606-20-2Cc1c([N+](=O)[O-])cccc1[N+](=O)[O-]XTRDKALNCIHHNI-UHFFFAOYSA-N2,6-Dinitrotoluene can cause cancer according to an independent committee of scientific and health experts. It can cause male reproductive toxicity according to The National Institute for Occupational Safety and Health (NIOSH) and The Environmental Protection Agency (EPA).
606-20-2DTXSID5020528CHEMBL1328508CHEBI:957Nitrogen Compounds -> Nitros, Aromatic
Carcinogens
Semi-Volatile Organic Compound (SVOC)
log Kow = 2.10
2.05
2.02
1.283 at 231.8 °F (USCG, 1999) - Denser than water; will sink
Density: 1.2833 g/cu cm at 111 °C
Relative density (water = 1): 1.283 (liquid)
1.32
1.2833 @ 111°C
Yellow rhombic crystals
Yellow to red solid
less than 1 mg/mL at 64 °F (NTP, 1992)
In water, 204 mg/L at 25 °C
Soluble in ethanol and chloroform
Solubility in water: very poor
Danger
H301: Toxic if swallowed [Danger Acute toxicity, oral]
P203, P260, P261, P262, P264, P270, P271, P273, P280, P301+P316, P302+P352, P304+P340, P316, P318, P319, P321, P330, P361+P364, P403+P233, P405, and P501 (click each P-code to see the statement)
Danger
H301+H311+H331 (54.8%): Toxic if swallowed, in contact with skin or if inhaled [Danger Acute toxicity, oral; acute toxicity, dermal; acute toxicity, inhalation]
P203, P260, P261, P262, P264, P270, P271, P273, P280, P301+P316, P302+P352, P304+P340, P316, P318, P319, P321, P330, P361+P364, P403+P233, P405, and P501 (click each P-code to see the statement)
Chemical: Benzene, 2-methyl-1,3-dinitro-
Hazard Traits - Carcinogenicity; Environmental tox; Reproductive Toxicity
Benzene, 2-methyl-1,3-dinitro- is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Benzene, 2-methyl-1,3-dinitro- are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)
The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)
Special Hazards of Combustion Products: Emits toxic fumes of oxides of nitrogen
Combustible. Gives off irritating or toxic fumes (or gases) in a fire. Finely dispersed particles form explosive mixtures in air. Risk of explosion on contact with many substances.
2,6-DNT is potent hepatocarcinogen in Fischer 344 rats, whereas 2,4-dinitrotoluene is believed to be noncarcinogenic. Neither 2,6-DNT nor 2,4-dinitrotoluene is carcinogenic in the strain A mouse lung bioassay. The ip administration of 2,6-DNT or 2,4-dinitrotoluene (150 mg/kg each) to Fischer 344 rats resulted, after 24 hr, in covalent binding to DNA of the liver (131.1 to 259.9 pmol 2,6-DNT/mg DNA; 215.4 to 226.8 pmol 2,4-dinitrotoluene/mg DNA), and lower binding to DNA of the lung and the intestine (14.9 to 22.7 pmol 2,6-DNT/mg DNA; 45.0 to 75.0 pmol 2,6-DNT/mg DNA). Similar treatment of A/J mice resulted in lower binding in the liver (25.9 to 31.9 pmol 2,6-DNT/mg DNA; 42.6 to 58.9 pmol 2,4-dinitrotoluene/mg DNA), no detectable binding of 2,6-DNT in extrahepatic tissues and low amounts of binding of 2,4-dinitrotoluene to lung and intestinal DNA (9.7 to 39.0 pmol/mg DNA). Covalent binding of the noncarcinogenic isomeric 2,4-dinitrotoluene to DNA of various tissues of both species suggests that factors other than binding to DNA determine the ultimate carcinogenic effect of these cmpd.
... Sprague-Dawley female rats were exposed via gavage to one of five concentrations of one of five nitrotoluenes [2,4,6-trinitrotoluene (TNT), 2-amino-4,6-dinitrotoluene (2ADNT) 4-amino-2,6-dinitrotoulene (4ADNT), 2,4-dinitrotoluene (2,4DNT) and 2,6-dinitrotoluene (2,6DNT)] with necropsy and tissue collection at 24 or 48 hr. Gene expression profile results correlated well with clinical data and liver histopathology that lead to the concept that hematotoxicity was followed by hepatotoxicity. Overall, 2,4DNT, 2,6DNT and TNT had stronger effects than 2ADNT and 4ADNT. Common functional terms, gene expression patterns, pathways and networks were regulated across all nitrotoluenes. These pathways included NRF2-mediated oxidative stress response, aryl hydrocarbon receptor signaling, LPS/IL-1 mediated inhibition of RXR function, xenobiotic metabolism signaling and metabolism of xenobiotics by cytochrome P450. One biological process common to all compounds, lipid metabolism, was found to be impacted both at the transcriptional and lipid production level. ...
