Dibromoacetic acid

217.84

217.84

211-165-5

7FUW62YY5L

DTXSID1023815

Hygroscopic crystals

2915900090

37.30000

1.18690

2.382 g/mL at 25ºC(lit.)

49 °C

125-135 °C @ Press: 10 Torr

>230 °F

1.598

In water, 2.11X10+6 mg/L at 25 deg C

0-6°C

2.3X10-2 mm Hg at 25 deg C (est)

4.42e-09 atm-m3/mole|Henry's Law constant = 4.42X10-9 atm-cu m/mole at 25 °C

pKa = 1.48 at 25 °C

When heated to decomposition it emits toxic fumes|Hydroxyl radical reaction rate constant = 6.3X10-13 cu cm/molecule-sec at 25 °C (est)

II

8

UN 3261 8/PG 2

3

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

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

AG5980000

C,Xi,F

P280-P305 + P351 + P338-P310

H302 + H312 + H332-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.|Contact a licensed professional waste disposal service to dispose of this material. ... Observe all federal, state, and local environmental regulations.

Environmental Health Criteria 216: Disinfectants and DIsinfectant By-Products (1999) by the International Programme on Chemical Safety (IPCS) under the joint sponsorship of the United Nations Environment Programme, the International Labour Organisation and the World Health Organization. Available at http://www.inchem.org/documents/ehc/ehc/ehc216.htm as of August 1, 2008|DHHS/NTP; Toxicology and Carcinogenesis Studies of Toxicology and Carcinogenesis Studies of Dibromoacetic Acid (CAS No. 631-64-1) in F344/N Rats and B6C3F1 Mice (Drinking Water Studies) 326 pp. (2007) Technical Rpt Series No. 537 NIH Pub No.07-4475

|Danger|H302 (92.68%): 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.

ENGINEERING CONTROLS. Safety shower and eye bath. Use only in a chemical fume hood.|PERSONAL PROTECTIVE EQUIPMENT. Respiratory: Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU). Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator.|Hand: Compatible chemical-resistant gloves. Eye: Chemical safety goggles. Other: Faceshield (8-inch minimum).

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

Emits toxic fumes under fire conditions.

Sweep up, place in a bag and hold for waste disposal. Avoid raising dust. Ventilate area and wash spill site after material pickup is complete.

Avoid breathing 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 leak or spill, 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 DIBROMOACETIC ACID (7 total), please visit the HSDB record page.

Dibromoacetic acid was detected in the Tres Rios Wetlands, which receive tertiary-treated sewage effluent from the 91st Ave Wastewater Treatment Plant southwest of Phoenix, AZ, at concentrations of not detected-0.4 ug/L(1).

SOURCE DOMINATED: Dibromoacetic acid was qualitatively identified as a component of smokestack emissions from a municipal incinerator in Boras, Sweden(1).

The disinfection by-product dibromoacetic acid (DBA) has been found in female rats to increase circulating concentrations of both estradiol (E2) and estrone (E1). This effect is apparently due, at least in part, to a suppression in hepatic catabolism. The present study investigated whether DBA, by increasing sex steroid levels, is able either to augment the hypothalamic up-regulation involved in triggering a luteinizing hormone (LH) surge, or to affect the ability of the neurotoxicant sodium dimethyldithiocarbamate (DMDC) to block the surge. Sprague-Dawley rats were gavaged for 14 days with DBA (0-150 mg/kg) and ovariectomized on dosing day 11, and at the same time implanted with an estradiol capsule to generate daily LH surges. An injection of 0.1 mM/kg DMDC was administered at 13:00 hr on day 14 and blood was sampled over the afternoon. DBA induced a dose-related increase in total estrogens. For identified surges, areas under the LH curve partitioned into two groups, comprising the two lower (0 and 37.5 mg/kg DBA) and the two higher (75 and 150 mg/kg) treatment groups. Consequently, low and high DBA groups were compared and found to be significantly different. At 150 mg DBA/0.1 mM DMDC, the timing of an identifiable LH peak was comparable to non-DMDC females, unlike the 37.5mg DBA/0.1 mM DMDC group in which the appearance of peak concentrations was delayed. A significant effect with DBA treatment alone was not present. Results indicated that this exposure to DBA induced a dose-related increase in total estrogen concentrations that paralleled a diminished DMDC blockade of the LH surge. The effect appeared to be attributable to an augmentation in the estrogen-associated up-regulation in brain mechanisms stimulating the surge.|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/

