クリスタルバイオレット

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.

In water & buffered water samples crystal violet was decomp & decolorized by photolysis & radiolysis.

1.5 g of water-insoluble poly-n-vinylpyrrolidone adsorbent was added to 15 mL waste water (absorbance 28.4) containing crystal violet at 20 deg, and after agitating the waste water was settled for 2 hr and centrifuged to remove pptd materials.

SMALL SPILLS AND LEAKAGE: You should dampen the solid spill material with acetone, then transfer the dampened material to a suitable container. Use absorbent paper dampened with acetone to pick up any remaining material. Seal your contaminated clothing and the adsorbent paper in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with acetone 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.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity 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 and plant life; and conformance with environmental and public health regulations.

Incineration: 1) Dissolve in such combustible solvent as alcohols, etc. Spray the soln into the furnace with afterburner and scrubber. 2) Pour into sodium bicarbonate or a mixture of sand and Na2CO3 /sodium carbonate/ (9:1). After mixing, transfer into a paper carton filled with packing paper. Burn in an open furnace, or more efficiently in the furnace with afterburner and scrubber.

1.3 [mg/m3]

14 [mg/m3]

83 [mg/m3]

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)

If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

LC50; Species: Oryzias latipes (Japanese Medaka) length 2 cm, weight 0.2 g; Conditions: freshwater, static, 25 °C; Concentration: 200 ug/L for 24 hr /formulation/

LC50; Species: Oryzias latipes (Japanese Medaka) length 2 cm, weight 0.2 g; Conditions: freshwater, static, 25 °C; Concentration: 100 ug/L for 48 hr /formulation/

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 6.1X10+5(SRC), determined from a structure estimation method(2), indicates that gentian violet is expected to be immobile in soil(SRC). The estimated pKa of gentian violet is 8.64(3), indicating that this compound will exist almost entirely in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization from moist soil is not expected because the compound exists as an cation and ions do not volatilize. Gentian violet is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.0X10-13 mm Hg at 25 °C(SRC), determined from a fragment constant method(5). Utilizing a river die-away test, transformation rates of 0.002 to 0.012/hour(6), corresponding to half-lives of 2.4 to 14.4 days(SRC), indicate that biodegradation may be an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 6.1X10+5, determined from a structure estimation method(2), indicates that gentian violet is expected to adsorb to suspended solids and sediment(SRC). The estimated pKa(3) indicates gentian violet will exist almost entirely in the cation form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process. According to a classification scheme(4), an estimated BCF of 3(SRC), from its log Kow of 0.51(5) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Utilizing a river die-away test, transformation rates of 0.002 to 0.012/hour(7), corresponding to half-lives of 2.4 to 14.4 days(SRC), indicate that biodegradation may be 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), gentian violet, which has an estimated vapor pressure of 1.0X10-13 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 gentian violet may be removed from the air by wet and dry deposition(SRC). Gentian violet absorbs light at wavelengths of 590 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

The CIR Expert Panel concluded that the data available on Basic Violet 1, Basic Violet 3, and Basic Violet 4 are insufficient to support the safety of these hair dye ingredients as used in cosmetic formulations.

Ingredients for which the data are insufficient and their use in cosmetics is not supported

Gentian Violet is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

Symptoms of low dose exposure include excessive salivation and eye-watering. Acute dose symptoms include severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Hypertension, hypoglycemia, anxiety, headache, tremor and ataxia may also result.

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from, as of November 6, 2012: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=548-62-9]

Using a structure estimation method based on molecular connectivity indices(1), the Koc of gentian violet can be estimated to be 6.1X10+5(SRC). According to a classification scheme(2), this estimated Koc value suggests that gentian violet is expected to be immobile. Gentian violet is a cationic dye(3). The estimated pKa of gentian violet is 8.64(4), indicating that this compound will exist almost entirely in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5).

