Tribromoacetic acid

296.740

296.74

200-919-9

71KTL99QJX

DTXSID6021668

Colorless crystals

2915900090

37.30000

3.33

3.1±0.1 g/cm3

132 °C

245.0±0.0 °C at 760 mmHg

97.0±25.9 °C

1.676

In water, 2.0X10+5 mg/L at 25 deg C

Keep tightly closed. Store in a cool dry place.

2.8X10-4 mm Hg at 25 deg C (est)

3.34e-09 atm-m3/mole|Henry's Law constant = 3.34X10-9 atm-cu m/mole at 25 °C

pKa = 0.72 at 25 °C

Decomposes in boiling water to bromoform.|Hydroxyl radical reaction rate constant = 5.2X10-13 cu cm/molecule-sec at 25 °C (est)

III

8

UN 3261 8/PG 2

3

R35

S26-S36/37/39-S45-S24/25-S36-S16

C:Corrosive;

Stable. Incompatible with strong oxidizing agents, bases.

P210-P403 + P235

H225-H315

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure 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, aquatic, and plant life; and conformance with environmental and public health regulations.|Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Observe all federal, state, and local environmental regulations.

NTP/NIEHS; Short Term Reproductive and Developmental Toxicity of Tribromoacetic Acid (CAS No. 75-96-7) Administered in Drinking Water to Sprague-Dawley Rats NTP Study Number: RDGT94009. NTIS#: PB98-165111.

|Danger|H314 (100%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]|P260, P264, P280, P301+P330+P331, P303+P361+P353, P304+P340, P305+P351+P338, P310, P321, P363, P405, and P501|Aggregated GHS information provided by 46 companies from 3 notifications to the ECHA C&L Inventory.

ENGINEERING CONTROLS. Safety shower and eye bath. Use only in a chemical fume hood.|PERSONAL PROTECTIVE EQUIPMENT. Wear appropriate government approved respirator, chemical-resistant gloves, safety goggles, other protective clothing.|Faceshield (8-inch minimum).

FIREFIGHTING. Protective Equipment: Wear self-contained breathing apparatus and protective clothing to prevent contact with skin and eyes.|EXTINGUISHING MEDIA. Suitable: Carbon dioxide, dry chemical powder, or appropriate foam.

Emits toxic fumes under fire conditions.

Cover with dry lime or soda ash, pick up, keep in a closed container, and hold for waste disposal. Ventilate area and wash spill site after material pickup is complete.

Do not breathe dust. Do not get in eyes, on skin, on clothing. Avoid prolonged or repeated exposure.|Wear self-contained breathing apparatus, rubber boots, and heavy rubber gloves. In case of spill or leak, evacuate the area.|Wash contaminated clothing before reuse. Discard contaminated shoes. Wash thoroughly after handling.|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. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning.|For more Preventive Measures (Complete) data for TRIBROMOACETIC ACID (7 total), please visit the HSDB record page.

Occupational exposure to tribromoacetic acid may occur through inhalation and dermal contact with this compound at workplaces where it is produced or used. Monitoring data indicate that the general population may be exposed to bromoacetic acid via ingestion of chlorinated or chloraminated drinking water, particularly when source waters contain high concentrations of bromide. (SRC)

Chlorination of drinking water generates disinfection by-products (DBPs) , which have been shown to disrupt spermatogenesis in rodents at high doses, suggesting that DBPs could pose a reproductive risk to men. ... A cohort study /was conducted/ to evaluate semen quality in men with well-characterized exposures to DBPs. ... The results of the present study do not support an association between exposure to DBPs at levels approaching regulatory limits and adverse sperm outcomes, although /there was/ an association between total organohalides and sperm concentration. ... The lone association of total organohalide exposure with sperm concentration may lend support to findings that have suggested that total organohalide is a stronger risk factor for adverse pregnancy outcomes than any of the regulated DBP groups or species and that the toxicity of total organohalides is greater than that of the individual or subclasses of DBPs. ... /Disinfection by-products/