LD50 Rat oral 1737 mg/kg

GENETIC TOXICOLOGY. Dibromoacetic acid was mutagenic in Salmonella typhimurium strain TA100 with and without rat or hamster liver metabolic activation enzymes (S9); no activity was detected in strain TA98, with or without S9. Increased frequencies of micronucleated normochromatic erythrocytes were observed in peripheral blood samples from male, but not female, mice administered dibromoacetic acid in drinking water for 3 months|2-WEEK STUDY IN RATS. Groups of five male and five female rats were exposed to 0, 125, 250, 500, 1,000, or 2,000 mg/L dibromoacetic acid in drinking water for 2 weeks, equivalent to average daily doses of approximately 17, 32, 67, 134, 270 (males), or 257 (females) mg dibromoacetic acid/kg body weight. All rats survived to the end of the study. Mean body weight gains of 1,000 mg/L males and of 500 mg/L females were significantly greater than those of the controls. Water consumption by exposed and control groups was similar. Liver weights of exposed males and females were significantly increased. Right testis weights of males exposed to 500 mg/L or greater were significantly decreased. The incidences of hepatocytic cytoplasmic alteration were significantly increased in males exposed to 500 mg/L or greater and in 2,000 mg/L females. Testicular lesions, characterized by a delay in spermiation and retained spermatids, were noted in males exposed to 500 mg/L or higher concentrations. 2-WEEK STUDY IN MICE. Groups of five male and five female mice were exposed to 0, 125, 250, 500, 1,000, or 2,000 mg/L dibromoacetic acid (equivalent to average daily doses of approximately 24, 47, 95, 178, or 370 mg/kg to males and 22, 53, 88, 166, or 309 mg/kg to females) in drinking water for 2 weeks. All mice survived to the end of the study. Mean body weight gains of 250 and 500 mg/L males were significantly greater than those of the controls. Water consumption by exposed and control groups was similar. Liver weights of males and females in the 1,000 and 2,000 mg/L groups were significantly increased. Thymus weights of males and females in the 1,000 and 2,000 mg/L groups were significantly less than those of controls. The incidences of thymus atrophy were significantly increased in 1,000 and 2,000 mg/L males and 2,000 mg/L females. The incidences of morphological changes to the germinal epithelium of the testes were increased in males exposed to 1,000 or 2,000 mg/L.|3-MONTH STUDY IN RATS. Groups of 10 male and 10 female rats were exposed to 0, 125, 250, 500, 1,000, or 2,000 mg/L dibromoacetic acid (equivalent to average daily doses of approximately 10, 20, 40, 90, and 166 mg/kg to males and 12, 23, 48, 93, and 181 mg/kg to females) in drinking water for 3 months. All rats survived to the end of the study. Mean body weights of male and female rats in the 2,000 mg/L group were significantly less than those of controls. Water consumption by the 2,000 mg/L males at weeks 1 and 13 and by females at week 13 was less than that by controls. Small decreases in the erythron and platelet counts occurred in rats exposed to 2,000 mg/L; minimally impaired erythropoiesis was also seen in 1,000 mg/L rats. Liver weights of all exposed groups of males and females were significantly increased. Male rats in the 2,000 mg/L group had significantly decreased testis weights. Testicular atrophy was noted in the 2,000 mg/L group, and retained spermatids were observed in the 500 and 1,000 mg/L groups. In the pituitary gland of male rats exposed to 2,000 mg/L, the incidence of cellular hypertrophy was significantly increased. The incidences of hepatocellular vacuolization were significantly increased in males exposed to 500 mg/L or greater and in females exposed to 2,000 mg/L. Hematopoietic cell proliferation was noted in females in the 2,000 mg/L group. 3-MONTH STUDY IN MICE. Groups of 10 male and 10 female mice were exposed to 0, 125, 250, 500, 1,000, or 2,000 mg/L dibromoacetic acid (equivalent to average daily doses of approximately 16, 30, 56, 115, and 230 mg/kg to males and 17, 34, 67, 132, and 260 mg/kg to females) in drinking water for 3 months. All mice survived to the end of the study. Mean body weights and body weight gains of female mice in the 2,000 mg/L group and the mean body weight gain of 2,000 mg/L males were significantly less than those of controls. Water consumption by males in the 2,000 mg/L group was decreased at weeks 1 and 13 relative to controls. Small decreases in mean cell hemoglobin and platelet counts occurred in 2,000 mg/L male mice. Liver weights of males and females exposed to 500 mg/L or greater were significantly increased. Hepatocellular cytoplasmic vacuolization was present in most mice and the severity was increased in 1,000 and 2,000 mg/L males and females. The incidences of abnormal testicular morphology were significantly increased in 1,000 and 2,000 mg/L males.|2-YEAR STUDY IN RATS. Groups of 50 male and 50 female rats were exposed to drinking water containing 0, 50, 500, and 1,000 mg/L dibromoacetic acid for 2 years (equivalent to average daily doses of approximately 2, 20, and 40 mg/kg to males and 2, 25, and 45 mg/kg to females). Survival of exposed rats was similar to that of the control groups. Mean body weights of 1,000 mg/L males and females were less than those of the controls after weeks 29 and 53, respectively, and those of 500 mg/L males and females were less after weeks 57 and 85, respectively. Water consumption by males and females exposed to 1,000 mg/L was less than that by controls during year 2 of the study. The incidence of malignant mesothelioma was significantly increased in 1,000 mg/L male rats. A positive trend in the incidence of mononuclear cell leukemia occurred in female rats, and the incidence in 1,000 mg/L females was significantly increased. The incidences of mononuclear cell leukemia were increased in 50 and 500 mg/L males. The incidences of cystic degeneration of the liver were significantly increased in all exposed groups of male rats. The incidences of alveolar epithelial hyperplasia were significantly increased in 500 and 1,000 mg/L females, and the incidences of nephropathy were significantly increased in all exposed groups of females. 