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Chlorine dioxide (ClO2), an alternative to chlorine for drinking water disinfection, has been implicated as a potential antithyroid agent (Bercz et al., 1982). Because antithyroid compounds are known to alter neurobehavioral development, the present study was designed to determine if perinatal exposure to ClO2 affects behavioral activity in rat pups. The activity cage system was designed to monitor the development of locomotor activity of a litter of pups between ages 14-21 d. Pups were exposed to ClO2 either directly, by gavaging 14 mg/kg . from age 5 to 20 d, or indirectly via their dams' drinking water in concentrations of 2, 20, or 100 mg/l from gestation to weaning (21 d postpartum). Although the activity of the indirectly exposed group was not different from controls, the gavaged group showed significantly depressed activity for d 18 and 19 postpartum. The T4 levels of the 21-d-old pups was significantly depressed in the 100-mg/l ClO2 group. The gavaged pups showed an even greater T4 depression, which correlates with their activity levels. These data support the hypothesis that ClO2 affects thyroid function and suggests that a slight
Depression in T4 can result in developmental delays.
http://www.ncbi.nlm.nih.gov/pubmed/4009737
Subchronic toxicities of ClO2, NaClO2, NaClO3 and NH2Cl were studied in the African Green monkeys (Cercopithecus aethiops). The chemicals were administered in drinking water during 30-60 days subchronic rising dose protocols. The only unexpected and significant toxic effect was elicited by ClO2; this chemical inhibited thyroid metabolism in the animals at a dose of ca. 9.0 mg/kg/day. A statistically significant decrease of serum thyroxine occurred after the fourth week of exposure to 100 mg/l.concentration. The extent of thyroid suppression was dose dependent in each individual monkey, and was reversible after cessation of exposure. NaClO2 and NaClO3 failed to elicit similar effects in doses up to ca. 60 mg/kg/day. Also, NaClO4 or NH2Cl did not cause T-4 suppression in doses of 10 mg/kg/day. The selective thyroid effect of ClO2 was unexplained and it appeared to be paradoxical since ClO2 was rapidly reduced by the oral and gastric secretions to nonoxidizing species (presumably Cl-). No evidence of thyroid effects were detected in the serum of human volunteers who ingested approximately 1 mg/l. of ClO2 in drinking water as a result of routine use in the community water treatment process. Sodium chlorite induced dose-dependent oxidative stress on hematopoesis, causing decreased hemoglobin and red cell count and increased methemoglobin content. At the same time, serum transaminase (SGPT) levels showed significant subclinical elevation. The hematologic effects of NaClO2 rebounded during exposure indicating compensatory hemopoietic activity taking effect during oxidative stress. Sodium chlorate and chloramine did not induce detectable hematologic changes in the animals.
http://www.ncbi.nlm.nih.gov/pubmed/7151767
In a previous study from this laboratory, chlorine dioxide (ClO2) treated drinking water depressed thyroxine (T4) levels in the African green monkey. The present study again demonstrated a decrease in T4 levels in the same species after 4 wk of oral exposure. However, after 8 wk of treatment T4 levels rebounded to above pretreatment levels, coinciding with an increase in thyroid radioiodide uptake. This T4 rebound phenomenon and increased
Iodide uptake may be due to a compensatory endocrinological mechanism. In rats, T4 levels dropped during the 8-wk ClO2 treatment period in a dose-dependent manner, and no rebound effect was observed.
Iodide uptake values in the rat were not affected. It appears that ClO2 may have an effect on thyroid function in both species.
http://www.ncbi.nlm.nih.gov/pubmed/3761383