Di(2-ethylhexyl) phthalate

Hazardous Air Pollutants (HAPs)

Carcinogens

Phthalate

Semi-Volatile Organic Compound (SVOC)

Plastics -> PUR; PVC (soft); ABS; (E)PS

Plastics -> Plasticisers

log Kow = 7.60

5.03

7.3

Plasticizers

Plasticizer

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

0.99

0.981 @25 °C

0.99

Liquid

Colorless, oily liquid

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

405 °F (NTP, 1992)

420 °F (215 °C) (Open cup)

215 °C o.c.

420 °F (open cup)

(oc) 420 °F

Danger

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.

Danger

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

Chemical: 1,2-Benzenedicarboxylic acid, 1,2-bis(2-ethylhexyl) ester

Hazard Traits - Bioaccumulation; Carcinogenicity; Developmental Toxicity; Endocrine Toxicity; Environmental Persistence; Hepatotoxicity and Digestive System Toxicity; Immunotoxicity; Reproductive Toxicity; Respiratory Toxicity

Regulation (EC) No 178/2002 (amended)

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

Status: Active Update: 19-01-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/15358

Restricted substance: Bis (2-ethylhexyl) phthalate (DEHP)

Special Hazards of Combustion Products: Irritating vapors and toxic gases, such as carbon dioxide and carbon monoxide, may be formed when involved in fire.

Combustible. Gives off irritating or toxic fumes (or gases) in a fire.

Di(2-ethylhexyl) phthlate (DEHP) is a manufactured chemical that is commonly added to plastics to make them flexible. DEHP is a colorless liquid with almost no odor. DEHP is present in plastic products such as wall coverings, tablecloths, floor tiles, furniture upholstery, shower curtains, garden hoses, swimming pool liners, rainwear, baby pants, dolls, some toys, shoes, automobile upholstery and tops, packaging film and sheets, sheathing for wire and cable, medical tubing, and blood storage bags.

Bis

NTP/CERHR; Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) phthalate (DEHP), 308 pp. (2006) NIH Publication No. 06-4476.[Available from, as of May 8, 2008: http://cerhr.niehs.nih.gov/evals/index.html]

European Chemicals Bureau; European Union Risk Assessment Report, Bis(2-ethylhexyl) phthalate (DEHP) (117-81-7) 2008) Prepared to evaluate information on health and the environment to determine the risks of exposure to humans and ecosystems..[Available from, as of December 29, 2009 http://ecb.jrc.it/documents/Existing-Chemicals/RISK_ASSESSMENT/REPORT/dehpreport042.pdf]

CA OEHHA/Reproductive and Cancer Hazard Assessment Section; Proposition 65 Maximum Allowable Dose Level (MADL) for Reproductive Toxicity for Di(2-ethylhexyl)phthalate (DEHP) by Oral Exposure p.3 (April 2006).

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

For more Special Reports (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (12 total), please visit the HSDB record page.

U028; As stipulated in 40 CFR 261.33, when 1,2-benzenedicarboxylic acid, bis(2-ethylhexyl) ester, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. 1,2-Benzenedicarboxylic acid, bis(2-ethylhexyl) ester is included on this list. Effective date: 10/04/82; Sunset date: 10/04/92.

As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of older pesticides to consider their health and environmental effects and make decisions about their continued use. Under this pesticide reregistration program, EPA examines newer health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether the use of the pesticide does not pose unreasonable risk in accordance to newer saftey standards, such as those described in the Food Quality Protection Act of 1996. Pesticides for which EPA had not issued Registration Standards prior to the effective date of FIFRA '88 were divided into three lists based upon their potential for human exposure and other factors, with List B containing pesticides of greater concern than those on List C, and with List C containing pesticides of greater concern than those on List D. Bis(2-ethylhexyl) phthalate is found on List C. Case No: 3112; Case Status: No products containing the pesticide are actively registered ... The case /is characterized/ as "cancelled." Under FIFRA, pesticide producers may voluntarily cancel their registered products. EPA also may cancel pesticide registrations if registrants fail to pay required fees or make/meet certain reregistration commitments, or if EPA reaches findings of unreasonable adverse effects.; Active ingredient (AI): Bis(2-ethylhexyl) phthalate; AI Status: The active ingredient is no longer contained in any registered pesticide products ... "cancelled."

Fire Extinguishing Agents Not to Be Used: Water.

Use water spray, foam, powder, carbon dioxide.