2-YEAR STUDY IN MICE. Groups of 50 male and 50 female mice were exposed to drinking water containing 0, 50, 500, and 1,000 mg/L dibromoacetic acid for 2 years (equivalent to average daily doses of approximately 4, 45, and 87 mg/kg to males and 4, 35, and 65 mg/kg to females). Survival of exposed mice was similar to that of the controls. Mean body weights of 50 and 500 mg/L male mice were greater than those of the controls after week 85. Water consumption by exposed mice was generally similar to that by controls throughout the study. The incidences of liver neoplasms occurred with positive trends in male and female mice. The incidences of multiple hepatocellular adenoma and hepatocellular adenoma or carcinoma (combined) were significantly increased in all exposed groups of males and in 500 and 1,000 mg/L females. The incidences of hepatoblastoma were significantly increased in 500 and 1,000 mg/L males, and the incidences of hepatocellular carcinoma were significantly increased in 1,000 mg/L males and 500 mg/L females. The incidences of alveolar/bronchiolar adenoma occurred with positive trends in males and females, and the incidence in 500 mg/L male mice was significantly greater than that in controls.|The National Toxicology Program (NTP) requested that a dose range-finding study be performed in order to establish the potential effects of dibromoacetic acid (DBA) on the immune system and to determine doses that could be used in a full immunotoxicology study. These studies were conducted in female B6C3F1 mice. The animals were exposed to DBA based on the concentration of the test article in the drinking water. Five DBA concentrations of 125, 250, 500, 1000 and 2000 mg/L for 28 days were utilized. DBA solutions were prepared fresh every two weeks in tap water and stored refrigerated. The in-life phase of these studies was carried out between 18 November 1997 and 6 February 1998. ... DBA was administered in the drinking water from water bottles for 28 days at 125, 250, 500, 100 and 2000 mg/L/day. There was no statistical difference in drinking water consumption from animals exposed to DBA as compared to the tap water controls. Exposure to DBA did not produce any signs of overt toxicity. There was no significant difference in body weight between the exposed and control animals during the experimental period; however, a 40% decrease in body weight gain was observed in the DBA high dose group. No gross pathological lesions were observed in DBA-exposed animals; furthermore, there were no differences observed in terminal body weight, brain or lung weight. Animals exposed to the high dose of DBA had a significant decrease (33%) in relative thymus weight and an increase (21%) in relative spleen weight. DBA produced a dose-related increase in liver weight which was significant at all dose levels with the greatest increase (51%) in relative liver weight being observed at the high dose group. In addition, a dose-related increase in kidney weight was also observed with the increase in the highest four dose levels reaching the level of statistical significance. The greatest increase (21%) in the relative kidney weights was also observed at the high dose group. The erythrocyte count, hemoglobin, hematocrit, MCV, MCH, MCHC, platelets, leukocyte counts and leukocyte differential were unaffected by DBA. While a statistically significant increase in MCH was observed at the 500 mg/L dose level, this increase (1%) was not considered to be biologically relevant. A dose-related increase in reticulocytes, significant at the three highest dose levels, was observed following exposure to DBA with the greatest increase (30%) being observed at the high dose level. The immunological studies are summarized in Table ES-2. As in the toxicological parameters, exposure to DBA produced marked changes in various immunological parameters. A dose-dependent increase in spleen cell number was observed in animals exposed to DBA. The maximum effect was observed in the 500 mg/L dose group where there was a 20% increase in spleen cell number compared to the vehicle (tap water) control animals. In addition, both the 1000 and 2000 mg/L dose groups have statistically significant increases in spleen cell numbers. In the phenotypic enumeration of the spleen cells, there were dose-related increases in the absolute number of B cells, total T cells, T helper cells, T suppresser/cytotoxic cells and natural killer cells. However, for each of these cell types, the increases appeared to be due primarily to an increase in spleen cell number since little effect was observed on the percentage values. In contrast, the dose-related increase (91%) in the splenic macrophage numbers appeared to be the result of an actual increase in the macrophage number. Exposure to DBA produced a dose-dependent decrease in the antibody-forming cell (AFC) response to sheep erythrocytes, which was significant at the three highest dose levels when evaluated either as specific activity or as total spleen activity. At the highest dose level, the decreases were 50% and 47%, respectively, for each of these parameters. No effect was observed on serum IgM antibody titer to sheep erythrocytes which may be the result of DBA having a greater effect on the spleen than on the bone marrow and lymph nodes. No effect was observed on the mixed leukocyte response (MLR) following DBA exposure. Overall, no effect was observed in the ability of thioglycolate-recruited peritoneal macrophages to kill and/or inhibit the growth of B16F10 tumor cells. In addition, exposure to DBA did not inhibit the ability of the macrophages to respond to a stimulus known to enhance macrophage function. In contrast to the suppression observed in the antibody-forming cell response, animals exposed to DBA had an increase in natural killer (NK) activity when the data were evaluated as lytic units. A statistically significant increase was observed in the three highest dose groups when the results were expressed as specific activity and in the four highest dose levels when expressed as total spleen activity. The greatest effects were observed at the high dose level where specific activity was increased 100% and the total spleen activity increased 143%.

