| Section 1. Identification | |||
|---|---|---|---|
| Chemical Name | carbazole | CAS No. | 86-74-8 |
| Synonyms | dibenzopyrrole | Chinese Name | 咔唑 |
| Molecular Formula | C12HgN | Molecular Weight | 167.2066 |
| UN No. | 1325 | Data Source | PubChem (NIH/NLM) |
| GHS Hazard Classification | |
|---|---|
| Signal Word | WARNING |
| Pictograms | GHS07 · Irritant GHS08 · Health Hazard GHS09 · Environmental Hazard |
| Hazard Statements | H315H341H351H400H411H413H373H410H340 |
| Precautionary Statements | P203P264P273P280P302+P352P318P321P332+P317P362+P364P391P405P501P260P319 |
| Contents | |||
|---|---|---|---|
| Section 2 | Hazards Identification | Section 4 | First-Aid Measures |
| Section 5 | Fire-Fighting Measures | Section 6 | Accidental Release Measures |
| Section 7 | Handling and Storage | Section 8 | Exposure Controls / Personal Protection |
| Section 9 | Physical and Chemical Properties | Section 10 | Stability and Reactivity |
| Section 11 | Toxicological Information | Section 12 | Ecological Information |
| Section 13 | Disposal Considerations | ||
This chemical does not meet GHS hazard criteria for 10.9% (25 of 229) of reports.
H315 (10%): Causes skin irritation [Warning Skin corrosion/irritation]
H341 (52.8%): Suspected of causing genetic defects [Warning Germ cell mutagenicity]
H351 (70.3%): Suspected of causing cancer [Warning Carcinogenicity]
H400 (16.2%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]
H411 (48%): Toxic to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]
H413 (23.1%): May cause long lasting harmful effects to aquatic life [Hazardous to the aquatic environment, long-term hazard]
P203, P264, P273, P280, P302+P352, P318, P321, P332+P317, P362+P364, P391, P405, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 229 reports by companies from 19 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Reported as not meeting GHS hazard criteria per 25 of 229 reports by companies.
There are 18 notifications provided by 204 of 229 reports by companies with hazard statement code(s).
Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.
H351: Suspected of causing cancer [Warning Carcinogenicity]
H373: May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]
H410: Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]
P203, P260, P273, P280, P318, P319, P391, P405, and P501 (click each P-code to see the statement)
H340: May cause genetic defects [Danger Germ cell mutagenicity]
P203, P280, P318, P405, and P501 (click each P-code to see the statement)
H413: May cause long lasting harmful effects to aquatic life [Hazardous to the aquatic environment, long-term hazard]
P203, P273, P280, P318, P405, and P501 (click each P-code to see the statement)
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. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. 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.
OTHER: Since this chemical is a known or suspected carcinogen you should contact a physician for advice regarding the possible long term health effects and potential recommendation for medical monitoring. Recommendations from the physician will depend upon the specific compound, its chemical, physical and toxicity properties, the exposure level, length of exposure, and the route of exposure. (NTP, 1992)
Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)
Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.
Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.
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: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. 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.
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.
SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.
Product: Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Offer surplus and non-recyclable solutions to a licensed disposal company; Contaminated packaging: Dispose of as unused product.
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: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.
Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.
Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.
Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.
For more Preventive Measures (Complete) data for Carbazole (8 total), please visit the HSDB record page.
SMALL SPILLS AND LEAKAGE: If a spill of this chemical occurs, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with acetone and 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 absorbent paper in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with acetone 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 material under ambient temperatures. (NTP, 1992)
Keep container tightly closed in a dry and well-ventilated place.
0.66 [mg/m3]
7.2 [mg/m3]
43 [mg/m3]
NIOSH considers coal tar pitch volatiles to be potential occupational carcinogens. /Coal tar pitch volatiles/
8 Hr Time Weighted Avg (TWA): 0.2 mg/cu m. /Coal tar pitch volatiles, as benzene soluble aerosol/
Peak Exposure Recommendation: Transient increases in workers' exposure levels may exceed 3 times the value of the TLV-TWA level for no more than 15 minutes at a time, on no more than 4 occasions spaced 1 hour apart during a workday, and under no circumstances should they exceed 5 times the value of the TLV-TWA level. In addition, the 8-hour TWA is not to be exceeded for an 8-hour work period. /Coal tar pitch volatiles, as benzene soluble aerosol/
A1; Confirmed human carcinogen. /Coal tar pitch volatiles, as benzene soluble aerosol/
Biological Exposure Index (BEI): Determinant: 1-Hydroxypyrene (1-HP) in urine (with hydrolysis); Sampling Time: end of shift at end of workweek. BEI: None.; Biological monitoring should be considered for this compound based on the review; however, a specific BEI could not be determined due to insufficient data. /Polycyclic aromatic hydrocarbons/
For more Threshold Limit Values (TLV) (Complete) data for Carbazole (6 total), please visit the HSDB record page.
RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with a combination filter cartridge, i.e. organic vapor/acid gas/HEPA (specific for organic vapors, HCl, acid gas, SO2 and a high efficiency particulate filter). (NTP, 1992)
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).
Skin protection: Handle with gloves.
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.
Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).
For more Personal Protective Equipment (PPE) (Complete) data for Carbazole (6 total), please visit the HSDB record page.
Carbazole appears as white crystals, plates, leaflets or light tan powder. Sublimes readily. Exhibits strong fluorescence and long phosphorescence on exposure to ultraviolet light. (NTP, 1992)
White solid; [Hawley] Sublimes readily; Exhibits strong fluorescence and long phosphorescence on exposure to ultraviolet light; [CAMEO] Faintly beige powder; [MSDSonline]
Crystals from alcohol, benzene, toluene, glacial acetic acid
White crystals
White crystals, plates, leaflets or light tan powder
Characteristic odor
671 °F at 760 mmHg (NTP, 1992)
354.6 °C
354.7 °C @760 [mm Hg]
473 to 475 °F (NTP, 1992)
244.8 °C
220.0 °C (428.0 °F) - closed cup
less than 1 mg/mL at 66 °F (NTP, 1992)
In water, 1.80 mg/L at 25 °C
In water, 1.20 mg/L at 20 °C
1 gram dissolves in 3 mL quinoline, 6 mL pyridine, 9 mL acetone, 2 mL acetone at 50 °C, 35 mL ether, 120 mL benzene, 135 mL absolute alcohol; slightly soluble in petroleum ether, chlorinated hydrocarbons, acetic acid; dissolves in concentrated sulfuric acid without decomposition
Slightly soluble in pyrimidine, carbon disulfide; soluble in hot chloroform, toluene
1.1 at 64 °F (NTP, 1992) - Denser than water; will sink
1.10 at 18 °C/4 °C
1.10 @18°C
400 mmHg at 613 °F (NTP, 1992)
0.00000137 [mmHg]
1.5X10-6 mm Hg at 25 °C (extrapolated)
400 [mm Hg] @323 °C
log Kow = 3.72
Henry's Law constant = 1.16X10-7 atm-cu m/mole at 25 °C
Stable under recommended storage conditions.
When heated to decomposition it emits toxic fumes of /nitrogen oxides/.
-3.719X10+4 kJ/kg at 25 °C
65.7 kJ/mol at 540 K
Extremely weak base
pKa = -6.0
An approximated pKa value for carbazole, between those of indole and pyrrole (-2.4 and -3.8), indicates that the environmental chemistry of carbazole will involve only the free base.
