Dicyclohexyl phthalate

330.42

330.42

201-545-9

CGD15M7H2N

0651

6101

3082

DTXSID5025021

White granular solid|White, crystalline solid|Prisms from alcohol

29173400

52.6

5.2

White Solid

1.383 g/cm³ @ Temp: 20 °C

66 °C

222-228 °C @ Press: 4 Torr

207 °C

1.544

H2O: insoluble

Store below +30°C.

0.1 mm Hg ( 150 °C)

11.6 (vs air)

LD50 oral in rat: 30mL/kg

Mildly aromatic odor

Henry's Law constant = 1.0X10-7 atm-cu m/mol at 25 °C (est)

Phthalate esters would be expected to have UV maxima in the 230 nm and 270 nm regions. /Phthalate esters/|IN MOLTEN STATE DISSOLVES NITROCELLULOSE & BENZYL CELLULOSE; WHEN HOT DISSOLVES VEGETABLE WAXES & PARAFFIN WAX|Nonvolatile|Pour point: 63.5 °C|For more Other Experimental Properties (Complete) data for DICYCLOHEXYL PHTHALATE (6 total), please visit the HSDB record page.

Insoluble in water.

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

DICYCLOHEXYL 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 reacts with oxidizers. It hydrolyzes under acid and basic conditions. (NTP, 1992)

NONH for all modes of transport

1

36/37/38

26-36

TI0889000

Xi

Store in an area without drain or sewer access. Separated from acids and bases.

Stable under recommended storage conditions.

P261-P305 + P351 + P338

H315-H319-H335

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. Contaminated packaging Dispose of as unused product.

Strong oxidizing agents

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

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|Phthalate Esters; Environ Health Perspect 45: 1-210 (1982)|USEPA/ECAO; Atlas Document for: Phthalate Esters (1980)|For more Special Reports (Complete) data for DICYCLOHEXYL PHTHALATE (6 total), please visit the HSDB record page.

This chemical is combustible. (NTP, 1992)|Combustible.

|Danger|H317: May cause an allergic skin reaction [Warning Sensitization, Skin]|P201, P202, P261, P272, P280, P281, P302+P352, P308+P313, P321, P333+P313, P363, P405, and P501|H315 (17.32%): Causes skin irritation [Warning Skin corrosion/irritation]|P201, P202, P261, P264, P271, P272, P273, P280, P281, P302+P352, P304+P340, P305+P351+P338, P308+P313, P312, P321, P332+P313, P333+P313, P337+P313, P362, P363, P403+P233, P405, and P501|Aggregated GHS information provided by 254 companies from 14 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H360Df: May damage the unborn child; Suspected of damaging fertility [Danger Reproductive toxicity]|P201, P202, P281, P308+P313, P405, and P501|Warning|H315: Causes skin irritation [Warning Skin corrosion/irritation]|P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, and P501|H335: May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]|P201, P202, P261, P271, P281, P304+P340, P308+P313, P312, P403+P233, 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: Should a spill occur while you are handling this chemical, you should dampen the solid spill material with alcohol, then transfer the dampened material to a suitable container. Use absorbent paper dampened with alcohol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, 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 contaminate area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should store this material in a refrigerator away from oxidizers. (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)|Skin protection Handle with gloves.|Eye/face protection Safety glasses with side-shields conforming to EN166 Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Respiratory protection For nuisance exposures use type P95 (US) or type P1 (EU EN 143) particle respirator.For higher level protection use type OV/AG/P99 (US) or type ABEK-P2 (EU EN 143) respirator cartridges. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).|Body Protection impervious clothing, The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Wear self-contained breathing apparatus for firefighting if necessary.|Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

ACCIDENTAL RELEASE MEASURES Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

Increased /room/ ventilation and /SRP: decreased/ aspiration of vapors and dusts. /Phathalic esters/|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.|SRP: Contaminated protective clothing should be segregated in a manner such that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. The completeness of the cleaning procedures should be considered before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at the end of shift, but should remain at employee's place of work for cleaning.|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.|For more Preventive Measures (Complete) data for DICYCLOHEXYL PHTHALATE (7 total), please visit the HSDB record page.

Neat dicyclohexyl phthalate (DCHP) was slightly irritant to the skin of guinea pigs and rabbits, and the eyes of rabbits.

Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting.

Store in an area without drain or sewer access. Separated from acids and bases.

A harmful contamination of the air will not or will only very slowly be reached on evaporation of this substance at 20 °C.