Dibromoacetic acid's formation as a chemical byproduct of chlorination and chloramination of drinking water(1) 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 1.5(SRC), determined from a water solubility of 2.11X10+6 mg/L(2) and a regression-derived equation(3), indicates that dibromoacetic acid is expected to have very high mobility in soil(SRC). The pKa of dibromoacetic acid is 1.48(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). Volatilization of dibromoacetic acid from moist soil surfaces is not expected to be an important fate process(SRC) given the compound's pKa(4). Dibromoacetic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.3X10-2 mm Hg(SRC), determined from a fragment constant method(6). Limited data are available regarding the biodegradation of dibromoacetic acid in soil. However, dibromoacetic acid (5 mM) was used as a carbon source by Xanthobacter autotrophicus GJ10 as measured by halide production after a period of 10 days at 30 °C(7).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.5(SRC), determined from a water solubility of 2.11X10+6 mg/L(2) and a regression-derived equation(3), indicates that dibromoacetic acid is not expected to adsorb to suspended solids and sediment(SRC). A pKa of 1.48(4) indicates dibromoacetic 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 0.17(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 dibromoacetic acid in water. However, dibromoacetic acid (5 mM) was used as a carbon source by Xanthobacter autotrophicus GJ10 as measured by halide production after a period of 10 days at 30 °C(8).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dibromoacetic acid, which has an estimated vapor pressure of 2.3X10-2 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 dibromoacetic 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 25.3 days(SRC), calculated from its rate constant of 6.3X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Dibromoacetic 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 dibromoacetic acid with photochemically-produced hydroxyl radicals has been estimated as 6.3X10-13 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 25.3 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Dibromoacetic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Dibromoacetic acid does not contain chromophores that absorb at wavelengths >290 nm(2) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 0.17 was calculated for dibromoacetic acid(SRC), using a water solubility of 2.11X10+6 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 dibromoacetic acid is estimated as 1.5(SRC), using a water solubility of 2.11X10+6 mg/L(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that dibromoacetic acid is expected to have very high mobility in soil. The pKa of dibromoacetic acid is 1.48(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 1.48(1) indicates dibromoacetic 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). The pKa of dibromoacetic acid indicates that volatilization from moist soil surfaces is unlikely to occur(SRC). Dibromoacetic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.3X10-2 mm Hg(SRC), determined from a fragment constant method(3).

