Bromochloroacetic acid

173.39

173.39

216-653-1

DTXSID4024642

2915400090

37.30000

1.14

DryPowder

2.1±0.1 g/cm3

31.5 °C

215 °C

>230 °F

1.539

In water, 2.5X10+5 mg/L at 25 deg C (est)

2-8°C

1.4X10-1 mm Hg at 25 deg C (est)

Henry's Law constant = 2.2X10-8 atm-cu m/mole at 25 °C (est)

pKa = 1.40 (est)

Hydroxyl radical reaction rate constant = 6.8X10-13 cu cm/molecule-sec at 25 °C (est)

III

8

UN 3265 8/PG 2

3

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

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

AF5957282

C,Xi,F

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

NTP/NIEHS; TR-549 Toxicology and Carcinogenesis Studies of Bromochloroacetic Acid (CAS No. 5589-96-8) in F344/N Rats and B6C3F1 Mice (Drinking Water Studies) (Draft abstract). Available at http://ntp.niehs.nih.gov/index.cfm?objectid=82F00224-F1F6-975E-7C0A4D903E12624D as of July 31, 2008|NTP/NIEHS; Abstract for RDGT96001 - Short Term Reproductive and Developmental Toxicity of Bromochloroacetic Acid (CAS No. 5589-96-8) Administered in the Drinking Water to Sprague-Dawley Rats NTP Study Number: RDGT9600. (August 1998). Full report available through NTIS#: PB98-172414

|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 45 companies from 2 notifications to the ECHA C&L Inventory.

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 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.|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 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.|Hand: Compatible chemical-resistant gloves. Eye: Chemical safety goggles. Other: Faceshield (8-inch minimum).

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 vapor. 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 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 BROMOCHLOROACETIC ACID (7 total), please visit the HSDB record page.