Fresh air, rest.

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

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

Rinse mouth. 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.

(General first aid procedures)

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.

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.

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.

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.

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.

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.

Bis(2-ethylhexyl) phthalate was detected in human adipose tissue at 0.30-1.15 ppm(1-2). Bis(2-ethylhexyl) phthalate was found in the serum of 25 of 41 young (12-83 months) Puerto Rican girls with premature breast development at 187-2,098 ug/L(3). Bis(2-ethylhexyl) phthalate had a mean concentration of 0.067 ug/g in breast milk(4). Bis(2-ethylhexyl) phthalate was found in 65 of 84 newborn cord blood samples at a mean concentration of 1.19 ug/mL(5). The median concentration of mono(2-ethylhexyl) phthalate in urine samples from 36 Japanese people collected May to June 2004 was 5.0 ug/L; this translates to an exposure rate of 2.7 ug/kg/day of the parent compound bis(2-ethylhexyl) phthalate(6).

Bis(2-ethylhexyl) phthalate was measured in personal air samples of pregnant New York women at 0.05-0.41 ug/cu m in samples taken Mar to Sept 2000 and in pregnant Krakow, Poland women at 0.08-1.1 ug/cu m in samples taken Nov 2000 to Mar 2001(1).

Bis(2-ethylhexyl) phthalate (DEHP) degradation products mono(2-ethyl-5-hydroxyhexyl) phthalate (MeHHP) and mono(2-ethyl-5-oxohexyl) phthalate (MeOHP) were analyzed in urine to determine exposure. The ug/g creatinine was used to determine the ug/kg/day of DEHP consumption(1).[Table#1083]

Bis(2-ethylhexyl) phthalate (DEHP) degradation products mono(2-ethylhexyl) phthalate (MEHP), 5-mono hydroxyl isononyl phthalate (5OH-MEHP), 2-ethyl-5-oxohexyl phthalate (5oxo-MEHP), 2-ethyl-5-carboxylpentyl phthalate (5cx-MEPP) and 2-mono carboxyl isononyl phthalate (2cx-MEPP) were analyzed in urine, breast milk and cord blood to determine exposure(1). Urine samples from 100 pregnant women were collected in the third trimester (Dec 2001-Nov 2002). From this same population, urine samples from 30 two to three year olds (2003-2004) and 59 five to six year olds (2006-2007) were collected. All samples were collected from residents of central Taiwan(1).[Table#1084]

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

Hepatic

[in animals: liver tumors]

In studies of the effects of DEHP ingestion on the metabolism of ethanol, there was a distinct difference between the action of single doses of 1,500-7,500 mg/kg DEHP and the same doses given over a 7-day period ... . The single dose appeared to decrease the metabolism of intraperitoneal ethanol, given 18 hours after DEHP, as reflected by an increase in the ethanol-induced sleeping time of the exposed rats and inhibition of hepatic alcohol dehydrogenase activity. On the other hand, when DEHP was given for 7 days before the ethanol, the ethanol-induced sleeping time was decreased and the activities of both alcohol and aldehyde dehydrogenase were increased. This indicates the changes in sleeping time were the result of more rapid metabolic removal of the alcohol from the system in the rats treated with repeated doses of DEHP and slower metabolism in the rats given one dose.

... One hypothesis is that altered zinc homeostasis is a cause of teratogenicity following DEHP exposure. On GD 9 (9 days post-coitus), CD-1 mice were given corn oil (vehicle) or DEHP 800 mg/kg bw by gavage. ... Maternal liver expression of metallothionein (MT)-I and MT-Il, enzymes that sequester zinc in liver and thus lower blood levels, were increased at 3.0-4.5 hours following DEHP exposure and then began returning to baseline levels at 6 hours following exposure. Maternal liver expression of zinc transporter-1 (ZnT-1), a transmembrane protein involved in zinc efflux, was not affected by DEHP exposure. Exposure to DEHP resulted in a down-regulation of MT-I, MT-Il, and ZnT-1 expression in embryonic brain from 3 to 6 hours following exposure. There was no effect on visceral yolk sac. A dose-response study was conducted in which pregnant mice were gavaged on GD 9 with 0, 50, 200, or 800 mg DEHP/kg bw. Dams were killed, and maternal liver and embryonic brains were collected at 3 hours following exposure. ... Up-regulation of MT-I ... in maternal liver reached statistical significance at 200 mg/kg bw/day DEHP ... /and/ MT-Il ... at 800 mg/kg bw. ... In embryonic brain, reductions in MT-I and ZnT-1 were significant at 200 mg/kg bw, and reductions in MT-Il were significant at 50 mg/kg bw. ... /It was/ concluded that exposure of dams to DEHP during periods of organogenesis can alter the expression of key fetal enzymes involved in zinc homeostasis.

