 38/49); necrosis (3/50, 4/49, 1/50, 6/50, 13/49); eosinophilic focus (4/50, 1/49, 7/50, 2/50, 11/49); basophilic focus (1/50, 1/49, 4/50, 4/50, 17/49)Testis: germinal epithelium, degeneration (includes bilateral) (16/49, 25/49, 21/50, 21/50, 44/49); interstitial cell, hyperplasia, focal (includes bilateral) (4/49, 3/49, 6/50, 5/50, 30/49); seminiferous tubule, dysgenesis (includes bilateral) (0/49, 0/49, 0/50, 0/50, 10/49)Epididymis: hypospermia (includes bilateral) (4/49, 5/49, 12/50, 8/50, 43/49)Kidney: papilla, edema (0/50, 0/49, 0/50, 0/50, 39/49); papilla, hemorrhage (0/50, 1/49, 0/50, 2/50, 12/49); epithelium, papilla, hyperplasia (9/50, 4/49, 4/50, 3/50, 17/49); infarct (2/50, 10/49, 9/50, 7/50, 17/49)Heart: valve, fibrosis (0/50, 2/49, 1/50, 3/50, 11/49); valve, thrombus (0/50, 0/49, 0/50, 0/50, 6/49)Bone marrow: hypercellularity (21/50, 17/49, 29/50, 34/50, 36/50)Pituitary gland: pars distalis, hypertrophy (3/50, 7/49, 5/50, 15/50, 37/49) Liver: hepatocyte, cytoplasmic alteration (0/49, 4/50, 7/50, 39/50, 39/48); hepatocyte, hypertrophy (0/49, 2/50, 5/50, 9/50, 34/48); pigment (0/49, 6/50, 14/50, 36/50, 40/48); necrosis (3/49, 9/50, 3/50, 7/50, 8/48); eosinophilic focus (3/49, 4/50, 4/50, 7/50, 12/48); basophilic focus (4/49, 5/50, 3/50, 2/50, 10/48); bile duct hyperplasia (9/49, 13/50, 13/50, 21/50, 8/48)Pancreas: acinus, hyperplasia (0/49, 0/50, 0/50, 2/50, 3/48)Kidney: papilla, edema (0/50, 0/50, 2/50, 0/50, 38/48); epithelium, papilla, hyperplasia (2/50, 1/50, 2/50, 4/50, 15/48); infarct (0/50, 3/50, 7/50, 5/50, 12/48); renal tubule, cyst (0/50, 0/50, 2/50, 0/50, 7/48); renal tubule, dilation (0/50, 0/50, 0/50, 0/50, 3/48) Liver: hepatocyte, cytoplasmic alteration (0/50, 1/50, 0/50, 38/50, 49/50); hepatocyte, hypertrophy (0/50, 0/50, 0/50, 2/50, 6/50); pigment (0/50, 0/50, 7/50, 45/50, 50/50); necrosis (0/50, 2/50, 4/50, 7/50, 8/50); eosinophilic focus (1/50, 0/50, 4/50, 2/50, 24/50); clear cell focus (29/50, 31/50, 33/50, 35/50, 39/50)Pancreas: acinus, hyperplasia (7/49, 8/50, 9/50, 24/50, 26/50)Testis: germinal epithelium, degeneration (includes bilateral) (31/50, 25/50, 21/50, 22/50, 50/50); edema (includes bilateral) (27/50, 23/50, 29/50, 24/50, 45/50); interstitial cell, hyperplasia, focal (includes bilateral) (1/50, 1/50, 0/50, 4/50, 4/50)Epididymis: hypospermia (includes bilateral) (4/50, 4/50, 4/50, 3/50, 43/50); duct, exfoliated germ cell (includes bilateral) (2/50, 3/50, 4/50, 4/50, 36/50)Heart: valve, fibrosis (2/50, 0/50, 0/50, 1/50, 9/50); valve, thrombus (0/50, 0/50, 0/50, 2/50, 6/50)Bone marrow: hypercellularity (18/50, 22/50, 30/50, 25/50, 34/50)Pituitary gland: pars distalis, hypertrophy (8/50, 10/50, 11/50, 14/50, 37/50) Liver: hepatocyte, cytoplasmic alteration (0/50, 2/50, 15/50, 38/50, 45/49); hepatocyte, hypertrophy (0/50, 0/50, 6/50, 14/50, 28/49); pigment (3/50, 0/50, 18/50, 30/50, 48/49)Pancreas: acinus, hyperplasia (0/50, 1/50, 1/50, 1/50, 5/47)Uterus: inflammation, chronic (2/50, 9/50, 6/50, 8/50, 8/49) Neoplastic effects Liver: hepatocellular adenoma (0/50, 1/49, 0/50, 3/50, 8/49); hepatocellular carcinoma (1/50, 0/49, 0/50, 0/50, 3/49); hepatocellular