The potential toxicity of tribromoacetic acid (TBA; CAS No. 75-96-7) was evaluated using a short-term reproductive and developmental toxicity screen. This study design was selected to identify the process (development; female reproduction; male reproduction; various somatic organs/processes) that is the most sensitive to tribromoacetic acid exposure. The dose range-finding study was conducted at concentrations of 0, 30, 100, 300, and 500 ppm of TBA in the drinking water for two weeks. Based on decreased water consumption in the 500 ppm males and females, the dose levels of 0, 10, 70, and 400 ppm (Groups 1, 2, 3, and 4, respectively) were selected for the main study, which utilized two groups of male rats designated as Group A (non-BrdU treated animals, 10 rats in Groups 1, 2, 3, and 4) and Group B (BrdU-treated, 5 rats in Groups 1, 2, and 3, and 8 rats in Group 4), and three groups of female rats designated as Group A (peri-conception exposure, 10 rats in Groups 1, 2, 3, and 4), Group B (gestational exposure), and Group C (peri-conception exposure, BrdU-treated, 5 rats in Groups 1, 2, and 3, and 8 animals in Group 4). Control animals received deionized water, the vehicle. During the treatment period, all animals survived to the scheduled necropsy and there were no clinical signs of general toxicity noted at any dose level. There were no treatment-related findings in body weights or feed consumption, but there was a slight and inconsistent decrease in water consumption in the 400 ppm animals. The overall calculated consumption of TBA for Groups 2-4 was 1, 7, and 39 mg/kg/day, respectively. Male and female gross necropsy findings were comparable across dose groups with the exception of a 40% incidence of mottled kidneys in the 400 ppm A males. Female and male reproductive findings were unremarkable. The visceral evaluation of the newborn heart and brain using Wilson's soft tissue free hand slicing technique did not reveal any treatment-related effects. Adult male organ weights, organ-to-body weight ratios, and clinical chemistry and hematology endpoints were unaffected by TBA treatment with the following exceptions: a 14 % increase in liver-to-body weight ratio in the 400 ppm A males, and an increase of 12% and 10%, respectively, in blood urea nitrogen and serum albumin in the 400 ppm A males. The increases in BUN and albumin represent a small, but possible biologically significant indicator of dehydration, probably attributable to decreased fluid consumption. The increase in BUN accompanied by the increase in mottled kidneys may also suggest mild kidney toxicity which could result in morphological changes with a longer term exposure. No treatment-related histopathology was noted in the organs of the A males or in cellular proliferation as measured by BrdU Labeling Index from the liver, kidney, or urinary bladder from the B males or C females. The results of this study indicate that TBA at up to 400 ppm marginally reduced water consumption and did not affect reproductive function or produce general toxicity. From these data, TBA is not a reproductive toxicant in males or females at doses up to 400 ppm. This conclusion rests heavily on the shortness of the current exposure, and should be replicated using a longer study before the data are relied on.

Tribromoacetic acid's formation as a chemical byproduct of chlorination and chloramination of drinking water(1), and its use as a brominating agent and catalyst for polymerization(2) may result in its release to the environment through various waste streams.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 5.3(SRC), determined from a water solubility of 2.0X10+5 mg/L(2) and a regression-derived equation(3), indicates that tribromoacetic acid is expected to have very high mobility in soil(SRC). The pKa of tribromoacetic acid is 0.72(4), indicating that this compound will primarily exist in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). Tribromoacetic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.8X10-4 mm Hg(SRC), determined from a fragment constant method(6). Limited data are available regarding the biodegradation of tribromoacetic acid in soil. However, tribromoacetic acid (0.1% w/v) was used as a carbon source by Pseudomonas and Nocardia when measured for halide released over a period of 20 days at 30 °C(7).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 5.3(SRC), determined from a water solubility of 2.0X10+5 mg/L(2) and a regression-derived equation(3), indicates that tribromoacetic acid is not expected to adsorb to suspended solids and sediment(SRC). A pKa of 0.72(4) indicates tribromoacetic acid will exist almost 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(5). According to a classification scheme(6), an estimated BCF of 0.63(SRC), from its water solubility(2) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Limited data are available regarding the biodegradation of tribromoacetic acid in water. However, tribromoacetic acid (0.1% w/v) was used as a carbon source by Pseudomonas and Nocardia when measured for halide released over a period of 20 days at 30 °C(8).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), tribromoacetic acid, which has an estimated vapor pressure of 2.8X10-4 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase tribromoacetic acid 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 30.9 days(SRC), calculated from its rate constant of 5.2X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Tribromoacetic acid does not contain chromophores that absorb at wavelengths >290 nm(4) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of tribromoacetic acid with photochemically-produced hydroxyl radicals has been estimated as 5.2X10-13 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 30.9 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Tribromoacetic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Tribromoacetic acid does not contain chromophores that absorb at wavelengths >290 nm(3) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 0.63 was calculated for tribromoacetic acid(SRC), using a water solubility of 2.0X10+5 mg/L(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).

The Koc of tribromoacetic acid is estimated as 5.3(SRC), using a water solubility of 2.0X10+5 mg/L(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that tribromoacetic acid is expected to have very high mobility in soil. The pKa of tribromoacetic acid is 0.72(4), indicating that this compound will primarily exist in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5).

A pKa of 0.72(1) indicates tribromoacetic acid will exist almost 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(2). Tribromoacetic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.8X10-4 mm Hg(SRC), determined from a fragment constant method(3).

DRINKING WATER: A mean concentration of 0.13 ug/L tribromoacetic acid was measured in post-treatment drinking water from disinfection utilities in Belgium, France, Germany, Spain, The Netherlands, and Italy(1). Tribromoacetic acid was measured in water samples taken from Barcelona's water treatment plant between November 1997 and March 1998; the compound was detected in prechlorinated water (2.3-10 ug/L), sand-filtered water (3-10 ug/L), ozonated water (3.1-10 ug/L), granulated activated carbon-filtered water (not detected-1.7 ug/L), and postchlorinated water (2.7-4.9 ug/L)(2).|DRINKING WATER: Water taken from 4 treatment plants in The Netherlands contained tribromoacetic acid concentrations between 0.3-2.1 ug/L; concentrations in water taken from 16 other treatment plants were less than 0.1 ug/L(1).