... Four-week-old /F344 rats/ ... were stimulated with diethyistilbestrol or with pregnant mare serum gonadotropin (PMSG) following which ovaries were removed and granulosa cells harvested. Cells were cultured in the presence of 500 nM testosterone and 200 ng/mL FSH. MEHP ... was added to cultures /for 48 hr/ ... A comparison with other phthalate monoesters showed a decrease in estradiol in the medium (controlled for protein content) with MEHP 100 or 200 uM (27.8 or 55.6 mg/L) but not with comparable molar concentrations of monomethyl, -ethyl, -propyl, -butyl, -pentyl, or -hexyl phthalate. Monopentyl phthalate was associated with a decrease in estradiol production at 400 uM. mRNA for aromatase was estimated in media after culture with MEHP 0, 25, 50, or 100 uM (0, 7.0, 13.9, or 27.8 mg/L). Graphically, there appeared to be a concentration-dependent decrease in estradiol concentration and in aromatase mRNA; pair-wise comparisons with control were statistically significant for the 100 uM concentration for estradiol and for the 50 and 100 uM concentrations for aromatase mRNA. The peroxisome proliferator Wy-14,643 also decreased estradiol and aromatase mRNA. Cholesterol side-chain cleavage enzyme was not altered by MEHP ... . Aromatase protein was decreased by MEHP at concentrations of 100 and 200 uM (27.8 and 55.6 mg/L). In a final experiment, granulosa cells were incubated for 48 hours with MEHP 0 or 200 uM (0 or 56 mg/L) and 8-bromo-cyclic adenosine monophosphate (8-Br-cAMP) added for the last 24 hours. mRNA for aromatase and cholesterol side-chain cleavage enzyme and medium progesterone levels were increased by 8-Br-cAMP in the absence of MEHP. In the presence of MEHP, mRNA for aromatase and medium estradiol levels were suppressed, but there was no suppression of P450 side-chain cleavage enzyme mRNA or progesterone. ... The results /were interpreted/ as consistent with transcriptional suppression of aromatase by MEHP independent of the FSH-cAMP pathway. ... A peroxisome proliferator-activated receptor (PPAR) pathway /was proposed/ as a candidate mechanism for MEHP suppression of granulosa cell steroidogenic function. /MEHP/

... Granulosa cells were harvested from 4-week-old Fisher rats 24 hours after injection of pregnant mare serum gonadotropin (PMSG). Cells were cultured for 48 hours with 500 nM testosterone and 200 ng/mL FSH with or without MEHP ... 50 uM (13.9 mg/L). ... MEHP in culture reduced aromatase mRNA by >40% compared to control. The addition of a peroxisome proliferator-activated receptor (PPAR)-gamma antagonist partially reversed the decrease in aromatase mRNA. PPAR-alpha and gamma agonists reduced aromatase mRNA to an extent similar to that after treatment with MEHP. To test the hypothesis that MEHP activated PPAR-gamma plus activated retinoic acid X receptor (RXR) results in aromatase suppression mediated by the PPAR-gamma:RXR heterodimer, cells were treated with MEHP plus RXR or RAR ligands. All treatments decreased aromatase, with significant additional suppression by MEHP when it was added with 9-cis-retinoic acid. To demonstrate that MEHP activity could be mediated through PPAR-alpha, MEHP treatment was shown to increase mRNA for 17 beta-hydroxysteroid dehydrogenase IV, which is inducible by PPAR-alpha. The addition of a PPAR-gamma antagonist did not alter the MEHP induction of 17 beta-hydroxysteroid dehydrogenase IV, suggesting MEHP activation of the alpha-isoform of PPAR. Both MEHP and a selective PPAR-alpha agonist, but not a selective PPAR-gamma agonist, increased the expression of Ah receptor, CYP1B1, and epoxide hydrolase. Cholesterol side-chain cleavage enzyme was not induced by MEHP or by either PPAR isoform agonist. Heart-type fatty acid-binding protein (H-FABP) was induced by MEHP and by each specific PPAR isoform agonist. ... /It was/ concluded that MEHP effects on granulosa cell gene expression, which would serve to decrease estrogen production, were mediated by both PPAR pathways. /MEHP/

For more Interactions (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (21 total), please visit the HSDB record page.