NO open flames.

Use local exhaust.

Protective gloves.

Wear safety spectacles.

Dicyclohexyl phthalate was identified in the stack emission from coal combustion, and in the fly ash of combined coal/refuse combustion(1). Dicyclohexyl phthalate was detected in the dissolved form in secondary municipal sewage treatment effluent (Tamagawa River, Tokyo, Japan) at 5.54, 5.43, and 1.19 ng/L on May 21, June 10, and Nov 15, 1999, respectively(2). Dicyclohexyl phthalate was also detected in the particulate form at 0.64 ug/L in the May 21, 1999 sample (detection limit 0.1 ng/L)(2). Dicyclohexyl phthalate was not detected (detection limit 119 ug/kg-dm) in 4 sewage samples containing predominantly domestic sewage(3). Dicyclohexyl phthalate was detected in 4 of 6 sewage samples comprised of domestic sewage, storm runoff and small amounts of industrial effluent at concentrations of 472, 470, 349 and 199 ug/kg-dm(3). Dicyclohexyl phthalate was detected in 2 sewage samples comprised of domestic sewage, storm runoff and higher amounts of industrial effluent at concentrations of 1047 and 955 ug/kg-dm(3).

SOIL: Dicyclohexyl phthalate was found as a complex with fulvic acid in soil obtained from Prince Edwards Island, Canada(1). Soil samples collected from 26 sites in the JiangHan plain, China contained dicyclohexyl phthalate at not detected (detection limit not reported) to 301.9 ng/g in 30.8% of the samples; samples were collected June 2007 and Jan 2008(2).

INDOOR AIR: Dicyclohexyl phthalate was measured in 6 residential homes in Tokyo; concentrations were <0.0012-0.17 ug/cu m(1). Dicyclohexyl phthalate was detected in air samples from 27 homes in Tokyo, Japan at <0.001-0.75 ug/cu m; samples were collected April 10 to May 12, 2000(2). Dicyclohexyl phthalate was not found in 6 residential and office air samples(3).

Dicyclohexyl phthalate was detected in 6 of 6 residential and office dust samples at 0.569-5.38 ug/g dust(1). Dicyclohexyl phthalate was not detected (detection limit not reported) in house dust samples from the Chinese cities of Beijing, Guangzhou, Jinan and Urumchi, but was detected in house dust samples from the cities of Qiqihaer and Shanghai at not detected to 0.3 and not detected to 0.1 ug/g dry weight, respectively; samples were collected May to July 2010(2). Dicyclohexyl phthalate was also found in house dust samples collected Dec 2007 to Jan 2008 from Albany, NY at not detected to 0.3 ug/g dry weight(2). Dicyclohexyl phthalate was detected in 1 of 3 bar soap samples at >1-100 ug/g; 213 commercial products representing 50 product types were analyzed(3).

IDENTIFICATION AND USE: Dicyclohexyl phthalate(DCHP) is a white granular solid. It is used as a plasticizer to modify the properties of synthetic resins, in alkyd resins and cellulose nitrate to increase their stability to light and weathering, and to improve the chemical and physical properties of plastics by preventing creep. It is very stable to heat and light and imparts a glossy finish to extruded materials. It is also used in paper finishes and makes printers ink water-resistant. HUMAN EXPOSURE AND TOXICITY: There is limited evidence that occupational exposure to DCHP fumes may have caused asthma. In vitro DCHP effectively inhibit the calcium signaling of human nicotinic acetylcholine receptors. In vitro assay of human breast cancer MCF-7 cell proliferation demonstrated DCHP estrogenic activities. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine. ANIMAL STUDIES: Neat dicyclohexyl phthalate (DCHP) was slightly irritant to the skin of guinea-pigs and rabbits, and the eyes of rabbits. Liver and testicular effects were seen following repeated administration in oral studies in rats. It was of low acute oral toxicity in rats and mice. DCHP gave no indication of genotoxicity in studies using bacteria, including Ames tests. Prolonged estrous cycle length was found in rats exposed to 6000 ppm DCHP in diet. A decrease in the survival of pups was seen after rats were exposed to 500 mg/kg/d during gestation. DCHP may have antiandrogenic effects on male reproductive development before and after birth. DCHP affected the developing rat brain, resulting in hyperactivity, probably as a result of degeneration of mesencephalic tyrosine hydroxylase rather than alteration of the level of gene expression. ECOTOXICITY STUDIES: DCHP significantly inhibited activities of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) in liver of freshwater goldfish Carassius.