132.9 Ų [M-H]- [CCS Type: DT; Buffer gas: N2; Ionization: ESI-; Dataset: TOXCAST; Source Identifier: DTXSID4020248]
130.2 Ų [M]+ [CCS Type: DT; Buffer gas: N2; Ionization: APCI+; Dataset: TOXCAST; Source Identifier: DTXSID4020248]
Exhibits strong fluorescence and long phosphorescence on exposure to UV light
Sublimes readily
Potassium hydroxide fusion yields n-potassium salt
Hydroxyl radical reaction rate constant = 4.0X10-11 cu cm/molecule-sec at 25 °C
Angular frequency
Insoluble in water.
Amines, Phosphines, and Pyridines
CARBAZOLE is an extremely weak base. It is incompatible with strong oxidizing agents. It reacts with nitrogen oxides. Potassium hydroxide fusion yields a salt. (NTP, 1992)
Incompatible materials: Oxidizing agents.
Exhibits strong fluorescence and long phosphorescence on exposure to ultraviolet light.
Strong oxidizers.
IDENTIFICATION AND USE: Carbazole is a solid. Carbazole occurs in the products of incomplete combustion of nitrogen-containing organic matter, e.g., tobacco. It is an important dye intermediate. It is also used in making photographic plates sensitive to ultraviolet light, and as reagent for lignin, carbohydrates, and formaldehyde. Carbazole exhibits wide range of biological activity upon modifications, including antibacterial, antimalarial, anticancer, and anti-Alzheimer properties. HUMAN EXPOSURE AND TOXICITY: There are no data available. ANIMAL STUDIES: Groups of 50 male and 50 female mice, six weeks of age, were fed a pellet diet containing technical grade carbazole at concentrations of 0.6, 0.3 or 0.15% or none (control group). The treatment was continued for 96 weeks; the animals were then fed a basal diet until killed in week 104. Neoplastic lesions were found in the liver and in the forestomach. The lesions in liver were classified as neoplastic nodules and hepatocellular carcinomas. The incidences of both types of lesion in livers of all the groups fed carbazole were significantly greater than that in the control group. In rats, no signs of maternal or developmental toxicity were noted after dermal administration of carbazole at doses of 2.5, 25.0, and 250.0 mg/kg. Carbazole was nonmutagenic with or without metabolic activation in the Ames assay. It is moderately clastogenic in mice when administered intraperitoneally. It induced dominant lathality and sperm-head abnormalities in male mice.
Carbazole
Semi-Volatile Organic Compound (SVOC) and(or) Waste-water effluent contaminant
Smith, C.D. and Nowell, L.H., 2024. Health-Based Screening Levels for evaluating water-quality data (3rd ed.). DOI:10.5066/F71C1TWP
Evaluation: There is sufficient evidence in experimental animals for the carcinogenicity of carbazole. Overall Evaluation: Carbazole is possibly carcinogenic to humans (Group 2B).
Group 2B: Possibly carcinogenic to humans
Volume 32: (1983) Polynuclear Aromatic Compounds, Part 1: Chemical, Environmental and Experimental Data
Volume Sup 7: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, 1987; 440 pages; ISBN 92-832-1411-0 (out of print)
Volume 71: (1999) Re-evaluation of Some Organic Chemicals, Hydrazine and Hydrogen Peroxide (Part 1, Part 2, Part 3)
Volume 103: (2013) Bitumens and Bitumen Emissions, and some N- and S-Heterocyclic Aromatic Hydrocarbons
IARC Carcinogen - Class 3: Chemicals are not classifiable by the International Agency for Research on Cancer.
PDF Document
Inadequate information to assess carcinogenic potential
HEAST Archive
LD50 Mice ip 200 mg/kg
LD50 Rat oral greater than 5000 mg/kg
A group of 40 Syrian golden hamsters [sex unspecified], six weeks of age, was given a single intraperitoneal injection of 20 mg/kg bw 2,2'-dioxo-N-nitrosodipropylamine (DOPN), while another group of 80 animals was left untreated. Beginning one week later, half of each group continued to receive basal diet alone, while the other half received basal diet containing 0.2% carbazole until they were killed at week 40. The numbers of GST-Ppositive foci, expressed as foci/sq cm, were: basal diet, 0; carbazole diet, 3.6 +/- 1.3 (p < 0.001); DOPN + basal diet, 9.2 +/- 4.1; DOPN + carbazole diet, 19.0 +/- 7.6 (p < 0.001).
Tobacco and coffee contain many compounds including azole group compounds, but a little information is available on the reproductive and teratogenic effects of them. In this study, we examined the single or the combination with ethanol effect(s) of some azole compounds on the embryo development. Gestation day 9.5 rat embryos were cultured for 48 hr with different doses of azole compounds (benzothiazole & carbazole (BZT & CBZ, 10(-6)-10(-4) M), 2-aminobenzothiazole (ABT, 10(-4)-5x1O(-4) M), thiazole (THZ, 10(-8)-10(-4) M), 2,5-dimethylbenzoxazole (DMBZ, 10(-6)-1O(-3) M)), alone or in combination with 0.3% ethanol. For evaluation of embryo development, morphological changes were observed and scored by the method of Van Maele-Fabry. Total protein and DNA content of the embryo were determined also. BZT, THZ and DMBZ inhibited otic and optic development. THZ and ABT inhibited the development of yolk sac circulatory system, and reduced yolk sac diameter and head length. THZ, CBZ and DMBZ inhibited brain development. All compounds caused significant reduction of total score and abnormal tail development. Ethanol also caused developmental toxicity in heart, brain, otic- and optic system and mandibular process. Except THZ, the embryotoxicity induced by the combination treatment of azole and ethanol was much greater than that by each chemical alone. These data suggest that some of azole compounds presented in tobacco or/and coffee aroma may cause embryotoxicity, and the addition of ethanol increased their toxicity in cultured rat embryos.
The present study examined photo-induced toxicity and toxicokinetics for acute exposure to selected polycyclic aromatic hydrocarbons (PAHs) in zebrafish. Photo-enhanced toxicity from co-exposure to ultraviolet (UV) radiation and PAHs enhanced the toxicity and exhibited toxic effects at PAH concentrations orders of magnitude below effects observed in the absence of UV. Because environmental exposure to PAHs is usually in the form of complex mixtures, the present study examined the photo-induced toxicity of both single compounds and mixtures of PAHs. In a sensitive larval life stage of zebrafish, acute photo-induced median lethal concentrations (LC50s) were derived for 4 PAHs (anthracene, pyrene, carbazole, and phenanthrene) to examine the hypothesis that phototoxic (anthracene and pyrene) and nonphototoxic (carbazole and phenanthrene) pathways of mixtures could be predicted from single exposures. Anthracene and pyrene were phototoxic as predicted; however, carbazole exhibited moderate photo-induced toxicity and phenanthrene exhibited weak photo-induced toxicity. The toxicity of each chemical alone was used to compare the toxicity of mixtures in binary, tertiary, and quaternary combinations of these PAHs, and a predictive model for environmental mixtures was generated. The results indicated that the acute toxicity of PAH mixtures was additive in phototoxic scenarios, regardless of the magnitude of photo-enhancement. Based on PAH concentrations found in water and circumstances of high UV dose to aquatic systems, there exists potential risk of photo-induced toxicity to aquatic organisms.
/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. /Aromatic hydrocarbons 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 ventilations 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 ... . 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. Administer activated charcoal ... . /Aromatic hydrocarbons 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. Consider drug therapy for pulmonary edema ... . 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 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. Watch for signs of fluid overload ... .Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Aromatic hydrocarbons and related compounds/
/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A group of ten male A strain mice, three to four months old, received six sc injections, in the left flank, of 10 mg crystallized carbazole moistened with glycerol. All ten mice were still alive after one year and four after 19 months. No tumor reported at the injection site.