Hydrolyzed urine from workers exposed to dinitrotoluene contained 2,4- and 2,6-DNT, 2,4- and 2,6-dinitrobenzoic acid, 2,4- and 2,6-dinitrobenzyl alcohol, 2-amino-4-nitrobenzoic acid, and 2-(N-acetyl)amino-4-nitrobenzoic acid. ... The percentages of 2,4- and 2,6-DNT metabolites in the urine of individual subjects ranged from 79% to 93%.
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404 °F (NTP, 1992)
404 °F (closed cup)
207 °C c.c.
404 °F
Decomposes (NTP, 1992)
285 °C
decomposes
285 °C @760 [mm Hg]
When heated to decomposition it emits toxic fumes of /nitrogen oxides/.
285 °C
151 °F (NTP, 1992)
66.0 °C
66 °C
151 °F
66 °C
6.28 (NTP, 1992) - Heavier than air; will sink (Relative to Air)
6.28 (Air = 1)
Relative vapor density (air = 1): 6.28
6.28
Can induce methemoglobinemia; May be toxic to human reproduction or development, based on animal studies; [ICSC] Comprises approximately 19% of technical grade dinitrotoluene; [HSDB] A mild skin sensitizer in guinea pigs; Evidence suggests that dinitrotoluene isomers can be significantly absorbed through human skin; [DOE] An irritant; Toxic by ingestion, inhalation, and skin absorption; May cause cancer; Possible hazard of impaired fertility and irreversible effects; [Alfa Aesar MSDS] See Dinitrotoluene, all isomers.
Chem Indus Inst of Tox Report: A Thirty Day Toxicology Study in Fischer-344 Rats Given Dinitrotoluene, Technical Grade Docket # 22397 (1977)
Rickert DE et al; CRC Crit Rev Toxicol 13 (3): 217-34 (1984). A review with 86 references on the toxicity, mutagenicity, carcinogenicity, and metabolism of 2,3- 2,4-, 2,5-, 2,6-, 3,4-, and 3,5-dinitrotoluene in man and laboratory animals.
NIOSH; Current Intelligence Bulletin 44 Dinitrotoluenes (DNT) 20 pp. (7/5/85) DHHS Pub No 85-109.
Turner MJ et al; Identification and Quantication of Urinary Metabolites of Dinitrotoluenes in Occupationally Exposed Humans. Toxicol Appl Pharmacol 80 (1): 166-74 (1985)
For more Special Reports (Complete) data for 2,6-DINITROTOLUENE (6 total), please visit the HSDB record page.
U106; As stipulated in 40 CFR 261.33, when 2,6-dinitrotoluene, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).
Fire Extinguishing Agents: Water, Carbon dioxide, dry chemical (USCG, 1999)
Use water spray, powder, foam, carbon dioxide. In case of fire: keep drums, etc., cool by spraying with water. Combat fire from a sheltered position.
Fresh air, rest. Artificial respiration may be needed. Refer for medical attention.
Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer for medical attention .
First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.
Rinse mouth. Give one or two glasses of water to drink. Refer for medical attention .
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.
Water, carbon dioxide, or dry chemical from protected location.
If material on fire or involved in fire: Use water in flooding quantities as fog. Use foam, dry chemical, or carbon dioxide. Apply water from as far a distance as possible. Keep run-off water out of sewers and water sources. /Dinitrotoluenes, molten/
If material on fire or involved in fire: Use water in flooding quantities as fog. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Solid streams of water may be ineffective. Use foam, dry chemical, or carbon dioxide. /Dinitrotoluene, liquid; dinitrotoluene, solid/
Storage temperture: Ambient
PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/
1) REMOVE ALL IGNITION SOURCES. 2) VENTILATE AREA OF SPILL. 3) FOR SMALL QUANTITIES, SWEEP ONTO PAPER OR OTHER SUITABLE MATERIAL & BURN IN SUITABLE COMBUSTION CHAMBER WHICH ALLOWS BURNING IN UNCONFINED CONDITION & IS EQUIPPED WITH APPROPRIATE EFFLUENT GAS CLEANING DEVICE. LARGE QUANTITIES MAY BE RECLAIMED ... IF ... NOT PRACTICAL, DISSOLVE IN FUEL OIL & ATOMIZE IN SUITABLE COMBUSTION CHAMBER EQUIPPED WITH APPROPRIATE EFFLUENT GAS CLEANING DEVICE. /DINITROTOLUENE/
PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab hoods, glove boxes or animal rooms ... Filter housing that is designed so that used filters can be transferred into plastic bag without contaminating maintenance staff is avail commercially. Filters should be placed in plastic bags immediately after removal ... The plastic bag should be sealed immediately ... The sealed bag should be labelled properly ... Waste liquids ... should be placed or collected in proper containers for disposal. The lid should be secured & the bottles properly labelled. Once filled, bottles should be placed in plastic bag, so that outer surface ... is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken glassware ... should be decontaminated by solvent extraction, by chemical destruction, or in specially designed incinerators. /Chemical Carcinogens/
Environmental considerations - water spill: Use natural deep water pockets, excavated lagoons, or sand bag barriers to trap material at bottom. Remove trapped material with suction hoses. If dissolved, in region of 10 ppm or greater concentration, apply activated carbon at ten times the spilled amount. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates. /Dinitrotoluene, liquid; dinitrotoluene, solid/
Environmental considerations - land spill: Cover solids with plastic sheet to prevent dissolving in rain or fire fighting water. /Dinitrotoluene, liquid; dinitrotoluene, solid/
SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with 60-70% ethanol and transfer the dampened material to a suitable container. Use absorbent paper dampened with 60-70% ethanol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with 60-70% ethanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.
