Fast Orange

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.3X10+5(SRC), determined from a structure estimation method(2), indicates that C.I. Pigment Orange 5 is expected to be immobile in soil(SRC). Volatilization of C.I. Pigment Orange 5 from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 9.1X10-15 atm-cu m/mole(SRC), using a fragment constant estimation method(3). C.I. Pigment Orange 5 is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 9.3X10-12 mm Hg(SRC), determined from a fragment constant method(4). Biodegradation data were not available(SRC, 2009).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.3X10+5(SRC), determined from a structure estimation method(2), indicates that C.I. Pigment Orange 5 is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 9.1X10-15 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 10(SRC), from an estimated log Kow of 5.7(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data were not available(SRC, 2009).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), C.I. Pigment Orange 5, which has an estimated vapor pressure of 9.3X10-12 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase C.I. Pigment Orange 5 may be removed from the air by wet or dry deposition(SRC). C.I. Pigment Orangee 5 contains functional groups that are typically chromophores which absorb at wavelengths >290 nm(3); therefore C.I. Pigment Orange 5 may be susceptible to direct photolysis by sunlight(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of C.I. Pigment Orange 5 can be estimated to be 1.3X10+5(SRC). According to a classification scheme(2), this estimated Koc value suggests that C.I. Pigment Orange 5 is expected to be immobile in soil.

/HUMAN EXPOSURE STUDIES/ Eight patients suffering from pigmented contact dermatitis caused by the commercial Brilliant Lake Red R were patch tested with purified Sudan I and its several chemical analogs. Positive reactions were observed to Sudan I, Orange SS, Brilliant Lake Red R, Vacanceine Red, Yellow OB and Sudan II. Negative patch tests were obtained with Toluidine Red, Permanent Orange /Pigment Orange 5/, Lithol Red and Sudan III. The commercial Brilliant Lake Red R, which is said to be the most important causative agent of pigmented contact dermatitis, contained Sudan I as a major impurity. The patients reacting to Brilliant Lake Red R always gave a positive reaction to Sudan I, but those reacting to Sudan I did not always give a positive reaction to Brilliant Lake Red R. ...

An estimated BCF of 10 was calculated for C.I. Pigment Orange 5(SRC), using an estimated log Kow of 5.7(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for C.I. Pigment Orange 5 is estimated as 9.1X10-15 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that C.I. Pigment Orange 5 is expected to be essentially nonvolatile from water surfaces(2). The Henry's Law constant of C.I. Pigment Orange 5 indicates that volatilization from moist soil surfaces is not expected(SRC). C.I. Pigment Orange 5 is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 9.3X10-12 mm Hg(SRC), determined from a fragment constant method(3).

/GENOTOXICITY/ The induction of DNA damage by commonly used printing ink pigment, CI pigment orange 5 (CI 12075) ... was investigated in freshly isolated rat hepatocytes with the comet assay. ... The /pigment is/ virtually insoluble in aqueous solutions, and /has/ not been tested extensively for toxicological effects. CI pigment orange 5 increased the levels of DNA damage at 5 ug/mL (P < 0.02) ... . (P < 0.002). The effect of incubation time (20, 40, and 80 min) of the same concentrations of the pigment was tested. The levels of DNA damage were increased up to 80 min...

/GENOTOXICITY/ This study involved 19 dyes, selected from a list of 34 colorants considered to be representative of those ... used in the trade ... . They were tested for their ability to create revertants in the Ames Salmonella typhimurium/mammalian microsome reversion test system. Two variations of the standard Ames test were also used: the colorants were mixed with the warm top agar before spreading on the minimal plates, and the colorants were added to mouse liver homogenate, generating solution, and bacteria and shaken at 37 °C for 30 min before plating. All colorants were dissolved in dimethyl sulfoxide and all were tested in the presence and absence of liver microsomes. Two colorants, para red (color index (CI) number 12070) and dinitroaniline orange (CI 12075), were weakly mutagenic. Para red requires the presence of liver homogenate to produce mutagenicity. Dinitroaniline orange is a direct mutagen. Both colorants revert only the frameshift strains that were tested (TA1538 and TA98).