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 bromochloroacetic acid (BCA) 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 bromochloroacetic acid exposure. The dose range-finding study was conducted at concentrations of 0, 30, 100, 300, and 500 ppm of bromochloroacetic acid in the drinking water for two weeks. Since no changes in body weight, feed or water consumption occurred, a higher top dose was selected for the main study, which used dose levels of 0, 60, 200, and 600 ppm (Groups 1, 2, 3, and 4, respectively). The main study utilized two groups of male rats designated as male Group A (non-BrdU treated animals, 10 per group in Groups 1-4) and male Group B (BrdU treated, 5 animals in Groups 1, 2, and 3, and 8 animals in Group 4, and three groups of female rats designated as female Group A (peri-conception exposure, 10 per group in Groups 1-4), female Group B (gestational exposure, 13 per group in Groups 1-4), and female Group C (peri-conception exposure, BrdU-treated, 5 animals in Groups 1, 2, and 3, and 8 animals in Group 4). BrdU exposure was included to help assess cell turnover. Control animals received deionized water, the vehicle. During the treatment period, all animals except one survived to the scheduled necropsy and there were no clinical signs of general toxicity noted at any dose level. There were no treatment-related effects on body weights or feed consumption. Water consumption was decreased by 21-34% at many of the intervals for the 600 ppm rats. The overall calculated consumption of BCA for Groups 2-4 was 7, 20, and 50 mg/kg/day, respectively. Clinical chemistry and hematology endpoints at necropsy were unaffected by BCA treatment except for a 16% increase in the albumin to globulin ratio in the 600 ppm A males; decreases of 15 and 20% in the alanine aminotransferase parameter in the 200 and 600 ppm A males, respectively; and increases of 5 and 9% in albumin in the 60 and 600 ppm A males, respectively. The increases in albumin to globulin ratio and albumin represent a small but possible biologically significant indicator of dehydration, probably attributable to decreased fluid consumption. The decreases in alanine aminotransferase are of little toxicological significance. Organ weights and organ-to-body weight ratios were comparable except for an increase of 13% and 10% in liver-to-body weight ratios in the 600 ppm A and B males, respectively. Gross findings were comparable across all groups. An increase in cytoplasmic vacuolization of hepatocytes was seen in all treated Group A males but was not observed in the corresponding Group B males examined for Labeling Index (LI). The Group C females had an apparent treatment-related increase in renal tubular dilatation/degeneration. The LI for the liver, kidney, and urinary bladder from the B males and C females showed small changes between treated and control groups, although these changes have no or questionable biological significance. Treatment-related findings noted in the male and female reproductive parameters were: a 16% decrease in total implants per litter in the 600 ppm A females and a 50% decrease in the number of live fetuses per litter in the 600 ppm C females. Other changes that occurred but were not statistically significant were: increases in % post-implantation loss in the 600 ppm C females and in the 60, 200, and 600 ppm B females; increases in % pre-implantation loss in the 600 ppm A females and in the 60, 200, and 600 ppm C females; an increase in total resorptions in the 600 ppm C females; and decreases in total implants in the 60, 200, and 600 ppm C females. Combining the data for the Group A and C females revealed decreases of 29% in live fetuses per litter and 25% in total implants per litter. The visceral evaluation of the heart and brain of the B female pups using Wilson's soft tissue free hand slicing technique did not reveal any treatment-related effects. Results of this study indicate that BCA at doses of 600 ppm produced a consistent decrease in water consumption in both sexes and affected reproductive function in females at a dose of 600 ppm. From these data, BCA is taste-aversive and a general toxicant in both sexes at 600 ppm and also a female reproductive toxicant at 600 ppm.|2-WEEK STUDY IN RATS. Groups of five male and five female rats were exposed to drinking water containing 0, 62.5, 125, 250, 500, or 1,000 mg/L bromochloroacetic acid for 2 weeks (equivalent to average daily doses of approximately 9, 18, 35, 75, or 140 mg bromochloroacetic acid/kg body weight to males and 8, 17, 35, 70, or 130 mg/kg to females). All rats survived to the end of the study. Mean body weights of exposed males and females were similar to those of the controls. Water consumption by exposed and control groups was similar. Right kidney weights of 1,000 mg/L males were significantly increased. No exposure-related gross or histopathologic lesions were observed.|3-MONTH STUDY IN RATS. Groups of 10 male and 10 female rats were exposed to drinking water containing 0, 62.5, 125, 250, 500, or 1,000 mg/L bromochloroacetic acid for 3 months (equivalent to average daily doses of approximately 5, 10, 20, 40, or 75 mg/kg to males and 5, 10, 20, 40, or 85 mg/kg to females). All rats survived to the end of the study. Mean body weights of exposed male and female rats were similar to those of the controls. Water consumption by exposed and control groups was similar. Liver weights of 500 and 1,000 mg/L males and females and kidney weights of 1,000 mg/L males were significantly increased. In the liver, there were significantly increased incidences of cytoplasmic vacuolization in 1,000 mg/L males and females. 3-MONTH STUDY IN MICE. Groups of 10 male and 10 female mice were exposed to drinking water containing 0, 62.5, 125, 250, 500, or 1,000 mg/L bromochloroacetic acid for 3 months (equivalent to average daily doses of approximately 8, 16, 32, 65, or 125 mg/kg to males and 8, 17, 35, 70, or 140 mg/kg to females). All mice survived to the end of the study. Mean body weight gains of females exposed to 250 mg/L or greater were significantly decreased. Water consumption by exposed and control groups was similar. Liver weights of 1,000 mg/L males and all exposed groups of females were significantly increased. All males and females exposed to 500 or 1,000 mg/L had periportal cytoplasmic vacuolization. In the spleen, there were increased incidences of hematopoietic cell proliferation in 62.5, 125, and 250 mg/L males and 125 and 1,000 mg/L females.|2-YEAR STUDY IN RATS. Groups of 50 male and 50 female rats were exposed to drinking water containing 0, 250, 500, or 1,000 mg/L bromochloroacetic acid for 2 years (equivalent to average daily doses of approximately 10, 20, or 40 mg/kg to males and 13, 25, or 50 mg/kg to females). Survival of exposed rats was similar to that of the control groups. Mean body weights of 500 mg/L males were 8% less than the control group after week 81, and those of 1,000 mg/L males were 10% less than the control group after week 69. Mean body weights of 1,000 mg/L females were 10% less than the control group after week 85. Water consumption by exposed and control groups was similar. The incidences of malignant mesothelioma in all exposed groups of male rats exceeded the historical control ranges and the incidence in the 500 mg/L group was significantly increased. Positive trends in the incidences of adenoma of the large intestine (colon or rectum) occurred in male and female rats, and the incidence in 1,000 mg/L females was significantly increased. Although the incidences of mammary gland fibroadenoma were not significantly increased in exposed female rats, the incidences of multiple fibroadenomas of the mammary gland were increased in 500 and 1,000 mg/L females. The incidence of pancreatic islet adenoma was significantly increased in 500 mg/L males. The incidences of hepatocellular adenoma occurred with a positive trend in females; the incidences in 500 mg/L males and 1,000 mg/L males and females exceeded the historical control ranges. In the liver, the incidences of eosinophilic focus in 500 mg/L females and 1,000 mg/L males and females and of mixed cell focus in 1,000 mg/L females were significantly increased. In the lung, the incidence of alveolar epithelium hyperplasia was significantly increased in 1,000 mg/L females 2-YEAR STUDY IN MICE. Groups of 50 male and 50 female mice were exposed to drinking water containing 0, 250, 500, or 1,000 mg/L bromochloroacetic acid for 2 years (equivalent to average daily doses of approximately 25, 50, or 90 mg/kg to males and 15, 30, or 60 mg/kg to females). Survival of 1,000 mg/L males was significantly less than that of the control group. Mean body weights of 1,000 mg/L males were 12% less than the control group after week 97, and those of 1,000 mg/L females were 8% less than the control group after week 21. Water consumption by exposed and control groups was similar. The incidences of hepatocellular adenoma in 250 and 500 mg/L males and all exposed groups of females, hepatocellular carcinoma in 500 and 1,000 mg/L males and 500 mg/L females, hepatocellular adenoma or carcinoma (combined) in all exposed groups of males and females, and hepatoblastoma in all exposed groups of males were significantly increased. The incidences of hepatocyte cytoplasmic vacuolization in all exposed groups, eosinophilic focus in 500 and 1,000 mg/L females, and centrilobular necrosis in 1,000 mg/L males were significantly increased. The incidences of hematopoietic cell proliferation of the spleen were significantly increased in 500 and 1,000 mg/L males, and the incidence of bone marrow hyperplasia was significantly increased in 1,000 mg/L males.

