1,2-Dibromo-3-chloropropane results

Chemical/Physical. The hydrolysis rate constant for 1,2,3-trichloropropane at pH 7 and 25 °C was determined to be 1.8 x lO Vh, resulting in a half-life of 43.9 yr (Ellington et ah, 1988). The hydrolysis half-lives decrease at varying pHs and temperature. At 87 °C, the hydrolysis half-lives at pH values of 3.07, 7.12, and 9.71 were 21.1, 11.6, and 0.03 d, respectively (Ellington et al, 1986). By analogy to l,2-dibromo-2-chloropropane, the following hydrolysis products would be formed 2,3-dichloro-l-propanol, 2,3-dichloropropene, epichlorohydrin, l-chloro-2,3-... 

Depletion of other cofactors such as UTP, NADH, and NADPH may also be involved in cell injury either directly or indirectly. Thus, the role of NADPH in maintaining reduced GSH levels means that excessive GSH oxidation such as caused by certain quinines, which undergo redox cycling, may in turn cause NADPH depletion (see below). Alternatively, NADPH may be oxidized if it donates electrons to the foreign compound directly. However, NADPH may be regenerated by inter conversion of NAD+ to NADP+. Some quinones such as menadione, l,2-dibromo-3-chloropropane (DBCP), and hydrogen peroxide also cause depletion of NAD, but probably by different mechanisms. Thus, with menadione, the depletion may be the result of... 

Use of l,2-dibromo-3-chloropropane as a pesticide, soil fumigant and a nematocide resulted in the direct release of this compound to the environment. Its production and use as an intermediate in organic synthesis also may have resulted in its release to the environment through various waste streams. It has been detected at low levels in ambient and urban air, groundwater, drinking-water and soil samples (United States National Library of Medicine, 1997). 

Brown (1992) conducted a cohort mortality study of workers employed at four pesticide manufacturing plants. The 1158 workers employed at Plant 3 of the study, which produced aldrin and dieldrin, were also potentially exposed to l,2-dibromo-3-chloropropane produced at the plant between 1975 and 1976. The cohort included all white males employed for six or more months before 1964 with follow-up through 1987. Although overall cancer mortality at Plant 3 was not elevated (SMR, 0.9 95% Cl, 0.7-1.1 = 72), an excess of liver and biliary tract cancer was observed (SMR, 3.9 95% Cl, 1.3-9.2 5 observed). All of the deaths occurred at least 15 years after first employment (SMR, 4.9), but no association was observed with duration of employment. The SMR for lung cancer was 0.7 (95% Cl, 0.4-1.0). Levels of exposure were not reported. Amoateng-Adjepong et al. (1995) reported the results of an update of the same cohort with three additional years of follow-up. No new association was reported. 

Necrosis and atrophy of the olfactory epithelium in the nasal cavity resulted from inhalation exposure to 5 and 25 ppm [50 and 240 mg/m l,2-dibromo-3-chloropropane for 6 h per day on five days per week for 13 weeks in both male and female Fischer 344 rats and B6C3Fi mice. At 1 ppm, respiratory changes were obsen ed that included cytomegaly, focal hyperplasia and, to lesser extents, squamous metaplasia and loss of cilia (Reznik et al., 1980). 

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