Cancer, Developmental (effects while organs are developing), Hepatic (Liver), Immunological (Immune System), Renal (Urinary System or Kidneys), Reproductive (Producing Children)

Hepatic

Eyes, respiratory system, central nervous system, liver, reproductive system, gastrointestinal tract

Chronic and/or high levels of DEHP exposure may cause reproductive and developmental damage. This includes damaged sperm, delayed sexual maturity, and deficiencies in the development of male babies. DEHP may also cause liver and kidney damage, and is potentially carcinogenic. (L181, L182)

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.

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).

Because bis(2-ethylhexyl) phthalate is used as a plasticizer in polyvinyl chloride (plastic wrap) which may contact food, some bis(2-ethylhexyl) phthalate in foods may be due to migration from packaging materials(1). In Japan, concentrations in foodstuffs that were in contact with packaging material varied from 0 to 68 ppm(1). Bis(2-ethylhexyl) phthalate concentrations in processed canned tuna and market place salmon in Canada were 40-60 ppb(2).

Bis(2-ethylhexyl) phthalate was detected in 16 of 16 samples of 80 proof vodka at 62-212 ppb and 8 of 8 samples of 100 proof vodka at 144-326 ppb(1). It was also detected in 23 of 26 samples of flavored vodka at 128-492 ppb(1). Bis(2-ethylhexyl) phthalate was detected in the following foods packaged in glass containers capped with twist-off caps, mg/kg: wild cherry jam, 0.13; pickled chillies, 0.65; ketchup, 0.12; hot ketchup, 0.05; tomato juice, 0.05; and orange juice, 0.02(2). Bis(2-ethylhexyl) phthalate in egg whites of chicken eggs collected from retail stores in Japan in 1977 ranged from 0.05 to 0.4 ppm(3). Bis(2-ethylhexyl) phthalate had mean concentrations of 0.077, 0.53, 1.5, 0.21, 4.1, 0.46, 0.03, 0.5, 0.35, 0.21, 1.1, 0.94, 0.17, 0.2, 0.007, 0.062, 0.12, and 0.28 ug/g in beverages, cereal, other dairy, eggs, fat and oils, fish, fruits, grains, meat, nuts and beans, poultry, processed meat, vegetables, infant formula powder, infant formula liquid, breast milk, baby food, and other foods, respectively(4). United Kingdom Ministry of Agriculture, Fisheries and Food's surveillance of phthalates found bis(2-ethylhexyl) phthalate in infant formula in all 12 powders tested at up to 1 ug/g(5). Bis(2-ethylhexyl) phthalate was detected in 15 of 16 different cheese packages from 13 US cities at 1-22 ug/g, and was found 2-4 times higher in cheese where packaging labels with color or printing were located(5). Bis(2-ethylhexyl) phthalate was found in baby food in Japan; milk powder (0.408-0.442 ug/g), liquid (0.008-0.024), solid (0.229-0.403 ug/g), granule (1.042-1.424 ug/g)(6). Food samples collected over four days from a university restaurant in Paris, France contained bis(2-ethylhexyl) phthalate at 453, 117, 349, 138, 189, 302, 645, 156, 41.1, 43.2, 3.4, 172.7, 105.7, 170, 211, 313 and 146 ng/g wet weight in fish terrine, mixed salad, corn salad, radishes, lasagne, roast beef, chicken leg, mixed steak, Basmati rice, fried vegetables, fried potatoes, plain yogurt, Gruyere cheese, Camembert cheese, granny apple, black grapes, stewed apples and fruit salad, respectively(7).

The substance can be absorbed into the body by inhalation, through the skin and by ingestion.

inhalation, ingestion, skin and/or eye contact

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

ENVIRONMENTAL: Bis(2-ethylhexyl) phthalate was detected in human breast milk sampled five times in 21 women from Kingston, Ontario, Canada; samples were collected 2003 to 2004(1).[Table#1091]

ENVIRONMENTAL: Bis(2-ethylhexyl) phthalate was detected at 80 mg/L of dairy milk (whole milk basis, one sample), not detected in later samples from the same farm(1). Bis(2-ethylhexyl) phthalate was detected at 34-281 ng/g in baby milk powders purchased 2001 to 2002 from 11 different countries (Japan, Taiwan, Vietnam, Thailand, Indonesia, Hong-Kong, Turkey, UK, Germany, US, Canada), however the products were produced in 12 different countries (Japan, Taiwan, Vietnam, Turkey, UK, Germany, US, Canada, Spain, Netherlands, New Zealand, Denmark, Ireland)(2). Bis(2-ethylhexyl) phthalate had a mean concentration of 0.08 ug/g in dairy milk and 0.067 ug/g in human breast milk(3).

