Dihexyl phthalate

334.45

334.45

201-559-5

42MAH1QFG5

4817

3082

DTXSID6025068

Clear, oily liuid

29173490

52.6

6.9

Di-n-hexyl phthalate is a yellow-brown oily viscous liquid with a slight aromatic odor. Insoluble in water. (NTP, 1992)

0.995 g/cm³

-58 °C

210 °C @ Press: 5 Torr

185-187°C/0.5mm

1.494

soluble in water (0.24 mg/L).

5 mm @ 20°C

11.5

Oral-Rat LD50: 29600 mg/kg

Combustible in case of open flame, high temperature and strong oxidant; burning emits irritating smoke

Slightly aromatic

Henry's Law constant = 2.57X10-5 atm-cu m/mol at 25 °C (est)

CONVERSION FACTORS: 13.65 MG/CU M= APPROX 1 PPM|Acidity (as phthalic acid) 0.01% max|Phthalate esters would be expected to have UV maxima in the 230 nm and 270 nm regions. /Phthalate esters/|... Resistance to migration from polymers, low temperature flexibility ... compatibility with polar polymers and additives over a wide range of compositions. /Phthalate esters/|Hydroxyl radical reaction rate constant = 1.49X10-11 cu cm/molec-sec at 25 °C (est)

Insoluble in water.

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

DI-N-HEXYL PHTHALATE is an ester. Esters react with acids to liberate heat along with alcohols and acids. Strong oxidizing acids may cause a vigorous reaction that is sufficiently exothermic to ignite the reaction products. Heat is also generated by the interaction of esters with caustic solutions. Flammable hydrogen is generated by mixing esters with alkali metals and hydrides. This compound can react with oxidizing materials and strong alkaline materials. (NTP, 1992)

Ⅲ

9

UN3082

36/37/38-62-63

26-36/37

TI1100000

Xi

Completely packed, lightly placed; storeroom ventilated, away from open flames, high temperature, and stored separately from oxidants

P201-P308 + P313

H360

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. 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 soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

... Can react with oxidizing materials.

Dihexyl phthalate is an indirect food additive for use only as a component of adhesives.

NTP/CERHR; Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Heptyl Phthalate (DnHP), 129 pp. (2003) NIH Publication No. 03-4489 includes: 1) the NTP Brief, 2) the Expert Panel Report on the Reproductive and Developmental Toxicity of DnHP, and 3) public comments received on the Expert Panel Report. As stated in the NTP Brief, ... the scientific evidence was insufficient to reach a conclusion regarding the potential for DnHP to adversely affect human development or reproduction. NTP-CERHR monographs are transmitted to federal and state agencies, interested parties, and the public and are available in electronic PDF format on the CERHR web site and in printed text or CD-ROM from the CERHR (National Institute of Environmental Health Sciences, P.O. Box 12233, MD EC-32, Research Triangle Park, NC; fax: 919-316-4511).|Nat'l Research Council Canada; Phthalate Esters in the Aquatic Environment (1980) NRCC No. 17583|USEPA; Ambient Water Quality Criteria Doc: Phthalate Esters (1980) EPA 440/5-80-067|USEPA/ECAO; Atlas Document for: Phthalate Esters (1980)|EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) Challenge Program's Robust Summaries and Test Plans. Available from the Database Query page at: http://www.epa.gov/hpv/pubs/hpvrstp.htm on Phthalate Esters Category, Dihexyl phthalate (84-75-3), 27 pp. (2007) as of April 29, 2008.

This chemical is combustible. (NTP, 1992)

|Danger|H360FD: May damage fertility; May damage the unborn child [Danger Reproductive toxicity]|P201, P202, P281, P308+P313, P405, and P501|H360 (100%): May damage fertility or the unborn child [Danger Reproductive toxicity]|Aggregated GHS information provided by 46 companies from 4 notifications to the ECHA C&L Inventory.|H360Df: May damage the unborn child; Suspected of damaging fertility [Danger Reproductive toxicity]|Warning|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P260, P264, P270, P273, P301+P312, P309+P311, P330, P391, P405, and P501|H360: May damage fertility or the unborn child [Danger Reproductive toxicity]|P201, P202, P260, P273, P281, P308+P313, P314, P391, P405, and P501

Excerpt from ERG Guide 171 [Substances (Low to Moderate Hazard)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

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 store this chemical under ambient temperatures, and keep it away from oxidizing materials. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

Combustible

To fight fire use, foam, carbon dioxide, dry chemical.

SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning.

SEDIMENT: The concentration of dihexyl phthalate in the 1 to 10 cm layer of a sediment core from Chesapeake Bay was 5.6 ppb (dry wt)(1). The concentration of dihexyl phthalate in the core layers between 60 and 100 cm ranged from 2.9 to 4.0 ppb(1). Dihexyl phthalate was found in sediment samples taken Jan to Aug 2000, from Zhonggang, Keya, Erren, Gaoping, Donggang and Danshui rivers in Taiwan at concentrations ranging from not detected to 1.9 ug/g(2).

INDOOR AIR: Dihexyl phthalate, several isomers, was identified in association with airborne particles in one or more office buildings(1). The representative indoor concentration of dihexyl phthalate was 5.0 ng/cu m(1).

Dihexyl phthalate was detected in 5 of 6 residential and office dust samples at concentrations of 0.308-3.14 ug/g dust(1).

practically nontoxic

The effects of phthalate esters of branched chain alcohols, typified by di-(2-ethylhexyl)phthalate (DEHP) differ from those of esters of straight chain alcohols typified by di-n-hexyl phthalate (DnHP). The former induce liver enlargement and proliferation of hepatic peroxisomes, while the latter cause no peroxisome proliferation but cause fat accumulation in the liver. Both classes of phthalate esters are hypolipidaemic and cause thyroid changes associated with an increased rate of thyroglobulin turnover. As phthalate esters are used as mixtures, ... the effect of mixtures of the compounds /were examined/. Groups of five male Wistar albino rats were administered either control diet or diets containing either 10,000 ppm of DEHP, 10,000 ppm of DnHP or 10,000 ppm DEHP plus 10,000 ppm DnHP for 14 days. Rats receiving diets containing DEHP showed the expected increase in relative liver weight, in "peroxisomal" fatty acid oxidation and in CYP4A1. Serum triglyceride and serum cholesterol were also reduced, and the thyroid showed the histological changes mentioned above. Rats consuming diets containing DnHP showed no increase in relative liver weight and no induction of peroxisomal fatty acid oxidation or CYP4A1. However, there was a marked accumulation of fat in the liver. The fall in serum cholesterol was similar to that in rats treated with DEHP, but the fall of serum triglyceride was more pronounced. Thyroidal changes were again observed. In general, changes in rats treated with a mixture of DEHP and DnHP were very similar to those found with rats treated with DEHP alone. The liver was enlarged, and peroxisomal fatty acid oxidation and CYP4A1 were both induced. The amount of fat in the liver was much less than in rats receiving DnHP alone. Thyroid changes were similar to those in rats receiving the individual compounds. The effect on serum cholesterol seemed additive, but the levels of serum triglyceride were intermediate between the groups receiving the single compounds. PMID:

LD50 Rabbit dermal 20000 mg/kg|LD50 Rat oral 29600 mg/kg|LD50 Rat (female) 38.9 mL/kg

