ピクリルスルホン酸

Other Uses -> Explosives

Flammable agents - 3rd degree

Trinitrobenzene sulfonic acid appears as a detonating explosive substance derived from an organic sulfonic acid. Primary hazard is blast of an instantaneous explosion, not flying projectiles or fragments. Under prolonged exposure to fire or heat the containers may explode violently.

Solid; [Sigma-Aldrich MSDS]

This chemical does not meet GHS hazard criteria for 46.2% (36 of 78) of reports.

Danger

H201 (53.8%): (Deleted) Explosive; mass explosion hazard [Danger Explosives]

P210, P230, P240, P250, P260, P261, P264, P270, P272, P280, P301+P316, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P316, P321, P330, P333+P317, P362+P364, P363, P370+P380, P372, P373, P401, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 78 reports by companies from 5 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Chemical: Benzenesulfonic acid, 2,4,6-trinitro-

Benzenesulfonic acid, 2,4,6-trinitro-: Does not have an individual approval but may be used under an appropriate group standard

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.)

A detonating explosive and strong oxidizing agent; [CAMEO] Explosive; Causes burns; Inhalation may cause corrosive injuries to upper respiratory tract; May cause skin sensitization; Toxic by ingestion; [Sigma-Aldrich MSDS] See Picryl chloride.

TRINITROBENZENE SULFONIC ACID is a nitroaryl oxidizing acid. If mixed with reducing agents, including hydrides, sulfides and nitrides, they may begin a vigorous reaction that culminates in a detonation. The aromatic nitro compounds may explode in the presence of a base such as sodium hydroxide or potassium hydroxide even in the presence of water or organic solvents. The explosive tendencies of aromatic nitro compounds are increased by the presence of multiple nitro groups.

Trinitrobenzenesulfonic acid

UN0386

Div 1.1 Explosives (with a mass explosion hazard) (49 eCFR § 173.50)

Expl. 1.1 (53.8%)

Flammable agents - 3rd degree, Reactive agents - 3rd degree

Trinitrobenzenesulfonic acid

A Commercial Grade

5,000

A Commercial Grade

400

Explosive chemical that can be released at a facility.

Fire-Fighting Measures. Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. Special protective equipment for fire-fighters: Wear self contained breathing apparatus for fire fighting if necessary.

ACCIDENTAL RELEASE MEASURES. Personal precautions: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

Wear protective gloves/ protective clothing/ eye protection/ face protection.

Handle with gloves. 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.

Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

If in eyes: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continue rinsing. Immediately call a POISON CENTER or doctor/ physician.

For more Preventive Measures (Complete) data for Picryl sulfonic acid (7 total), please visit the HSDB record page.

Excerpt from ERG Guide 112 [Explosives - Division 1.1, 1.2, 1.3 or 1.5]:

Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multi-purpose combination (US) or type ABEK (EN 14387) 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).

Tightly fitting safety goggles. Faceshield (8-inch minimum). Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

For skin and body protection, complete suit protecting against chemicals, The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

The aim of the present study is to investigate the treatment efficiency of intra-rectal (IR) and intra-peritoneal (IP) application of Origanum onites essential oil (OOEO), which is a well-known antioxidant, in the colitis model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS) and ethanol (E) in comparison with dexamethasone therapy through the morphologic damage score. Monoclonal antibodies against intercellular adhesion molecule-1 (ICAM-1, CD54), anti-rat granulocytes, and myeloperoxidase (MPO), were also investigated immunohistochemically. There was a significant difference in terms of ulceration, mucus cell depletion, inflammatory cell infiltration, vascular dilatation (p<0.001), crypt abscesses (p<0.01), and edema (p<0.05) between OOEO-1mg/kg-IR and control colitis groups. A significant difference was encountered in terms of mucus cell depletion, crypt abscesses, inflammatory cell infiltration, vascular dilatation (p<0.01), and ulceration (p<0.05) between the OOEO-0.1mg/kg-IR and control colitis groups. A significant difference was noticed in terms of ulceration, inflammatory cell infiltration, mucus cell depletion (p<0.001), vascular dilatation (p<0.01), and mucosal atrophy (p<0.05) between the OOEO-1mg/kg-IP and control colitis groups. There was a significant difference in terms of ulceration, mucus cell depletion, inflammatory cell infiltration (p<0.001), crypt abscesses, vascular dilatation (p<0.01), and mucosal atrophy (p<0.05) between the OOEO-0.1mg/kg-IP and control colitis groups. No significant difference was determined in terms of ulceration, inflammatory cyst, mucosal atrophy, edema, and vascular dilatation between the dexamethazone and control colitis groups (p>0.05) ...