The mechanisms associated with the carcinogenic effects of HAAs include those identified for DCA and TCA. It is apparent that more than one mechanism is responsible for the effects of this class and that the importance of these mechanisms to the activity of individual members of the class varies. In part, these differences in mechanism can be related to the differences in tumor phenotypes that are induced. One phenotype seems to be associated with prior characterizations of tumors induced by peroxisome proliferators and is induced by TCA. The second phenotype involves glycogen-poor tumors that stain heavily with antibodies to c-Jun and c-Fos. This phenotype is produced by DCA. These effects are probably produced by selection of lesions with differing defects in cell signalling pathways that control the processes of cell division and cell death.|The brominated HAAs are about 10-fold more potent than their chlorinated analogues in their ability to induce point mutations. This does not establish that they are inducing cancer by mutagenic mechanisms in vivo, but this activity will have to be taken into account as data on their carcinogenic activity become more complete.|The HAAs vary widely in their ability to induce oxidative stress and to elevate the 8-OH-dG content of nuclear DNA of the liver. This property becomes increasingly apparent with the brominated compounds. It is notable that the brominated analogues are not more potent inducers of hepatic tumors than the corresponding chlorinated HAAs. Therefore, it is doubtful that this mechanism is the most important determinant of this effect.

/SIGNS AND SYMPTOMS/ Corrosive.|/SIGNS AND SYMPTOMS/ ... Symptoms of exposure may include burning sensation, coughing, wheezing, laryngitis, shortness of breath, headache, nausea, and vomiting. Inhalation may result in spasm, inflammation and edema of the larynx and bronchi, chemical pneumonitis, and pulmonary edema. Material is extremely destructive to tissue of the mucous membranes and upper respiratory tract, eyes, and skin.|/EPIDEMIOLOGY STUDIES/ Chlorination of drinking water generates disinfection by-products (DBPs) , which have been shown to disrupt spermatogenesis in rodents at high doses, suggesting that DBPs could pose a reproductive risk to men. ...This study ...assessed DBP exposure and testicular toxicity, as evidenced by altered semen quality. ... A cohort study /was conducted/ to evaluate semen quality in men with well-characterized exposures to DBPs. Participants were 228 presumed fertile men with different DBP profiles. They completed a telephone interview about demographics, health history, water consumption, and other exposures and provided a semen sample. Semen outcomes included sperm concentration and morphology, as well as DNA integrity and chromatin maturity. Exposures to DBPs were evaluated by incorporating data on water consumption and bathing and showering with concentrations measured in tap water. ... Multivariable linear regression /was used/ to assess the relationship between exposure to DBPs and adverse sperm outcomes. ... The mean (median) sperm concentration and sperm count were 114.2 (90.5) million/mL and 362 (265) million, respectively. The mean (median) of the four trihalomethane species (THM4) exposure was 45.7 (65.3) ug/L, and the mean (median) of the nine haloacetic acid species (HAA9) exposure was 30.7 (44.2) ug/L. These sperm parameters were not associated with exposure to these classes of DBPs. For other sperm outcomes, we found no consistent pattern of increased abnormal semen quality with elevated exposure to trihalomethanes (THMs) or haloacetic acids (HAAs) . The use of alternate methods for assessing exposure to DBPs and site-specific analyses did not change these results. ... Overall, the results of the present study do not support an association between exposure to DBPs at levels approaching regulatory limits and adverse sperm outcomes, although /there was/ an association between total organohalides and sperm concentration that was in line with /the/ hypothesis.... The lone association of total organohalide exposure with sperm concentration may lend support to findings that have suggested that total organohalide is a stronger risk factor for adverse pregnancy outcomes than any of the regulated DBP groups or species ... and that the toxicity of total organohalides is greater than that of the individual or subclasses of DBPs. ... Previous studies have suggested that exposures to THMs via bathing and showering may be more strongly associated with adverse reproductive outcomes than other exposure indicators... /These/ results did not support these findings. /Disinfection by-products/

tribromoacetate

Acetic acid, 2,2,2-tribromo-: ACTIVE|Haloacetic acids ... are chemical byproducts of chlorination and chloramination of drinking water. /Haloacetates/

Method: EPA-OGWDW/TSC 552.2; Procedure: liquid-liquid extraction, derivitization and gas chromatography with electron capture detection; Analyte: tribromoacetic acid; Matrix: drinking water, ground water, raw source water, and water at any intermediate treatment stage; Detection Limit: 0.82 ug/L.|Method: EPA-OGWDW/TSC 552.3rev1.0; Procedure: liquid-liquid microextraction, derivitization, and gas chromatography with electron capture detection; Analyte: tribromoacetic acid; Matrix: drinking water; Detection Limit: 0.097 ug/L.