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.
Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U106, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.[
A potential candidate for rotary kiln incineration at a temperature range of 820 to 1,600 °C and residence times of seconds for liquids and gases, and hours for solids. A potential candidate for fluidized bed incineration at a temperature range of 450 to 980 °C and residence times of seconds for liquids and gases, and longer for solids.
1) BY MAKING PACKAGES OF DINITROTOLUENE IN PAPER OR OTHER FLAMMABLE MATERIAL & BURNING IN SUITABLE COMBUSTION CHAMBER WHICH ALLOWS BURNING IN UNCONFINED CONDITION & IS EQUIPPED WITH APPROPRIATE EFFLUENT GAS CLEANING DEVICE. 2) BY DISSOLVING IN FUEL OIL & ATOMIZING IN SUITABLE COMBUSTION CHAMBER EQUIPPED WITH APPROPRIATE EFFLUENT GAS CLEANING DEVICE. /DINITROTOLUENE/
For more Disposal Methods (Complete) data for 2,6-DINITROTOLUENE (10 total), please visit the HSDB record page.
Consult an expert! Personal protection: chemical protection suit including self-contained breathing apparatus. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.
SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. The completeness of the cleaning procedures should be considered before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at the end of shift, but should remain at employee's place of work for cleaning.
Eating and smoking should not be permitted in areas where dinitrotoluene or liquids containing dinitrotoluene are handled, processed, or stored. Employees who handle dinitrotoluene or liquids containing dinitrotoluene should wash their hands thoroughly with soap or mild detergent and water before eating, smoking, or using toilet facilities. /Dinitrotoluene/
If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. Build dikes to contain flow as necessary. /Dinitrotoluene, liquid; dinitrotoluene, solid/
If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. Build dikes to contain flow as necessary. Attempt to stop leak if without undue personnel hazard. /Dinitrotoluenes, molten/
For more Preventive Measures (Complete) data for 2,6-DINITROTOLUENE (24 total), please visit the HSDB record page.
Following oral exposure, immediately dilute with 4 to 8 ounces (120 to 240 mL) of water or milk (not to exceed 4 ounces/120 mL in a child). Administer charcoal as a slurry. Gastric lavage and oxygen administration is recommended. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Following eyes exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water, and administer a benzodiazepine IV in case of irritation. In all those cases, a physician may need to examine the area if irritation or pain persists. (T36)
The influence of diets varying in pectin content on intestinal microfloral metabolic capacity of rats has been investigated as a possible mechanism for the alteration of toxicity of 2,6-DNT produced by these diets. Male F-344 rats were fed a purified diet (AIN)-76A), AIN-76A plus 5% or 10% citrus pectin, or either of 2 cereal-based diets that vary in pectin content, NIH-07 or Purina Chow 5002. After 28 days, rats were given tritium-labeled 2,6-DNT (10 or 75 mg/kg per os) and killed 12 hr later. Total hepatic macromolecular covalent binding was determined by exhaustive extraction. The macromolecular covalent binding of 2,6-DNT was independent of diet at 10 mg/kg. At 75 mg/kg, marcomolecular covalent binding was increased 40% by feeding 5% pectin in the purified diet and 90% by feeding 10% pectin in the purified diet. Animals fed Purina 5002 and NIH-07 had 135 and 150% higher macromolecular covalent binding, respectively, than animals fed the purified diet alone and significantly greater macromolecular covalent binding than animals fed the pectin supplemented diets. Elevated (2 to 3-fold) beta-glucuronidase and nitroreductase activities, microfloral enzymes proposed to be involved in the activation of 2,6-DNT to toxicant, were found in the cecal contents of animals fed the pectin-containing diets which correlated with a 2 to 3-fold increase in total number of cecal anaerobes.
