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Toxicogenic theory
Published in Herman Staudenmayer, Environmental Illness, 2018
Limbic kindling was the first of several CNS mechanisms incorporated by the toxicogenic theory. In the scientific literature, limbic kindling was defined by an animal model for seizure disorders induced by low levels of stimulation or high doses of a pharmacologic agent (Gilbert, 1992a,b; Wada, 1990). In 1969, Goddard (1969) reported that daily electrical stimulation of limbic and cortical brain structures sensitized the animals so that they would convulse in response to smaller stimuli. The sensitizing current did not damage the site where it was applied, so that the effect was not detectable by anatomical brain-imaging techniques. The lowered seizure threshold was observed to last as long as one year (Wada et al., 1974). The effect does not remain localized but gradually spreads to brain structures beyond those stimulated, typically the corresponding cortical site in the other hemisphere, thus the term “kindling” (Racine, 1978). The theory that limbic kindling contributes to non-experimentally-induced human seizure activity is controversial (Wada, 1990). EI advocates suggest that low-level chemicals serve as the inducing agents.
Risk assessment of lithium-ion battery explosion: chemical leakages
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Yoo Jung Park, Min Kook Kim, Hyung Sik Kim, Byung Mu Lee
The lethal dose, 50% (LD50) for rats during an intratracheal test was found to be 8200 µg/kg, at which, lung, thoracic or respiration changes, and hemorrhage were noted (NIOSH 2012) (Table 5). The oral LD50 for mouse was 363 mg/kg at which, general depressed activity, convulsions, weight loss or decreased weight gain occurred (NIOSH 2012) (Table 5). The oral LD50 for rat was 210 mg/kg produced depression, convulsions or lower seizure threshold and weight loss or decreased weight gain (NIOSH 2012) (Table 5).