Diisononyl phthalate

Fires involving this material should be controlled using a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)

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

Rinse and then wash skin with water and soap.

Rinse with plenty of water for several minutes (remove contact lenses if easily possible).

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.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapours, 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, use absorbent paper to pick up all liquid spill material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with alcohol followed by washing with a strong soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

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

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

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

Avoid inhalation of vapor or mist.

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.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

Diisononyl phthalate metabolites, mono carboxyl isononyl phthalate (MCINP), mono hydroxyl isononyl phthalate (MHINP), mono oxo isononyl phthalate (MOINP) and mono isononyl phthalate (MINP) were analyzed in urine of 129 US adults with no documented exposure to diisononyl phthalate(1). Samples were collected in 2005 from a diverse demographic population(1).[Table#4948]

The diisononyl phthalate metabolites, monocarboxyl isononyl phthalate (MCOP) and mono isononyl phthalate (MiNP), were detected in 95.2 and 12.9% of 2548 urine samples at 0.7-4961 and 0.8-148.1 ug/L, respectively; samples were collected by the United States National Health and Nutrition Examination Survey (2005-2006)(1). MiNP was not detected in the serum of 501 female and 502 male seniors from Uppsala, Sweden(2). MiNP was detected in <20% of the urine samples collected from 3236 people (ages 6-49 years old) during the Canadian Health Measures Survey 2007-2009(3).

Diisononyl phthalate metabolites, mono hydroxyl isononyl phthalate (OH-MiNP), mono oxo isononyl phthalate (oxo-MiNP) and mono carboxyl isononyl phthalate (cx-MiNP) were analyzed in urine, breast milk and cord blood to determine exposure; all samples were collected from residents of central Taiwan(1). OH-MiNP and cx-MiNP were detected in 1 and 4 of 30 cord blood samples that were collected upon delivery at 1.79 and <0.25-4.05 ug/L, respectively. oxo-MiNP was not detected in cord blood samples. None of the metabolites were detected in 30 breast milk samples collected from this same population. Urine samples from 100 pregnant women were collected in the third trimester (Dec 2001-Nov 2002), along with urine from 30 two to three year olds (2003-2004) and 59 five to six year olds (2006-2007), and had the following results(1).

Diisononyl phthalate metabolites, mono-4-methyl-7-hydroxyl octyl phthalate (7OH-MMeOP), mono-4-methyl-7-oxo octyl phthalate (7oxo-MMeOP) and mono-4-methyl-7-carboxyl heptyl phthalate (7cx-MMeHP) were analyzed in serum of 938 pregnant women and 401 of their spouses from Greenland, Poland and the Ukraine(1).[Table#4950]

Diisononyl phthalate metabolites, monoisononyl phthalate (MiNP), monohydoxyl isononyl phthalate (MHiNP), monooxo isononyl phthalate (MOiNP) and monocarboxyl isooctyl phthalate (MCiOP) were analyzed in serial urine samples of 58 full term and 67 pre-term infants from birth to 14 months of age(1). Samples were collected at a hospital in Finland Aug 2006 to Mar 2008; collection was done at 1-3 days old, 7 days, at each month of age from 1 to 6 months, and again at 14 months. Results were(1):[Table#4951]

Phthalates, widely used in flexible plastics and consumer products, have become ubiquitous contaminants worldwide. This study evaluated the acute toxicity and estrogenic endocrine disrupting activity of butyl benzyl phthalate (BBP), di(n-butyl) phthalate (DBP), bis(2-ethylhexyl) phthalate (DEHP), diisodecyl phthalate (DIDP), diisononyl phthalate (DINP), di-n-octyl phthalate (DNOP) and their mixtures. Using a 72 h zebrafish embryo toxicity test, the LC50 values of BBP, DBP and a mixture of the six phthalates were found to be 0.72, 0.63 and 0.50 ppm, respectively. The other four phthalates did not cause more than 50% exposed embryo mortality even at their highest soluble concentrations. The typical toxicity symptoms caused by phthalates were death, tail curvature, necrosis, cardio edema and no touch response. Using an estrogen-responsive ChgH-EGFP transgenic medaka (Oryzias melastigma) eleutheroembryos based 24 h test, BBP demonstrated estrogenic activity, DBP, DEHP, DINP and the mixture of the six phthalates exhibited enhanced-estrogenic activity and DIDP and DNOP showed no enhanced- or anti-estrogenic activity. These findings highlighted the developmental toxicity of BBP and DBP, and the estrogenic endocrine disrupting activity of BBP, DBP, DEHP and DINP on intact organisms, indicating that the widespread use of these phthalates may cause potential health risks to human beings. /Mixture/

Diisononyl phthalate (DINP) has been widely used in polyvinyl chloride (PVC) products and is ubiquitous as a substitute; however, its toxicity due to exposure remains to be determined. This study investigated the oxidative damage induced by DINP and the induced production of the pro-inflammation cytokines interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-a). Oral exposure to DINP induced oxidative damage and inflammatory responses in liver and kidney tissues through the accumulation of ROS, which may be an underlying mechanism for its toxicity. These changes may contribute to hepatic and renal histopathological alterations. Our data suggest that oxidative stress is involved in DINP-induced toxicity and that the co-administration of melatonin exerts a protective effect against DINP-induced toxicity.