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)

U028; As stipulated in 40 CFR 261.33, when 1,2-benzenedicarboxylic acid, bis(2-ethylhexyl) ester, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. 1,2-Benzenedicarboxylic acid, bis(2-ethylhexyl) ester is included on this list. Effective date: 10/04/82; Sunset date: 10/04/92.

As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of older pesticides to consider their health and environmental effects and make decisions about their continued use. Under this pesticide reregistration program, EPA examines newer health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether the use of the pesticide does not pose unreasonable risk in accordance to newer saftey standards, such as those described in the Food Quality Protection Act of 1996. Pesticides for which EPA had not issued Registration Standards prior to the effective date of FIFRA '88 were divided into three lists based upon their potential for human exposure and other factors, with List B containing pesticides of greater concern than those on List C, and with List C containing pesticides of greater concern than those on List D. Bis(2-ethylhexyl) phthalate is found on List C. Case No: 3112; Case Status: No products containing the pesticide are actively registered ... The case /is characterized/ as "cancelled." Under FIFRA, pesticide producers may voluntarily cancel their registered products. EPA also may cancel pesticide registrations if registrants fail to pay required fees or make/meet certain reregistration commitments, or if EPA reaches findings of unreasonable adverse effects.; Active ingredient (AI): Bis(2-ethylhexyl) phthalate; AI Status: The active ingredient is no longer contained in any registered pesticide products ... "cancelled."

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Bis(2-ethylhexyl)phthalate is included on this list.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

(ME) MAINE 25 ug/L

(MN) MINESOTA 6 ug/L

Maximum contaminant levels (MCL) for synthetic organic contaminants apply to community water systems and non-transient, non-community water systems: Di(2-ethylhexyl) phthalate, MCL 0.006 mg/L.

EPA 6 ug/L

... A single dose of 1000 mg/kg bw MEHP (> 97% purity) in corn oil was administered by gavage to 5-week-old Sprague-Dawley rats, 28-day-old wild-type C57CL/6 mice, or 28-day-old gld mice. The gld mice express a dysfunctional fasL protein, which cannot bind to the fas receptor to initiate apoptosis. ... Following MEHP exposure, apoptosis was found to occur primarily in spermatocytes in both wild-type and gld mice. In wild-type mice, germ cell apoptosis was significantly increased from 6 to 48 hours following MEHP exposure. Apoptotic activity peaked between 12 and 24 hours with 5-fold increases compared to baseline levels. A significant ~2-fold increase in apoptosis compared to baseline levels was observed at 12 and 48 hours following MEHP exposure of gld mice. In both groups of mice, apoptotic activity returned to baseline levels by 96 hours following exposure. Western blot analyses revealed that fas expression significantly increased in wild-type mice (~ 3-fold) at 3 hours following MEHP exposure. There was no significant alteration in fas expression following MEHP exposure in gld mice. Expression of DR4, DR5, and DR6 proteins /which are fas-independent death receptors in the tumor necrosis factor (TNF) superfamily/ occurred in both wild-type and gld mice, but MEHP exposure did not increase expression in either strain. DR5 but not DR4 expression significantly increased in Sprague-Dawley rat testes (~1.5-fold) at 1.5 and 3 hours following MEHP exposure. Procaspase 8 cleavage products, downstream receptor-mediated signals of apoptotic pathways, were detected in testes of wild-type and gld mice, but expression was significantly increased only in gld mice at 6 hours following MEHP exposure. Electrophoretic mobility shift assays demonstrated that DNA binding of NFkappa3, a receptor-mediated downstream signal possibly involved in cell death or survival, was generally reduced in wild-type mice but upregulated in gld mice following MEHP exposure. ... /It was/ concluded that these findings demonstrate that germ-cell related death receptors and downstream signaling products appear to respond to MEHP-induced cell injury ... /MEHP/