Pectin-induced changes in microflora have been shown to elevate the covalent binding of 2,6-DNT-related materials to total rat hepatic macromolecules. Therefore, the effect of diets varying in pectin content on the induction of foci and hepatic tumors induced by 2,6-DNT was studied in male F344 rats. 2,6-DNT (3.0-3.5 and 0.6-0.7 mg/kg/day) was incorporated into NIH-07, an open formula cereal-based diet high in pectin content, AIN-76A, a purified pectin-free diet, or AIN-76A supplemented with 5% pectin. Hepatic foci were scored after histochemical staining for gamma-glutamyl transpeptidase, canalicular adenosine triphosphatase or glucose-6-phosphatase following administration of test diets for 3,6 and 12 months. The number of foci per cu m of liver increased in a dose and time dependent manner following incorporation of 2,6-DNT into test diets with NIH-07 > pectin greater than AIN-76A. In the NIH-07 diet, 2,6-DNT did not alter the phenotypic distribution of foci. Animals fed control or 2,6-DNT-containing AIN-76 and pectin diets had few or no gamma-glutamyl transpeptidase foci throughout the study. Hepatocellular carcinomas and neoplastic nodules were observed only in rats fed NIH-07 containing 2,6-DNT. The concentrations of 2,6-DNT-related material covalently bound to hepatic macromolecules after a single oral dose of radiolabeled 2,6-DNT given after 12 months on the diets increased in control rats and in rats receiving low dose 2,6-DNT in the diet with AIN-76A < pectin < NIH-07. The results suggest that diet-induced alterations in the covalent binding of 2,6-DNT are not the sole factor in determining the carcinogenic response to 2,6-DNT.
The sulfotransferase inhibitors 2,6-dichloro-4-nitrophenol and pentachlorophenol were used to investigate the role of sulfate ester formation during the in vivo bioactivation of 2,4- and 2,6-dinitrotoluene. Male F-344 rats were administered one of the sulfotransferase inhibitors (40 umol/kg ip) 45 min prior to oral administration of 28 mg/kg ring-(14)C-2,4-DNT or 3-(3)H-2,6-DNT and killed 12 hr later. Pentachlorophenol had no significant effect on the urinary excretion of the benzyl glucuronide or benzoic acid metabolites of 2,6-DNT. The sulfotransferase inhibitors decreased the total hepatic macromolecular covalent binding of 2,4-DNT by 33%, and of 2,6-DNT by 69%. Hepatic DNA showed covalent binding of 2,4- and 2,6-DNT of 45 and 94 pmol equivalents/mg DNA, respectively. The sulfotransferase inhibitors decreased the binding of the hepatocarcinogen 2,6-DNT to hepatic DNA by greater than 95%. These results suggest that sulfation is important in the biotransformation of 2,4- and 2,6-DNT to reactive metabolites which covalently bind to DNA. (3)H2O was detected in the urine of rats administered 3-(3)H-2,6-DNT. Pentachlorophenol decreased (3)H2O formation to the same extent as it decreased the total hepatic macromolecular covalent binding of 2,6-DNT, suggesting that (3)H exchange at the 3 position of 2,6-DNT occurs following sulfate ester formation.
To determine what effect 2,4,5-trichlorophenoxyacetic acid had on 2,6-dinitrotoluene metabolism, intestinal enzymes, microbial populations, and urine mutagenicity were examined during 2,4,5-trichlorophenoxyacetic acid treatment. Weanling Fischer 344 male rats were treated daily with 54.4 mg/kg 2,4,5-trichlorophenoxyacetic acid by gavage for 4 wk. One, two, and four wk after the initial 2,4,5-trichlorophenoxyacetic acid dose, rats were administered (orally) 2,6-dinitrotoluene (75 mg/kg) and urine was collected for 24 hr in metabolism cages. Azo reductase, nitroreductase, beta-glucuronidase, dechlorinase, and dehydrochlorinase activities were examined concurrently. Treatments of rats for 1 wk reduced the transformation of 2,6-dinitrotoluene to mutagenic urinary metabolites. This was accompanied by a decrease in the fecal anaerobic microorganisms. The elimination of Lactobacillus ermentum from the small intestine and cecum of treated animals accompanied a significant increase in oxygen-tolerant lactobacilli and other unidentified aerobic microorganisms. However, there were no significant alterations in the intestinal enzyme activities examined. By 2 wk of 2,4,5-trichlorophenoxyacetic acid treatment, microbiota and urine genotoxicity returned to the levels observed in control animals. This trend continued for the duration of the experiment. After 2 wk, while cecal nitroreductase and azo reductase activities increased, small intestinal beta-glucuronidase activity decreased. By 4 wk, treated and untreated animal intestinal enzyme activities were indistinguishable. The transient increase in azo reductase and nitroreductase after treatment with 2,4,5-trichlorophenoxyacetic acid for 2 wk may have been counteracted by the reduced beta-glucuronidase activity, thus resulting in no change in 2,6-dinitrotoluene-derived urin mutagenicity. However, other environmental chemicals, unaffected by beta-glucuronidase, potentially could be activated by 2,4,5-trichlorophenoxyacetic acid exposure.
For more Interactions (Complete) data for 2,6-DINITROTOLUENE (6 total), please visit the HSDB record page.