Bromochloroacetic 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 1.9(SRC), determined from a structure estimation method(2), indicates that bromochloroacetic acid is expected to have very high mobility in soil(SRC). The pKa of bromochloroacetic acid is 1.40(3), indicating that this compound will primarily exist 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). Bromochloroacetic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.4X10-1 mm Hg(SRC), determined from a fragment constant method(5). Biodegradation data were not available(SRC, 2008).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.9(SRC), determined from a structure estimation method(2), indicates that bromochloroacetic acid is not expected to adsorb to suspended solids and sediment(SRC). An estimated pKa of 1.40(3) indicates bromochloroacetic 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(4). According to a classification scheme(5), an estimated BCF of 3.2(SRC), from an estimated log Kow of 0.61(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low. Biodegradation data were not available(SRC, 2008).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), bromochloroacetic acid, which has an estimated vapor pressure of 1.4X10-1 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 bromochloroacetic 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 23.8 days(SRC), calculated from its rate constant of 6.8X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Bromochloroacetic 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 bromochloroacetic acid with photochemically-produced hydroxyl radicals has been estimated as 6.8X10-13 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 23.8 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Bromochloroacetic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Bromochloroacetic 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 3.2 was calculated for bromochloroacetic acid(SRC), using an estimated log Kow of 0.61(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).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of bromochloroacetic acid can be estimated to be 1.9(SRC). According to a classification scheme(2), this estimated Koc value suggests that bromochloroacetic acid is expected to have very high mobility in soil. The estimated pKa of bromochloroacetic acid is 1.40(3), 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(4).

An estimated pKa of 1.40(1) indicates bromochloroacetic 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). Bromochloroacetic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.4X10-1 mm Hg(SRC), determined from a fragment constant method(3).

DRINKING WATER: Bromochloroacetic 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 or chlorine dioxide was used to disinfect the water(1). Bromochloroacetic 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 (6.4-15 ug/L), sand-filtered water (7.1-11 ug/L), ozonated water (8-11.4 ug/L), granulated activated carbon-filtered water (not detected-3.2 ug/L), and postchlorinated water (1-3.9 ug/L)(2). Bromochloroacetic acid was detected at 32 of 35 Finnish waterworks between January and October 1994 with concentrations between 0.3 and 19 ug/L; levels at all other facilities were below quantitation limits(3).|DRINKING WATER: Bromochloroacetic acid was detected in US groundwater and surface water distribution systems at mean concentrations of 1.47 and 3.61 ug/L, respectively(1). Levels in finished drinking water samples from the Philadelphia, PA Suburban Water Co., Houston, TX, the Metropolitan Water District of Southern California and Corpus Christi, TX were below detection limit (not specified), 4.68, 10.8 and 6.73 ug/L, respectively(2).|SURFACE WATER: Between October 1994 and April 1996, a mean concentration of 0.6 ug/L bromochloroacetic acid was measured in the Santa Ana River downstream of a discharge point for highly treated municipal wastewater effluent(1).