/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Groups of 50 male and 50 female B6C3 F1 mice, six weeks of age, were fed a pellet diet containing technical grade carbazole (purity, 96%) at concentrations of 0.6, 0.3 or 0.15% or none (control group). The treatment was continued for 96 weeks; the animals were then fed a basal diet until killed in week 104. Neoplastic lesions were found in the liver and in the forestomach. The lesions in liver were classified as neoplastic nodules and hepatocellular carcinomas. The incidences of both types of lesion in livers of all the groups fed carbazole were significantly (p <0.05) greater than that in the control group. The incidences of neoplastic nodules and hepatocellular carcinomas were, respectively: in the high-dose group, females: 16/46 (34.8%) and 30/46 (65.2%) with 3 (10%) lung metastases; males: 10/48 (20.9%) and 37/48 (77.1%) with 11 (29.7%) lung metastases; mid-dose group, females: 21/43 (48.8%) and 24/43 (55.8%) with 3 (12.5%) lung metastases; males: 22/42 (52.4%) and 20/42 (47.4%) with 7 (35%) lung metastases; low-dose group, females: 13/49 (26.5%) and 35/49 (71.4%) with 5 (14.3%) lung metastases, males: 30/42 (71.4%) and 12/42 (28.6%) with 2 (16.7%) lung metastases. In control animals, with a mean survival time of about 100 weeks, the incidences of neoplastic nodules and hepatocellular carcinomas were, respectively, 4.4% (2/45) and 4.4% (2/45) in females and 28.2% (13/46) and 19.6% (9/46) in males. The numbers of papillomas in the forestomach in groups of mice given 0.6% carbazole were 4/46 in females (p <0.05) and 4/48 in males (p < 0.05); in mice given 0.3%, 7/43 in females (p < 0.01) and 1/42 in males; in mice given 0.15%, 5/49 in females (p < 0.05) and 0/42 in males, whereas no such tumor was observed in the respective control groups (female 0/45, male 0/46). Squamous cell carcinoma incidence was increased significantly (p < 0.01) in males fed 0.6% carbazole (7/48, 14.6%). No squamous cell carcinoma was observed in the forestomachs of male or female controls.
/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A solution of 0.5% carbazole in benzene was applied 120 times to the skin of 50 mice. Epilation of the treated area was the only reaction observed after 276 days.
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The objectives of this study were (1) to determine the developmental toxicity of carbazole and benzo(a)carbazole following daily dermal administration to female Sprague-Dawley rats on days 0 through 20 of gestation and (2) to determine the mutagenicity of these two compounds using a modified version of the Ames assay. These chemicals are of concern because they are found in a variety of environmental matrices including crude oil mixtures. No signs of maternal or developmental toxicity were considered to be related to dermal administration of carbazole at doses of 2.5, 25.0, and 250.0 mg/kg. Signs of maternal toxicity considered to be related to administration of benzo(a)carbazole included significantly decreased body-weight gain and decreased absolute-food consumption at a dose of 250.0 mg/kg. Signs of developmental toxicity considered to be related to administration of benzo(a)carbazole included significantly decreased number of total (live and dead combined) and live pups on lactation day 0 as well as significantly decreased average pup weight on lactation days 0 and 4 at a dose of 250.0 mg/kg. Because developmental toxicity following benzo(a)carbazole treatment was observed only at a dose at which maternal toxicity was observed, it is likely that the effects on the offspring are secondary to the treatment effects on the dam. Evidence of toxic effects with benzo(a)carbazole in the absence of effects with carbazole suggests that the substituted benzene ring enhances the biological activity of this compound. Carbazole was nonmutagenic with or without S-9 activation, whereas benzo(a)carbazole showed a clear dose-response with S-9 activation. Without S-9 activation, benzo(a)carbazole was nonmutagenic. Apparently benzo(a)carbazole must be enzymatically activated in order to be mutagenic.
For more Non-Human Toxicity Excerpts (Complete) data for Carbazole (9 total), please visit the HSDB record page.
EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPA; ICSS Dashboard Application; Available from, as of April 4, 2017: http://actor.epa.gov/dashboard/]
The following link will take the user to the National Toxicology Program (NTP) Test Status of Agents Search page, which tabulates the results and current status of tests such as "Short-Term Toxicity Studies", "Long-term Carcinogenicity Studies", "Developmental Studies", "Genetic Toxicology Studies", etc., performed with this chemical. Testing status for carbazole is available.[Available from, as of March 24, 2017: https://ntpsearch.niehs.nih.gov/?e=True&ContentType=Testing+Status]
LC50; Species: Daphnia magna (Water flea) neonate <24 hr; Conditions: freshwater, renewal, 21.2 (21-21.4) °C, pH 8.31 (8.1-8.6), hardness 159.6 (113-200) mg/L CaCO3, alkalinity 102.3 (81-117) mg/L CaCO3, dissolved oxygen 96.1 (93.5-113) mg/L; Concentration: 3350 ug/L for 48 hr (95% confidence interval: 2300-4880 ug/L) /98.9% purity/
LC50; Species: Pimephales promelas (Fathead Minnow) age 30 days, length 17 mm, weight 0.043-0.125 g; Conditions: freshwater, static, 22.6 (22-23) °C, pH 7.23 (6.82-7.51), hardness 53.9 (51.9-55.9) mg/L CaCO3, alkalinity 44 (43-45) mg/L CaCO3, dissolved oxygen 75.6% (62.2-85.1%); Concentration: <1500 ug/L for 96 hr /98.9% purity/
LC50; Species: Pimephales promelas (Fathead Minnow) age 30 days, length 17 mm, weight 0.043-0.125 g; Conditions: freshwater, flow through, 23.2 (21-24.4) °C, pH 7.06 (6.84-7.35), hardness 48.9 (47.9-49.9) mg/L CaCO3, alkalinity 42.5 (42-43) mg/L CaCO3, dissolved oxygen 78.1% (68.9-83.2%); Concentration: 930 ug/L for 96 hr /98.9% purity/
/AQUATIC SPECIES/ The present study examined photo-induced toxicity and toxicokinetics for acute exposure to selected polycyclic aromatic hydrocarbons (PAHs) in zebrafish. Photo-enhanced toxicity from co-exposure to ultraviolet (UV) radiation and PAHs enhanced the toxicity and exhibited toxic effects at PAH concentrations orders of magnitude below effects observed in the absence of UV. Because environmental exposure to PAHs is usually in the form of complex mixtures, the present study examined the photo-induced toxicity of both single compounds and mixtures of PAHs. In a sensitive larval life stage of zebrafish, acute photo-induced median lethal concentrations (LC50s) were derived for 4 PAHs (anthracene, pyrene, carbazole, and phenanthrene) to examine the hypothesis that phototoxic (anthracene and pyrene) and nonphototoxic (carbazole and phenanthrene) pathways of mixtures could be predicted from single exposures. Anthracene and pyrene were phototoxic as predicted; however, carbazole exhibited moderate photo-induced toxicity and phenanthrene exhibited weak photo-induced toxicity. The toxicity of each chemical alone was used to compare the toxicity of mixtures in binary, tertiary, and quaternary combinations of these PAHs, and a predictive model for environmental mixtures was generated. The results indicated that the acute toxicity of PAH mixtures was additive in phototoxic scenarios, regardless of the magnitude of photo-enhancement. Based on PAH concentrations found in water and circumstances of high UV dose to aquatic systems, there exists potential risk of photo-induced toxicity to aquatic organisms.