A targeted delivery system for inflammatory bowel disease (IBD), Eudragit L100 (EuL)-coated chitosan (Ch)-succinyl-prednisolone (SP) conjugate microspheres (Ch-SP-MS/EuL), was designed and examined in vivo for efficacy and toxicity ... Experimental colitis was induced by instillation of 2,4,6-trinitrobenzenesulfonic acid (TNBS) into the colon in rats. Drugs were administered once or twice a day intragastrically for three consecutive days. Visible colitis severity, colon/body weight ratio and myeloperoxidase activity were measured as inflammatory indices. Toxicity was examined from the decrease in the thymus/body weight ratio. Efficacy was dose-dependent and the greatest in the order Ch-SP-MS/EuL>Ch-SP-MS>prednisolone (PD) alone, and Ch-SP-MS/EuL showed excellent recovery of colitis states. Toxicity was the greatest in the order PD>>Ch-SP-MS>Ch-SP-MS/EuL. Ch-SP-MS and Ch-SP-MS/EuL reduced significantly the thymic atrophy caused by PD. It was demonstrated that Ch-SP-MS/EuL enhanced effectiveness of PD and reduced toxic side effects of PD greatly ...

/The aim of the study was/ to evaluate the protective effects of ilomastat, an exogenous matrix metalloproteinase (MMP) inhibitor, on trinitrobenzenesulfonic acid (TNB)-induced ulcerative colitis (UC) in rats. Male SD rats were randomly divided into model group, protective groups A and B, and normal control group. Rats in the model group received only intra-colonic TNB. Rats in the protective groups A and B received intra-peritoneal ilomastat of 10 mg/kg and 20 mg/kg, respectively, beside TNB. Rats in the normal control group received only intra-colonic normal saline. After 3 wk, segments of colon were obtained. RT-PCR and immunohistochemistry were used to examine the expression of MMP-1 and TIMP-1. Hematoxylin-eosin (HE) staining was used for pathological study. The model of UC was successfully induced in rats. Inflammation of colonic mucosa greatly improved in protective groups A and B. Expression of MMP-1 and TIMP-1 in the model group, protective groups A and B was significantly higher than that in the normal control group (P < 0.0001) with MMP-1 expression increased more significantly than TIMP-1 expression. Expression of MMP-1 in protective groups A and B was significantly lower than that in the model group (P < 0.0001) . Expression of MMP-1 in protective group B was significantly lower than that in protective group A (P < 0.0001). Ilomastat /thus/ improves TNB-induced UC in rats by inhibiting the MMP-1 activity.

... The trinitrobenzenesulfonic acid model of colitis in the rat was used. Rats were treated orally with alendronate and its efficacy compared with that of oral sulfasalazine or vehicle, starting 2 h after colitis induction. The status of the animals was assessed 5 days later ... Alendronate treatment (25 or 75 mg/kg/day) resulted in a decrease in the colonic damage score and loss of body weight (at 25 mg/kg/day only). This was associated to a dramatic reduction in the mRNA levels of interleukin 1 beta (IL-1 beta), monocyte chemoattractant protein 1 (MCP-1) and interleukin 1 receptor antagonist (IL-1 ra). The magnitude of the beneficial effect was comparable to that of sulfasalazine (at a 6-20 fold higher dose) ...

