Dibromochloroacetic acid

252.29

252.29

216-653-1

AMD03B602V

DTXSID3031151

2903799090

37.30000

1.75340

2.684 g/cm3

99-102 °C(lit.)

217.7ºC at 760mmHg

85.5ºC

1.623

In water, 2.4X10+3 mg/L at 25 deg C (est)

2-8°C

5.2X10-3 mm Hg at 25 deg C (est)

Henry's Law constant = 2.6X10-9 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

36/37/38-40-34-38-11

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

F,Xi,C

P280-P305 + P351 + P338-P310

H314

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; Final report on the short term reproductive and developmental toxicity of dibromochloro-acetic acid (CAS No. 5278-95-5) administered in drinking water to Sprague-Dawley rats. NTIS Technical Report (NTIS/PB2000-103420) 2000 Jan;:442 pp.

|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 41 companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

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. Evacuate area in case of spill or leak.|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 DIBROMOCHLOROACETIC ACID (7 total), please visit the HSDB record page.

The potential toxicity of Dibromochloroacetic acid (DBCA, CAS No.: 5278-95-5) was evaluated using a short-term reproductive and developmental toxicity screen. This study design was selected to identify the physiologic process (development; female reproduction; male reproduction; various somatic organs/processes) that is the most sensitive to DBCA exposure. The first range-finding study was conducted at concentrations of 0, 30, 100, 300, and 500 ppm of DBCA in the drinking water for two weeks, with no significant test-article related effects observed at any dose level including 500 ppm. Following two weeks of a wash-out period, the second range-finding study was conducted at concentrations of 0, 750, 1000, and 1500 ppm of DBCA in the drinking water for two weeks. Based on decreases in water consumption, dose levels of 0, 500, 1000, and 1500 ppm (Groups 1, 2, 3, and 4, respectively) were selected for the main study. The main study utilized two groups of male rats designated as A males (Main study, non-BrdU treated, 10 per group in Groups 1-4) and B males (Main study, BrdU treated, 5 animals in Groups 1, 2, and 3, and 8 animals in Group 4), and three groups of female rats designated as A females (peri-conception exposure, 10 per group in Groups 1-4), Group B (gestational exposure, 13 per group in Groups 1-4), and Group C (peri-conception exposure, BrdU-treated, 5 animals 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. Body weights were 10-14% less than controls in the 1500 ppm A and C females. Water consumption was decreased at several of the intervals for the 1000 and 1500 ppm dose groups. Water consumption was decreased by 12-49% at 1000 and 1500 ppm in both males and females throughout the course of the study. The overall calculated mean consumption of DBCA for Groups 2, 3, and 4 was 51, 89, and 112 mg/kg body weight/day, respectively. There were no treatment-related findings noted in male clinical pathology parameters, female reproductive parameters, gross visceral observations, or male reproductive parameters except for a decrease of 11% in sperm velocity and ALH max in the 1500 ppm A males. Necropsy organ weights and organ-to-body weight ratios were evaluated in A and B males, and the ratios were comparable to the controls in both A and B males. Gross findings and histopathologic findings were comparable across all groups in both males and females. The BrdU Labeling Index (LI) for the liver of the B males, and liver and kidney of C females, was significantly increased at 1500 ppm dose level. Although not statistically significant, LI was increased in the kidney of C females at 500 and 1000 ppm dose levels. The LI for the 500, and 1000 ppm groups was generally increased with a corresponding increase in water consumption, however, the LI for the 1500 ppm group was increased as compared to the controls with similar or decreased water consumption. The nature of the response suggests a mitogenic mode of action for DBCA, although, histopathologic evaluation did not identify any changes which would result from the cell proliferative effects observed in the liver and kidney of B males and C females. Results of this study indicate that DBCA at doses at and above 1000 ppm produced consistent decreases in food and water consumption in both sexes, but did not result in any female reproductive toxicity or any visceral malformation or variations in any pups. In the male reproductive data, a decrease of 11% in the male sperm velocity samples and in the male ALH max were observed in the 1500 ppm A male; no changes in fertility were noted. From these data, DBCA is: taste-aversive, a possible mitogen and a general toxicant in both male and female rats at 1500 ppm, and a male reproductive toxicant at 1500 ppm.

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). /Haloacetic acids/

DRINKING WATER: Dibromochloroacetic 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 below detection limit (not specified), 2.60, 5.37 and 3.52 ug/L, respectively(1).

Chloro, bromo, and mixed bromochloro haloacetates (HAs) are by-products of drinking water disinfection and are hepatocarcinogenic in rodents. ... The toxicokinetics of a series of di-HAs, dichloro (DCA), bromochloro (BCA), dibromo (DBA) and tri-HAs: trichloro (TCA), bromodichloro (BDCA), chlorodibromo (CDBA), and tribromo (TBA) /were compared/ after iv and oral dosing (500 um/kg) in male F344 rats. The blood concentrations of the HAs after iv injection declined in a bi-exponential manner with a short but pronounced distributive phase. The structural features that had the greatest influence on the disposition of HAs were substitution of a halogen for a hydrogen and the degree of bromine substitution. All di-HAs and blood elimination half lives of less than 4 hours (DCA > DBA, BCA) compared to the tri-HAs, which had half lives that varied from 0.6 to 8.0 hours (TCA > BDCA > TBA). The urinary excretion of all di-HAs was low and accounted for less than 3% of the dose in contrast to the tri-HAs, where urinary excretion accounted for at least 30% of the dose. Toxicokinetic analysis indicated the steady-state apparent volume of distribution varied between 301 and 881 mL/kg among the HAs, but the variation was not statistically significant (P > 0.17). The blood concentration-time profiles for all di-HAs after oral dosing was complex and exhibited multiple peaks.

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.|/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 ... 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/

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: chlorodibromoacetic acid; Matrix: drinking water, ground water, raw source water, and water at any intermediate treatment stage; Detection Limit: 0.468 ug/L.|Method: EPA-OGWDW/TSC 552.3rev1.0; Procedure: liquid-liquid microextraction, derivitization, and gas chromatography with electron capture detection; Analyte: chlorodibromoacetic acid; Matrix: drinking water; Detection Limit: 0.035 ug/L.