DRINKING WATER: Dibromoacetic acid was qualitatively detected in water from two Israeli drinking water treatment plants using the Sea of Galilee (Lake Kinereth) as a source(1). The compound was observed when chlorine, chlorine dioxide, or a combination of chlorine dioxide and monochloramine was used to disinfect the water(1). Water collected from fifty-three Canadian drinking water treatment facilities in winter of 1993 contained dibromoacetic acid(2). When bromide concentrations were low (0.06 mg/L), the water contained 0.9 ug/L dibromoacetic acid; when bromide was moderate (0.5 mg/L), the water contained 0.8 ug/L dibromoacetic acid(2).|DRINKING WATER: A mean concentration of 6.95 ug/L dibromoacetic acid was measured in post-treatment surface water from disinfection utilities in Belgium, France, Germany, Spain, The Netherlands, and Italy; post-treatment groundwater from disinfection utilities contained a mean 3.0 ug/L dibromoacetic acid(1). Dibromoacetic 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 (3.1-10 ug/L), sand-filtered water (5-8.4 ug/L), ozonated water (5.2-10 ug/L), granulated activated carbon-filtered water (not detected-3.1 ug/L), and postchlorinated water (2.1-5.7 ug/L)(2).|DRINKING WATER: The median concentration of dibromoacetic acid measured at 35 American drinking water utilities was 0.9 ug/L in spring 1988, 1.5 ug/L in summer 1988, 1.4 ug/L in fall 1988, and 1.0 ug/L in winter 1989(1). At a drinking water utility with high bromide levels, clearwell effluent contained dibromoacetic acid concentrations of 19 ug/L in summer 1988, 13 ug/L in fall 1988, and 7.8 ug/L in winter 1989; at a utility with seasonally-varying bromide levels, dibromoacetic acid was 14 ug/L in summer of 1988, 17 ug/L in fall of 1988, and 13 ug/L in winter of 1989(1). Dibromoacetic acid was detected at 6 of 35 Finnish waterworks between January and October 1994 with concentrations between 1.3 and 27 ug/L; levels at all other facilities were below quantitation limits(2).|DRINKING WATER: Water taken from 15 treatment plants in The Netherlands contained dibromoacetic acid concentrations between 0.1-6.5 ug/L; concentrations in water taken from 5 other treatment plants were less than 0.1 ug/L(1).|For more Environmental Water Concentrations (Complete) data for DIBROMOACETIC ACID (6 total), please visit the HSDB record page.

Monitoring data indicate that the general population may be exposed to dibromoacetic acid via ingestion of chlorinated or chloraminated drinking water, particularly when source waters contain high concentrations of bromide. (SRC)

Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases. (See all compounds classified as Alkylating Agents.)

