“... oral ingestion by monkeys, chlorine dioxide was rapidly converted into chloride ion and, to a lesser extent, chlorite and chlorate.. In rats, excretion of chloride and, to a lesser extent, chlorite ion is mainly via the urine, smaller amounts being excreted in faeces... At typical low drinking-water levels, chlorine dioxide would be decomposed by oxidation–reduction reactions with saliva and stomach contents...” “Drinking-water containing chlorine dioxide at a concentration of 0, 10 or 100 mg/L (equivalent to approximately 0, 1.5 and 15 mg/kg bw per day) was administered to mice... with no apparent effects on blood parameters... “ “study with Sprague-Dawley rats at drinking-water concentrations ranging from 0 to 200 mg/L...enzymatic changes suggested liver toxicity; the principal effect was histopathology of nasal turbinates from inhalation of the gas. Although chlorine dioxide is water soluble, it is a gas at room temperature, so there can be difficulty in interpreting toxicity findings.” “In a 2-year study in rats at drinking-water concentrations up to 100 mg/L, the NOAEL was 10 mg/L (1.3 mg/kg bw per day)” "Currently, there is no readily available and low-cost treatment available to remove chlorate ion once it has been formed in drinking-water. "

(1978)

****!!!!*** {Collection of extensive safety data} "Vacated 1989 OSHA PEL TWA 0.1 ppm (0.3 mg/cu m); STEL 0.3 ppm (0.9 mg/cu m) is still enforced in some states."

{Extensive data, studies, dosages}

2002

****!!!!**** The main lesion induced by ClO2 is the destruction of alveolar walls, which creates pulmonary emphysema lesions. This emphysema was found on all rats of the study (except control) whatever the tested concentration. The severity of the lesion is proportional to the dose. Animals died by respiratory deficiency. LC50combined = 89 mg/m3air

{includes Toxicity levels}