/BIRDS and MAMMALS/ The effects of dihexyl phthalate (DHP) on weight and food consumption in captive starlings (Sturnus vulgaris) were studied. All phthalate fed starlings had greater lipid means in the carcass homogenates than controls ... Differences in food consumption existed only in groups fed 250 ppm (other groups given 25 ppm).|/AQUATIC SPECIES/ Tests were performed with the freshwater invertebrates Hyalella azteca, Chironomus tentans, and Lumbriculus variegatus to determine the acute toxicity of six phthalate esters, including dimethyl phthalate (DMP), diethyl phthalate (DEP), di-n-butyl phthalate (DBP), butylbenzyl phthalate (BBP), di-n-hexyl phthalate (DHP), and di-2-ethylhexyl phthalate (DEHP). It was possible to derive 10-d LC50 (lethal concentration for 50% of the population) values only for the four lower molecular weight esters (DMP, DEP, DBP, and BBP), for which toxicity increased with increasing octanol-water partition coefficient (Kow) and decreasing water solubility. ... No significant survival reductions were observed when the three species were exposed to either DHP or DEHP at concentrations approximating their water solubilities.|/AQUATIC SPECIES/ Seven phthalate esters /including di-n-hexyl phthalate (DHP) were evaluated for their 10-d toxicity to the freshwater invertebrates Hyalella azteca and Chironomus tentans in sediment. ... All seven esters were tested in a sediment containing 4.80% total organic carbon (TOC) ... The five higher molecular weight phthalate esters /including DHP which was tested/ .... and found to be nontoxic in water-only tests ... were tested at single concentrations between 2,100 and 3,200 mg/kg dry weight. Preliminary spiking studies were performed to assess phthalate ester stability under test conditions. The five higher molecular weight phthalate esters in sediment had no effect on survival or growth of either C. tentans or H. azteca, consistent with predictions based on water-only tests and EqP theory. ...|/AQUATIC SPECIES/ A previous in vitro study has indicated that four phthalate esters (PAEs) could damage hemocytes and decreases the cellular immunity of prawns ... . The aim of this study was to investigate the in vivo effect of ... diethyl phthalate (DEP), dihexyl phthalate (DHP), dipropyl phthalate (DPrP) and diphenyl phthalate (DPP) on the defense system of the giant freshwater prawn, M. rosenbergii. PAE dissolved in corn oil was continuously fed to prawns for 8 days and five immune parameters (total hemocyte count, THC; ratio of granulocytes to hyalinocytes, G/H; intrahemocytic total phenoloxidase activity, PO(T); intracellular superoxide anion (O2-) production; transglutaminase (TGase) activity) were separately detected on days 1, 4 and 8. In addition, mortality was determined on days 4 and 8 after challenging the prawns with Lactobacillus garvieae. ... DHP demonstrated the lowest toxicity in that it only influenced the PO activity and O2- production before 4 days after treatment and caused 6.6% mortality on day 8. DEP decreased G/H, PO(T) and TGase activity on day 1 and reduced THC, G/H and PO(T) and caused 16.6% mortality on day 4; however, on day 8, it increased O2- production and caused no mortality. In the DPrP-treated group, a reduction of all the immune reactions apart from TGase activity and 22.2% mortality were detected on day 4. ... DPP ... decreased all the immune parameters apart from THC on days 1 and 4, but caused no mortality on day 4; but on day 8, an increase of O2- production and 17.7% mortality were detected. These results indicated that the immune reactions of prawns were variable due to the different toxic effects of PAEs. In addition, ... on day 8 after treatment, ... DHP, DPrP and DPP increased O2- production and did not influence the other four reactions, but mortality was detected in these groups.|/AQUATIC SPECIES/ Five phthalate esters, dimethyl phthalate, diethyl phthalate, dibutyl phthalate, dihexyl phthalate, and dioctyl phthalate, were tested for the hatching of brine shrimp (Artemia salina) eggs. Dibutyl phthlate ester was the most toxic of the phthalates tested. The toxic order of 3 of the esters was dibutyl phthalate greater than diethyl phthalate greater than dimethyl phthalate. Concentrations were 10, 20, and 50 ppm.

Di-N-hexylphthalate (DHP) was tested using the standard RACB protocol in both sexes of Swiss CD-1 mice. Data on food & water consumptions, body weights, & clinical signs collected in the Task 1 dose-range-finding study, were used to set doses for the continuous breeding part of the study at 0.0, 0.3, 0.6, & 1.2% in feed. Food consumption was not altered by the presence of DHP. These concns yielded calculated consumption estimates of nearly equal to 0.38, 0.80, & 1.67 g DHP/kg/day. In the continuous breeding phase, there were no live pups at the high dose & 1 litter of 4 pups at the middle dose. At the low dose, there was a significant reduction in the mean number of litters/pair (3.4, vs. 4.9 for the controls). Also at the low dose, the number of live pups/litter was reduced from 12.3 (controls) to 3.4, the proportion born alive was reduced by 14%. Pup weight adjusted for litter size was unchanged. These effects occurred in the absence of an effect on post-partum dam body weights. These significant reproductive effects prompted the determination of the affected sex in the Task 3 crossover mating trial using the control & 1.2% DHP-treated mice. Each group had 17-20 pairs of mice. The mating index (proportion of pairs showing copulatory plugs) in groups with 2 control partners, with a DHP-treated male, or a DHP-treated female, was 90%, 56%, & 88%, showing that the treated females were cycling & could be receptive, & that mating capability was reduced in the group of treated males . However, no treated females bore any litters, & only 1 of 18 treated males sired a litter. Effectively, both sexes were infertile at this level of DHP exposure. After the litters from the crossover were examined & discarded, the F0 adults from the control & 1.2% DHP groups were killed & necropsied. Body weight in the high dose males was 10% less than controls, & absolute testis weight was 70% less. Body-weight-adjusted liver weights were increased by 34%, & adjusted weights of kidney, epididymis, & seminal vesicles were reduced by 9, 23, & 18%, respectively. Body weight of DHP-exposed F0 females was 6% less than controls, while adjusted weights of liver was increased by 32% & adjusted kidney weights were decreased by 6%. Not surprisingly, epididymal sperm concn was reduced by 93%, & motility was reduced by 80%. Morphologic abnormalities were unchanged. There were insufficient animals from any DHP-treated group to provide F1 mice for an evaluation of the second generation. These data clearly demonstrate that DHP is a reproductive toxicant in mice. The relative sensitivity of the liver & the reproductive system cannot be judged from these data, but the reproductive effects occured in the absence of large changes (at the top dose) or any changes (low & middle doses) in body weight.