LD50 Rat oral > 3200 mg/kg|LD50 Rat oral 30 mL/kg|LD50 Rat ip > 3200 mg/kg|LD50 Mouse oral > 3200 mg/kg|For more Non-Human Toxicity Values (Complete) data for DICYCLOHEXYL PHTHALATE (6 total), please visit the HSDB record page.

/AQUATIC SPECIES/ Phthalates (PAEs) are chemical agents typically used as plasticizers in numerous industrial products. They have become ubiquitous contaminants due to their tendency to release into the environment. The present study was conducted to investigate the comparative antioxidant responses in liver of freshwater goldfish Carassius auratus injected intraperitoneally with 17 different PAEs at a concentration of 10 mg/kg for 10 days. The results indicated that these PAEs can adversely affect the antioxidant status, confirmed by the significantly inhibited activities of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase). Especially, the latter two enzymes constituted the most affected antioxidant enzymes after the exposure, and the lowest values were recorded for the catalase activity. The toxicity order was proposed via the integrated biomarker response, with dicyclohexyl phthalate the most toxic and diethyl phthalate the least. Overall, these findings may contribute to the risk assessments of these chemicals on aquatic species.

Phthalates are semivolatile organic compounds with a ubiquitous environmental distribution. Their presence in indoor environments is linked to their use in a variety of consumer products such as children's toys, cosmetics, food packaging, flexible PVC flooring among others. The goal of this study was to investigate the occurrence and concentration of phthalates in dust from homes in Kuwait and to assess non-dietary human exposure to these phthalates. Dust samples were randomly collected from 21 homes and analyzed for eight phthalates. The concentrations of total phthalates were log normally distributed and ranged from 470 to 7800 ug/g. Five phthalates [Di(2-ethylhexyl) phthalate (DEHP), Di-n-octyl phthalate (DnOP), Di-n-butyl phthalate (DBP), Benzyl butyl phthalate (BzBP), and Dicyclohexyl phthalate (DcHP)] were routinely detected. The major phthalate compound was DEHP at a geometric mean concentration of 1704 ug/g (median, 2256 ug/g) accounting for 92% of the total phthalates measured. Using the measured concentrations and estimates of dust ingestion rates for children and adults, estimated human non-dietary exposure based on median phthalate concentrations ranged from 938 ng/kg-bd/day for adults to 13362 ng/kg-bd/day for toddlers. The difference in exposure estimates between children and adults in this study supports previous reports that children are at greater risk from pollutants that accumulate indoors.

Dicyclohexyl phthalate's production and use as a plasticizer for nitrocellulose, ethyl cellulose, chlorinated rubber, polyvinyl acetate, polyvinyl chloride and other polymers(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), estimated log Koc values of 4.12-4.47(2-3), indicate that dicyclohexyl phthalate is expected to be immobile in soil(SRC). Volatilization of dicyclohexyl phthalate from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.0X10-7 atm-cu m/mole(SRC), based upon its vapor pressure, 8.69X10-7 mm Hg(4), and water solubility, 4 mg/L(5). Dicyclohexyl phthalate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). Dicyclohexyl phthalate reached 68.5% of its theoretical BOD in the Japanese MITI test(6), suggesting that biodegradation is an important environmental fate process in soil(SRC).|AQUATIC FATE: Based on a classification scheme(1), estimated log Koc values of 4.12-4.47(2-3), indicate that dicyclohexyl 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 1.0X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 8.69X10-7 mm Hg(5), and water solubility, 4 mg/L(6). Dicyclohexyl phthalate is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(4). According to a classification scheme(7), an estimated BCF of 5750(SRC), from an estimated log Kow of 6.2(2) and a regression-derived equation(2), 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(8). Hydrolysis is not expected to be an important process(SRC) based on estimated hydrolysis half-lives of 12 and 1.2 years at pHs 7 and 8, respectively(2). Dicyclohexyl phthalate had average biodegradation half-lives of 11.1 and 26.4 days under aerobic and anaerobic conditions, respectively, in river sediment samples(9), suggesting that biodegradation is an important environmental fate process in water(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dicyclohexyl phthalate, which has a vapor pressure of 8.69X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase dicyclohexyl 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 2.4X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase dicyclohexyl phthalate may be removed from the air by wet and dry deposition(SRC). Dicyclohexyl phthalate contains 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 dicyclohexyl phthalate with photochemically-produced hydroxyl radicals has been estimated as 2.4X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 16 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). A base-catalyzed second-order hydrolysis rate constant of 0.019 L/mole-sec(SRC) was estimated using a structure estimation method(1); this corresponds to half-lives of 12 and 1.2 years at pH values of 7 and 8, respectively(1). Dicyclohexyl phthalate contains chromophores that absorb at wavelengths >290 nm(2) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 5750 was calculated in fish for dicyclohexyl phthalate(SRC), using an estimated log Kow of 6.2(1) and a regression-derived equation(1). According to a classification scheme(2), 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(3).