adenoma or carcinoma (combined) (1/50, 1/49, 0/50, 3/50, 11/49)Pancreas: acinar adenoma (10/50, 7/49, 8/50, 36/50, 22/49); acinar carcinoma (0/50, 0/49, 0/50, 3/50, 1/49); acinar adenoma or carcinoma (combined) (10/50, 7/49, 8/50, 38/50, 22/49) Liver: hepatocellular adenoma (1/49, 0/50, 5/50, 9/50, 5/48); hepatocellular carcinoma (0/49, 0/50, 0/50, 0/50, 8/48); hepatocellular adenoma or carcinoma (combined) (1/49, 0/50, 5/50, 9/50, 13/48)Pancreas: acinar adenoma or carcinoma (combined) (0/49, 0/50, 0/50, 2/50, 1/48) Liver: hepatocellular adenoma (0/50, 2/50, 0/50, 1/50, 6/50); hepatocellular carcinoma (0/50, 0/50, 0/50, 0/50, 6/50); hepatocellular adenoma or carcinoma (combined) (0/50, 2/50, 0/50, 1/50, 12/50)Pancreas: acinar adenoma (1/49, 4/50, 5/50, 23/50, 30/50); acinar carcinoma (0/49, 1/50, 0/50, 1/50, 5/50); acinar adenoma or carcinoma (combined) (1/49, 5/50, 5/50, 23/50, 33/50) Liver: hepatocellular adenoma (0/50, 0/50, 1/50, 1/50, 13/49); hepatocellular carcinoma (0/50, 0/50, 0/50, 0/50, 2/49); hepatocellular adenoma or carcinoma (combined) (0/50, 0/50, 1/50, 1/50, 14/49)Pancreas: acinar adenoma or carcinoma (combined) (0/50, 0/50, 0/50, 1/50, 2/47)Uterus: adenoma, adenocarcinoma, squamous cell carcinoma, or squamous cell papilloma (combined) (2/50, 4/50, 1/50, 6/50, 13/50) Equivocal findings None Uterus: adenoma, adenocarcinoma, squamous cell carcinoma, or squamous cell papilloma (combined) (3/50, 1/50, 1/50, 3/50, 7/50) Testis: interstitial cell, adenoma (7/50, 3/50, 3/50, 6/50, 15/50) None Level of evidence of carcinogenic activity Clear evidence Clear evidence Clear evidence Clear evidence Genetic toxicology Bacterial gene mutations: Negative in Salmonella typhimurium strains TA100, TA1535, TA1537, TA97, and TA98, with and without S9 Mouse lymphoma L5178Y tk+/− cells: Negative with and without S9 In vitro CHO cell chromosomal aberration test: Negative with and without S9 In vitro CHO cell sister chromatid exchange test: Without rat liver S9: Positive or equivocal in 7 out of 9 studies With rat liver S9: Negative in 9 out of 9 studies In vivo chromosome aberration test: Negative in female B6C3F1 mice exposed via dosed feed for 14 days In vivo micronucleus test in mice: B6C3F1 mice: Equivocal in females exposed via dosed feed for 14 days TgAC (FVB/N) mice: Equivocal in males and positive in females exposed via dosed feed for 26 weeks TgAC (FVB/N) mice: Negative in males and females exposed dermally for 26 weeksDrosophila melanogaster sex-linked recessive lethal test: Adult injection: Negative Larval feeding: Negative Introduction Back to TopChemical and Physical PropertiesDi(2-ethylhexyl) phthalate (DEHP) is the diester of phthalic acid and the branched-chain 2-ethylhexanol. DEHP is a pale-yellow to colorless viscous liquid at room temperature and can have a slight odor. DEHP has a boiling point of 384°C, a melting point of −55°C, and a flash point of 215°C.1 At 25°C, DEHP has a limited water solubility of approximately 0.3 mg/L and a vapor pressure ranging from 1.42 × 10−7 to 9.75 × 10−6 mm Hg.2 DEHP has an estimated log Kow of 7.63 and is miscible in organic solvents, such as hexane.

