"Trinitrobenzene, wetted, with not less than 10% water by mass" is a yellowish moist mass of crystals or a slurry. An explosive, but wetting lowers the risk of detonation. Dangerously explosive if allowed to dry out. The dry compound has a melting point of 122.5°C and is only slightly soluble in water (40 mg / L at 20°C). Store tightly sealed (to protect from drying out) in a cool, ventilated place, away from acute fire hazards and easily oxidized materials. May be toxic by ingestion.
颜色/状态：
Yellow crystals
气味：
Odorless
味道：
Tasteless
蒸汽压力：
6.44X10-6 mm Hg at 25 °C (extrapolated)
分解：
When heated to decomposition it emits toxic fumes of /nitrogen oxides/ and explodes.
... Trinitrobenzene (TNB) and its metabolites /were determined/ in the biological fluids of rats exposed to TNB in the diet and identified reductive metabolites, 1,3-dinitro,5-aniline (urine), 1,3-diamino-5-nitrobenzene (urine, feces and blood) and 1,3,5-triaminobenzene (urine and feces). No TNB was found in the checked samples by a GC/MS method. ... The metabolism of (14)C-TNB /was studied/ in an in vitro rat liver microsomal system and found that TNB (43 ug) is metabolized in 5 minutes. No parent compound and three metabolites were detected by HPLC. The two major peaks were identified as 3-amino-5-nitroaniline (3,5-diamino-nitrobenzene) and 3,5-dinitroaniline by either spiking or coelution with authentic standards. (14)C-TNB when administered orally (single dose, 225 mg/kg) to Fischer rats formed stable adducts with blood proteins and tissue DNA. Hemoglobin binding persisted throughout the life span of red blood cells (65 days); 10 weeks later, a significant amount of radioactivity was associated with spleen and kidney DNA.
The fluid in the receptor cell from human or rat skin contained 3,5-dinitroaniline and 1,3,5-triacetylaminobenzene. Guinea pig skin also metabolized TNB to 1-nitro-3,5-diacetamidobenzene and 3,5-diaminonitrobenzene to a minor extent ... TNB was absorbed and metabolized to a similar extent by human and rodent skin. Liver microsomes from male F344 rats produced 3,5-diaminobenzene as a major metabolite of TNB.
1,3,5-Trinitrobenzene is absorbed via oral, inhalation, and dermal routes and is believed to penetrate the red blood cell membrane. The metabolism of 1,3,5-TNB includes both oxidative and reductive biotransformations, followed by conjugation. The main route of excretion of 1,3,5-TNB metabolites is the urine. (L199)
IDENTIFICATION AND USE: 1,3,5-Trinitrobenzene (TNB) is a solid. It is used as an explosive, as a vulcanizing agent for natural rubber, and as an indicator for pH 12.0-14.0. HUMAN STUDIES: TNB is alleged to have caused optic neuritis and amblyopia. Chronic intoxication also is said to have caused yellowing of the conjunctiva or sclera. These reports of intoxication and ocular disturbances have come from the munitions industry where commonly there is exposure to a variety of substances, and it is difficult to be sure of the individual substance responsible. TNB was found toxic in TK6 human lymphoblastic cells. ANIMAL STUDIES: Male rats were gavaged with TNB at 35.5 and 71 mg/kg in corn oil. Blood was collected 5 hr and 24 hr after a single oral dose or 24 hr after daily oral doses for 4 or 10 d in four different sets of experiments. A dose-dependent methemoglobinemia was present only in blood collected 5 hr after a single dose. A highly significant dose-dependent anemia with reduced red cells, hemoglobin, and hematocrit was present in rats receiving TNB for 4 or 10 d. In a 90-day oral toxicity study of TNB, kidneys in male rats receiving TNB at dose levels of 67, 400 and 800 ppm TNB had an increased incidence of cytoplasmic hyaline droplets in proximal cortical tubular epithelial cells at all treatment levels. However, a diagnosis of alpha-2-u-globulin nephropathy was not deemed appropriate since there was no significant increase in single cell necrosis, no presence of granular casts or linear papillary mineralization or increased tubular hyperplasia. A 90-day toxicity test of TNB in mice revealed treatment-related changes in spleen (erythroid cell hyperplasia) and in testis (seminiferous tubule degeneration) in the 750 ppm TNB group. The carcinogenic activity of TNB was studied in mouse skin and lung tumor assays. A single application of 10 or 50 mg of TNB to the skin of mice increased the incidence of inflammation, epidermal hyperplasia and dark cells. TNB was found negative in assay for initiation-promotion of skin carcinogenicity. In rats, TNB-mediated tissue damage is accompanied by breakdown of the blood-brain barrier. The presence of vacuolation and associated extravasated serum proteins in TNB-treated rats is an indication of vasogenic brain edema, which appears to be a critical event in TNB toxicity. Sperm depletion and degeneration of the seminiferous tubules were noted in a reproduction study in rats. Mutagenicity was evaluated with the Salmonella fluctuation test (FT) and the V79 Chinese hamster lung cell mutagenicity assay. The fluctuation test results indicated that TNB was mutagenic. However, TNB was not mutagenic for the V79 mammalian cells with or without metabolic activation. ECOTOXICITY STUDIES: Slight irritant effects suggesting respiratory distress upon short term exposure to marine fish Kuhlia sandvicensis were observed at exposure levels of 100 ug/L, while moderate and violent reactions to the chemical were produced at exposures of 1,000 and 10,000 ug/L. Results from the hydra assay of TNB indicated the minimal affective concentrations required to elicit a toxic response in the adult hydra and in the regenerating hydra were 3.8 ug/mL and 1.8 ug/mL, respectively.