Using a structure estimation method based on molecular connectivity indices(1), the log Koc of dicyclohexyl phthalate can be estimated to be 4.12(SRC). An estimated log Koc of 4.47 was reported for dicyclohexyl phthalate(2). According to a classification scheme(3), these log Koc values suggest that dicyclohexyl phthalate is expected to be immobile in soil.

The Henry's Law constant for dicyclohexyl phthalate is estimated as 1.0X10-7 atm-cu m/mole(SRC) derived from its vapor pressure, 8.69X10-7 mm Hg(1), and water solubility, 4.0 mg/L(2). This Henry's Law constant indicates that dicyclohexyl phthalate is expected to be essentially nonvolatile from moist soil and water surfaces(3). Dicyclohexyl phthalate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

GROUNDWATER: Dicyclohexyl phthalate was detected in groundwater at an unrestricted municipal land fill in Oklahoma at an estimated concentration of 0.2 ug/L, but not in an upgradient control well(1,2).

In April 2011, 72 commonly consumed foods were purchased from super markets in Albany, NY; dicyclohexyl phthalate was not detected (detection limit 0.2 ng/g) in beverages, milk, fish, fruits/vegetables, grain, beef, pork, poultry or meat and meat products(1). It was detected in 1 of 9, 1 of 3, 1 of 6 and 1 of 7 samples of other dairy, vegetable oils, condiments and infant food, respectively(1). Dicyclohexyl phthalate was detected in 11% of foods and beverages purchased from Norwegian grocery stores(2). Dicyclohexyl phthalate was detected at <0.01-18.6 mg/kg in 47 confectionary, snack products and biscuits wrapped in printed polypropylene film; a good correlation was found between the ink concentration and the food products(3). Dicyclohexyl phthalate was not detected in raw cow's milk collected from farms in Belgium(4).

Dicyclohexyl phthalate was not detected (detection limit 0.2 ng/g) in 2 milk samples purchased from super markets in Albany, NY in April 2011(1). Dicyclohexyl phthalate was not detected in raw cow's milk collected from farms in Belgium(2).|This survey determined the levels of eight phthalates - i.e. dimethyl phthalate (DMP), diethyl phthalate (DEP), diisobutyl phthalate (DiBP), di-n-butyl phthalate (DnBP), benzylbutyl phthalate (BzBP), di(2-ethylhexyl) phthalate (DEHP), dicyclohexyl phthalate (DCHP) and di-n-octyl phthalate (DnOP) - in several Belgian milk and dairy products. Samples were obtained from various farms, a dairy factory and from different shops in order to investigate phthalate contamination "from farm to fork". At several stages in the milk chain, product contamination with phthalates - mostly DiBP, DnBP, BzBP and DEHP - was observed. At farm level, the mechanical milking process and the intake of phthalate containing feed by the cattle were found to be possible contamination sources. At industry and retail level, contact materials including packaging materials were additional contamination sources for phthalates in milk and dairy products.|This study investigated the occurrence of dimethyl phthalate (DMP), diethyl phthalate (DEP), diisobutyl phthalate (DiBP), di-n-butyl phthalate (DnBP), benzylbutyl phthalate (BBP), di(2-ethylhexyl) phthalate (DEHP), dicyclohexyl phthalate (DCHP) and di-n-octyl phthalate (DnOP) in raw cow's milk and feed from Belgian farms in order to determine their most relevant contamination pathways in milk. Measurable levels of DMP, DEP, DnBP, DCHP and DnOP were found in various feed samples, although they were not observed in milk. A plausible explanation for this is that they are rapidly metabolised in cows. DEHP and in a smaller degree also DiBP and BBP levels in milk seemed to vary across seasons and farms. DiBP and BBP levels were lower in summer than in winter milk, which was in contrast with what was observed for DEHP. This is possibly due to another feed composition during summer and winter. Comparing BBP and DEHP concentrations in manually with those in mechanically obtained milk revealed that, besides environmental contamination via feed ingestion, contact materials used during the mechanical milking process is another important contamination pathway. Concentrations observed in this study confirm the decreasing trend of DEHP in European cow's milk owing to the substitution of DEHP by other plasticisers.