Back to TopProduction, Use, and Human ExposureDEHP is a widely used member of the phthalate ester chemical class. Phthalates are employed predominantly as plasticizers to provide flexibility in products composed of polyvinyl chloride (PVC) plastic or vinyl chloride resins. DEHP is produced by the esterification of phthalic anhydride with 2-ethylhexanol in the presence of an acid catalyst, such as sulfuric acid or para-toluenesulfonic acid.4 DEHP is considered a high-production volume chemical with an estimated 10 to 50 million pounds produced in the United States in 2015, as reported to the U.S. Environmental Protection Agency (EPA),5 a production level consistent with annual production reports from 1986 to 2014, indicating that DEHP use remained consistent.

Globally, between 90% and 95% of DEHP is used as a plasticizer in the manufacture of PVC polymers and corresponding products.6,7 DEHP is used in a variety of plastic consumer products, including construction materials, shower curtains, garden hoses, floor tiles, automobile upholstery, and food packaging materials. Plastics may contain 1% to 40% DEHP by weight, with materials that exhibit increased softness or flexibility likely containing higher levels of DEHP or other phthalates. DEHP is used in the production of medical devices, such as blood bags, enteral/parenteral nutrition bags, peritoneal dialysis bags, and medical tubing.8,9 Because DEHP is not covalently bonded to the PVC polymer, potential exists for DEHP to leach into contact media. Migration from PVC storage bags into collected blood, blood products, and other biological products is likely associated with the lipophilic nature of DEHP.

LC50; Species: Daphnia magna (Water flea) age <24 hr; Conditions: freshwater, static, 22 °C pH 8.0 (7.4-9.4), hardness 173 mg/L CaCO3; Concentration: 68,000 ug/L for 24 hr />80% purity/

LC50; Species: Daphnia magna (Water flea) age <24 hr; Conditions: freshwater, static, 22 °C pH 8.0 (7.4-9.4), hardness 173 mg/L CaCO3; Concentration: 11,000 ug/L for 48 hr (95% confidence interval: 7500-16000 ug/L) />80% purity/

LC50; Species: Daphnia magna (Water flea); Concentration: 1,000-5,000 ug/L for 48 hr /Conditions of bioassay not specified/

EC50; Species: Daphnia magna (Water flea) age <24 hr; Conditions: freshwater, static, 20-23 °C, pH 7.0-8.5, hardness 120-250 mg/L CaCO3, alkalinity 120-250 mg/L CaCO3, dissolved oxygen 6.0-9.3 mg/L; Concentration: 9500 ug/L for 24 hr; Effect: intoxication, immobilization /formulated product/

For more Ecotoxicity Values (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (42 total), please visit the HSDB record page.