Dibromoacetic acid (DBA) ... /was/ provided in drinking water in range-finding reproductive/developmental toxicity studies (rats) ... Studies included absorption and biodisposition of DBA ... including passage into placentas, amniotic fluid, fetuses ... or milk ... . The DBA ... range-finding reproductive/developmental toxicity studies each included 50 Sprague-Dawley rats/sex/group. DBA (0, 125, 250, 500, or 1000 ppm) ... was provided in drinking water 14 days premating through gestation and lactation (63 to 70 days). ... Satellite groups (6 male, 17 female rats/group/study ... were used for bioanalytical sampling. Rats ... had exposure-related reduced water consumption caused by apparent taste aversion to DBA ..., especially in the parental animals at the two highest exposure levels (500 and 1000 ppm DBA ... . Female rats consumed slightly higher mg/kg/day doses of DBA than male rats, especially during gestation and lactation; weanling rats consumed the highest mg/kg/day doses. DBA produced detectable and quantifiable concentrations in plasma, placentas, amniotic fluid, and milk. Plasma samples confirmed that rats drink predominately during the dark; this drinking pattern, not accumulation, produced detectable plasma concentrations for 18 to 24 hours/day...|Dibromoacetate was measured in the testicular interstitial fluid of male Sprague-Dawley rats given five daily gavage doses of 250 mg dibromoacetate/kg body weight ... . The level of dibromoacetate in testicular fluid peaked at 79 ug/mL (approximately 370 uM) 30 minutes after the last dose, and the half-life was approximately 1.5 hours.|Dibromoacetate was administered to Sprague-Dawley rats in drinking water at concentrations ranging from 125 to 1,000 ppm (mg/L) with exposures beginning 14 days before cohabitation and continuing through gestation and lactation ... Quantifiable levels of dibromoacetate were measured in parental and fetal plasma, placental tissue, amniotic fluid, and milk. Thus, dibromoacetate crosses the placenta and is taken up by fetal tissue.|The oral bioavailability of dibromoacetate was reported to be 30% in male F344/N rats ... . The lower bioavailability of dibromoacetate compared to dichloroacetate is due to greater first-pass metabolism of dibromoacetate in the liver.

Dibromoacetate was measured in the testicular interstitial fluid of male Sprague-Dawley rats given five daily gavage doses of 250 mg dibromoacetate/kg body weight ... . The half-life was approximately 1.5 hours.