/GENOTOXICITY/ ... As a sequel to an earlier study of food colorants and related compounds, the Salmonella/mammalian microsome assay was used to test a number of colorants commonly used in drugs and cosmetics. These agents were mostly lakes, which are dye-alumina complexes, or insoluble salts from which the dyes were solubilized prior to mutagenicity testing. Agents causing mutations in Salmonella typhimurium were D & C Red No. 19, D & C Red No. 36 and D & C Orange No. 17. Rat liver microsomes were used.

/GENOTOXICITY/ Dyes (37) including 3 anthraquinone, 22 azo; 5 xanthene, 5 fluorandiol and 2 thioindigo dyes were tested for mutagenic potential with the Salmonella/mammalian-microsome test. Two frame-shift histidine mutants (TA1537 and TA98) and 2 base-pair substituted histidine mutants (TA1535 and TA100) of S. typhimurium were employed. Both the spot test and the plate-incorporation assay indicated that 1 azo dye, D&C Orange No. 17, was mutagenic with 3 of the bacterial test strains. The mutagenic response of D&C Orange No. 17 was depressed by the addition of the microsomal fraction from rat livers. Of the chemicals used to synthesize D&C Orange No. 17, beta-naphthol was not mutagenic but 2,4-dinitroaniline was mutagenic to the same Salmonella strains as D&C Orange No. 17. Dimethyl sulfoxide extracts of lipsticks of similar formula but with and without D&C Orange No. 17 were tested in the plate incorporation assay. Only those containing D&C Orange No. 17 were mutagenic and the dye was mutagenic at concentrations consumed in normal (human) daily use.

C.I. Pigment Orange 5 is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). C.I. Pigment Orange 5 contains functional groups which are typically chromophores and absorb at wavelengths >290 nm(1); therefore C.I. Pigment Orange 5 may be susceptible to direct photolysis by sunlight(SRC).

Occupational exposure to C.I. Pigment Orange 5 may occur through inhalation of dust and dermal contact with this compound at workplaces where C.I. Pigment Orange 5 is produced or used. Use data indicate that the general population may be exposed to C.I. Pigment Orange 5 via dermal contact with consumer products containing this compound. (SRC)

C.I. Pigment Orange 5's production and use in paints and printing inks may result in its release to the environment through various waste streams. If released to air, an estimated vapor pressure of 9.3X10-12 mm Hg at 25 °C indicatesC.I. Pigment Orange 5 will exist solely in the particulate phase in the atmosphere. Particulate-phase C.I. Pigment Orange 5 will be removed from the atmosphere by wet or dry deposition. C.I. Pigment Orange 5 contains functional groups that are typically chromophores which absorb at wavelengths >290 nm; therefore C.I. Pigment Orange 5 may be susceptible to direct photolysis by sunlight. If released to soil, C.I. Pigment Orange 5 is expected to be immobile based upon an estimated Koc of 1.3X10+5. Volatilization from moist soil surfaces is not expected to be an important fate process based upon an estimated Henry's Law constant of 9.1X10-15 atm-cu m/mole. C.I. Pigment Orange 5 is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Biodegradation data were not available. If released into water, C.I. Pigment Orange 5 is expected to adsorb to suspended solids and sediment based upon the estimated Koc. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated Henry's Law constant. An estimated BCF of 10 suggests bioconcentration in aquatic organisms is low. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. Occupational exposure to C.I. Pigment Orange 5 may occur through inhalation of dust and dermal contact with this compound at workplaces where C.I. Pigment Orange 5 is produced or used. Use data indicate that the general population may be exposed to C.I. Pigment Orange 5 via dermal contact with consumer products containing this compound. (SRC)

/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 if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the 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. /Poisons A and B/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. 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 ... . Anticipate seizures 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 ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

/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 ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/