For more Interactions (Complete) data for Picryl sulfonic acid (11 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 120(SRC), determined from a structure estimation method(2), indicates that picryl sulfonic acid is expected to have high mobility in soil(SRC). The pKa of picryl sulfonic acid is estimated as 0.31(3), indicating that this compound will exist entirely in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of picryl sulfonic acid from moist soil surfaces is not expected to be an important fate process(SRC) given its estimated pKa(3). Picryl sulfonic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.2X10-12 mm Hg at 25 °C(SRC), determined from a fragment constant method(5). Biodegradation data were not available(SRC, 2010).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 120(SRC), determined from a structure estimation method(2), indicates that picryl sulfonic acid is not expected to adsorb to suspended solids and sediment(SRC). An estimated pKa of 0.31(3) indicates picryl sulfonic acid will exist entirely in the anion form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from an estimated log Kow of -1.71(5) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Picryl sulfonic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(7). Biodegradation data were not available(SRC, 2010).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), picryl sulfonic acid, which has an estimated vapor pressure of 5.2X10-12 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase picryl sulfonic acid may be removed from the air by wet or dry deposition(SRC). Picryl sulfonic acid contains chromophores that absorb at wavelengths >290 nm(3) and may be susceptible to direct photolysis by sunlight(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of picryl sulfonic acid can be estimated to be 120(SRC). According to a classification scheme(2), this estimated Koc value suggests that picryl sulfonic acid is expected to have high mobility in soil. The pKa of picryl sulfonic acid is estimated as 0.31(3), indicating that this compound will exist entirely in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

/SIGNS AND SYMPTOMS/ Skin sensitiser, Toxic by ingestion, Corrosive

/SIGNS AND SYMPTOMS/ May be harmful if inhaled. Material is extremely destructive to the tissue of the mucous membranes and upper respiratory tract. May be harmful if absorbed through skin. Causes skin burns. Causes eye burns.

An estimated BCF of 3 was calculated in fish for picryl sulfonic acid(SRC), using an estimated log Kow of -1.71(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

An estimated pKa of 0.31(1) indicates picryl sulfonic acid will exist entirely in the anion form at pH values of 5 to 9 and therefore volatilization from water surfaces and moist soil is not expected to be an important fate process(SRC). Picryl sulfonic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.2X10-12 mm Hg(SRC), determined from a fragment constant method(2).

/LABORATORY ANIMALS: Acute Exposure/ ... Models of acute colitis in animals have been achieved by intrarectal administration of agents such as 2,4,6-trinitrobenzenesulfonic acid (TNBS) into rat colon. This agent induces focal inflammation and alterations in the colon with features similar to those found in chronic inflammatory diseases in humans. The aim of this study was to assess the effect of TNBS administration on histological and ultrastructural features of the rat colon ... In areas without transmural inflammation, ... a significant increase in crypt diameter and in the number and area of the goblet cells /were observed/, as well as alterations in the contents of mucin in goblet cells. /It was concluded/ that TNBS treatment in rats led to severe changes in normal architecture of the colon and also in damaged areas where no direct inflammation was produced.

/LABORATORY ANIMALS: Acute Exposure/ ... The objective of this study was to investigate mechanisms of free radical formation from the colitis inducer 2,4,6-trinitrobenzene sulfonic acid (TNBS) /It was shown that/ TNBS was rapidly metabolized to TNBS nitro radical anion via metabolic reduction by flavinmononucleotide/NADPH, xanthine/xanthine oxidase as well as the rat small intestine and colon. TNBS nitro radical anion was directly detected with electron paramagnetic resonance (EPR) spectroscopy. EPR spectra of TNBS nitro radical anion showed hyperfine coupling constants from the proximal nitrogen, two hydrogens and the two distal nitrogens with respective magnitudes of a(N)(4) = 9.7 G; a(H)(3,5) = 3.2 G (2); and a(N)(2,6) = 0.25 G. EPR spin trapping using 5.5-dimethyl-1-pyrroline N-oxide in aerobic incubations of isolated enterocytes (or colonocytes, or red blood cells) and TNBS, in the presence or absence of NADPH, produced radical adducts characteristic of superoxide and hydroxyl radicals. /The/ EPR data showing generation of TNBS nitro and superoxide radical anions demonstrate that one-electron reduction of TNBS may be an initial step in the cascade of the in vivo inflammatory events in TNBS-induced colitis.

