Bromodichloroacetic acid

207.84

207.84

216-653-1

SJ84PTP2HD

DTXSID4024644

37.3

1.53 (est)

2.3±0.1 g/cm3

108-110 °C

200.7±35.0 °C at 760 mmHg

75.2±25.9 °C

1.571

In water, 4.9X10+3 mg/L at 25 deg C (est)

2-8°C

3.6X10-2 mm Hg at 25 deg C (est)

Henry's Law constant = 7.9X10-9 atm-cu m/mole at 25 °C

pKa = 0.03 (est)

Hydroxyl radical reaction rate constant = 5.2X10-13 cu cm/molecule-sec at 25 °C (est)

UN23983/PG2

3

36/37/38-40-34-20/21/22-38-11

16-26-36-45-36/37/39-27-24-9

AF5958500

F,Xi,C

Stable

P280-P305 + P351 + P338-P310

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.

|Danger|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P260, P261, P264, P270, P271, P280, P301+P312, P301+P330+P331, P302+P352, P303+P361+P353, P304+P312, P304+P340, P305+P351+P338, P310, P312, P321, P322, P330, P363, P405, and P501|Aggregated GHS information provided by 41 companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H350: May cause cancer [Danger Carcinogenicity]|P201, P202, P260, P281, P308+P313, P314, P405, and P501

ENGINEERING CONTROLS. Safety shower and eye bath. Use only in a chemical fume hood.|PERSONAL PROTECTIVE EQUIPMENT Other: Wear appropriate government approved respirator, chemical-resistant gloves, safety goggles, other protective clothing. Faceshield (8-inch minimum).|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. Evacuate area in case of spill.|Wash thoroughly after handling. Wash contaminated clothing before reuse. Discard contaminated shoes.|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 BROMODICHLOROACETIC ACID (7 total), please visit the HSDB record page.

... When administered to rodents, haloacetates have been shown to increase formation of thiobarbituric acid-reactive substances and 8-hydroxydeoxyguanosine levels in the liver. These responses appear to be modified by prior treatment. To examine potential mechanisms that account for these modifications in oxidative stress, the ability of trichloroacetate (TCA) or dichloroacetate (DCA) pretreatment to alter the metabolism of bromodichloroacetate (BDCA) and the disposition of its metabolites was examined in male B6C3F1 mice. Two-week pretreatment with 1 g/L DCA and TCA in the drinking water of mice alters the initial hepatic metabolism of BDCA and the further metabolism of its metabolite DCA. DCA pretreatment inhibits cytosolic metabolism of both 1 mM DCA or BDCA up to 70%. In contrast, DCA pretreatment stimulates hepatic microsomal BDCA metabolism 1.3-fold but has little effect on microsomal metabolism of DCA. Increased microsomal metabolism of BDCA appears to be attributable to the induction of a metabolic pathway that produces CO2 and bromodichloromethane (BDCM) as metabolites. TCA pretreatment inhibits BDCA metabolism up to 70% in the cytosol and 30% in microsomes but has little effect on DCA metabolism. These results indicate that the hepatic metabolism of the haloacetate becomes quite complex at the high doses that have been employed in cancer bioassays...

Studies suggest that bromochloro haloacetic acid species are formed from the chlorination of water containing aquatic humic substances in the presence of bromide ion(1). At high bromide concentrations in the range of 6-15 uM bromide ion, bromodichloroacetic acid was the principal species formed when using model water prepared from extracted aqautic humic substances(1).

DRINKING WATER: Bromodichloroacetic acid levels in finished drinking water samples from the Philadelphia, PA Suburban Water Co., Houston, TX, Metropolitan Water District of Southern California and Corpus Christi, TX were 6.55, 5.28, 12.2 and 8.75 ug/L, respectively(1).