/AQUATIC SPECIES/ Herocyclic derivatives of polycyclic aromatic hydrocarbons (PAHs) are often significant components of environmental contaminant mixtures; however, their contribution to the toxicity of these mixtures is not well characterized. These heterocycles commonly co-occur in PAH mixtures, which contain agonists for the aryl hydrocarbon receptor (AHR). /The/ goal for these studies was to explore the effects of two PAH heterocycles, carbazole (CB) and dibenzothiophene (DBT), alone and in combination with a PAH-type agonist for the AHR (Beta-naphthoflavone [BNF]) on AHR-mediated cytochrome P4501A (CYP1A) activity and on fish embryotoxicity. Embryos of Fundulus heteroclitus were exposed to CB or DBT, with and without coexposure to BNF. Carbazole alone slightly induced, whereas DBT alone slightly reduced, in ovo CYP1A-mediated ethoxyresorufin-O-deethylase (EROD) activity compared to control values. However, exposure to CB or DBT reduced in ovo EROD activity in embryos coexposed to BNF. Carbazole and DBT were characterized in vitro as noncompetitive CYP1A inhibitors. Carbazole and DBT enhanced the embryotoxicity of BNF, although neither compound was embryotoxic by itself. The co-occurrence of CB and DBT with PAH-type AHR inducers in contaminated ecosystems may increase the toxicity of PAH-type AHR agonists in these settings and may need to be considered when estimating the embryotoxicity of PAH mixtures.
/AQUATIC SPECIES/ ... The present study focuses on possible implications NSO-HET have for ecotoxicity (algae and daphnids) and mutagenicity (Salmonella/microsome test). A combination of bioassays and chemical-analytical quantification of the test compounds during toxicity assays should aid in determination of the hazard potential. Samples of the test concentrations of 14 NSO-HET were taken at the beginning and end of the bioassays; these samples were then quantified by high-performance liquid chromatography. The toxicity potential of the substances was evaluated and compared with the toxicity calculated with the nominal concentrations. Significantly different results were obtained primarily for volatile or highly hydrophobic NSO-HET. The concentration of heterocyclic hydrocarbons can change significantly during the algae and Daphnia test. The EC50 values (effective concentration value: the concentration of a chemical that is required to produce a 50% effect) calculated with the nominal concentrations underestimate the toxicity by a factor of up to 50. Prioritizing the tested compounds according to toxicity, the mutagenic and toxic compounds quinoline, 6-methylquinoline, and xanthene have to be listed first. The greatest ecotoxic potential on algae and daphnids was determined for dibenzothiophene followed by acridine. In the Daphnia magna immobilization test, benzofuran, dibenzofuran, 2-methylbenzofuran, and 2,3-dimethylbenzofuran and also carbazole are ecotoxicologically relevant with EC50 values below 10 mg/L.
/OTHER TERRESTRIAL SPECIES/ The effects of eight polycyclic aromatic compounds on the survival and reproduction of the collembolan Folsomia fimetaria L. were investigated in a well-characterized Danish agricultural soil. With the exception of acridine, polycyclic aromatic hydrocarbons (PAHs) and neutral N-, S-, and O-monosubstituted analogues showed similar toxicities to soil collembolans when the results were expressed in relation to total soil concentrations (mg/kg). The estimated concentrations resulting in a 10% reduction of reproductive output (EC10 values) were based on measured initial concentrations and were for acridine 290 mg/kg, carbazole 10 mg/kg, dibenzofuran 19 mg/kg, dibenzothiophene 7.8 mg/kg, fluoranthene 37 mg/kg, fluorene 7.7 mg/kg, phenantrene 23 mg/kg, and pyrene 10 mg/kg. When the EC10 values were converted to soil pore-water concentrations, they showed a highly significant correlation (r2 = 0.71, p < 0.01) to no-observed-effect concentrations for the freshwater crustacean Daphnia magna, as estimated by a quantitative structure activity relation (QSAR) for baseline toxicity (nonpolar narcosis). Only carbazole and acridine were more than two times more toxic (4.9 and 3.1, respectively) than expected from the Daphnia QSAR data. The latter result indicates that the toxicity of the tested substances is close to that expected for compounds with nonpolar narcosis as the mode of action. However, the relatively large uncertainties in the extrapolation method prevent final conclusions from being drawn.
/OTHER TERRESTRIAL SPECIES/ The effects of eight polycyclic aromatic compounds (PACs) on the survival and reproduction of the enchytraeid worm Enchytraeus crypticus were investigated in an agricultural soil with an organic carbon content of 1.6%. With the exception of acridine, which showed a strong binding to the test soil and a subsequent low toxicity, polycyclic aromatic hydrocarbons and neutral N-, S-, O-monosubstituted analogues showed a similar toxicity to the enchytraeids. Concentrations estimated to give a 10% reduction of reproductive output (EC10 values) were based on measured initial concentrations and were, for acridine, 310 mg/kg; for carbazole, 19 mg/kg; for dibenzofuran, 36 mg/kg; for dibenzothiophene, 40 and 45 mg/kg (two tests); for fluoranthene, 15 mg/kg; forfluorene, 25 mg/kg; for phenanthrene, 40 mg/kg; and for pyrene, 11 mg/kg. Using reported soil-pore-water partitioning coefficients for the substances in question, equilibrium pore-water concentrations could be estimated from the total soil concentrations. Calculated EC10 values, expressed as log10(mmol/L pore water), were negatively related to the lipophilicity (log KOW) of the compounds (r2 = 0.58; p = 0.027, n = 8), thus indicating a rather nonspecific (narcotic) mode of toxic action for these compounds. When compared with literature ecotoxicity data for a springtail (Folsomia fimetaria) tested in the same soil type, enchytraeids generally seem less sensitive.
Carbazole's production and use as an intermediate in the manufacture of dyes, insecticides, lubricants and rubber antioxidants and as a UV sensitizer for photographic plates may result in its release to the environment through various waste streams. Emissions from waste incineration and tobacco smoke will result in its direct release to the environment. Carbazole occurs in coal, petroleum, peat, crude oils and coal tar. Carbazole occurs in products of incomplete combustion of nitrogen containing organic matter. If released to air, a vapor pressure of 1.5X10-6 mm Hg at 25 °C indicates carbazole will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase carbazole will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 9.6 hours. Particulate-phase carbazole will be removed from the atmosphere by wet and dry deposition. Carbazole absorbs strongly at wavelengths >290 nm and, therefore, is expected to be susceptible to direct photolysis by sunlight. In the particulate phase, photolysis is highly dependent on the adsorbing substrate. Photolytic half-lives of 64.5 to >1000 hours were observed for carbazole adsorbed to 15 different types of coal fly ash. If released to soil, carbazole can have high to no mobility based upon a Koc range of 114-4980, with most values suggesting low mobility to immobility. Volatilization from moist soil surfaces is not expected to be an important fate process based upon a Henry's Law constant of 1.16X10-7 atm-cu m/mole. Carbazole is not expected to volatilize from dry soil surfaces based upon its vapor pressure. A 2.8% of theoretical BOD using activated sludge in the Japanese MITI test suggests that carbazole is not readily biodegradable. However, results of screening studies indicate that carbazole is biodegradable by adapted microorganisms in water and soil. Photodegradation is expected to occur on surfaces exposed to sunlight. If released into water, carbazole is expected to adsorb to suspended solids and sediment based upon the Koc. In a model ecosystem including degradation and distribution processes, >99.5% of initial carbazole disappeared from the water phase within 33 days. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's Henry's Law constant. A BCF range of 34-500 suggests the potential for bioconcentration in aquatic organisms is moderate to high, provided the compound is not metabolized by the organism. A measured fish biotransformation half-life of 1.15 days has been reported for carbazole. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. A direct photolysis half-life of 2.9 hours was measured for carbazole in pure water for midday late January sunlight. Occupational exposure to carbazole may occur through inhalation and dermal contact with this compound at workplaces where carbazole is produced or used. Monitoring data indicate that the general population may be exposed to carbazole via inhalation of ambient air and tobacco smoke, ingestion of char-broiled or smoke-cured food and drinking water, and dermal contact with consumer products containing carbazole. (SRC)
Carbazole occurs in coal, petroleum, peat(1), crude oils and coal tar(2). Carbazole occurs in products of incomplete combustion of nitrogen containing organic matter(1,2).