/AQUATIC SPECIES/ ... The effects of several organic chemicals including DEHP on the synthesis of vertebral collagen and hydroxyproline /were studied/. Three fish species were used: brook trout (Salvelinus fontinalis), fathead minnow (Pimephales promelas) and rainbow trout (Onchorhynchus mykiss). Adult brook trout (1.5 yr at initiation of exposure) were continuously exposed to DEHP concentrations ranging from 0 - 52 ug/L for 150 days. The fathead minnows were 10 days old at initiation of exposure and were continuously exposed to concentrations ranging from 0 - 100 ug/L for 127 days. In the rainbow trout study eyed eggs were continuously exposed from 10 days before hatching to 80 days post hatch to DEHP concentrations ranging from 0 - 54 ug/L. In all studies acetone was used as a solvent. ... In the brook trout study the collagen content in backbone was significantly reduced and the level of hydroxyproline in collagen was significantly increased (p = 0.05) already at the lowest DEHP exposure (3.7 ug/L). However, there was no dose response relationship and the level of reduction/increase was approximately the same at all exposure levels. Also in the fathead minnow study the collagen content of backbone was significantly reduced and the hydroxyproline content in collagen significantly increased at the lowest DEHP exposure (11 ug/L). The reduction in collagen content was dose dependent but the increase in hydroxyproline was not. In the embryo-larval study with rainbow trout collagen content was significantly reduced at next lowest exposure level, 14 ug/L, whereas hydroxyproline content did not differ significantly from the control. There was no mortality and no significant effects on growth in any of the three fish species tested. ...

/AQUATIC SPECIES/ In the Atlantic cod (Gadus morhua), the synthesis of steroid hormones such as testosterone and 11-ketotestosterone was affected by exposures as low as 1 mg/L.

/AQUATIC SPECIES/ ... The concentrations /of phthalate esters/ that inhibit growth are high /and have/ been shown to act as heartbeat depressors in goldfish (Crassius auratus). Reductions of approximately 60% were recorded for 12 mg/L DnBP and 200 mg/L benzylbutylphthalate (BBP), respectively. A reduction of 33% was recorded for 200 mg/L DEHP.

/AQUATIC SPECIES/ Fathead minnows, exposed to DEHP, converted this material to mono-2-ethylhexyl phthalate (MEHP) and a glucose conjugate. The same metabolites were observed in rainbow trout. Liver microsomes converted DEHP and DBP to the mono esters and 2 polar metabolites. In sediment, after hydrolysis to MEHP, decarboxylation and ring cleavage occurred.

For more Ecotoxicity Excerpts (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (28 total), please visit the HSDB record page.

3.90e+01

1.60e+02

1.20e+00

5.10e+00

5.60e+00

6.00e+00

1.30e+00

1.40e+00

1.40e-02

2.00e-02

Volatile

3.80e+03

1.60e+04

1.20e+02

5.10e+02

5.60e+02

Bioaccumulation of this chemical may occur in seafood.

Bis(2-ethylhexyl)phthalate's production and use as a plasticizer in polyvinyl chloride (PVC) resins for fabricating flexible vinyl products may result in its release to the environment through various waste streams. If released to air, a vapor pressure of 1.42X10-7 mm Hg at 25 °C indicates bis(2-ethylhexyl) phthalate will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase bis(2-ethylhexyl) 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 16 hours. Particulate-phase bis(2-ethylhexyl) phthalate will be removed from the atmosphere by wet and dry deposition. Bis(2-ethylhexyl) phthalate contains chromophores that absorb at wavelengths >290 nm and, therefore, may be susceptible to direct photolysis by sunlight. If released to soil, bis(2-ethylhexyl) phthalate is expected to have no mobility based upon Koc values of 87,420 to 510,000. Volatilization from moist soil surfaces is not expected to be an important fate process based upon an estimated Henry's Law constant of 2.7X10-7 atm-cu m/mole. Bis(2-ethylhexyl) phthalate is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Utilizing the Japanese MITI test, 69% of the theoretical BOD was reached in 4 weeks. Mineralization rates of 15 to 50% were reported after 80 days. 22 to 32% (14)CO2 evolution was observed in three soils after 60 days incubation. These studies suggest that biodegradation is an important environmental fate process. If released into water, bis(2-ethylhexyl) phthalate is expected to adsorb to suspended solids and sediment based upon the Koc values. In unacclimated aquatic systems no biodegradation was observed; however, a biodegradation half-life of 60 to 70 hours was observed in groundwater impacted by bis(2-ethylhexyl) phthalate. These results suggest that biodegradation is dependent to a large extent on acclimation of aquatic environments. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated Henry's Law constant. BCF values of <0.1 to 850 in carp, bluegill and fathead minnows, suggest bioconcentration of bis(2-ethylhexyl) phthalate in aquatic organisms is low to very high; this range may indicate the ability of aquatic organisms to readily metabolize this class of compounds. Bis(2-ethylhexyl) phthalate is not expected to undergo hydrolysis in the environment based on an aqueous hydrolysis half-life of 2000 years that was determined at pH 7. Occupational exposure to bis(2-ethylhexyl) phthalate may occur through inhalation of aerosols and dust, and dermal contact with this compound at workplaces where bis(2-ethylhexyl) phthalate is produced or used. Monitoring data indicate that the general population may be exposed to bis(2-ethylhexyl) phthalate via inhalation of ambient air, ingestion of food and drinking water, and dermal contact with household dust and products containing bis(2-ethylhexyl) phthalate. (SRC)