Plasticizers are additives used to increase the flexibility or plasticity of the material to which they are added, normally rigid plastic and as additives in paint and adhesives. They are suspected to interfere with the endocrine system, including the estrogen and the thyroid hormone (TH) systems. We investigated in vitro the thyroid hormone-like and estrogenic activities of a range of widely used plasticizers and phenols including benzyl butyl phthalate (BBP), dibutyl phthalate (DBP), dioctyl phthalate (DOP), diisodecyl phthalate (DIDP), diisononyl phthalate (DINP), di(2-ethylhexyl) phthalate (DEHP), bis(2-ethylhexyl) adipate (DEHA), 4-tert-octylphenol (tOP), 4-chloro-3-methylphenol (CMP), 2,4-dichlorophenol (2,4-DCP), 2-phenylphenol (2-PP) and resorcinol. The TH disrupting potential was determined by the effect on the TH-dependent rat pituitary GH3 cell proliferation (T-screen). The estrogenic activities of the compounds were assessed in MVLN cells, stably transfected with an estrogen receptor (ER) luciferase reporter vector. Furthermore, the combined effect of a multi-components mixture of six plasticizers was evaluated for its estrogenic and TH-like activities. All the tested compounds, but 2-PP, significantly affected the GH3 cell proliferation. tOP, BBP and DBP activated ER transactivity, whereas DEHP antagonized the 17beta-estradiol induced ER function. The mixture significantly induced ER transactivity in an additive manner, whereas in the T-screen, the observed mixture effect was lower than predicted, suggesting a potential antagonizing effect of the mixture. In conclusion, the tested plasticizers and phenols elicited endocrine-disrupting potential that can be mediated via interference with the estrogen and TH systems. Moreover, the observed mixture effect stresses the importance of considering the combined effect of the compounds for risk assessment of human health. /Mixture/

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

EC50; Species: Pseudokirchneriella subcapitata (Green algae) 2-3 instar; Conditions: freshwater, static, 22-24 °C, pH 7.6-7.9, hardness 25-50 mg/L CaCO3, alkalinity 25-50 mg/L CaCO3; Concentration: 1800 ug/L for 96 hr; Effect: decreased population abundance /> or = 95% purity/

LC50; Species: Pimephales promelas (Fathead minnow); Conditions: flow through, 20-24 °C, pH 6.6-7.2; Concentration: >0.19 mg/L for 96 hr

LC50; Species: Pimephales promelas (Fathead minnow); Conditions: static, 20+/-1 °C, pH 6.6-7.2; Concentration: >0.14 mg/L for 96 hr

LC50; Species: Lepomis macrochirus (Bluegill sunfish); Conditions: static, 20-23 °C, pH 6.6-7.2; Concentration: >0.17 mg/L for 96 hr

For more Ecotoxicity Values (Complete) data for DIISONONYL PHTHALATE (16 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), estimated log Koc values of 5.49-5.52(2-3), indicate that diisononyl phthalate is expected to be immobile in soil(SRC). Volatilization of diisononyl phthalate from moist soil surfaces is expected given an estimated Henry's Law constant of 1.5X10-6 atm-cu m/mole(SRC), based upon its vapor pressure, 5.4X10-7 mm Hg(4), and water solubility, 0.2 mg/L(4). However, adsorption to soil is expected to attenuate volatilization(SRC). Diisononyl phthalate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). A 74% of theoretical BOD using activated sludge in the Japanese MITI test(5) suggests that biodegradation is an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), estimated log Koc values of 5.49-5.52(2-3), indicate that diisononyl phthalate is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(4) based upon an estimated Henry's Law constant of 1.5X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 5.4X10-7 mm Hg(5), and water solubility, 0.2 mg/L(5). Using this Henry's Law constant and an estimation method(4), volatilization half-lives for a model river and model lake are 50 and 370 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond is 1640-1670 years if adsorption is considered(6). Diisononyl phthalate is not expected to undergo hydrolysis based on estimated hydrolysis half-lives of 3.4 years and 125 days at pHs 7 and 8, respectively(3). According to a classification scheme(7), an estimated BCF of 230(SRC), from an estimated log Kow of 9.37(3) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is high(SRC). However, bioconcentration studies on compounds which are structurally similar suggest that bioconcentration may be lower than that indicated by the regression-derived equations due to the ability of aquatic organisms to readily metabolize this class of compounds(8). Using a freshwater inoculum, >95% biodegradation was reached in 12 days(8), indicating that biodegradation is an important environmental fate process in water(SRC). However a much lower rate of <1 to 8% biodegradation in 28 days was observed using a freshwater sediment inoculum(9).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), diisononyl phthalate, which has a vapor pressure of 5.4X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase diisononyl 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 2.3X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase diisononyl phthalate may be removed from the air by wet and dry deposition(SRC). Diisononyl phthalate contains chromophores that absorb at wavelengths >290 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Diisononyl phthalate was detected in 84% of foods and beverages purchased from Norwegian grocery stores(1). In 1996, dinonyl phthalate (isomer not specified) was identified, not quantified, in 4 of 12 infant formulas from the UK(2). In a follow-up survey, diisononyl phthalate was not detected in 39 infant formula samples from the UK(2).