According to the 2012 TSCA Inventory Update Reporting data, 3 reporting facilities estimate the number of persons reasonably likely to be exposed in the manufacturing, processing, or use of dicyclohexyl phthalate in the United States may be as low as 25-49 workers up to the range of 50-99 workers per plant; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 3565 workers (967 of these are female) were potentially exposed to dicyclohexyl phthalate in the US(1). Occupational exposure to dicyclohexyl phthalate may occur through inhalation of aerosols and dermal contact with this compound at workplaces where dicyclohexyl phthalate is produced or used. Monitoring and use data indicate that the general population may be exposed to dicyclohexyl phthalate via inhalation of ambient air, ingestion of food and beverages, and dermal contact with consumer products containing dicyclohexyl phthalate(SRC).

The degradation product of dicyclohexyl phthalate, monocyclohexyl phthalate (MCHP), was detected (detection limit 0.7 ug/L) in <16% of 2540 urine samples collected in the United States National Health and Nutrition Examination Survey (1999-2000)(1). MCHP was not detected in the serum of 501 female and 502 male seniors from Uppsala, Sweden(2). MCHP 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).

The phthalic acid esters and/or their metabolites are readily absorbed from the intestinal tract, the intraperitoneal cavity, and the lung. There is also evidence indicating that these esters can be absorbed through the skin. The vehicle can play an important role in the absorption, distribution, and elimination of the ester. /Phthalic acid esters/|Absorbed esters of phthalic acid esters (or their metabolites) distribute quite repidly to various organs and tissues both in animals and humans, especially the liver, kidney, and bile. /Phthalic acid esters/|Pharmacokinetic studies have been performed using ingestion, absorption through skin, and injection. Phthalates were readily taken up, distributed, metabolized, and excreted by all three routes of exposure. /Phthalates/

Hepatic preparation from rat, baboon and ferret hydrolyzed dicyclohexyl phthalate to its corresponding monoester derivative. Intestinal preparation from the 3 animals and from man catalyzed the monohydrolysis of phthalate diester.|The phthalate diesters are rapidly metabolized to the monoester both in the intestine and following absorption. The rate of hydrolysis is greater for the lower molecular weight esters. The monoester may undergo further oxidation of the alcohol side chain, but further hydrolysis is minimal. Suggest that the half hydrolysis of diester substrates is due to the anionic charge of the free carbonyl group inhibiting formation of the enzyme-substrate complex. /Phthalate diesters/|Orally administered phthalic acid esters are most probably absorbed from the gut primarily as monoesters. The hydrolysis of dimethyl phthalate, di-n-butyl phthalate, dioctyl phthalate, di-2-ethylhexyl phthalate, diethyl phthalate, and dicyclohexyl phthalate was studied. Hepatic preparations from the rat, ferret, baboon, and intestinal preparations from these species and from humans hydrolyzed these diesters to the monoesters. With the exception of dicyclohexyl phthalate, all of the diesters were hydrolyzed faster than di-2-ethylhexyl phthalate by intestinal preparations.|After 16 hr incubation, 1% dicyclohexylphthalate at 1 mg/mL was metabolized to the monoester by intestinal contents of rats and humans. The hydrolysis by stomach contents was negligible.|For more Metabolism/Metabolites (Complete) data for DICYCLOHEXYL PHTHALATE (8 total), please visit the HSDB record page.