Sprague-Dawley male rats were treated orally with 250, 500, or 750 mg/kg/d Di(2-ethylhexyl) phthalate (DEHP) for 28 days, while control rats were given corn oil. The levels of cell cycle regulators (pRb, cyclins, CDKs, and p21) and apoptosis-related proteins were analyzed by Western blot analysis. The role of PPAR-gamma (PPAR-gamma), class B scavenger receptor type 1 (SR-B1), and ERK1/2 was further studied to examine the signaling pathway for DEHP-induced apoptosis. Results showed that the levels of pRB, cyclin D, CDK2, cyclin E, and CDK4 were significantly lower in rats given 500 and 750 mg/kg/d DEHP, while levels of p21 were significantly higher in rat testes. Dose-dependent increases in PPAR-gamma and RXRalpha proteins were observed in testes after DEHP exposure, while there was a significant decrease in RXRgamma protein levels. In addition to PPAR-gamma, DEHP also significantly increased SR-B1 mRNA and phosphorylated ERK1/2 protein levels. Furthermore, DEHP treatment induced pro-caspase-3 and cleavage of its substrate protein, poly(ADP-ribose) polymerase (PARP), in a dose-dependent manner. Data suggest that DEHP exposure may induce the expresson of apoptosis-related genes in testes through induction of PPAR-gamma and activation of the ERK1/2 pathway.

Global gene expression profiling combined with an evaluation of Gene Ontology (GO) and pathway mapping tools /was used/ ... for identifying the molecular pathways and processes affected /to examine/ ... the acute effects caused by the non-genotoxic carcinogen and peroxisome proliferator (PP) diethylhexylphthalate (DEHP) in the mouse liver as a model system. Consistent with what is known about the mode of action of DEHP, /the/ GO analysis of transcript profiling data revealed a striking overrepresentation of genes associated with the peroxisomal cellular component, together with genes involved in carboxylic acid and lipid metabolism. Furthermore ... gene expression changes associated with additional biological functions, including complement activation, hemostasis, the endoplasmic reticulum overload response, and circadian rhythm /were revealed/. Together, these data reveal potential new pathways of PP action and shed new light on the mechanisms by which non-genotoxic carcinogens control hepatocyte hypertrophy and proliferation. ...

... Peroxisome proliferator-activated receptor alpha (PPAR-alpha), the nuclear receptor, is a member of the steroid hormone receptor superfamily and binds to DNA as a heterodimer with the retinoid X receptor (RXR). Peroxisome proliferator response elements (PPREs) have been found in genes for both peroxisomal and microsomal fatty acid-oxidizing enzymes. ... The species differences /responding to peroxisome proliferators, eg DEHP/, particularly with respect to humans compared to rats and mice, can be potentially attributed to ... the level of expression and functional capability of PPAR-alpha, the presence or absence of active PPREs in the promoter region of specific genes, and other aspects of interaction with transcriptional regulatory proteins. ... Marked species differences in the expression of PPAR-alpha mRNA have been demonstrated between rodent and human liver, with the latter expressing 1-10% of the levels found in mouse or rat liver ... PPAR-alpha protein expression /in human livers/ contained less than 10% of the level in mice. ... In most human samples studied, it was found that PPREs are mainly bound by other competing proteins that may block peroxisome proliferator responsiveness. In addition, the low levels of PPAR-alpha protein detected in human liver were lower than those estimated from RNA analysis and this was explained by the finding that a significant fraction of PPAR-alpha mRNA is mis-spliced in human liver. ... The truncated PPAR-alpha mRNA accounted for 25-50% of total PPAR-alpha mRNA in 10 human liver samples, while no truncated PPAR-alpha mRNA was found in livers of rats and mice. The truncated human PPAR-alpha mRNA was expressed in vitro, where it was shown to (a) fail to bind to PPRE, a necessary step for gene activation and (b) interfere with gene activation by expressed full-length human PPAR-alpha, in part due to titration of coactivator CREB-binding protein, an additional element of transcriptional regulation. ... Differential species sensitivity to peroxisome proliferators could depend on gene-specific factors. In the case of peroxisomal acyl-coenzyme A oxidase, the promoter regions containing PPRE responsible for transcriptional activation of the rodent gene are not present in the promoter region of the human gene ... The absence of a significant response of human liver to induction of peroxisome proliferation and hepatocellular proliferation is explained by several aspects of PPAR-alpha-mediated regulation of gene expression. ... Overall, these findings indicate that the increased incidence of liver tumors in mice and rats treated with di(2-ethylhexyl) phthalate results from a mechanism that does not operate in humans.