EC50; Species: Scenedesmus subspicatus (Green Algae) exponential growth phase; Conditions: freshwater, static; 24 °C, pH 8.0-9.3; Concentration: 16000 ug/L for 48 hr; Effect: population, decreased biomass /formulation/
EC50; Species: Scenedesmus subspicatus (Green Algae) exponential growth phase; Conditions: freshwater, static; 24 °C, pH 8.0-9.3; Concentration: 11000 ug/L for 72 hr; Effect: population, decreased biomass /formulation/
EC50; Species: Scenedesmus subspicatus (Green Algae) exponential growth phase; Conditions: freshwater, static; 24 °C, pH 8.0-9.3; Concentration: 12000 ug/L for 96 hr; Effect: population, decreased biomass /formulation/
EC50; Species: Scenedesmus subspicatus (Green Algae) exponential growth phase; Conditions: freshwater, static; 24 °C, pH 8.0-9.3; Concentration: 22000 ug/L for 48 hr; Effect: decreased population, population changes, general /formulation/
For more Ecotoxicity Values (Complete) data for 2,6-DINITROTOLUENE (10 total), please visit the HSDB record page.
TERRESTRIAL FATE: Based on a classification scheme(1), measured Koc values of 19 and 72(2) and 197(3) indicate that 2,6-dinitrotoluene is expected to have very high to moderate mobility in soil(SRC). Leaching of 2,6-dinitrotoluene has been observed in soil column transport studies(4) and it has been observed to migrate large distances in subsurface soils during a field monitoring study(5). Volatilization of 2,6-dinitrotoluene from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 6.7X10-7 atm-cu m/mole at 25 °C(SRC), derived from its vapor pressure, 5.67X10-4 mm Hg(6), and water solubility, 204 mg/L(7). 2,6-Dinitrotoluene is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure. Photolysis of 2,6-dinitrotoluene on surfaces exposed to sunlight is expected to be an important fate process since 2,6-dinitrotoluene is susceptible to photodegradation(8-10). Biodegradation of 2,6-dinitrotoluene is expected to be an important fate process based on results of various screening tests that demonstrated microbial degradation(11-17). 2,6-Dinitrotoluene was degraded in two soils, with half-lives of 92 and 73 days reported(18).
AQUATIC FATE: Based on a classification scheme(1), measured Koc values of 19 and 72(2) and 197(3) indicate that 2,6-dinitrotoluene is expected to have little to moderate adsorption to suspended solids and sediment in water(SRC). Volatilization from water surfaces is expected to be slow(4) based upon an estimated Henry's Law constant of 6.7X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 5.67X10-4 mm Hg(5), and water solubility, 204 mg/L(6). Using this Henry's Law constant and an estimation method(4), volatilization half-lives for a model river and model lake are 66 and 486 days, respectively(SRC). According to a classification scheme(7), a measured BCF range of 0.6 to 21.2 in carp for dinitrotoluene isomers(8) suggests the potential for bioconcentration in aquatic organisms is low. 2,6-Dinitrotoluene is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(4). In aqueous solution, 2,6-dinitrotoluene has a quantum yield of 0.00188 at 313 nm(9) indicating that it is susceptible to direct photolysis by sunlight(SRC). The half-life for 2,6-dinitrotoluene in river water exposed to sunlight was 12 minutes and was determined to be an indirect photoreaction(10). Phototransformation tests of 2,6-dinitrotoluene in seawater under simulated solar radiation found that 89% of initial 2,6-dinitrotoluene was photodegraded within 24 hours and 100% after 72 hours(11). Biodegradation of 2,6-dinitrotoluene is expected to be an important fate process based on results of various screening tests that demonstrated microbial degradation(12-18).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 2,6-dinitrotoluene, which has a vapor pressure of 5.67X10-4 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. However, at 15 °C, 2,6-dinitrotoluene has a vapor pressure which indicates it will exist in both the vapor and particulate phases in the ambient atmosphere. Dinitrotoluenes have been detected in atmospheric particulate matter(3). Vapor-phase 2,6-dinitrotoluene 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 75 days(SRC), calculated from its rate constant of 2.2X10-13 cu cm/molecule-sec at 25 °C(SRC), determined using a structure estimation method(3). Particulate-phase 2,6-dinitrotoluene may be removed from the air by wet or dry deposition(SRC). 2,6-Dinitrotoluene is susceptible to direct photolysis in sunlight(5).
The substance can be absorbed into the body by inhalation, through the skin and by ingestion.
Dermal (T44) ; eye contact (T44) ; inhalation (T44) ; oral (T44)
Dinitrotoluene may cause conversion of oxyhemoglobin to methemoglobin via oxidation of iron(II) to iron(III) by its metabolites. High levels of methemoglobin are removed by catabolism, leading to the development of anemia. Some metabolites of dinitrotoluene are also transported back from the bile to the liver, where the amine group is N-hydroxylated by cytochrome P-450 to form an unstable sulfate conjugate. The sulfate conjugate is degraded into carbonium or nitrenium ions. These ions covalently bind to hepatic macromolecules (DNA, RNA), leading to mutations and subsequently liver tumors. They also bind to DNA of the lung and the intestine. (L276)
/BIRDS and MAMMALS/ ...The effects from oral exposures of 2,6-dinitrotoluene (2,6-DNT) and 1,3,5-trinitro-1,3,5-triazine (RDX) were tested using a controlled dosing regime in northern bobwhite (Colinus virginianus). Nine groups of birds of mixed sex received either corn oil or 50, 100, 190, or 350 mg 2,6-DNT/kg body weight/day or 20, 80, 125, or 180 mg RDX/kg body weight/day mixed in corn oil via gavage for 14 days. Etiology of disease was markedly different between compounds. Increased RDX exposure caused an inverse relationship to time of death, symptoms including clonic followed by tonic convulsions, and death shortly thereafter. Brain concentrations of RDX postmortem, however, were relatively consistent (mean +/- standard error, 20.5 +/- 2.9 mg/kg tissue). Observations of 2,6-DNT effects included gastrointestinal distress, dehydration, and a reduction in body mass and feed consumption. Together, these data suggest that RDX is more toxic from short, repeated exposures than 2,6-DNT, resulting in central nervous system-related effects, whereas 2,6-DNT causes gastrointestinal disturbances at higher exposures.