Dihexyl phthalate's production and use as a plasticizer(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an average Koc value of 5.26X10+5(2), indicates that dihexyl phthalate is expected to be immobile in soil(SRC). Volatilization of dihexyl phthalate from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.6X10-5 atm-cu m/mole(SRC) based upon its vapor pressure, 1.4X10-5 mm Hg(3), and water solubility, 0.05 mg/L(4). Dihexyl phthalate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). However, adsorption to soil is expected to attenuate volatilization(SRC). Biodegradation in soil may be important(SRC) based on a study using an acclimated inoculum of soil, sewage and activated sludge; >99% of dihexyl phthalate was lost and 77% of theoretical carbon dioxide was evolved after 28 days(5).|AQUATIC FATE: Based on a classification scheme(1), an average Koc value of 5.26X10+5(2), indicates that dihexyl phthalate is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 2.6X10-5 atm-cu m/mole(SRC), derived from its vapor pressure, 1.4X10-5 mm Hg(4), and water solubility, 0.05 mg/L(5). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 2.8 and 26 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 15 years if adsorption is considered(6). According to a classification scheme(7), an estimated BCF of 1,100(SRC), from a log Kow of 6.82(8) and a regression-derived equation(9), suggests the potential for bioconcentration in aquatic organisms is very 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(10). Estimated hydrolysis half-lives of 3.4 years and 130 days at pHs 7 and 8, respectively, suggest that hydrolysis is not expected to be an important process(11). In a river die-away test, it took 1 day to achieve 90% degradation(12). An initial concn of dihexyl phthalate of 25 mg/L was degraded 30 to 95% in fresh water after a 14 day incubation(10).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dihexyl phthalate, which has a vapor pressure of 1.4X10-5 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase dihexyl 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 26 hours(SRC), calculated from its rate constant of 1.5X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase dihexyl phthalate may be removed from the air by wet or dry deposition(SRC). Dihexyl phthalate does contain chromophores that absorb at wavelengths >290 nm(4) and therefore may be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of dihexyl phthalate with photochemically-produced hydroxyl radicals has been estimated as 1.5X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 26 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). A base-catalyzed second-order hydrolysis rate constant of 0.064 L/mole-sec(SRC) was estimated using a structure estimation method(2); this corresponds to half-lives of 3.4 years and 130 days at pH values of 7 and 8, respectively(2). Dihexyl phthalate does contain chromophores that absorb at wavelengths >290 nm(3) and therefore may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 1,100 was calculated in fish for dihexyl phthalate(SRC), using a log Kow of 6.82(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is very 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(4).|The bioconcentration of ring-labeled (14)C-dihexyl phthalate in Daphnia was determined for Daphnia exposed to the ester in water only (48 hr), food and water (48 hr), and in a mixed model system (14 days) in which the Daphnia was subject to predation by bluegill sunfish (1). The resulting BCF's were 1066, 1486, and 3254, respectively(1). No (14)C-dihexyl phthalate was detected in any Daphnia samples where the ester was introduced only as food(1). No definitive explanation was offered for the three-fold variation in BCF in the different systems, however the length of exposure rather than the complexity of the system, was considered the probable cause(1). The BCF in Daphnia are within the same order of magnitude and one order of magnitude less than that previously reported for two species of planktonic marine fish(1).

5.25e+04 L/kg|The average Koc of (14)C-dihexyl phthalate using three standard USEPA sediments (supplied and characterized by the EPA) was measured at 5.26X10+5(1). According to a classification scheme(2), this Koc value suggests that dihexyl phthalate is expected to be immobile in soil.