In the red blood cell, 1,3,5-TNB induces formation of methemoglobin, leading to cyanosis. Reduction of the nitrogroup(s) of 1,3,5-TNB produces reactive nitroaromatic radical anions which redox cycle to produce other reactive species such as superoxide anion. Redox cycling of these intermediates probably causes the methemoglobinemia. 1,3,5-TNB may also exert neurotoxic effects by damaging the blood-brain barrier.(L199, A136)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌物分类
对人类不具有致癌性（未被国际癌症研究机构IARC列名）。
No indication of carcinogenicity to humans (not listed by IARC).
Chronic exposure to 1,3,5-trinitrobenzene can cause a reduction (or loss) in the number of red blood cells (anemia). 1,3,5-TNB may also have neurotoxic effects. (L199, A136)
Male Wistar rats injected intraperitoneally with 100 umol/kg body weight (21.3 mg/kg) of TNB (in propylene glycol) excreted approximately 3.24-3.42 mg p-aminophenol equivalents per kilogram in the urine 5 hours after dosing... Since these levels were twice the base line levels excreted by vehicle-only treated animals, it was concluded that absorption and metabolism of TNB is slow. Additional details on TNB deposition were not included in the study.
The toxicokinetics (absorption, distribution and elimination) of (14)C-trinitrobenzene (TNB) were studied in Fischer 344 rats following a single oral dose. Male (4) and female (4) rats were dosed with (14)C-TNB (152 mg/kg, 6-8 mCi) in DMSO. Groups of 2 male and 2 female rats were used in experiments to determine (14)C-TNB elimination through expired CO2. (14)C-TNB levels in urine and feces were measured at 24, 48, 72 and 96 hours after dosing. Approximately 10% of the dose was eliminated in the urine of male and female rats in the first 24 hours. Approximately 21% and 36% of the dose appeared in the urine in 4 days in male and female rats, respectively. Excretion via feces was approximately 4% in the same period in both sexes. The expired (14)C-CO2 was about 3% and 5% of the dose in 2 days in male and female rats, respectively. At 4 days after treatment, the radioactive residues were about 0.02-0.03%/g of tissue in the liver, kidney, skin and lungs, whereas other tissues showed lower levels of residues (about 0.001%/g or less). The results showed that a single dose of TNB in the rat was absorbed in the gut (administered in DMSO) and was eliminated mainly in the urine, with low levels in feces in 4 days. The results from this study did not show bioaccumulation of TNB in rats.
The percutaneous absorption of 1,3,5-trinitrobenzene (TNB) was studied in viable skin from hairless guinea pigs (HGP), Fischer 344 rats and humans. Skin was dermatomed and assembled in flow-through diffusion cells followed by TNB application in either an acetone or a water vehicle. Skin absorption was expressed as the percentage of applied dose absorbed into skin and receptor fluid within 24 hr. Rapid absorption of TNB by rodent skin was obtained with both vehicles. For HGP skin, TNB absorption was 72.7+/-5.5% in the acetone vehicle and 82.3+/-4.5% in the water vehicle. For rat skin, TNB absorption was 61.0+/-4.1% (acetone) and 66.5+/-4.1% (water). Absorption of TNB from acetone was significantly reduced (38.0+/-11.0%, P = 0.0118) in human skin, but absorption from water remained high (75.5+/-10.8%). Little TNB remained in skin when a thin (200 um) dermatome section was used (HGP and human skin). A thicker dermatome section was required (350 um) with haired rat skin, and 13-21% of the absorbed radioactivity remained in the skin at 24 hr. Rodent skin did not simulate satisfactorily the barrier properties of human skin when TNB absorption was reduced by application in a volatile solvent.