/BIRDS and MAMMALS/ ...The oral toxicity of 2,6-dinitrotoluene (DNT) /was evaluated/ in a representative ground-foraging species of management concern. Adult male and female northern bobwhite (Colinus virginianus) were exposed to either 0, 5, 10, 40, or 60 mg/kg/day via gavage for 60 days (subchronic) following determination of the median acute lethal dose (320 mg/kg). Circulating levels of red blood cells and hemoglobin were significantly decreased in a dose-dependent manner; however, levels remained within normal ranges. Plasma concentrations of total protein, albumin, globulin, aspartate aminotransferase, and potassium, sodium, and chlorine ions were significantly decreased, and circulating levels of uric acid were significantly increased. Decreased body weight, enlarged gallbladders, edematous gastrointestinal tracts, pale kidneys, pale and fibrous livers, and loose stools were consistent observations. The effects found in the clinical chemistries taken together with histopathological abnormalities observed in sections of hepatic and renal tissue suggest that the liver and kidneys are major targets for 2,6-DNT. Oral exposures to 2,6-DNT appear to affect northern bobwhite in a manner similar to that of the other main DNT isomer, 2,4-DNT, but in more subtle ways, adversely affecting the gastrointestinal system and leading to diarrhea and, ultimately, emaciation. The lowest-observed-adverse-effect level is 40 mg/kg/day based on hematological measures, and the no-observed-adverse-effect level is 10 mg/kg/day based on the absence of results indicative of adverse effects.
/AQUATIC SPECIES/ 2,4,6-Trinitrotoluene (TNT) is one of the most prevalent high explosives in the environment. 2,4-Dinitrotoluene (2,4-DNT) and 2,6-dinitrotoluene (2,6-DNT) are the most common isoforms of dinitrotoluene. The goal of this study was to determine the acute toxic effects of TNT, 2,4-DNT, and 2,6-DNT in adult male bullfrogs (Lithobates catesbeiana). The /oral/ LD(50) for TNT was 1,060 mg/kg BW while the LD(50 )for 2,4-DNT and 2,6-DNT was 1,098 mg/kg BW. All three compounds elicited similar symptoms of toxicity including changes of skin color, body weight, development of seizures, liver and kidney necrosis, and lung cyanosis. Relative organ weights did not show significant change.
2,6-Dinitrotoluene concentrations of 17.4 to 536.5 g/kg dry wt were detected in the birds eggs collected from the Lake Baikal region (Selenga River estuary, Russia)(1).[Table#4288]
2,6-Dinitrotoluene concentrations of 17.4 to 536.5 ug/kg dry wt were detected in the eggs of wild birds collected from the Lake Baikal region, Russia(1).
Blue lips, fingernails and skin. Headache. Dizziness. Nausea. Confusion. Convulsions. Unconsciousness.
MAY BE ABSORBED! See Inhalation.
See Inhalation.
Symptoms of 2,4-dinitrotoluene poisoning include blue lips or finger nails, blue skin, vertigo, fatigue, dizziness, weakness, nausea, vomiting, dyspnea, arthralgia, insomnia, tremor, paralysis, unconsciousness, chest pain, shortness of breath, palpitation, anorexia, and loss of weight. (T45, L940)
2,6-Dinitrotoluene concentration in raw wastewater from a textile plant was 50 mg/cu m(1) and was an average of 4.3 mg/L in the wastewater from 2,4,6-trinitrotoluene production(2). 2,6-Dinitrotoluene was detected in 100% of the samples of condensate water collected from a TNT manufacturing facility at a range of 0.06-14.9 mg/L; a minimum of one sample per week was collected over a one year period (n=54)(3).
U106; As stipulated in 40 CFR 261.33, when 2,6-dinitrotoluene, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).
This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Dinitrotoluene is produced, as an intermediate or a final product, by process units covered under this subpart. /Dinitrotoluene/
Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).
2,6-Dinitrotoluene is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.
Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Dinitrotoluene/
(FL) FLORIDA 0.05 ug/Ll
(ME) MAINE 0.5 ug/l
(WI) WISCONSIN 0.05 ug/l
Bioactivation of dinitrotoluene in the rat is thought to occur by the following processes: The methyl group is oxidized to an alcohol by a cytochrome p450 dependent pathway; the benzyl alcohol is conjugated with glucoronic acid and excreted in the bile. Intestinal microflora hydrolyze the glucuronide and reduce one nitro group, forming an aminonitrobenzyl alcohol which can be readsorbed from the intestine. The amino group oxidized to an hydroxylamine by hepatic enzymes and conjugated with sulfate. Decomposition of the sulfate ester yields a highly electrophilic nitrenium (or carbonium) ion which can react with DNA and other biological nucleophiles.
Urine specimens were collected over 72 hr from workers at a dinitrotoluene manufacturing plant. Samples were analyzed for 2,4- and 2,6-DNT and putative metabolites by GC/MS. Urine from workers exposed to dinitrotoluene contained 2,4- and 2,6-DNT, 2,4- and 2,6-dinitrobenzoic acid, 2,4-and 2,6-dinitrobenzyl glucuronide, 2-amino-4-nitrobenzoic acid and N-(acetyl)amino-4-nitrobenzoic acid. Excretion of these metabolites peaked near the end of the workshift, but declined to low or undetectable concentrations by the start of work the following day. The calculated half-times for elimination of total dinitrotoluene-related material detected in urine ranged from 1.0-2.7 hr, and those of individual metabolites from 0.8-4.5 hr. The most abundant metabolites were 2,4-dinitrobenzoic acid and 2-amino-4-nitrobenzoic acid, collectively accounting for 74-86% of the dinitrotoluene metabolites detected.
The metabolism and excretion of the hepatocarcinogen 2,6-DNT was investigated in Fischer 344 rats in vivo and in isolated perfused livers. Urinary excretion accounted for half of the dose (10 mg/kg) 72 hr after administration of (14)C-2,6-DNT. 2,6-Dinitrobenzoic acid, 2,6-dinitrobenzyl alcohol glucuronide, and 2-amino-6-nitrobenzoic acid accounted for 95% of the urinary (14)C. Fecal excretion accounted for 1/5 of the dose in 72 hr. 2,6-Dinitrobenzyl alcohol glucoronide was the major metabolite found in the perfusate and bile of isolated perfused rat livers. Biliary excretion of 2,6-dinitrobenzyl alcohol glucoronide by livers from male rats was 3.3 and 8.6-fold that of female rats on perfusion with 20 and 70 uM (14)C 2,6-DNT, respectively. No sex-dependent differences in biliary flow rates were observed. Twice as much (14)C was found to be covalently bound to hepatic macromolecules in male than female rat livers in vivo. Decreased biliary excretion of 2,6-dinitrobenzyl alcohol glucoronide may account for the lesser amount of (14)C found to be covalently bound in female rat livers. Observations with 2,6-DNT parallel those made with 2,4-DNT, suggesting that both isomers are metabolized by the liver, excreted in the bile, deconjugated and further metabolized by the intestinal microflora, and transported back to the liver for, perhaps, additional metabolism and covalent binding to an endogenous component of the liver.
For more Metabolism/Metabolites (Complete) data for 2,6-DINITROTOLUENE (11 total), please visit the HSDB record page.
The metabolism of 2,6-DNT occurs in the liver and also in the intestine by microflora. Both oxidized and reduced metabolites are excreted in the urine after oral administration of the compound. Oxidative metabolism by cytochrome P450 predominates in the liver, leading to the formation of dinitrobenzyl alcohol which is either converted to glucuronide conjugate or further oxidized to dinitrobenzoic acid. Dinitrobenzyl alcohol glucuronide is partially excreted into the bile, followed by metabolism by gut microflora and enterohepatic cycling (nitroreductase). Thus, 2,6-DNT appears to be first metabolized by the liver with the metabolites being excreted into the bile; the biliary metabolites are hydrolyzed and further metabolized in the intestine; after reabsorption and circulation back to the liver, a portion of the metabolites (2-amino-6-nitrobenzyl) are oxidized to a hydroxylamine by hepatic enzymes. The hydroxylamine is then conjugated with sulfate by hepatic sulfotransferase. The unstable N-sulfate decomposes to form an electrophilic nitrenium ion, which can react with cellular nucleophiles such as DNA. 2,6-Dinitrobenzyl alcohol glucuronide, 2-amino-6-nitrotoluene, and 2,6-dinitrobenzaldehyde can be detected in the bile. Some amounts of 2,6-dinitrobenzylalcohol and 2-amino-6nitrobenzyl alcohol can also be found. (L276)
After ip and oral administration of 2,6-DNT, the distribution and elimination were determined in strain A mice. In a 30 wk bioassay and at total ip doses of 600, 1500, or 3000 mg/kg, or total oral doses of 1200, 3000, or 6000 mg/kg, the urine was the major route of elimination of both ip and orally administered (3)H-labeled 2,6-DNT, with 87.6, 55.2 and 49.1% of ip doses of 1, 10 and 100 mg/kg, respectively, excreted within 4 hr. The corresponding amounts excreted after oral administration were 33.6, 25.2 and 24.3%, which increased to 53.7, 53.5 and 48.6% after 8 hr. The distribution of 2,6-DNT in various tissues (blood, liver, kidneys, lungs, small and large intestine) showed no evidence for preferential uptake or retention at any of the ip or po doses. Terminal half-lives of radioactive material in the liver were 1.11, 0.95 and 1.16 hr after ip doses of 1, 10 and 100 mg/kg, respectively.