Endocrine disrupting chemicals (EDCs) may potentially worsen infectious diseases because EDCs disturb human immune function by interfering with endocrine balance. To evaluate the influence of EDCs on the innate immune function of macrophages, we investigated the effects of 37 possible EDCs on lipopolysaccharide-induced activation of the IFN-beta promoter. Alachlor, atrazine, benomyl, bisphenol A, carbaryl, diethyl phthalate, dipropyl phthalate, kelthane, kepone, malathion, methoxychlor, octachlorostyrene, pentachlorophenol, nonyl phenol, p-octylphenol, simazine and ziram all inhibited the activation. Kepone and ziram showed strong inhibitory effects. Aldicarb, amitrole, benzophenone, butyl benzyl phthalate, 2,4-dichlorophenoxy acetic acid, dibutyl phthalate, 2,4-dichlorophenol, dicyclohexyl phthalate, diethylhexyl adipate, diethylhexyl phthalate, dihexyl phthalate, di-n-pentyl phthalate, methomyl, metribuzin, nitrofen, 4-nitrotoluene, permethrin, trifluralin, 2,4,5-trichlorophenoxyacetic acid and vinclozolin had no significant effects at 100 muM. These results indicate that some agrochemicals and resin-related chemicals may potentially inhibit macrophage function, which suggests that endocrine disruptors may influence the development of infectious diseases.|Xenoestrogen dialkyl phthalates, C(6)H(4)(COOC(n)H(m))(2), lack the phenolic hydroxyl group that is an essential structural component of the steroid A ring of 17 beta-estradiol. In order to examine whether dialkyl phthalates imitate the steroid structure, we have synthesized a series of 4-hydroxyl derivatives of dialkyl phthalates. The compounds were examined for their ability to displace [(3)H]17 beta-estradiol from the recombinant human estrogen receptor, which was expressed on Sf9 cells using the vaculovirus expression system. Dialkyl 4-hydroxyl phthalates were found to exhibit several-fold higher binding affinities compared to phthalates without the 4-hydroxyl group. From the analyses of receptor binding modes of dialkyl phthalates with and without the 4-hydroxyl group, it was deduced that the phthalic benzene ring mimics the steroid A ring. A biphasic binding curve observed for dicyclohexyl phthalate was also depicted by its 4-hydroxyl derivative, but it increased binding affinity only at the high affinity binding site. These data suggest that the phthalate benzene moiety recognizes the core of the estrogen receptor binding site and the hydrophobic interaction of the dialkyl moiety substantiates the binding characteristics of the phthalates. The present data indicate that even chemicals with slight structural analogy and weak receptor affinity can perturb the endocrine system when administered in high concentrations.

ACUTE/CHRONIC HAZARDS: This compound may cause irritation on contact. (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)

Fresh air, rest.

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.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Esters and related compounds/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilation if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Esters and related compounds/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Esters and related compounds/

/SIGNS AND SYMPTOMS/ There was limited evidence that occupational exposure to dicyclohexyl phthalate fumes may have caused asthma.|/CASE REPORTS/ A meat cutter experienced wheezing when working in area where price labels were heated. Only exposure to the emissions from the heated price labels evoked a response. Emissions contained phthalic anhydride, 2,5-di-tert-amyl quinone and dicyclohexylphthalate.|/ENDOCRINE MODULATION/ Phthalates are suspected to disrupt the endocrine system, especially through estrogenic effects. In the present study, we investigated the effects of various phthalates and compared them with those of estrogenic compounds that disrupt the female reproductive system. To assess the effects of these phthalates, alteration of the Calbindin-D9k (CaBP-9k) gene was measured as a biomarker because rat CaBP-9k gene carries an estrogen response element (ERE) which is involved in estrogen responsiveness of the gene during the estrous cycle. In this study, phthalates were tested for estrogenic properties in in vitro and in vivo models. First, the E-Screen assay was used to measure the proliferation of MCF-7 cells, a human breast cancer cell line. Treatments with 17beta-estradiol (E2; 9-fold) and 17alpha-estradiol (EE; 9-fold) induced MCF-7 cell proliferation at concentrations of 10(-9) M. Phthalates induced an increase in MCF-7 proliferation at concentration of 10(-6) M up to 10(-4) M. Nbutyl benzyl phthalate (BBP; 6-fold vs. vehicle), dicyclohexyl phthalate (DCHP; 8-fold), 2-ethylhexyl phthalate (DEHP; 6-fold) and di-n-butyl phthalate (DBP; 7-fold) at the concentration of 10(-4) M induced in an increase in MCF-7 proliferation after 6 d of treatment compared to vehicle. However, significant increase in MCF-7 proliferation was induced by diethyl phthalate (DEP). Second, we investigated the expression of CaBP-9k in the uterus of immature rats after oral treatment with BBP, DCHP, DEHP, DBP or DBP (600 mg/kg per day) in this in vivo model, because the immature rat model is highly sensitive to exposure to estrogenic chemicals. None of the phthalates induced the expression of CaBP-9k mRNA and its protein in the neonatal uterus as analysed by Northern and Western blot analyses, respectively. Although phthalates induced an increase in MCF-7 cell proliferation by an estrogenic effect, they could not induce CaBP-9k expression in the in vivo system, suggesting that the assays of estrogenic effects of various phthalates conducted in vitro and in vivo expression of CaBP-9k may produce conflicting results.|/ALTERNATIVE and IN VITRO TESTS/ Phthalates are widely used in industry and cause public concern since they have genomic estrogenic-like effects via estrogen receptors. We previously found that some phthalates have nongenomic effects, exerting inhibitory effects on the functional activities of nicotinic acetylcholine receptors (nAChRs) in bovine chromaffin cells. In this study, we 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 microM, 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 microM, were 10-50 lower than those for bovine nAChR. We suggest that some phthalates effectively inhibit the calcium signaling of human nAChR, and these nongenomic effects are cause for concern.|For more Human Toxicity Excerpts (Complete) data for DICYCLOHEXYL PHTHALATE (14 total), please visit the HSDB record page.

