Chronic neurotoxic effect

London, L. and J.E. Meyers (1998). Use of a crop and job specific exposure matrix for retrospective assessment of long term exposure in studies of chronic neurotoxic effects of agrichemicals, Occup. Environ. Med., 55, 194-201. 

Ray, D.E. (1998). Organophosphorus Esters An Evaluation of Chronic Neurotoxic Effects. Institute for Environment and Health, Leicester, UK, 62 pp. 

The chronic neurotoxic effects of methylmercury in animals are similar to those seen after intermediate exposure. Mice administered methylmercuric chloride in the diet for 2 years at approximately 0.6 mg Hg/kg/day showed posterior paralysis and sensory neuropathy, characterized by cerebral and cerebellar necrosis, as well as degeneration of spinal dorsal nerve roots and the sciatic nerve (Hirano et al. 1986 Mitsumori et al. 1990). Cats fed contaminated fish or contaminated fish and methylmercury at doses as low as 0.046 mg Hg/kg/day for 2 years exhibited neurobehavioral toxic signs, including mild impairment of motor activity and diminished sensitivity to pain (Charbonneau et al. 1976). These effects began after 60 weeks of exposure but did not progress during the remainder of the 2 years of exposure. 

CHRONIC HEALTH RISKS a rubber solvent induced chromosomal aberrations in human whole-blood cultures repeated exposure can damage the nervous system, including headache, fatigue, poor concentration, emotional instability, impaired memory and other intellectual functions chronic neurotoxic effects include motor polyneuropathy prolonged contact can cause drying and cracking of skin. 

In a cross-sectional study, exposure and effect are studied simultaneously. This approach contains an inherent problem because exposure must precede the effect. However, it can he used to investigate acute effects and also mild chronic effects (which do not force people to leave their jobs) if exposure has remained rather stable for a long time. When the prevalence of the effects studied are compared with the prevalence in other worker groups (controls or references) which correspond otherwise with the study group but are not exposed to the agent investigated, indicative evidence of possible causality may be obtained. For example, cross-sectional studies have been applied successfully to reveal the associations between mild neurotoxic effects and exposure to organic solvents. ... 

Intake can be expressed either as a pollutant mass per unit time, as discussed above, or as a mass per kg of body weight per unit time. The latter expression facilitates comparison to health effects data, especially laboratory animal data, which are commonly reported in equivalent units. Similarly, depending on the route of exposure, intake may be estimated on an annual basis to address chronic effects, or on a smaller time scale for addressing acute effects including lethality, teratogenesis, reproductive and neurotoxic effects. 

Chronic exposure to Pb has been shown to cause anaemia, neurotoxic effects, such as reduced cognitive performance and reduced peripheral nerve conduction velocity, and nephrotoxicity. Children are more sensitive to exposure to Pb than adults, especially during the first 2 years of life [41], For children, exposure to lead can cause growth retardation, affect the neuropsychological development and cause encephalopathy [39]. Adverse reproductive effects due to lead exposure have been observed for both men and women. Exposure of pregnant women to low concentrations of lead is associated with miscarriages and low birth weights [40],... 

ATSDR has derived a chronic oral MRL of 0.0003 mg/kg/day based on a laboratory animal study showing neurotoxic effects in dogs (Kettering Lab 1969). The EPA reference dose for endrin is 3xl0 4 mg/kg/day, and the critical dose is 0.025 mg/kg/day (IRIS 1995). Critical effects were occasional convulsions and mild histological lesions in the liver (Kettering Lab 1969). No EPA reference concentration exists for the compound. 

Chronic elevation of corticosteroids has been shown to impair cognitive processes and have neurotoxic effects (Sheline et al. 1996 de Kloet et al. 1999). The cumulative effects of elevated cortisol levels are associated with cognitive impairments in human aging (Lupien et al. 1999). Thus, the cognitive and neuroprotective effects of ginkgo may be partly mediated through its neuroendocrine effects. 

An occasional common side effect of capsaicin exposure is bronchoconstriction, in asthmatic people, caused by inhaled airborne particles. In nonasthmatic people, this induces a cough. This is prevented by washing the skin surface where capsaicin was applied after 30-40 minutes of exposure. Chronic overdosage can cause chronic gastritis, kidney and liver toxicity, and neurotoxic effects. 

Anger, W. K. (1981). Effects of carbaiyl on variable interval response rates in rats. Neurobehavioral Toxicology 2 21-24. Bear, D. M. (1986). Aggression in cat and human precipitated by a cholinesterase inhibitor. Psychosomatics 27 535-536. Branch, R. A. (1986). Is carbaryl as safe as its reputation Does it have a potential for causing chronic neurotoxicity in humans American Journal cf Medicine 80 659-664. 

De Haro L, Gastaut J-L, Jouglard J, et ah Central and peripheral neurotoxic effects of chronic methyl bromide intoxication. J Toxicol Clin Toxicol 35(l) 29-34, 1997... 

Neurotoxicity. Little information was available to determine the neurotoxicity of HDI after inhalation, oral or dermal exposure. Neurotoxic effects may occur if concentrations reach high levels in the air (Haskell Laboratoiy 1961) however, since HDI is metabolized quiekly in a biological matrix (Berode et al. 1991), little intact HDI is expected to reach the nervous tissue to elicit a toxic response, except possibly at very high concentrations. No neurological effects have reported in laboratoiy animals, or in humans exposed chronically to low concentrations of HDI (Mobay Corporation 1989) therefore the data need for determining the neurotoxicity of HDI is a low priority. 

Neurotoxicity. No histopathological effects on organs and tissues of the neurological systems of animals were found in subchronic and chronic oral studies, but signs of central nervous system toxicity were reported in inhalation, oral, and dermal studies. A battery of tests for neurotoxicity would provide further information of the neurotoxicity in animals, which then might be related to possible neurotoxic effects in humans. 

Available intermediate- and chronic-duration oral studies in animals indicate that the thyroid and liver are the main systemic targets of PBDE toxicity as shown by effects mainly including enlargement and histological alterations in both organs and changes in serum levels of thyroid hormones. Several acute-duration studies of pentaBDE suggest that immunosuppression may also be an important health end point. Very little information is available on potential neurotoxic effects of PBDEs, mainly the results of three... 

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