Carbazole's production and use as an intermediate in the manufacture of dyes, insecticides, lubricants and rubber antioxidants(1-3) and as a UV sensitizer for photographic plates(1,2) may result in its release to the environment through various waste streams(SRC). Carbazole may be released to the environment in effluents from coal processing(4), wood-treatment facilities(5), and aluminum manufacturing(6). Emissions from waste incineration(7) and tobacco smoke(8) will result in its direct release to the environment(SRC). Polyaromatic hydrocarbons, such as carbazole, are found in food as a result of char-broiling and smoking(9).
LC50; Species: Daphnia magna (Water flea) neonate <24 hr; Conditions: freshwater, renewal, 21.2 (21-21.4) °C, pH 8.31 (8.1-8.6), hardness 159.6 (113-200) mg/L CaCO3, alkalinity 102.3 (81-117) mg/L CaCO3, dissolved oxygen 96.1 (93.5-113) mg/L; Concentration: 3350 ug/L for 48 hr (95% confidence interval: 2300-4880 ug/L) /98.9% purity/
LC50; Species: Pimephales promelas (Fathead Minnow) age 30 days, length 17 mm, weight 0.043-0.125 g; Conditions: freshwater, static, 22.6 (22-23) °C, pH 7.23 (6.82-7.51), hardness 53.9 (51.9-55.9) mg/L CaCO3, alkalinity 44 (43-45) mg/L CaCO3, dissolved oxygen 75.6% (62.2-85.1%); Concentration: <1500 ug/L for 96 hr /98.9% purity/
LC50; Species: Pimephales promelas (Fathead Minnow) age 30 days, length 17 mm, weight 0.043-0.125 g; Conditions: freshwater, flow through, 23.2 (21-24.4) °C, pH 7.06 (6.84-7.35), hardness 48.9 (47.9-49.9) mg/L CaCO3, alkalinity 42.5 (42-43) mg/L CaCO3, dissolved oxygen 78.1% (68.9-83.2%); Concentration: 930 ug/L for 96 hr /98.9% purity/
/AQUATIC SPECIES/ The present study examined photo-induced toxicity and toxicokinetics for acute exposure to selected polycyclic aromatic hydrocarbons (PAHs) in zebrafish. Photo-enhanced toxicity from co-exposure to ultraviolet (UV) radiation and PAHs enhanced the toxicity and exhibited toxic effects at PAH concentrations orders of magnitude below effects observed in the absence of UV. Because environmental exposure to PAHs is usually in the form of complex mixtures, the present study examined the photo-induced toxicity of both single compounds and mixtures of PAHs. In a sensitive larval life stage of zebrafish, acute photo-induced median lethal concentrations (LC50s) were derived for 4 PAHs (anthracene, pyrene, carbazole, and phenanthrene) to examine the hypothesis that phototoxic (anthracene and pyrene) and nonphototoxic (carbazole and phenanthrene) pathways of mixtures could be predicted from single exposures. Anthracene and pyrene were phototoxic as predicted; however, carbazole exhibited moderate photo-induced toxicity and phenanthrene exhibited weak photo-induced toxicity. The toxicity of each chemical alone was used to compare the toxicity of mixtures in binary, tertiary, and quaternary combinations of these PAHs, and a predictive model for environmental mixtures was generated. The results indicated that the acute toxicity of PAH mixtures was additive in phototoxic scenarios, regardless of the magnitude of photo-enhancement. Based on PAH concentrations found in water and circumstances of high UV dose to aquatic systems, there exists potential risk of photo-induced toxicity to aquatic organisms.
/AQUATIC SPECIES/ Herocyclic derivatives of polycyclic aromatic hydrocarbons (PAHs) are often significant components of environmental contaminant mixtures; however, their contribution to the toxicity of these mixtures is not well characterized. These heterocycles commonly co-occur in PAH mixtures, which contain agonists for the aryl hydrocarbon receptor (AHR). /The/ goal for these studies was to explore the effects of two PAH heterocycles, carbazole (CB) and dibenzothiophene (DBT), alone and in combination with a PAH-type agonist for the AHR (Beta-naphthoflavone [BNF]) on AHR-mediated cytochrome P4501A (CYP1A) activity and on fish embryotoxicity. Embryos of Fundulus heteroclitus were exposed to CB or DBT, with and without coexposure to BNF. Carbazole alone slightly induced, whereas DBT alone slightly reduced, in ovo CYP1A-mediated ethoxyresorufin-O-deethylase (EROD) activity compared to control values. However, exposure to CB or DBT reduced in ovo EROD activity in embryos coexposed to BNF. Carbazole and DBT were characterized in vitro as noncompetitive CYP1A inhibitors. Carbazole and DBT enhanced the embryotoxicity of BNF, although neither compound was embryotoxic by itself. The co-occurrence of CB and DBT with PAH-type AHR inducers in contaminated ecosystems may increase the toxicity of PAH-type AHR agonists in these settings and may need to be considered when estimating the embryotoxicity of PAH mixtures.
/AQUATIC SPECIES/ ... The present study focuses on possible implications NSO-HET have for ecotoxicity (algae and daphnids) and mutagenicity (Salmonella/microsome test). A combination of bioassays and chemical-analytical quantification of the test compounds during toxicity assays should aid in determination of the hazard potential. Samples of the test concentrations of 14 NSO-HET were taken at the beginning and end of the bioassays; these samples were then quantified by high-performance liquid chromatography. The toxicity potential of the substances was evaluated and compared with the toxicity calculated with the nominal concentrations. Significantly different results were obtained primarily for volatile or highly hydrophobic NSO-HET. The concentration of heterocyclic hydrocarbons can change significantly during the algae and Daphnia test. The EC50 values (effective concentration value: the concentration of a chemical that is required to produce a 50% effect) calculated with the nominal concentrations underestimate the toxicity by a factor of up to 50. Prioritizing the tested compounds according to toxicity, the mutagenic and toxic compounds quinoline, 6-methylquinoline, and xanthene have to be listed first. The greatest ecotoxic potential on algae and daphnids was determined for dibenzothiophene followed by acridine. In the Daphnia magna immobilization test, benzofuran, dibenzofuran, 2-methylbenzofuran, and 2,3-dimethylbenzofuran and also carbazole are ecotoxicologically relevant with EC50 values below 10 mg/L.