Bis(2-ethylhexyl) phthalate's production and use as a plasticizer in polyvinyl chloride (PVC) resins for fabricating flexible vinyl products(1,2) may result in its release to the environment through various waste streams(SRC). Bis(2-ethylhexyl) phthalate is found in table cloths, shower curtains, furniture and automobile upholstery, imitation leather, garden hoses, floor tiles, swimming-pool liners, sheathing for wire and cable, rainwear, shoes, toys, dolls, baby pants, food packaging materials, tubing used in commercial milking equipment, and weather stripping(2). Bis(2-ethylhexyl) phthalate is also used in medical devices such as blood and intravenous solution bags, catheters, tubing for dialysis and parenteral solutions, oxygen masks, and urine and colostomy bags(2).

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values ranging from 87,420(2) to 510,000(3), indicate that bis(2-ethylhexyl) phthalate is expected to be immobile in soil(SRC). Volatilization of bis(2-ethylhexyl) phthalate from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.7X10-7 atm-cu m/mole(SRC), based upon its vapor pressure, 1.42X10-7 mm Hg(4), and water solubility, 0.27 mg/L(5). Bis(2-ethylhexyl) phthalate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). Mineralization rates of 15 to 50% remaining after 80 days(6) and 22 to 32% (14)CO2 in three soils after 60 days incubation(7) suggest that biodegradation proceeds slowly in soil environments(SRC).

AQUATIC FATE: Based on a classification scheme(1), Koc values ranging from 87,420(2) to 510,000(3), indicate that bis(2-ethylhexyl) phthalate is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 2.7X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 1.42X10-7 mm Hg(5), and water solubility, 0.27 mg/L(6). Bis(2-ethylhexyl) phthalate is not expected to undergo hydrolysis in the environment based on an aqueous hydrolysis half-life of 2000 years that was determined at pH 7(3). According to a classification scheme(7), BCF values of <0.1(8) to 850(9) in carp, bluegill and fathead minnows, suggest bioconcentration in aquatic organisms is low to very high; this range may indicate the ability of aquatic organisms to readily metabolize this class of compounds(3). In unacclimated aquatic systems no biodegradation was observed(10), but a biodegradation half-life of 60 to 70 hours in groundwater impacted by bis(2-ethylhexyl) phthalate was reported(11), suggesting that biodegradation is dependent to a large extent on acclimation of aquatic environments(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), bis(2-ethylhexyl) phthalate, which has a vapor pressure of 1.42X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase bis(2-ethylhexyl) 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 16 hours(SRC), calculated from its rate constant of 2.2X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase bis(2-ethylhexyl) phthalate may be removed from the air by wet and dry deposition(SRC). Bis(2-ethylhexyl) phthalate contains chromophores that absorb at wavelengths >290 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). Gas-phase hydroxyl radicals reacted with bis(2-ethylhexyl) phthalate adsorbed onto silicon dioxide, aluminum oxide, iron(III) oxide and coal fly ash(5), exhibiting half-lives of 1.1, 1.2, 1.3 and 2.0 days, respectively(SRC).