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

The chloro- and bromohaloacetates are drinking water disinfection by-products and rodent carcinogens. Chloro-bromo dihaloacetates are also mechanism-based inhibitors of glutathione S-transferase-zeta (GSTZ1-1). ... The stereospecific toxicokinetics and in vitro metabolism of two chiral dihaloacetates /were studied/ in male F344 rats: (-),(+)-bromochloroacetate (BCA) and racemic chlorofluoroacetate (CFA), a non-GST-zeta-inhibiting dihaloacetate. These experiments were repeated in animals that had previously been treated with dichloroacetate (DCA) to deplete GST-zeta activity. Results indicated that the elimination half-life of (-)-BCA was 0.07 compared to 0.40 hr for (+)-BCA in naive rats. A comparable difference in elimination half-life was also observed for the CFA stereoisomers (0.79 vs 0.11 hr). In GST-zeta-depleted rats, stereospecific elimination of (-),(+)-BCA was absent, with both stereoisomers having an elimination half-life of approximately 0.4 hr. This finding was in contrast to results for CFA, which still maintained the same relative difference in elimination rate between its stereoisomers, although overall elimination was diminished in GST-zeta-depleted rats. Results of in vitro metabolism experiments indicated (-)-BCA was affected by modulating GST-zeta activity, with the intrinsic metabolic clearance decreasing from 2.81 to 0.15 mL/hr/mg protein (naive, GST-zeta depleted) compared with values for (+)-BCA (0.30 and 0.31 mL/hr/mg.protein). Incubations with 350 uM diethyldithiocarbamate preferentially decreased (+)-BCA metabolism in naive and GST-zeta-depleted cytosol. These results indicate (+)-BCA is a poor substrate for GST-zeta and its metabolism is controlled by an additional GST isoenzyme.

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. /Halogenated acetic acids/|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. Lachrymator.|/SIGNS AND SYMPTOMS/ Material is extremely destructive to tissue of the mucous membranes and upper respiratory tract, eyes, and skin. Inhalation may result in spasm, inflammation and edema of the larynx and bronchi, chemical pneumonitis, and pulmonary edema. 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/|/GENOTOXICITY/ Research was initiated to develop an in vitro system to identify disinfection by-products with a potential to transform normal human colonocytes into malignant cells. Tribromomethane and bromochloroacetic acid, rodent colon carcinogens, dibromonitromethane and tribromonitromethane, recently identified in drinking water, and azoxymethane, a classic colon carcinogen, were tested for the ability to transform NCM460 cells. The chronic toxicity was determined for the series of trihalomethanes, haloacetic acids and halonitromethanes as well as NCM460 cell enzymatic capabilities. The order of cytotoxicity was halonitromethanes > haloacetic acids > trihalomethanes. Cytotoxicity within a series increased with the degree of bromination and decreased with the molecular weight. The genotoxicity profile was similar to that for cytotoxicity. Enzymatic analysis demonstrated that NCM460 cells possess glutathione-S transferase-1-1 and CYP450 activity similar to that measured in the large intestine. NCM460 cells were exposed to 10-6 M of the test chemicals for three days. While NCM460 cells from all treatments had the ability to grow in soft agar to some extent, only cells exposed to azoxymethane or tribromomethane were able to grow in media lacking serum and growth factors. When sub cultured, NCM460 cells exposed to 10-9 M azoxymethane for three weeks formed colonies with morphology distinct from untreated cells.

bromochloroacetate

Keratins: ACTIVE|Haloacetic acids ... are chemical byproducts of chlorination and chloramination of drinking water. /Haloacetates/

Fatty Acyls [FA] -> Fatty Acids and Conjugates [FA01] -> Halogenated fatty acids [FA0109]|Cosmetics -> Antistatic; Film forming; Hair conditioning; Humectant; Skin conditioning