/HUMAN EXPOSURE STUDIES/ /Investigators/ patch tested 11 patients with clinical signs of contact sensitivity to therapeutically used triphenylmethane dyes. Seven dyes were used, including Basic Violet 3. The patch tests were applied for 20 to 24 hours and were evaluated for 6 to 7 days. Because the skin was colored by the tested dyes, it was not possible to evaluate the erythematous reaction. Positive test reactions (itching +/-; isolated papules + ; edema, confluent papules, and infiltration ++; or vesicular reaction +++) were observed in 8 of the patients for Basic Violet 3.

/SIGNS AND SYMPTOMS/ Gentian Violet is a weak sensitizer when used as an antiseptic therapeutic dye, except when used on ulcers and eczematized skin. Gentian Violet may produce not only allergic contact dermatitis but also necrosis in the interiginous areas.

/SIGNS AND SYMPTOMS/ ... No serious side effects have been reported when used externally. However, oral administration can cause gastrointestinal irritation, and intravenous injection can cause depression in the white blood cell count. ...

/SIGNS AND SYMPTOMS/ Ingestion of gentian violet causes nausea, vomiting, diarrhea & abdominal pain even in therapeutic doses... severe systemic poisonings have not been reported in man.

For more Human Toxicity Excerpts (Complete) data for Gentian Violet (18 total), please visit the HSDB record page.

Crystal violet (CV) and leucocrystal violet (LCV) were found in the tissues of wild eels caught from surface waters under the influence of effluents discharged by municipal sewage treatment plants (STPs). LCV was the dominant residue detected with total concentrations up to 6.7 ug kg-1 fresh weight in tissues of eels /Anguilla anguilla/ caught from lakes, rivers and a canal in Berlin, Germany. The occurrence of the residues found in 35 out of 45 samples could directly be linked to the presence of discharges by municipal STPs into the receiving surface waters. CV is a multiple-use compound that is also used as a biological stain and to colour materials such as textiles, paints and printing inks. Thus, it seems very likely that the residues of CV found in the eel samples originate from such uses and from legal uses of CV as a veterinary drug for the treatment of ornamental fish. The results obtained from this study are the first report of background contamination by CV found in samples of fish not intentionally treated with this agent. Although the residues of CV and LCV measured in the tissues of the eels were very low, an oral exposure to residues of CV or LCV should be avoided with regard to their mutagenic and carcinogenic potential. According to European Union law, zero tolerance applies to all residues of CV and LCV found in food for human consumption, as CV is not registered for use as a veterinary drug.

Gentian violet's production and use as a dye for wood, silk, paper, in inks; as a biological stain(1), and as an antiseptic(2) may result in its release to the environment through various waste streams(SRC). Its use as a veterinary drug for the treatment of ornamental fish infected with the parasitic protozoa Ichthyophthirius multifiliis(3) may result in its direct release to the environment(SRC).

The Food and Drug Administration has determined that gentian violet is not generally recognized as safe for use in animal feed and is a food additive subject to section 409 of the Federal Food, Drug, and Cosmetic Act (the act), unless it is intended for use as a new animal drug, in which case it is subject to section 512 of the act. The Food and Drug Administration has determined that gentian violet is not prior sanctioned for any use in animal feed.

The Food and Drug Administration (FDA) has determined that gentian violet is not generally recognized as safe and effective for any veterinary drug use in food animals and is a new animal drug subject to section 512 of the Federal Food, Drug, and Cosmetic Act. FDA has determined that gentian violet is not exempted from new animal drug status under the "grandfather" provisions of the Drug Amendments of 1962 (21 U.S.C. 342).

The Food and Drug Administration has determined that gentian violet has not been shown by adequate scientific data to be safe for use in animal feed. Use of gentian violet in animal feed causes the feed to be adulterated and in violation of the Federal Food, Drug, and Cosmetic Act (the act), in the absence of a regulation providing for its safe use as a food additive under section 409 of the act, unless it is subject to an effective notice of claimed investigational exemption for a food additive under section 570.17 of this chapter, or unless the substance is intended for use as a new animal drug and is subject to an approved application under section 512 of the act, or an index listing under section 572 of the act, or an effective notice of claimed investigational exemption for a new animal drug under part 511 of this chapter or section 516.125 of this chapter.