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

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

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

In 1996, dinonyl phthalate (isomer not specified) was identified, not quantified in 4 of 12 non-maternal infant formulas from the UK. In a follow-up survey, diisononyl phthalate was not detected in 39 non-maternal infant formula samples from the UK(1).

IDENTIFICATION AND USE: Di-isononyl phthalate (DiNP) is a mixture of phthalates with branched alkyl side chains of varying length (C8, C9, and C10). DiNP is primarily used to produce flexible plastics and has replaced di-2-ethylhexyl phthalate (DEHP) in some plastics, though not in medical products. DiNP is widely used in such products as toys, flooring, gloves, drinking straws, garden hoses, and in sealants used for food packaging. HUMAN EXPOSURE AND TOXICITY: No evidence of clinical sensitization or irritation was observed in human subjects. People exposed to DiNP will excrete small amounts of mono-isononyl phthalate (MiNP) and other secondary oxidative metabolites. These metabolites can be used to monitor occupational exposure to DiNP, as well as in epidemiological studies. ANIMAL STUDIES: The pivotal toxicological effect for DINP is considered to be the hepatic changes seen in various studies. In a two-year chronic toxicity study in rats, there was an increased incidence of spongiosis hepatis, accompanied by increased serum levels of liver enzymes and increases in absolute and relative liver and kidney weights in both sexes. DiNP administered to rodents produced liver and kidney toxicity. DINP is clearly carcinogenic to the rodent, inducing hepatocellular carcinoma in rats and mice of both sexes and mononuclear cell leukemia in male and female rats. There is limited evidence of carcinogenicity based upon renal tubular carcinoma in male rats. The carcinogenic effects in the liver of rodent species are linked to peroxisome proliferation and are no longer considered as relevant to humans. DINP appears to act by an alpha2u-globulin mechanism to cause renal tubular carcinoma, which is considered to be a rodent specific mechanism and unlikely to be relevant to a determination of human risk. In a developmental study in rats at dose levels up to 1000 mg/kg bw/day, visceral variations (dilated renal pelvis and hydroureter) were observed. In another study in rats, skeletal variations (rudimentary cervical and accessory 14th ribs) were observed. In chronic rat studies relative testis weights were statistically significantly increased with or without concurrent increase of absolute testis weights and decrease of body weights at high doses. DNIP produced behavioral changes in developmental studies. DINP is not mutagenic in vitro in bacterial mutation assays or mammalian gene mutation assay (with and without metabolic activation) and is not clastogenic in one cytogenetic assay in vitro on CHO cells and in one in vivo assay on bone marrow cell of rats. This suggests that DINP is not genotoxic in vivo or in vitro. ECOTOXICITY STUDIES: The observed toxicity to daphnids with most of the higher-molecular-weight phthalate esters appeared to be due to surface entrapment or a mode of toxicity that is not due to exposure to the dissolved aqueous-phase chemical. This pattern of observed toxicity with the lower-molecular-weight phthalate esters and not the higher-molecular-weight phthalate esters is consistent with previously reported acute toxicity studies for several aquatic species.

The average daily intake of diisononyl phthalate was estimated as 400-500 ng/kg body weight/day in studies of foods and beverages purchased from Norwegian grocery stores(1). The average daily intake of diisononyl phthalate can be >100 ug/kg body weight/day in infants and toddlers due to mouthing of soft plastic toys, eating food and dust(2). An analysis of indirect exposure models and urinary biomonitoring data of various population segments indicate an average daily intake of 1-2 ug/kg/day of diisononyl phthalate(3). The exposure of 37 workers from two companies that use diisononyl phthalate in the manufacturing of polyvinyl chloride film or compounding was assessed by monitoring of metabolites in urine; the highest daily intake was 26 ug/kg body weight/day(4).