The levels of DEHP and MEHP in plasma have been studied in newborn infants given blood exchange transfusions. In one case the MEHP half-life was the same as for DEHP (about 12 hr), indicating that the hydrolysis of DEHP was the rate-limiting metabolic step. However, in other children the half-time of MEHP was longer than that of DEHP ... .

After the iv admin of radiolabelled DEHP, at least two elimination phases of radioactivity, with short half-lives (4.5-9 and 22 min, respectively), were observed in rat blood ... After 7 wk of oral admin, the elimination phase in the liver was considerably slower, the half-life being 3-5 days ... No accumulation of DEHP or MEHP was observed when the dosage was 2.8 g/kg/day for 7 days ... nor was there any in a long-term (5-7 weeks) feeding study at a dose level of 1 or 5 g/kg diet (corresponding to a daily dose of about 50 and 250 mg/kg bw) ... .

... The mean plasma elimination halflives of MEHP were 3.9, 3.1 and 2.8 hours, respectively for 25, 40 and 60 days old /Sprague-Dawley/ rats. ...

Two healthy male volunteers (47 and 34 years old) received 30 mg DEHP (> 99% pure) as a single dose or 10 mg/day of DEHP for 4 days ... A urinary elimination half-life of about 12 hours was estimated. ...

For more Biological Half-Life (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (9 total), please visit the HSDB record page.

It is hypothesized that the teratogen di(2-ethylhexyl) phthalate (DEHP) acts by in vivo hydrolysis to 2-ethylhexanol (2-EXHO), which in turn is metabolized to 2-ethylhexanoic acid (2-EXHA), the proximate teratogen. Teratological studies were conducted with Wistar rats, with administration of these agents on day 12 of geatation. On an equimolar basis DEHP was least potent, 2-ethylhexanol was intermediate, and 2-ethylhexanoic acid was the most potent of the three agents, which is consistent with the hypothesis. Similarity in the types of defects found with these agents also suggests a common mechanism, with 2-ethylhexanoic acid as the proximate teratogen.

When admin either iv or orally, it is rapidly metabolized to derivatives of mono-(2-ethylhexyl)-phthalate. ...

Rats have been reported to metabolize di(2-ethylhexyl) phthalate to 5-keto-2-ethylhexyl phthalate, 5-carboxyl-2-ethylpentyl phthalate, 5-hydroxy-2-ethylhexyl phthalate & 2-carboxymethylbutyl phthalate after initial hydrolysis to mono(2-ethylhexyl) phthalate.

African green monkeys & ferrets, in contrast to rats, excrete di(2-ethylhexyl) phthalate metabolites in urine as glucuronide derivatives of mono(2-ethylhexyl) phthalate. Glucuronidation appears to occur at the free carboxyl group, while 2-ethylhexyl substituent is oxidized to an alcohol.

For more Metabolism/Metabolites (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (41 total), please visit the HSDB record page.

DEHP is mainly absorbed via ingestion. It is hydrolyzed in the small intestine and absorbed as monoethylhexylphthalate (MEHP) and 2-ethylhexanol, then likely distributed to the adipose tissues and kidneys. MEHP is further metabolized via numerous oxidative reactions, resulting in the formation of 30 or more metabolites, some of which can be conjugated with glucuronic acid for excretion. Oxidation of 2-ethylhexanol primarily yields 2-ethylhexanoic acid and several keto acid derivatives. Most DEHP metabolites are excreted in the urine as glucuronide conjugates, while unmetabolized DEHP is excreted in the faeces. (L181)

When administered either IV or orally ... it is mainly excreted in urine and bile.

It appeared to be rapidly cleared from blood, most being removed within 5-7 hr of completion of dialysis.

In one study of subjects who received hemodialysis, blood transfusions or blood that had previously been in contact with polyvinyl chloride medical products, di(2-ethylhexyl) phthalate was found at the following levels (ug/g wet tissue): brain (1.9), heart (0.5), kidney (1.2-2.2), liver (1.5-4.6), lung (1.4-2.2) & spleen (2.2-4.7).

The levels of di(2-ethylhexyl) phthalate in neonatal heart tissue from infants who had undergone umbilical catheterization, either alone or with admin of blood products, were reported to be higher than those in similar tissue from untreated infants.

For more Absorption, Distribution and Excretion (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (67 total), please visit the HSDB record page.

