Dibromochloroacetic acid

/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/

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The potential toxicity of dibromochloroacetic acid (DBCA, CAS No.: 5278-95-5) was evaluated /in male and female rats/. ... 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 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.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... The effects of exposing neurulation staged (3-6 somite pairs) CD-1 mouse conceptuses to bromochloro- (BCA), dibromochloro- (DBCA) and bromodichloro-acetic (BDCA) acids in whole embryo culture /were examined/ at concentrations ranging from 50 to 2500 uM. Morphological development was assessed after a 26 hr exposure period. Exposure of conceptuses to these HAAs produced dysmorphogenesis, including prosencephalic and pharyngeal arch hypoplasia as well as eye and heart tube abnormalities. Benchmark concentrations for induction of neural tube dysmorphogenesis were 63, 500 and 536 uM for BCA, DBCA and BDCA, respectively. /A/ previously developed HAA QSAR accurately predicted placement of these three chemicals in the larger context of the previously tested di- and tri-HAAs, also correctly predicting that BCA would be more potent than DBCA and BDCA, and that the latter two HAAs would be near equi-potent...

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).

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.