Neurobehavioral

Preventive Measures. The intake uptake biokinetic model (lUBK) projects the impact of lead in the environment on blood lead. This model assumes conservatively high levels of intake and cannot account for chemical speciation, thus over-predictions of blood lead levels often occur. Nonetheless, because of the allegations of the impact of blood lead and neurobehavioral development, blood lead levels in children are being reduced adrninistratively to below 10 //g/dL. In order to do so, soil leads are being reduced to a level of between 500—1000 ppm where remediation is required. 

Grandjean, P., White, R. E, and Weihe, P. (1996). Neurobehavioral epidemiology Application in risk assessment. Enniron. Health Perspect. 104(2), 397- 00. 

BAYK8644 is a DHP with Ca2+ channel activating properties. Although some therapeutic effects can be envisaged for such drugs (such as stimulation of glucose-dependent insulin secretion, positive inotropy), severe side effects are also predicted from animal studies (dystonic neurobehavioral syndrome, hypertension, arrhythmias), which currently prevents their clinical development. 

Dick RB, Ahlers H. 1998. Chemicals in the workplace Incorporating human neurobehavioral testing into the regulatory process. Am J Ind Med 33 439-453. 

Hansen E, Meyer O. 1980. Neurobehavioral effects of prenatal exposure to parathion-methyl on rats. Acta Morphol Acad Sci Hung 28 210. 

Rodnitzky RL, Levin HS, Morgan PP. 1978. Effects of ingested parathion on neurobehavioral functions. Clin Toxicol 13 347-359. 

In summary, neurotoxic effects of endosulfan are usually apparent only after acute ingestion of relatively high doses. Cumulative neurotoxicity does not appear to be significant. If the animal survives the acute toxic effects, then no long-term neurotoxic effects are evident from behavioral, gross, and microscopic observations. However, some impairment may occur that can be detected only by specialized neurobehavioral testing. 

Paul V, Balasubramaniam E, Jayakumar AR, et al. 1995. A sex-related difference in the neurobehavioral and hepatic effects following chronic endosulfan treatment in rats. Eur J Pharmacol 293(4) 355-360. 

MasUah E, Heaton RK, Marcotte TD, EUis RJ, Wiley CA, MaUory M, Achim CL, McCutchan JA, Nelson JA, Atkinson JH, Grant I (1997) Dendritic injury is a pathological substrate for human immunodeficiency virus-related cognitive disorders. HNRC Group. The HIV Neurobehavioral Research Center. Ann Neurol 42(6) 963-972... 

EUis RJ, Deutsch R, Heaton RK, Marcotte TD, McCutchan JA, Nelson JA, Abramson I, Thai LJ, Atkinson JH, Wallace MR, Grant 1 (1997) Neurocognitive impairment is an independent risk factor for death in HIV infection. San Diego HIV Neurobehavioral Research Center Group. Arch Neurol 54 416-424... 

Experimental exposure studies have attempted to associate various neurological effects in humans with specific trichloroethylene exposure levels. Voluntary exposures of 1 hours resulted in complaints of drowsiness at 27 ppm and headache at 81 ppm (Nomiyama and Nomiyama 1977). These are very low exposure levels, but the results are questionable because of the use of only three test subjects per dose, lack of statistical analysis, sporadic occurrence of the effects, lack of clear dose-response relationships, and discrepancies between the text and summary table in the report. Therefore, this study is not presented in Table 2-1. No effects on visual perception, two-point discrimination, blood pressure, pulse rate, or respiration rate were observed at any vapor concentration in this study. Other neurobehavioral tests were not performed, and the subjects were not evaluated following exposure. 

Amler RW, Anger WK, Sizemore OJ, eds. 1995. Adult environmental neurobehavioral test battery. 

Annau Z. 1981. The neurobehavioral toxicity of trichloroethylene. Neurobehav Toxicol Teratol 3 417-424. 

Baker EL, Letz R, Fidler AT, et al. 1985. A computer-based neurobehavioral evaluation system for occupational and environmental epidemiology Methodology and validation studies. Neurobehav Toxicol Teratol 7 369-377. 

Grasso P. 1988. Neurotoxic and neurobehavioral effects of organic solvents on the nervous system. Occupational Medicine State of the Art Reviews. 3 525-539. 

Kilbum KH, Warshaw RH. 1993. Effects on neurobehavioral performance of chronic exposure to chemically contaminated well water. Toxicol Ind Health 9 391 -404. 

Kulig BM. 1987. The effects of chronic trichloroethylene exposure on neurobehavioral functioning in the rat. Neurotoxicol Teratol 9 171-178. 

Moser VC, Cheek BM, MacPhail RC. 1995. A multidisciplinary approach to Toxicological screening III. Neurobehavioral toxicity. J Toxicol Environ Health 45 173-210. 

WHO. 1990. WHO neurobehavioral core test battery. In Johnson BL, ed. Proceedings of the Third International Symposium on Neurobehavioral Methods in Environmental and Occupational Health, Washington, DC, Dec 14-17, 1988. Chelsea, Ml Lewis Publishers 225-244. 

Effects noted in study and corresponding doses Mild subjective neurological effects (eye and throat irritation, headache, fatigue, drowsiness) were reported at 200 ppm (LOAEL). No objective effects, as measured by dexterity and coordination tests, were seen. However, 50% of the subjects reported that the neurobehavioral tests required greater mental effort for them to perform. 

Neurobehavioral effects of dietary soy phytoestrogens. Neurotoxicol Teratol. 24 (1) 5-16. 

Echeverria D, Woods JS, Heyer NJ, Rohhnan D, Farin FM, Li T, Garabedian CE. 2006. The association between a genetic polymorphism of coproporphyrinogen oxidase, dental mercury exposure and neurobehavioral response in humans. Neurotoxicol Teratol 28 39-48. 

Kim CY, Nakai K, Kasanuma Y, Satoh El. 2000. Comparison of neurobehavioral changes in three inbred strains of mice prenatally exposed to methylmercury. Neurotoxicol Teratol 22 397 03. 

My answer always is that no one has yet done a detailed neurobehavioral study of these individuals and the deficit that they may have. It may be very subtle in nature, and 1 am not sure that we have the methods available to detect and quantify those deficits. The fact that these people are not walking in with overt behavioral disturbances as the people with MPTP did. 1 think, is related to the fact that, one, they may not have the kind of neurotoxicity we are suspecting, and two, if they do, the kind of functional consequences that you may get from serotonergic dysfunction may be much more subtle than the kind of functional consequences you get with dopamine dysfunction, where it is very easy to recognize the parkinsonian patient... 

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