Congress has permanently banned three types of phthalates (DEHP, DBP, BBP) in any amount greater than 0.1 percent (computed for each phthalate, individually) in (1) children's toys and (2) certain child care articles. di-(2-ethylhexyl) phthalate (DEHP), dibutyl phthalate (DBP), or benzyl butyl phthalate (BBP).

For bis(2-ethylhexylphthalate) (USEPA/OPP Pesticide Code: 295200) there are 0 labels match. /SRP: 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./

The active ingredient is no longer contained in any registered pesticide products ... "cancelled."

Plastics may contain from 1 to 40% di(2-ethylhexyl) phthalate 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. ... Di(2-ethylhexyl) phthalate is also used as a hydraulic fluid and as a dielectric fluid (a non-conductor of electric current) in electrical capacitors.

For more Uses (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (19 total), please visit the HSDB record page.

Plastics -> Typical concentration range in plastic materials -> 2.0 - 35.0%

2023: 10,000,000 - <25,000,000 lb

(1982) 251,067,000 lbs

(1977) 1.77X10+11 G

(1982) 1.14X10+11 G

(1986) 1.30X10+11 g

For more U.S. Production (Complete) data for BIS(2-ETHYLHEXYL) PHTHALATE (9 total), please visit the HSDB record page.

PLASTICIZER FOR POLYVINYL CHLORIDE, 87%; PLASTICIZER FOR OTHER VINYL RESINS, 7%; OTHER PLASTICIZER USE, 3%; OTHER NON-PLASTICIZER USE, 3% (1979 EST)

Polyvinyl chloride, 95%; other, 5% (1986) /estimated/

Reaction of 2-ethylhexanol and phthalic anhydride.

DEHP is commercially produced from esterification of phthalic acid anhydride and 2-ethylhexanol. Esterification is completed with an acid or metal catalyst or with no catalyst at high temperature.

Preparation: P. J. Garner, G. Watson, United States of America patent 2508911 (1950 to Shell).

Di(2-ethylhexyl) phthalate is produced commercially by the reaction of excess 2-ethylhexanol with phthalic anhydride in the presence of an acid catalyst such as sulfuric acid or para-toluenesulfonic acid.

Nonvolatile esters such as bis(2-ethylhexyl) phthalate can be obtained continuously by the following procedure: The mixture of acid or anhydride and alcohol together with sulfuric acid is introduced at the top of a plate column. An entrainer, e.g., benzene, is distilled through the column from below. The azeotrope of water and entrainer is drawn off the top and the ester accumulates in the sump.

Trade names: FLEXOL Plasticizer DOP, Essochem DOP ... Palatinol AH-L (med., 99.5%), Genomoll 100 (99.7%), Vestinol AH (99.5%)

USEPA/OPP Pesticide Code 295200; Trade Names: Bisoflex dop, Celluflex dop, Compound 889, Eviplast 80, Fleximel, Flexol dop, Hercoflex 260, Kodaflex dop, NCI-C52733, Octoil, Palatinol AH, Pittsburgh PX-138, Polycizer 162, PX-138, RC Plasticizer DOP, Sicol 150, Staflex DOP, Truflex DOP, Union Carbide flexol 380, Vestinol AH, Vinicizer 80, Witcizer 312.

Jayflex DEHP

Di(2-ethylhexyl) phthalate is available in a variety of technical grades (including a special grade for capacitor applications and a low residuals grade). Typical specifications are: minimal ester content, 99.0-99.6%; maximal moisture content, 0.1%; and acidity (as acetic acid or phthalic acid), 0.007-0.01%.

Trade names for di(2-ethylhexyl) phthalate include: Bisoflex; Compound 889; Diacizer DOP; DOP; Eastman DOP Plasticizer; Ergoplast; Etalon; Eviplast; Fleximel; Flexol DOP; Good-rite GP 264; Hatco-DOP; Kodaflex DOP; Monocizer DOP; Octoil; Palatinol AH; Pittsburgh PX 138; Plasthall DOP; Platinol AH; Reomol D 79P; Sicol 150; Staflex DOP; Truflex DOP; Vestinol AH; Vinycizer; Witcizer 312.

Chemical Classes -> Phthalates

Food Contaminant -> CONTAMINANT -> JECFA Functional Classes

Food Contaminant -> CONTAMINANT -> JECFA Functional Classes

Plastics -> Plasticisers

Plastics -> Polymer Type -> PUR; PVC (soft); ABS; (E)PS

PLASTICIZERS