... The ability of dibromoacetic acid (DBA) to cause DNA hypomethylation, glycogen accumulation, and peroxisome proliferation /was examined/ ... Female B6C3F1 mice and male Fischer 344 rats were administered 0, 1,000, and 2,000 mg/L DBA in drinking water. The animals were euthanized after 2, 4, 7, and 28 days of exposure. Dibromoacetic acid caused a dose-dependent and time-dependent decrease of 20% to 46% in the 5-methylcytosine content of DNA. Hypomethylation of the c-myc gene was observed in mice after 7 days of DBA exposure. Methylation of 24 CpG sites in the insulin-like growth factor 2 (IGF-II) gene was reduced from 80.2% +/- 9.2% to 18.8% +/- 12.9% by 2,000 mg/l DBA for 28 days. mRNA expression of the c-myc and IGF-II genes in mouse liver was increased by DBA. A dose-dependent increase in the mRNA expression of the c-myc gene was also observed in rats. In both mice and rats, DBA caused dose-dependent accumulation of glycogen and an increase of peroxisomal lauroyl-CoA oxidase activity. Hence, DBA, like dichloroacetic acid and trichloroacetic acid, induced hypomethylation of DNA and of the c-myc and IGF-II genes, increased mRNA expression of both genes, and caused peroxisome proliferation. Again like DCA, DBA also induced glycogen accumulation. These results indicate that DBA shares biochemical and molecular activities in common with dichloroacetic acid and/or trichloroacetic acid, suggesting that it might also be a liver carcinogen.|Haloacetic acids (HAs) are embryotoxic contaminants commonly found in drinking water. The mechanism of HA embryotoxicity ... may be mediated in part by protein kinase C (PKC) inhibition. This study was conducted to evaluate the pathogenesis of HA embryotoxicity, and to compare these data with those from specific (Bis I) and non-specific (staurosporine) inhibitors of PKC. Embryos were incubated for varying times with several HAs, Bis I, staurosporine, or Bis V (a negative control). Cell cycle analysis was performed by flow cytometry following nuclear staining with propidium iodide; apoptosis was evaluated by fluorescence microscopy following LysoTracker staining. At concentrations producing 100% embryotoxicity with no embryolethality, only staurosporine perturbed the cell cycle. However, flow cytometry revealed accumulation of sub-G1 events (an apoptotic indicator) across time with bromochloroacetic acid, dichloroacetic acid, and staurosporine, but not dibromoacetic acid, Bis I, or Bis V. Sub-G1 events were particularly prominent in the head region, and remained at control levels in the heart. LysoTracker staining confirmed a similar pattern of apoptosis in the intact embryo; BCA and DCA produced intense staining in the prosencephalon, with virtually no staining in the heart. These data indicate that while cell-cycle perturbation may not mediate the pathogenesis of HA embryotoxicity, these agents do induce embryonic apoptosis. In addition, the lack of Bis I-induced apoptosis indicates that PKC inhibition is unlikely to be the sole mediator of HA embryotoxicity.|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/ Skin Contact: Causes burns. Skin Absorption: Harmful if absorbed through skin. Eye Contact: Causes burns. Inhalation: Material is extremely destructive to the tissue of the mucous membranes and upper respiratory tract. Harmful if inhaled. Ingestion: Harmful if swallowed.|/SIGNS AND SYMPTOMS/ 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. Symptoms of exposure may include burning sensation, coughing, wheezing, laryngitis, shortness of breath, headache, nausea, and vomiting.|/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/|/EPIDEMIOLOGY STUDIES/ ... A retrospective cohort study /was conducted/ to examine the effects of exposure to THMs and HAAs during the third trimester and during individual weeks and months of late gestation on the risks for term low birth weight, intrauterine growth retardation, and very preterm and preterm births. The study population (n = 48,119) included all live births and fetal deaths occurring from January 1998 through March 2003 to women whose residence was served by one of three community water treatment facilities. ... Evidence /was found/ of associations between exposure to specific HAAs and term low birth weight as well as intrauterine growth retardation and for exposure to the five regulated HAAs (HAA5) and term low birth weight. /These/ findings suggest a critical window of exposure with respect to fetal development during weeks 33-40 for the effects of dibromoacetic acid and during weeks 37-40 for the effects of dichloroacetic acid. Adjustment for potential confounders did not affect the conclusions.

dibromoacetic acid

Acetic acid, 2,2-dibromo-: ACTIVE|Haloacetic acids (five) (HAA5) mean the sum of the concentrations in milligrams per liter of the haloacetic acid compounds (monochloroacetic acid, dichloroacetic acid, trichloroacetic acid, monobromoacetic acid, and dibromoacetic acid), rounded to two significant figures after addition. /Haloacetic Acids (five) (HAA5)/|Haloacetic acids ... are chemical byproducts of chlorination and chloramination of drinking water. /Haloacetates/

Method: EPA-NERL 552.1; Procedure: ion-exchange liquid-solid extraction and gas chromatography with an electron capture detector; Analyte: dibromoacetic acid; Matrix: drinking water, ground water, raw source water, and water at any intermediate treatment stage; Detection Limit: 0.09 ug/L.|Method: EPA-OGWDW/TSC 552.2; Procedure: liquid-liquid extraction, derivitization and gas chromatography with electron capture detection; Analyte: dibromoacetic acid; Matrix: drinking water, ground water, raw source water, and water at any intermediate treatment stage; Detection Limit: 0.066 ug/L.|Method: EPA-OGWDW/TSC 552.3rev1.0; Procedure: liquid-liquid microextraction, derivitization, and gas chromatography with electron capture detection; Analyte: dibromoacetic acid; Matrix: drinking water; Detection Limit: 0.021 ug/L.|Method: Standard Methods 6251B; Procedure: micro liquid-liquid extraction gas chromatography with electron capture detector; Analyte: dibromoacetic acid; Matrix: water; Detection Limit: 0.06 ug/L.

Fatty Acyls [FA] -> Fatty Acids and Conjugates [FA01] -> Halogenated fatty acids [FA0109]