dicyclohexyl phthalate

Adhesive manufacturing|1,2-Benzenedicarboxylic acid, 1,2-dicyclohexyl ester: ACTIVE

Method: EPA-RCA 8061A; Procedure: gas chromatography with electron capture detection; Analyte: dicyclohexyl phthalate; Matrix: groundwater, leachate, soil, sludge, and sediment; Detection Limit: 0.022 ug/L.|Dicyclohexyl phthalate was extracted from water with petroleum ether alone or with ethanol, purified on florisil and determined by gas chromatography/ electron capture detection. The sensitivity for phthalates was 1-10 ng.|A simple, rapid and efficient method, the dispersive liquid-liquid microextraction (DLLME) in conjunction with gas chromatography-mass spectrometry (GC-MS), has been developed for the extraction and determination of phthalate esters (dimethyl phthalate, diallyl phthalate, di-n-butyl phthalate, benzyl butyl phthalate, dicyclohexyl phthalate and di-2-ethylhexyl phthalate) in water samples. Factors relevant to the microextraction efficiency, such as the kind of extraction, the disperser solvent and their volume, the salt effect and the extraction time were investigated and optimized. Under the optimized extraction conditions (extraction solvent: chlorobenzene, volume, 9.5microL; disperser solvent: acetone, volume, 0.50mL, without salt addition and extraction time below 5s), the figures of merit of the proposed method were evaluated. The values of the detection limit of the method were in the range of 0.002-0.008microgL(-1), while the RSD% value for the analysis of 1microgL(-1) of the analytes was below 6.8% (n=4). A good linearity (0.9962>/=r(2)>/=0.9901) and a broad linear range (0.02-100microgL(-1)) were obtained. The method exhibited enrichment factors and recoveries, ranging from 681 to 889 and 68.1 to 88.9%, respectively, at room temperature (25+/-1 degrees C). Finally, the proposed method was successfully utilized for the preconcentration and determination of the phthalate esters in different real water samples and satisfactory results were obtained.|Methodology for the determination of 15 phthalate diesters (dimethyl phthalate, diethyl phthalate, diisopropyl phthalate, diallyl phthalate, diisobutyl phthalate, di-n-butyl phthalate, di-n-pentyl phthalate, di-n-hexyl phthalate, benzyl butyl phthalate, dicyclohexyl phthalate, di-(2-ethylhexyl) phthalate, di-n-octyl phthalate, diisononyl phthalate, diisodecyl phthalate, and di-n-decyl phthalate) is described. The method was validated in-house and its broad applicability demonstrated by the analysis of high-fat, high-carbohydrate and high-protein foodstuffs as well as combinations of all three major food constituents. Following on from the analysis of the 20 UK Total Diet Study samples, 261 foodstuffs were purchased and tested for their phthalate levels. Phthalate diesters were confirmed to be present in 77 samples. Di-(2-ethylhexyl) phthalate was the most frequently detected (66 samples), although the highest levels found were for the isomeric mixture diisononyl phthalate. Additional studies confirmed that, for some foodstuffs, packaging materials did contribute to the phthalate diester concentration in the foodstuff and one example is presented.

The kovats retention index dicyclohexyl phthalate was determined by glass capillary column gas chromatography for identification of the esters in biological fluids. Column parameters were: 0.5% ov-101 coatings, 230 °C, helium or nitrogen as carrier gas; 0.5% se-30 coating, 250 °C; a flame ionization detector was used with both columns.