The Henry's Law constant for dihexyl phthalate is estimated as 2.6X10-5 atm-cu m/mole(SRC) derived from its vapor pressure, 1.4X10-5 mm Hg(1), and water solubility, 0.05 mg/L(2). This Henry's Law constant indicates that dihexyl phthalate is expected to volatilize from water surfaces(3). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(3) is estimated as 2.8 days(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(3) is estimated as 26 days(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 15 years if adsorption is considered(4). Dihexyl phthalate's estimated Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). Dihexyl phthalate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

SURFACE WATER: Dihexyl phthalate was detected at a concentration of 8 parts per trillion in the Mississippi River at Cairo, IL, but was not detected near its source, Lake Itasco, MN, or at sites near Memphis, TN and New Orleans, LA(1). Dihexyl phthalate was also found, but not quantified in rivers in Europe(2). Dihexyl phthalate was not found in river water samples taken Jan to Aug 2000, from Zhonggang, Keya, Erren, Gaoping, Donggang, Danshui, Puzi, Bazhang, Jiangiun, Jishui, Zengwin, Agongdian, Beinan and Waishuang rivers in Taiwan at a detection limit of 0.8 ug/L(3).|DRINKING WATER: Dihexyl phthalate has been identified in drinking water(1,2). It was found in drinking water from the Carrollton water plant in New Orleans, LA at a level of 0.03 ppb(3).|RAIN/SNOW: Snow surface analysis were done on seven sites in the Antarctic in 1993/1994 season, results for dihexyl phthalate are; Wood Bay at sea level (4 ng/L), Mt Melbourne at 200 meters above sea level (below detection limit), Vegetation Island at 220 meters above sea level (20 ng/L), Mt Melbourne at 600 meters above sea level (11 ng/L), McCarthy Ridge at 790 meters above sea level (2 ng/L), Mt Melbourne at 1130 meters above sea level (below detection limit) and Hercules Neve at 2960 meters above sea level (below detection limit)(1). Subsurface snow samples at McCarthy Ridge analyzed for dihexyl phthalate found concentrations of 29 ng/L at 1 meter deep and below detection limit at 2 and 3 meters deep(1). Subsurface snow samples taken at Hercules Neve gave dihexyl phthalate results of 67 ng/L at 1 meter deep, 32 ng/L at 2 meters deep and 5 ng/L at 3 meters deep(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 7149 workers (1974 of these were female) were potentially exposed to dihexyl phthalate in the US(1). Occupational exposure to dihexyl phthalate may occur through inhalation of aerosols and dermal contact with this compound at workplaces where dihexyl phthalate is produced or used. Use data indicate that the general population may be exposed to dihexyl phthalate via inhalation of ambient air and dust, ingestion drinking water, and dermal contact with products containing dihexyl phthalate(SRC).

No accumulation of dihexyl phthalate (25 or 250 ppm in the diet) occurred in starlings fed DHP for 30 days.|This study examined the extent of dermal absorption of a series of phthalate diesters in the rat. Those tested were dimethyl, diethyl, dibutyl, diisobutyl, dihexyl, di(2-ethylhexyl), diisodecyl, and benzyl butyl phthalate. Hair from a skin area (1.3 cm in diameter) on the back of male F344 rats was clipped, the 14(C)phthalate diester was applied in a dose of 157 mumol/kg, and the area of application was covered with a perforated cap. The rat was restrained and housed for 7 days in a metabolic cage that allowed separate collection of urine and feces. Urine and feces were collected every 24 hr, and the amount of (14)C excreted was taken as an index of the percutaneous absorption. At 24 hr, diethyl phthalate showed the greatest excretion (26%). As the length of the alkyl side chain increased, the amount of (14)C excreted in the first 24 hr decreased signficantly. The cumulative percentage dose excreted in 7 days was greatest for diethyl, dibutyl, and diisobutyl phthalate, about 50-60% of the applied (14)C; and intermediate (20-40%) for dimethyl, benzyl butyl, and dihexyl phthalate. Urine was the major route of excretion of all phthalate diesters except for diisodecyl phthalate. This compound was poorly absorbed and showed almost no urinary excretion. After 7 days, the percentage dose for each phthalate that remained in the body was minimal showed no specific tissue distribution. Most of the unexcreted dose remained in the area of application. These data show that the structure of the phthalate diester determines the degree of dermal absorption. Absorption maximized with diethyl phthalate and then decreased significantly as the alkyl side chain length increased.|Dermally absorbed DnHP was widely distributed throughout the body with no tissue containing >0.6% of the applied dose. There was no evidence for accumulation in any tissue.