Used to make TNT, urethane polymers, flexible and rigid foams, surface coatings, dyes, and other chemicals; Also used as a gelatinizing and waterproofing agent for explosives; [HSDB]
CHEM INT FOR TOLUENE-2,6-DIAMINE, A TOLUENE DIISOCYANATE INT; GELATINIZING & WATERPROOFING AGENT IN EXPLOSIVES
Intermediate in the manufacture of toluene diisocyanate and polyurethanes, ingredient in the manufacture of dyes and military and commercial explosives.
Dinitrotoluenes are used as intermediates for the production of toluene diisocyanate and dyestuffs; they also are used as explosives. Dinitrotoluene (including 2,6-dinitrotoluene) as an isomeric mixture is manufactured in large scale continuous plants for direct conversion to toluylene diamine (TDA) for production of toluene diisocyanate.
It is a high explosive and one of the precursors for trinitrotoluene (TNT), which is synthesized through three separate nitrations of toluene. 2,6-Dinitrotoluene can affect the body if it is inhaled, comes in contact with the eyes or skin, is swallowed, or is absorbed through the skin. Even a small amount absorbed from clothes or shoes may cause toxic symptoms. It is assumed that oral ingestion could be a secondary route for occupationally exposed humans. (L270, T44)
2023: 50,000,000 - <100,000,000 lb
(1977) AT LEAST 2.27X10+10 G
(1982) 3.27X10+4 G (INCLUDES 2,4-ISOMER)
(1975) ... Combined production of 272,610,000 lb for 2,4- and 2,6-dinitrotoluene.
Benzene, 2-methyl-1,3-dinitro- is listed as a High Production Volume (HPV) chemical (65FR81686). Chemicals listed as HPV were produced in or imported into the U.S. in >1 million pounds in 1990 and/or 1994. The HPV list is based on the 1990 Inventory Update Rule. (IUR) (40 CFR part 710 subpart B; 51FR21438).
Production volumes for non-confidential chemicals reported under the Inventory Update Rule. [Table#4291]
Dinitration of toluene results in the formation of a number of isomeric products, and with a typical sulfuric-nitric acid nitrating mixture the following mixture of isomers is obtained: 75 wt% 2,4-dinitrotoluene, 19 wt% 2,6-dinitrotoluene, 2.5 wt% 3,4-dinitrotoluene, 1 wt% 2,3-dinitrotoluene, and 0.5 wt% 2,5-dinitrotoluene.
NITRATION OF TOLUENE WITH NITRIC ACID IN THE PRESENCE OF CONCENTRATED SULFURIC ACID PRODUCES A MIXTURE OF ABOUT 80% 2,4- AND ABOUT 20% 2,6-ISOMERS, FROM WHICH THE 2,6-ISOMER IS NOT USUALLY ISOLATED
All Other Basic Organic Chemical Manufacturing
Benzene, 2-methyl-1,3-dinitro-: ACTIVE
A VAPOR GENERATOR WAS CONSTRUCTED TO PRODUCE KNOWN VAPOR CONCN OF EXPLOSIVES SUCH AS 2,6-DINITROTOLUENE GREATER THAN 1 PPB BY VOL FOR CALIBRATING TRACE EXPLOSIVES VAPOR DETECTORS.
Dinitrification of toluene typically yields 19% 2,6-dinitrotoluene by weight.
DefinitionChEBI: 2,6-dinitrotoluene is a dinitrotoluene carrying nitro substituents at positions 2 and 6. It has a role as a genotoxin.
/AQUATIC SPECIES/ Chronic aqueous exposures were conducted using bullfrog (Rana catesbeiana) tadpoles (8 day old) exposed to TNT (0-4 mg/L), 2,4-DNT (0-4 mg/L), and 2,6-DNT (0-8 mg/L) for 90 days. Survival of tadpoles examined using Cox proportional hazard models was reduced at all concentrations tested. Percent of abnormal swimming and other morphological abnormalities after sublethal exposure to TNT, 2,4-DNT, and 2,6-DNT at 2 mg/L were also evaluated. The effects of TNT, 2,4-DNT, and 2,6-DNT on wet body mass, snout vent length (SVL), and developmental stage of surviving tadpoles were examined. Only 2,4-DNT did not have a significant effect on body mass or SVL, but all three compounds tested had significant effects on survival. Long-term continuous exposure to these compounds at concentrations of 0.25 mg/L could lead to significant changes in growth and survival of larval amphibians.
For more Ecotoxicity Excerpts (Complete) data for 2,6-DINITROTOLUENE (8 total), please visit the HSDB record page.