/OTHER TERRESTRIAL SPECIES/ The effects of eight polycyclic aromatic compounds on the survival and reproduction of the collembolan Folsomia fimetaria L. were investigated in a well-characterized Danish agricultural soil. With the exception of acridine, polycyclic aromatic hydrocarbons (PAHs) and neutral N-, S-, and O-monosubstituted analogues showed similar toxicities to soil collembolans when the results were expressed in relation to total soil concentrations (mg/kg). The estimated concentrations resulting in a 10% reduction of reproductive output (EC10 values) were based on measured initial concentrations and were for acridine 290 mg/kg, carbazole 10 mg/kg, dibenzofuran 19 mg/kg, dibenzothiophene 7.8 mg/kg, fluoranthene 37 mg/kg, fluorene 7.7 mg/kg, phenantrene 23 mg/kg, and pyrene 10 mg/kg. When the EC10 values were converted to soil pore-water concentrations, they showed a highly significant correlation (r2 = 0.71, p < 0.01) to no-observed-effect concentrations for the freshwater crustacean Daphnia magna, as estimated by a quantitative structure activity relation (QSAR) for baseline toxicity (nonpolar narcosis). Only carbazole and acridine were more than two times more toxic (4.9 and 3.1, respectively) than expected from the Daphnia QSAR data. The latter result indicates that the toxicity of the tested substances is close to that expected for compounds with nonpolar narcosis as the mode of action. However, the relatively large uncertainties in the extrapolation method prevent final conclusions from being drawn.
/OTHER TERRESTRIAL SPECIES/ The effects of eight polycyclic aromatic compounds (PACs) on the survival and reproduction of the enchytraeid worm Enchytraeus crypticus were investigated in an agricultural soil with an organic carbon content of 1.6%. With the exception of acridine, which showed a strong binding to the test soil and a subsequent low toxicity, polycyclic aromatic hydrocarbons and neutral N-, S-, O-monosubstituted analogues showed a similar toxicity to the enchytraeids. Concentrations estimated to give a 10% reduction of reproductive output (EC10 values) were based on measured initial concentrations and were, for acridine, 310 mg/kg; for carbazole, 19 mg/kg; for dibenzofuran, 36 mg/kg; for dibenzothiophene, 40 and 45 mg/kg (two tests); for fluoranthene, 15 mg/kg; forfluorene, 25 mg/kg; for phenanthrene, 40 mg/kg; and for pyrene, 11 mg/kg. Using reported soil-pore-water partitioning coefficients for the substances in question, equilibrium pore-water concentrations could be estimated from the total soil concentrations. Calculated EC10 values, expressed as log10(mmol/L pore water), were negatively related to the lipophilicity (log KOW) of the compounds (r2 = 0.58; p = 0.027, n = 8), thus indicating a rather nonspecific (narcotic) mode of toxic action for these compounds. When compared with literature ecotoxicity data for a springtail (Folsomia fimetaria) tested in the same soil type, enchytraeids generally seem less sensitive.
Carbazole's production and use as an intermediate in the manufacture of dyes, insecticides, lubricants and rubber antioxidants and as a UV sensitizer for photographic plates may result in its release to the environment through various waste streams. Emissions from waste incineration and tobacco smoke will result in its direct release to the environment. Carbazole occurs in coal, petroleum, peat, crude oils and coal tar. Carbazole occurs in products of incomplete combustion of nitrogen containing organic matter. If released to air, a vapor pressure of 1.5X10-6 mm Hg at 25 °C indicates carbazole will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase carbazole will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 9.6 hours. Particulate-phase carbazole will be removed from the atmosphere by wet and dry deposition. Carbazole absorbs strongly at wavelengths >290 nm and, therefore, is expected to be susceptible to direct photolysis by sunlight. In the particulate phase, photolysis is highly dependent on the adsorbing substrate. Photolytic half-lives of 64.5 to >1000 hours were observed for carbazole adsorbed to 15 different types of coal fly ash. If released to soil, carbazole can have high to no mobility based upon a Koc range of 114-4980, with most values suggesting low mobility to immobility. Volatilization from moist soil surfaces is not expected to be an important fate process based upon a Henry's Law constant of 1.16X10-7 atm-cu m/mole. Carbazole is not expected to volatilize from dry soil surfaces based upon its vapor pressure. A 2.8% of theoretical BOD using activated sludge in the Japanese MITI test suggests that carbazole is not readily biodegradable. However, results of screening studies indicate that carbazole is biodegradable by adapted microorganisms in water and soil. Photodegradation is expected to occur on surfaces exposed to sunlight. If released into water, carbazole is expected to adsorb to suspended solids and sediment based upon the Koc. In a model ecosystem including degradation and distribution processes, >99.5% of initial carbazole disappeared from the water phase within 33 days. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's Henry's Law constant. A BCF range of 34-500 suggests the potential for bioconcentration in aquatic organisms is moderate to high, provided the compound is not metabolized by the organism. A measured fish biotransformation half-life of 1.15 days has been reported for carbazole. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. A direct photolysis half-life of 2.9 hours was measured for carbazole in pure water for midday late January sunlight. Occupational exposure to carbazole may occur through inhalation and dermal contact with this compound at workplaces where carbazole is produced or used. Monitoring data indicate that the general population may be exposed to carbazole via inhalation of ambient air and tobacco smoke, ingestion of char-broiled or smoke-cured food and drinking water, and dermal contact with consumer products containing carbazole. (SRC)
Carbazole occurs in coal, petroleum, peat(1), crude oils and coal tar(2). Carbazole occurs in products of incomplete combustion of nitrogen containing organic matter(1,2).
Carbazole's production and use as an intermediate in the manufacture of dyes, insecticides, lubricants and rubber antioxidants(1-3) and as a UV sensitizer for photographic plates(1,2) may result in its release to the environment through various waste streams(SRC). Carbazole may be released to the environment in effluents from coal processing(4), wood-treatment facilities(5), and aluminum manufacturing(6). Emissions from waste incineration(7) and tobacco smoke(8) will result in its direct release to the environment(SRC). Polyaromatic hydrocarbons, such as carbazole, are found in food as a result of char-broiling and smoking(9).
TERRESTRIAL FATE: Based on a classification scheme(1), a Koc range of 114 to 4980(2,3) indicates that carbazole can have high mobility to being immobile in soil, with most values suggesting low mobility to immobility(SRC). The variation of Koc values in 21 different soil horizons was thought to result from variation of organic matter sorbent in structure and content(2). Volatilization of carbazole from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 1.16X10-7 atm-cu m/mole(4). Carbaozle is not expected to volatilize from dry soil surfaces(SRC) based upon an extrapolated vapor pressure of 1.5X10-6 mm Hg at 25 °C(5). A 2.8% of theoretical BOD using activated sludge in the Japanese MITI test suggests that carbazole is not readily biodegradable(6). In contrast, OECD test guideline 301E using a mixed inoculum of a domestic sewage plant effluent and an aqueous bacterial solution extracted from local soil found carbazole to be readily biodegradable(7). Results of screening studies suggest that carbazole is biodegradable by adapted microorganisms in water and soil(8-10). Carbazole absorbs strongly at wavelengths >290 nm(10,11) and, therefore, is expected to be susceptible to direct photolysis on soil surfaces exposed to sunlight(SRC).