/LABORATORY ANIMALS: Acute Exposure/ ... In vivo, /Sprague-Dawley/ rats were given 2,4,6-trinitrobenzenesulfonic acid (TNBS), TNBS in ethanol, or TNBS coupled with dipalmitoylphosphatidylcholine by enema. On the 11th day, mucosal hydrophobicity damage score, colon weight, and myeloperoxidase activity were measured ... TNBS acutely (5 minutes) reduced the contact angle of the rat colonic mucosa ... when administered in 50% ethanol. Surface mucosal hydrophobicity was significantly reduced 11 days after intracolonic inoculation with TNBS in ethanol and appeared to be associated with colonic inflammation. The ability of TNBS to decrease mucosal hydrophobicity and induce colitis was attenuated if the hapten was coupled with dipalmitoylphosphatidylcholine. TNBS may reduce mucosal hydrophobicity by reacting with the surface-active phospholipids of the colonic mucosa. Reduced hydrophobic integrity of the colonic mucosa may contribute to TNBS-induced colonic inflammation.

Picryl sulfonic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Picryl sulfonic acid contains chromophores that absorb at wavelengths >290 nm(1) and therefore may be susceptible to direct photolysis by sunlight(SRC).

Picryl sulfonic acid's production and use as a laboratory reagent and detonator may result in its release to the environment through various waste streams. If released to air, an estimated vapor pressure of 5.2X10-12 mm Hg at 25 °C indicates picryl sulfonic acid will exist solely in the particulate phase in the atmosphere. Particulate-phase picryl sulfonic acid will be removed from the atmosphere by wet or dry deposition. Picryl sulfonic acid contains chromophores that absorb at wavelengths >290 nm and therefore may be susceptible to direct photolysis by sunlight. If released to soil, picryl sulfonic acid is expected to have high mobility based upon an estimated Koc of 120. The pKa of picryl sulfonic acid is estimated as 0.31, indicating that this compound will exist entirely in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts. Volatilization from moist soil is not expected because the acid exists as an anion and anions do not volatilize. Biodegradation data were not available. If released into water, picryl sulfonic acid is not expected to adsorb to suspended solids and sediment based upon the estimated Koc. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated pKa. An estimated BCF of 3 suggests the potential for bioconcentration in aquatic organisms is low. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. Occupational exposure to picryl sulfonic acid may occur through dermal contact with this compound at workplaces where picryl sulfonic acid is produced or used. (SRC)

Trinitrobenzenesulfonic acid

A Commercial Grade

5,000

A Commercial Grade

400

Explosive chemical that can be released at a facility.

Peroxynitrite, derived from the reaction of nitric oxide (NO) with superoxide (O(2)), is a potent nitrating and oxidizing agent that can induce apoptosis in a variety of different cell types. /This/ study ... investigated the possible role of peroxynitrite as a mediator of colon epithelial cell death in rat colitis. Rat colon inflammation was induced by intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid (TNBS) and rats were sacrificed 24 hr after TNBS administration. Expression of inducible nitric-oxide synthase (iNOS) was detected by reverse transcription-polymerase chain reaction and immunohistochemistry. The enzymatic activities of Ca(2+)-independent iNOS and Ca(2+)-dependent constitutive nitric oxide synthase were determined biochemically. Evidence of peroxynitrite-mediated cell injury was detected by immunostaining of nitrotyrosine. Apoptosis was examined by in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and DNA gel electrophoresis. To evaluate the specific contribution of peroxynitrite to the observed cell injury, a selective iNOS inhibitor, L-N(G)-[1-iminoethyl]lysine (L-NIL), was administered after TNBS induction. Morphological examination and analysis of TUNEL/cytokeratin double immunofluorescence revealed significant apoptosis in mucosal epithelial cells. Nitrotyrosine was colocalized with TUNEL, strongly demonstrating the association of peroxynitrite with the apoptotic death of colon epithelial cells. The administration of L-NIL reduced iNOS activity in 24 hr lesions by 92% and also significantly attenuated both nitrotyrosine staining and apoptotic cell counts in the colon epithelium. These results strongly suggest that local elevated level of peroxynitrite produced from increased iNOS expression and activity is a major contributor to colon epithelial apoptosis during colon inflammation.

Used as a reagent to neutralize peptide terminal amino groups; [ChemIDplus]

Bioreagent ... determination of primary amines

Detonator