The oral and iv elimination kinetics were investigated for bromodichloroacetate (BDCA) ... BDCA was administered at a dose of 5, 20 and 100 mg/kg to B6C3F1 mice and appears to distribute to the total body water with a mean volume of distribution of 427 +/- 79 mL/kg. It is subject to first-pass hepatic metabolism with a range of bioavailabilities of 0.28-0.73. A mean terminal half-life of 1.37 +/- 0.21 hr was calculated from the two lower doses of both iv and oral administration. Non-linear behavior was exhibited at doses greater than 20 mg/kg, with a much higher than expected area under the curve (AUC), a decrease in total body clearance (CL(b)) and an increase in the terminal half-life to 2.3 hr at the highest dose. The average CL(b) was 220 mL/hr/kg for the lower two doses but decreased to 156 mL/hr/kg at the high dose. The BDCA is primarily eliminated by metabolism, with only 2.4% of the parent dose being recovered in the urine at the high dose. The unbound renal clearance, as calculated from the high dose, was 15.0 mL/hr/kg. The BDCA is moderately bound to plasma proteins (f(u) = 0.28) and preferentially distributes to the plasma with a blood/plasma ratio of 0.88.|As the bromodichloroacetic (BDCA) acid dose is increased from 20 to 100 mg/kg of body weight in the rat, the fraction of the dose that is eliminated in the urine as dichloroacetic acid (DCA) increases from about 2% to 13%, whereas in mice the increase is from 0.2% to approximately 3%.

... /Unlike some other trihaloacetates/ bromodichloroacetate (BDCA) ... does not induce peroxisome proliferation even at high doses. This study attempts to determine whether differences in the metabolism of the trihaloacetates (THAs) may contribute to their differing toxicological properties. Studies were performed in male B6C3F1 mice given (14C1,2) trichloroacetic acid (TCA), (14C1)BDCA, and (14C1,2) dichloroacetic acid (DCA) by gavage. The replacement of a Cl by a Br greatly enhances THA metabolism. Much less radiolabel from BDCA is retained in the carcass after 24 hr than from TCA. Radiolabel from BDCA is largely found in the urine, with oxalate being the major metabolite. TCA is largely eliminated unchanged in the urine. There are dose-related changes in the rate of CO2 production from BDCA. The initial rate of CO2 production is reduced from 4.1 +/- 0.3 hr-1 at 5 and 20 mg/kg to 2.7 +/- 0.6 hr-1 at 100 mg/kg, but the net conversion to CO2 in 24 hr is greater at the highest dose. As would be predicted, substitution Br for Cl on TCA greatly increased its metabolism.|/Investigators/ studied the metabolism of BDCA in male B6C3F1 mice. As predicted, substitution of a bromine for a chlorine in TCA resulted in a substantially greater extent of trihaloacetate metabolism. Whereas 45% of a 100 mg/kg of body weight dose of TCA was eliminated unchanged in the urine of mice within 24 hr, less than 4% of the same dose of BDCA was found in the urine. At lower doses, only a fraction of a percent of the BDCA was eliminated unchanged.|The metabolism of BDCA is differentially modified in mice and rats as doses are increased. /Investigators/ found that the kinetics of carbon dioxide production from 1-(14)C-BDCA suggested an efficient conversion of BDCA to carbon dioxide through DCA at low doses, but a direct decarboxylation reaction became important as doses approached 100 mg/kg of body weight. This complex activity was not observed in rats, in that a progressively smaller fraction of the dose is converted to carbon dioxide as dose is increased. This suggests that direct decarboxylation plays a less important role in the metabolism of BDCA in rats than in mice.|The ratios of urinary metabolites produced by mice and rats suggest that there are some substantive differences in the metabolism of BDCA in the two species. Mice produce much higher amounts of oxalate (about 30% of the orally administered dose) than do rats (about 20%). The much greater conversion of BDCA to oxalate than for equivalent doses of DCA suggests that much of the extra oxalate seen in mouse urine arises from reductive dehalogenation of BDCA, followed by peroxy radical formation and decomposition to oxalate.|For more Metabolism/Metabolites (Complete) data for BROMODICHLOROACETIC ACID (6 total), please visit the HSDB record page.

... Bromodichloroacetate (BDCA) was administered at a dose of 5, 20 and 100 mg/kg... A mean terminal half-life of 1.37 +/- 0.21 hr was calculated from the two lower doses of both iv and oral administration. Non-linear behavior was exhibited at doses greater than 20 mg/kg, with ... an increase in the terminal half-life to 2.3 hr at the highest dose...|In the rat, increasing the dose from 5 mg/kg of body weight to 20 or 100 mg/kg of body weight was associated with a significantly extended half-life of both BDCA and DCA (from 0.9 to 3.7 hr).

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. Causes burns. Harmful by inhalation, in contact with skin and if swallowed.|/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 larynxand 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...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/

bromodichloroacetate

Haloacetic acids ... are chemical byproducts of chlorination and chloramination of drinking water. /Haloacetates/