AQUATIC FATE: Based on a classification scheme(1), an average Koc value of 637 in nine soils(2) and a Koc of 4980(3) indicates that carbazole is expected to adsorb to suspended solids and sediment(SRC). The variation of Koc value in different soils was thought to result from variation of organic matter sorbent in structure and content(2). Volatilization from water surfaces is not expected(4) based upon a Henry's Law constant of 1.16X10-7 atm-cu m/mole(5). According to a classification scheme(6), a measured BCF range of 34-500 in fish(7,8), suggests the potential for bioconcentration in aquatic organisms is moderate to high, provided the compound is not metabolized by the organism(SRC). A measured fish biotransformation half-life of 1.15 days has been reported for carbazole(9). A 2.8% of theoretical BOD using activated sludge in the Japanese MITI test suggests that carbazole is not readily biodegradable(7). In contrast, OECD test guideline 301E using a mixed inoculum of a domestic sewage plant effluent and an aqueous bacterial solution extracted from local soil found carbazole to be readily biodegradable(10). Results of screening studies suggest that carbazole is biodegradable by adapted microorganisms in water and soil(11-13). In a model ecosystem including degradation and distribution processes, >99.5% of initial carbazole disappeared from the water phase within 33 days, resulting in a spectrum of unidentified polar and nonpolar conversion products(14). A direct photolysis rate constant of 0.000066/sec was measured for carbazole in pure water for midday late January sunlight which corresponds to a half-life of 2.9 hr(14,15). Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions(4).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), carbazole, which has an extrapolated vapor pressure of 1.5X10-6 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase carbazole 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 9.6 hours(SRC), calculated from its rate constant of 4.0X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase carbazole may be removed from the air by wet and dry deposition(SRC). Carbazole has been detected in rain and snow samples(4). Carbazole absorbs strongly at wavelengths >290 nm(5,6) and, therefore, is expected to be susceptible to direct photolysis by sunlight(SRC). In the particulate phase, photolysis is highly dependent on the adsorbing substrate(7). Photolytic half-lives of 64.5 to >1000 hours were observed for carbazole adsorbed to 15 different types of coal fly ash(7).
AEROBIC: Carbazole, present at 100 mg/L, reached 2.8% of its theoretical BOD in 2 weeks using an activated sludge inoculum at 30 mg/L in the Japanese MITI test which classified the compound as not readily biodegradable(1). In a test for ready biodegradability according to OECD test guideline 301 E (Modified OECD Screening Test) using a mixed inoculum of a domestic sewage plant effluent and an aqueous bacterial solution extracted from local soil, carbazole was degraded to 86% within 7 days and to 93% within 28 days which passed criteria for being readily biodegradable(2). Carbazole is reported to be biodegradable by adapted microorganisms in water and soil(3).
AEROBIC: Based on pseudo-first order biodegradation rate constants of 2.7-9.7 per hr from batch fermentation screening studies using sewage inocula and 700-800 ppm carbazole, half-lives of 4.3 min-15.4 min can be estimated for carbazole(1). After 14 days of incubation at 30 °C, indigenous microorganisms removed 66% of carbazole (initial concentration of 2.9 ug/mL) from contaminated groundwater taken from the American Creosote Works Superfund site, Pensacola, FL(2). Levels of indigenous carbazole mineralization varied from 0 to 46% after 60 days in mineralization experiments using C14 labeled carbazole in 3 southern Illinois soils(3). In the same experiment, the carbazole-degrading bacterium, Xanthamonas sp., was reintroduced and enhanced mineralization to 45% after 7 days in a soil where little indigenous mineralization occurred(3). Carbazole initial concentrations of 500 and 5 ppm did not degrade after 90 and 15 days, respectively, in Chernozen loamy soil at 19 °C based on thin layer chromatography(4). Using soils collected from an abandoned coal tar refinery in Ohio, carbazole was mineralized over a 64-day incubation period in serum bottle respirometry studies(5).
ANAEROBIC: Carbazole was completely degraded under anaerobic conditions in a methane potential assay; however, there was no evidence of the degradation of carbazole in groundwater suggesting that the microorganisms responsible for the degradation of carbazole under anaerobic conditions were not able to degrade carbazole in the subsurface(1). Static serum bottle tests using an anaerobic sludge inoculum taken from digester tanks at a municipal wastewater treatment plant in Beijing found that carbazole was poorly degraded over a 50-day incubation period(2).
The rate constant for the vapor-phase reaction of carbazole with photochemically-produced hydroxyl radicals has been estimated as 4.0X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 9.6 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Carbazole absorbs strongly at wavelengths >290 nm(2,3) and, therefore, is expected to be susceptible to direct photolysis by sunlight(SRC). A direct photolysis rate constant of 0.000066/sec was measured for carbazole in pure water for midday late January sunlight which corresponds to a half-life of 2.9 hr(3,4). Photolysis experiments carried out at 313 nm on 1 ug/mL carbazole in pure water, lake water, creek water, pond water, and humic acid in pure water yielded photolysis rates ranging from 2.46X10-5 to 7.69X10-5/sec which correspond to half-lives of 2.5 to 7.8 hr(3,4). The second-order rate constant for the reaction of carbazole with free radical oxygen was measured to be 291/M-sec which corresponds to a half-life of 280 days at an alkyl peroxy concentration of 1X10-9 M in water; therefore, this photooxidation is not expected to be environmentally important(3). Carbazole is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(5).
Photolysis studies with 15 different types of coal fly ash found that half-lives for polyaromatic hydrocarbons (PAHs), such as carbazole, are highly dependent upon substrate(1); photolytic half-lives varied from 64.5 to >1000 hr(1). The dominant factor in preventing atmospheric photodegradation is the color of the absorbing substrate(1); fly ash samples that stabilize PAH reaction absorb the most light and prevent light from getting to the PAH(1); PAHs are stabilized when the carbon content of the fly ash is greater than 5%(1).
A BCF range of 34-412 was measured in fish for carbazole using carp (Cyprinus carpio) which were exposed over an 6-week period to 0.05 and 0.005 ppm carbazole(1). A BCF of 125 was measured in mosquito fish (Gambusia affinis) in a model ecosystem(2). A static experimental method using guppies (Poecilia reticulata) determined a carbazole BCF of 500(3). According to a classification scheme(4), these BCF values suggest the potential for bioconcentration in aquatic organisms is moderate to high, provided the compound is not metabolized by the organism(SRC). A measured fish biotransformation half-life of 1.15 days has been reported for carbazole(5). Log BCFs for carbazole in alga (Oedogonium cardiacum), snail (Physa sp.) and mosquito larvae (Culex pepiens) were measured to be 1.69, 2.13 and 2.05, respectively; however, carbazole was metabolized to N-methyl and N-acetyl derivatives(2). The log BCF for carbazole in Daphnia pulex was experimentally determined to be 2.06(6).
Based on an experimental Koc range of 114 to 1180, the average Koc value in 21 soil horizons comprised of nine different soils was determined to be 637(1). The variation of Koc value in different soils was thought to result from variation of organic matter sorbent in structure and content(1). Experimentally determined Koc values 2500(2) and 4980(3) have also been reported. In CA-Montmorillonite soil (0.06% organic content) and Coyote Creek sediment (1.4% organic content), Koc values of 5300 and 12500 were measured for carbazole(4). According to a classification scheme(5), the Koc range suggests that carbazole mobility can range from high mobility to being immobile in soil, with most values suggesting low mobility to immobility(SRC).
The Henry's Law constant for carbazole has been measured as 1.16X10-7 atm-cu m/mole at 25 °C(1). This Henry's Law constant indicates that carbazole is expected to be essentially nonvolatile from water surfaces(2). Carbazole's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Carbazole is not expected to volatilize from dry soil surfaces(SRC) based upon an extrapolated vapor pressure of 1.5X10-6 mm Hg at 25 °C(3).