AEROBIC: Bis(2-ethylhexyl) phthalate was degraded with gradual adaptation; 0, 43, 80, and 95% biodegradation were observed in the original culture, first, second, and third weekly subcultures, respectively, in static flask screening tests using a settled domestic wastewater inoculum(1). A biodegradation half-life of 0.8 days has been reported for bis(2-ethylhexyl) phthalate in activated sludge(2). Bis(2-ethylhexyl) phthalate subjected to static culture flask biodegradability tests was almost completely bio-oxidized at the end of 3 weeks(3). Greater than 64% removal of bis(2-ethylhexyl) phthalate was observed in a low-loaded activated sludge reactor and a biological aerated filter(4). In a biodegradability screening test using an activated sludge inoculum based on carbon dioxide evolution, bis(2-ethylhexyl) phthalate reached 4 to 5% theoretical amount of CO2 after 28 days at an initial carbon content of 34.1 to 38.7 mg/L(5). In a trickling filter system and an activated sludge system, 76 and 71% removal of bis(2-ethylhexyl) phthalate was observed, respectively(6). A mean of 81.5% biodegradation of bis(2-ethylhexyl) phthalate was observed after 24 hours in semi-continuous activated sludge tests; 4 days were required to reach >90% biodegradation in the activated sludge die-away portion of this test(7). Bis(2-ethylhexyl) phthalate had a half-life of 23 days in wastewater treatment plants(8). Bis(2-ethylhexyl) phthalate was degraded 82% in 28 days using the modified Sturm test(9). Aerobic biodegradation products of bis(2-ethylhexyl) phthalate incubated in sewage sludge include 2-ethylhexanol, 2-ethylhexanal and 2-ethylhexanoic acid(10).

AEROBIC: In three soils, (14)C-bis(2-ethylhexyl) phthalate present at 10 mg/kg, mineralization ranged from 22 to 32% (14)CO2 after 60 days incubation(1). Bis(2-ethylhexyl) phthalate was decomposed slowly in soil with amounts of 15 to 50% remaining after 80 days(2). Bis(2-ethylhexyl) phthalate was biodegraded 30% in 189 days from a starting concentration of 127.32 mg/kg outdoors with controlled watering(3). Bis(2-ethylhexyl) phthalate was biodegraded over a 63 day period 34-50% in Neuherburg soil (24% clay, 2.6% organic carbon, pH 7.2), 28-41% in Ebersberger Forest soil (15% clay, 5.4% organic carbon, pH 3.4), and 24-36% in Baierbrunn soil (24% clay, 5.4% organic carbon, pH 4.5)(4). Observed biological half-lives for bis(2-ethylhexyl) phthalate under aerobic conditions in soil was 31 to 98 days(5). Bis(2-ethylhexyl) phthalate was biodegraded 75% in 42 days in sandy soil and sandy soil mixed with gravel/till taken from a plasticizer manufacturing site(6). Bis(2-ethylhexyl) phthalate, present at 1.5 ug/g, had half-lives of 158, 86, and 52 days at temperatures of 5, 10, and 20 °C, respectively, in sandy loam (clay 9.8% silt 11.3%, sand 78.9%, organic carbon 2.5%) and half-lives of 301, 125, and 55 days at temperatures of 5, 10, and 20 °C, respectively, in the same loam amended with sludge(7). Bis(2-ethylhexyl) phthalate had initial phase half-lives of 39, 58, 58, and 9 days and late phase half-lives of 51, 84, 147, and 35 days in sludge amended with quartz, sludge slurry, sludge amended soil, and sludge amended soil with strain SDE 2 bacteria, respectively(8). In general, biodegradation of bis(2-ethylhexyl) phthalate occurs in soil, but at a slower rate than in water, since adsorption onto the soil organic matter reduces the availability of this compound for degradation(9). Bis(2-ethylhexyl) phthalate, present at 100 mg/L, reached 69% of its theoretical BOD in 4 weeks using an activated sludge inoculum at 30 mg/L in the Japanese MITI test(10).

