Protecting Children from Toxic Waste: Data-Usability Evaluation Can Deter Flawed Cleanup.

Nearly 25 percent of US children live within 2 km of toxic-waste sites, most of which are in urban areas. They face higher rates of cancer than adults, partly because the dominant contaminants at most US hazardous-waste sites include genotoxic carcinogens, like trichloroethylene, that are much more harmful to children. The purpose of this article is to help protect the public, especially children, from these threats and to improve toxics-remediation by beginning to test our hypothesis: If site-remediation assessments fail data-usability evaluation (DUE), they likely compromise later cleanups and public health, especially children's health. To begin hypothesis-testing, we perform a focused DUE for an unremediated, Pasadena, California toxic site. Our DUE methods are (a) comparing project-specific, remediation-assessment data with the remediation-assessment conceptual site model (CSM), in order to identify data gaps, and (b) using data-gap directionality to assess possible determinate bias (whether reported toxics risks are lower/higher than true values). Our results reveal (1) major CSM data gaps, particularly regarding Pasadena-toxic-site risks to children; (2) determinate bias, namely, risk underestimation; thus (3) likely inadequate remediation. Our discussion shows that if these results are generalizable, requiring routine, independent, DUEs might deter flawed toxic-site assessment/cleanup and resulting health threats, especially to children.

Effects of AMPA/kainate receptor blockade on responses to dopamine receptor agonists in the core and shell of the rat nucleus accumbens.

The present experiments were conducted to investigate effects of alpha-amino-3-hydroxy-5-methyl-4-isoxazoleprionic acid (AMPA)/kainate receptor blockade (CNQX, NBQX) on locomotor responses to D2/3 (7-OH-DPAT) and D1 [(+)-SKF 38393] dopamine receptor agonists in the nucleus accumbens (NAS) core and shell. CNQX (0.25-0.5 microgram) microinjected into the NAS core or shell did not affect baseline locomotor activity. 7-OH-DPAT (2.5-5 micrograms) decreased locomotor activity. Co-administration of CNQX (0.5 microgram) increased the effects of 7-OH-DPAT (5 micrograms) in the NAS core and shell. A similar increase was observed with NBQX (0.5 microgram) in the NAS shell. (+)-SKF 38393 (5 micrograms) into the NAS core and shell increased locomotor activity after 30 min; this effect was not altered by CNQX (0.5 microgram). As the D2/3 dopamine agonist (-)-quinpirole (2 micrograms) increased effects of (+)-SKF 38393 (5 micrograms) in NAS shell but not core, lack of site-selective effects of (+)-SKF-38393 and of 7-OH-DPAT within NAS is not attributable to drug diffusion. The previous observation that glutamate effects on locomotor activity depend on the relative involvement of D1 or D2/3 dopamine receptors in the NAS was based on the dopamine-depletion model. The present results demonstrate differential interactions of AMPA receptor blockade with dopamine agonists in "dopamine-intact" animals.