n-Hexanol is a metabolite of DnHP. Hexanol is oxidized to the fatty acid and metabolized by the fatty acid oxidation pathway.|Strains of Mycobacterium and Nocardia isolated because of their ability to use di(2-ethylhexyl) phthalate (DEHP) as sole carbon source also grew on diethyl, diisooctyl, and butyl benzyl phtalates. As the two bacteria grew on di(2-ethylhexyl) phthalate , they excreted products that increased the solubility of di(2-ethylhexyl) phthalate and diisoctyl, dihexyl, and diisodecyl but not butyl benzyl or di-n-butyl phthalates. The solubilizer was produced by Mycobacterium sp even when grown on a water soluble substrate such as acetate. Addition of the solubilizer to culture media enhanced the degradation of di(2-ethylhexyl) phthalate and diisooctyl phthalate by Mycobacterium sp and Nocardia sp but not butyl benzyl phthalate. The extent of di(2-ethylhexyl) phthalate degradation by Mycobacterium sp in media amended with the solubilizer was reduced and the initiation of degradation was delayed if the solubilizer was first treated with protease. The effect of protease was not a result of its toxicity to Mycobacterium or use of the enzyme preparation for growth of the organism. The results thus show that microbial products increase the solubility of certain phthalates and enhance their degradation.

SYMPTOMS: Symptoms of exposure to this compound may include eye irritation, skin irritation or drying progressing to dermatitis, nausea, vomiting and dizziness. (NTP, 1992)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

/ALTERNATIVE and IN VITRO TESTS/ ... /It was/ previously found that some phthalates have nongenomic effects, exerting inhibitory effects on the functional activities of nicotinic acetylcholine receptors (nAChRs) in bovine chromaffin cells. ... This study ... investigated the effects of eight phthalates on the calcium signaling of human nAChR by using human neuroblastoma SH-SY5Y cells. All eight phthalates, with different potency, have inhibitory roles on the calcium signaling coupled with human nAChR, but not muscarinic acetylcholine receptors (mAChRs). For inhibition of human nAChR, the strongest to weakest potencies were observed as di-n-pentyl phthalate (DPP) --> butyl benzyl phthalate (BBP) --> di-n-butyl phthalate (DBP) --> dicyclohexyl phthalate (DCHP) --> di-n-hexyl phthalate (DHP) --> di-(2-ethyl hexyl) phthalate (DEHP) --> di-n-propyl phthalate (DPrP) --> diethyl phthalate (DEP). The potencies of phthalates were associated with their structures such that the most effective ones had dialkyl group carbon numbers of C4 or C5, with shorter or longer numbers resulting in decreased potency. At as low as 0.1 uM, DPP, DBP, BBP, DCHP and DHP significantly inhibited the calcium signaling of human nAChR. The IC50 of phthalates on human nAChR, ranging from 0.32 to 7.96 uM, were 10-50 lower than those for bovine nAChR. ...

di-n-hexyl phthalate

Grade: Technical

Plastics product manufacturing|1,2-Benzenedicarboxylic acid, 1,2-dihexyl ester: ACTIVE|1,2-Benzenedicarboxylic acid, 1,2-dihexyl ester, branched and linear: ACTIVE|1,2-Benzenedicarboxylic acid, C6-12-alkyl esters: INACTIVE|DnHP is often found as a minor component (less than 1%) of C6-10- phthalate mixtures; it may also be an isomer in mixtures of diisohexyl phthalates (DIHP) (CAS RN 68515-50-4) at levels of 25% or lower.

Method: EPA-OSW 8061A; Procedure: gas chromatography with electron capture detection; Analyte: dihexyl phthalate; Matrix: groundwater, leachate, soil, sludge, and sediment; Detection Limit: 0.068 ug/L.|Method: OSHA PV2076; Procedure: gas chromatography with flame ionization detector; Analyte: di-n-hexyl phthalate; Matrix: air; Detection Limit: 0.21 mg/cu m.

DETERMINATION OF DIHEXYL PHTHALATE IN FISH BY GAS CHROMATOGRAPHY-MASS SPECTROSCOPY (GS-MS) IS DESCRIBED.|THIS COMPOUND WAS ISOLATED FROM EXTRACTED LIPIDS BY A COMBINATION OF GEL PERMEATION, HIGH PERFORMANCE LIQUID, AND COLUMN CHROMATOGRAPHY, AND SELECTIVE PRECIPITATION OF IMPURITIES. CONCLUSIVE PROOF OF ITS STRUCTURE WAS OBTAINED FROM GAS CHROMATOGRAPHIC-MASS SPECTROMETRIC ANALYSIS AND PROTON NWR SPECTROSCOPY.