AEROBIC: River die-away tests have resulted in half-lives for bis(2-ethylhexyl) phthalate of 2 to 3 weeks(1-3). In oligotrophic lake samples, no degradation occurs(4). Observed biological half-lives for bis(2-ethylhexyl) phthalate under aerobic conditions in river water was 4.5 weeks and hydrosoil was 14 days(5). Bis(2-ethylhexyl) phthalate was biodegraded with a half-life of 60 to 70 hours in groundwater impacted by this compound, ethylbenzene, and xylenes(6). Bis(2-ethylhexyl) phthalate had an average aerobic biodegradation half-life of 14.8 days calculated in 6 river sediment samples taken from Taiwan rivers(7). In a 13-month (Jun 2006 to Jul 2007) experiment using sludge reed beds, bis(2-ethylhexyl) phthalate degradation half-life was 289-578 days(8).

AEROBIC: Using sewage sludge from a waste water treatment plant in Taoyaun, Taiwan, aerobic biodegradation rate constants under varying pH and temperature were analyzed for bis(2-ethylhexyl) phthalate(1):[Table#1081]

For more Environmental Biodegradation (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (6 total), please visit the HSDB record page.

The rate constant for the vapor-phase reaction of bis(2-ethylhexyl) phthalate with photochemically-produced hydroxyl radicals has been estimated as 2.2X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 16 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Bis(2-ethylhexyl) phthalate is not expected to undergo hydrolysis in the environment based on an aqueous hydrolysis half-life of 2000 years that was determined at pH 7(2). Bis(2-ethylhexyl) phthalate contains chromophores that absorb at wavelengths >290 nm and has been shown to undergo direct photolysis(3). Irradiation of bis(2-ethylhexyl) phthalate with a 300 W xenon lamp resulted in the decomposition of this compound with gaseous carbon dioxide being one of the main products; after 14 hours irradiation, evolved carbon dioxide reached 0.5 to 0.7 mg/g bis(2-ethylhexyl) phthalate(3). 2-Ethyl-1-hexene, 2-ethylhexanol, and phthalic acid were found in the residue of the irradiated bis(2-ethylhexyl) phthalate(3). Bis(2-ethylhexyl) phthalate exhibited a photodegradation half-life of <2 days(4).

Experimental BCF values range from a log 2 to 4 in fish and invertebrates(1-7). Log BCFs of 2.93 and 2.06 were measured in fathead minnows (Pimephales promelas)(2) and bluegill sunfish (Lepomis macrochirus), respectively(3). BCF values of <0.7-29.7 and 1-3.4 were reported using carp (Cyprinus carpio) which were exposed over an 8-week period to bis(2-ethylhexyl) phthalate concentrations of 0.1 and 1.0 ppm, respectively(8). According to a classification scheme(9), these BCFs suggest that bioconcentration in aquatic organisms is low to very high(SRC). Experiments with rainbow trout (Salmo gairdneri) showed that the majority of (14)C-bis(2-ethylhexyl) phthalate did not reach the systemic circulation of the fish, but was present in the exposure water as metabolites as a result of pre-systemic branchial metabolism of this compound during uptake from the water to the blood(10). Biota-sediment accumulation factors were 1.0, 0.5 and 1.3 in roach (Rutilus rutilus), chub (Leuciscus cephalus) and perch (Perca fluviatilis), respectively; fish were collected from the Orge River, France from Jul 2009 to Apr 2010(11). BCFs of 0.02-0.11 were reported for bis(2-ethylhexyl) phthalate in water spinach (Ipomoea aquatica) grown under different conditions on sludge from waste water treatment plants in China(12). BCFs of 6.71-93.70 L/kg were reported for bis(2-ethylhexyl) phthalate in the submerged water plant Potamogeton crispus L.; plants were grown in the Haihe River, China from Mar to May 2008(13).

Bis(2-ethylhexyl) phthalate bioconcentration factor for rainbow trout: 42-113; duration, 36 days, whole body. Bioconcentration factor for fathead minnow 155-886; duration, 56 days, whole body. Bioconcentration factor for Gammarus pseudolimnaeus (scud): 54-2,680 (from dry to wet weight); duration, 14-21 days, whole body. Bioconcentration factor for Aselius brevicaudus (sowbug): 14-50 (from dry to wet weight); duration, 21 days, whole body.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U028, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

/Contaminated packaging/ Dispose of as unused product.

/Product/ Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Offer surplus and non-recyclable solutions to a licensed disposal company.

Symbol: T; R: 60-61; S: 53-45