GROUNDWATER: Carbazole was detected at a concentration of 4.3 mg/L in groundwater at a depth of 21 meters below the surface near an abandoned wood-treatment facility near Pensacola, FL(1). Concentrations ranging from 7.1 to 299 ug/L were detected in 16 of 23 groundwater samples near the abandoned wood-treatment facility near Pensacola, FL(2). Carbazole was detected at concentrations ranging from 0.01 to 24 mg/L in groundwater wells near an abandoned coal-tar distillation and wood-treatment facility in St. Louis Park, MN at depths of about 0.9 to 11 meters(3). Carbazole was detected in December, 1986 at concentration of 0.03, 0.03, 0.06, and 0.59 mg/L in 4 of 10 groundwater wells at Gas Works Park (a coal and oil gasification plant that ceased operation in 1956), Seattle, WA(4). Carbazole was qualitatively detected in a contaminated water plume moving away from a creosote waste disposal site in Texas(5).
DRINKING WATER: Carbazole was qualitatively identified in 2 of 14 drinking water samples collected from surface waters in the United Kingdom on March 19 and April 24, 1979(1,2). Source drinking water collected from three rivers in eastern Jiangsu Province, China in June 2002 contained carbazole concentrations of not detected (limit: 2.0 ng/L), 0.0005 ug/L and and 0.0053 ug/L respectively(3).
SURFACE WATER: Carbazole was detected at a concentration of 0.0194 mg/L in stream water collected near an abandoned wood-treatment facility near Pensacola, FL(1). Carbazole was not detected (limit: 0.5 ug/L) in water samples collected from 18 sites on seven selected streams in Arkansas during Mar-Aug 2004(2). Carbazole was not detected (limit: 0.5 ug/L) in 76 stream water samples collected upstream and downstream from select cities in Iowa in 2001(3).
RAIN/SNOW: Carbazole was detected at concentrations ranging from 0.002 to 0.05 ug/cu m in 4 of 8 aerosol samples collected during September, 1972 in Pasadena, CA(1).
Carbazole was qualitatively detected in stack emissions and condensate from waste incineration(1,2) and identified at a concentration of 38,400 ug-emission/kg-rubber from a rubber combustion operation(3). Carbazole was detected in wastewater effluents from the Timber products industry at a concentration of 1083 ng/uL extract, an Auto Laundry industry at a concentration of <1 ng/uL extract, and Public Owned Treatment Works (POTWs) at a concentration of 66 ng/uL extract(4). Carbazole was identified in municipal wastewater treatment sludge from Ontario Water Pollution Control plants at concentrations ranging from 520 to 2770 ug/L(5). Carbazole (plus methylphenanthrenes) comprise 9.6% (by weight) of fumes emitted by coal tar pitch(6).
SEDIMENT: Carbazole was detected in 10 of 12 sediment samples taken from St. Mary's River, connecting Lake Superior with Lake Huron, in 1985 at concentrations ranging from 0.04 to 14.0 mg/kg(1). Carbazole was detected at concentrations ranging from 3.1 to 80 ug/g in 4 of 7 sediment samples taken from the Nervion River, Spain at an uncontrolled hazardous waste dump(2). Carbazole was qualitatively detected in Black River (Lorain, OH) sediment near the outfall of a coking plant associated with a steel production facility(3). Carbazole was identified at average concentrations of 79 (+ or - 34) and 1700 (+ or - 1300) ng/g in 4 and 9 sediment samples, respectively at two separate sites from Eagle Harbor, WA(4). Sediments collected from the Newark Bay Estuary, New Jersey between 1991-1993 had median carbazole levels (dry wt) of 0.70 mg/kg (Arthur Kill site), 0.65 mg/kg (Hackensack River), 0.40 mg/kg (Kill Van Kull), 0.55 mg/kg (Newark Bay) and 0.70 mg/kg (Passaic River)(5). Carbazole was detected in 100% of 18 sediment samples from the Great Lakes basin at a median concentration of 50 ng/g dry wt (range of 20-130 ng/g)(6). Streambed sediment samples collected from 494 sites in 20 major river basins across the US during 1992-1995 had positive carbazole detections in 12.6% of all samples; concentrations of <50, 81, 180 and 1400 ug/kg dry wt at the 75th, 90th, 95th and maximum value, respectively, were reported(6).
SOIL: Soil samples collected from Xi'an, China contained a mean carbazole concentration of 7.5 ng/g (range of 4.0-14.2 ng/g)(1).
URBAN/SUBURBAN: Carbazole was qualitatively identified in background air south of Oslo, Norway in the fall of 1977, suburban air in a town east of Oslo, and Urban air in Oslo(1). Carbazole was detected in May of 1985 at a concentration of 0.8 ng/cu m in ambient air at Kokkola, Finland in the center of the city where traffic is dense; however, it was not detected in ambient air adjacent to an industrial area located outside the city(2). Carbazole was qualitatively detected in airborne particle samples collected from Washington, DC in the late 1970s(3).
RURAL/REMOTE: Carbazole was found at a concentration of 0.08 ng/cu m on aerosols 20 m over the North Atlantic Ocean(14). An average ambient concentration was reported to be 2-50 ng/cu m for carbazole(2).
SOURCE DOMINATED: Carbazole was identified at concentrations of 14.4, 23.2, and 332.7 ng/cu m in 3 of 8 air samples taken near the Urx chemical factory, Valasske Mezirici, Czechoslovakia on August 31 and September 2, 1989(1).
Carbazole has been reported to occur in curing smoke used to cure foods at level of 0-0.1 ppm(1). Polyaromatic hydrocarbons, such as carbazole, are found in food as a result of char-broiling and smoking(2).
Carbazole was detected at concentrations of 402.8, 1277.8, 750, 902.8, 2541.7, 3515.3, and 223.7 ng/g in 7 of 12 vegetation samples (mosses and needles) taken near the Urx chemical factory, Valasske Mezirici, Czechoslovakia on September 13, 1989(1).
Carbazole was detected, not quantified in the Indian Curry Tree (Murraya koenigii (Rutaceae))(1).
Carbazole was detected at a concentration of 110 ppb in a bullhead catfish (Ictalurus nebulosus) from the Black River, OH(1).
Carbazole was identified at a concentration of 448.8 ng/g in 1 of 10 soil and earthworm samples taken near the Urx chemical factory, Valasske Mezirici, Czechoslovakia on August 31, 1989(1).
Carbazole has been identified as a constituent of tobacco smoke(1,2). Carbazole concentrations in cigarette smoke of 100 ug/100 cigarettes have been reported(3). Carbazole has been reported to occur in curing smoke used to cure foods at level of 0-0.1 ppm(4).
The concentration of carbazole in creosote has been reported as 3 g/kg creosote(1). Carbazole is a constituent of coal tar creosote at 0.1% by weight(2). Carbazole has been reported to occur in diesel fuels(3,4). Road dust samples collected from Xi'an, China contained a mean carbazole concentration of 235 ng/g (range of 67.9-535.7 ng/g)(5).
NIOSH (NOES Survey 1981-1983) has statistically estimated that 78 workers are potentially exposed to carbazole in the USA(1). Occupational exposure to carbazole may occur through inhalation and dermal contact with this compound at workplaces where carbazole is produced or used. Monitoring data indicate that the general population may be exposed to carbazole via inhalation of ambient air and tobacco smoke, ingestion of char-broiled or smoke-cured food and drinking water, and dermal contact with consumer products containing carbazole(SRC). A carbazole concentration of 0.96 ug/cu m was detected in workroom air inside a Norwegian aluminum manufacturing plant(2). Air monitoring in a Norwegian plant producing electrode pastes for use in electric smelting furnaces found upper limit carbazole concentrations of 3.9 ug/cu m(3).
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.
SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.
Product: Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Offer surplus and non-recyclable solutions to a licensed disposal company; Contaminated packaging: Dispose of as unused product.