/AQUATIC SPECIES/ A two-generation feeding study has been carried out with Oryzias latipes (Japanese killifish) ... . DINP1 /1,2-benzenedicarboxylic acid, di-C8-10-branched alkyl esters, C9-rich/ was added to dry flake food at 20 mg/kg. DINP, control (no treatment) and acetone control were divided into five replicate tanks (N = 50) per treatment. In the F0 generation 14-day old fish were fed at 5% body weight per day. The F0 adults were terminated at day 123. There were no statistically significant changes in mortality or fecundity between the treatment groups. There was no reduced egg production. There was a slight but statistically insignificant increase in egg viability in the DINP treated group when compared to the no treatment control. Evaluation of F1 and F2 embryos showed normal development except for a transient decrease in red blood cell pigmentation. This effect was observed in both the DINP treatment and the acetone control group. The only histopathological change observed in the F0 adults was a minor alteration in hepatocellular staining around the central vein. The male to female ratios (3:1) in all groups were similar. Phenotypic gender classification of male and female fish were histopathologically confirmed to be 100% correct. Ale somatic gonadal index and liver somatic index were not significantly different in any group. /1,2-Benzenedicarboxylic acid, di-C8-10-branched alkyl esters, C9-rich/

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

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

Used as a plasticizer for PVC and flexible vinyls; [Merck Index]

General purpose plasticizers for PVC applications and flexible vinyls.

Dialkyl phthalate ester plasticizer used to impart softness and flexibility to PVC products.

... Plasticizers, ... adhesives, plastisols, and nitrocellulose lacquer coatings. ...

... Nonplasticizer products, such as perfumes and cosmetics, and plasticizer products, such as vinyl swimming pools, plasticized vinyl seats (on furniture and in cars), and clothing (jackets, raincoats, boots, etc). /Phthalate esters/

For more Uses (Complete) data for DIISONONYL PHTHALATE (8 total), please visit the HSDB record page.

Phthalates are produced with a high degree of purity (> 99.5%), in terms of ester content. Trace impurities have been summarised from producers' data ... i-nonanol ca 0.04%, isononylbenzoate ca 0.03%, n-butylisononyl phthalate ca 0.1%, Water 0.02 - 0.03% ... Bisphenol-A may be included upon request by customer /From table/

2023: 10,000,000 - <50,000,000 lb

(1984) /PROBABLY/ LESS THAN 2.27X10+6 G

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. [Table#4954]

1,2-Benzenedicarboxylic acid, diisononyl ester is listed as a High Production Volume (HPV) chemical (65FR81686). Chemicals listed as HPV were produced in or imported into the U.S. in >1 million pounds in 1990 and/or 1994. The HPV list is based on the 1990 Inventory Update Rule. (IUR) (40 CFR part 710 subpart B; 51FR21438).

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: 1,2-Benzenedicarboxylic acid, 1,2-diisononyl ester. Aggregated National Production Volume: 100 to < 500 million pounds.

Non-confidential 2012 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: 1,2-Benzenedicarboxylic acid, 1,2-diisononyl ester. National Production Volume: 108,497,785 lb/yr.

DINP is produced by esterification of phthalic anhydride with isononyl alcohol in a closed system. Isononyl alcohol used in the synthesis of DINP is produced via ... the dimerization of butene ... . The reaction rate is accelerated by elevated temperatures (140-250 °C) and catalyst. Following virtually complete esterification, excess alcohol is removed under reduced pressure and the product is then typically neutralised, water washed and filtered.

DINP is manufactured by reaction of phthalic anhydride with iso-nonanol in the presence of an acid catalyst.

Regular and electrical grades /available from Badische /SRP: now BASF//

Commercially, diisononyl phthalate, DiNP, is not a pure compound but rather a mixture of materials with an average side chain length of 9. ...

Trade names: Palatinol N, Vestinol 9, Jayflex DINP-S (Production stopped in 1992). /From table/

Computer and Electronic Product Manufacturing

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

Commercially, diisononyl phthalate, DiNP, is not a pure compound but rather a mixture of materials with an average side chain length of 9. ...

DINP is not a pure substance, but a complex mixture containing mainly C9-branched isomers, with mean formula C26H42O4 ... /In a good quality chromatogram/ up to 40 peaks are attributed to DINP ... (37 after partial distillation) ... 5 constituents may be considered as principal (from ca 6 to ca 20%).

THE PROCESS OF COATING PVC OVER METAL IS DESCRIBED. GAS FUMES & POWDERS ESCAPE INTO THE AIR CONSISTING OF TDOP, DIISONONYL PHTHALATE (DINP), & PVC. TO PURIFY EMISSIONS, A PACKED COLUMN WITH BACK CRASHING IS PROPOSED.

Best estimate in content (%) of the different chain structures of the DINP: Methyl ethyl hexanols 5-10, Dimethyl heptanols 40-45, Methyl octanols 35-40, n-Nonanol 0-10 /From table/