This laboratory focuses on understanding the contribution of environmental chemical exposures to human diseases and disorders of the nervous system in order to evaluate human health risks and to determine effective strategies for treatment.

Ongoing studies focus on three areas. One involves determination of the neurochemical mechanisms in rodent models by which chronic low level lead (Pb) exposures disrupt complex cognitive/executive functions, including learning and attention. This will allow development of behavioral and/or pharmacological therapeutic strategies for such deficits.

Our studies of behavioral deficits in lead-exposed children facilitate direct translation of findings from experimental models. Related studies are now examining the combined impacts of low level lead exposures and stress in both rat and mouse models, since these are co-occurring risk factors that both target the mesolimbic dopamine system of the brain, and our previous studies show that Pb exposure permanently alters HPA axis function.

Another line of research in this laboratory continues to explore the contribution of pesticide exposures to the etiology of the ParkinsonŐs disease phenotype, particularly when such exposures occur in combination with other risk factors, including developmental period of exposure, aging, genetic background and gender. Future studies aim to examine both the role of pesticides in addition to the paraquat + maneb model as etiological factors and to begin to determine mechanisms and markers that are common across models of the PD phenotype.

Recent Publications

Bronstein J, Carvey P, Chen H, Cory-Slechta D, DiMonte D, Duda J, English P, Goldman S, Grate S, Hansen J, Hoppin J, Jewell S, Kamel F, Koroshetz W, Langston JW, Logroscino G, Nelson L, Ravina B, Rocca W, Ross GW, Schettler T, Schwarzschild M, Scott B, Seegal R, Singleton A, Steenland K, Tanner CM, Van Den Eeden S, Weisskopf M. Meeting report: consensus statement-Parkinson’s disease and the environment: collaborative on health and the environment and Parkinson’s Action Network (CHE PAN) conference 26-28 June 2007. Environ Health Perspect. 2009 Jan;117(1):117-121.

Virgolini MB, Rossi-George A, Weston D, Cory-Slechta DA. Influence of low level maternal Pb exposure and prenatal stress on offspring stress challenge responsivity. Neurotoxicology. 2008 Nov;29(6):928-939.

Rossi-George A, Virgolini MB, Weston D, Cory-Slechta DA. Alterations in glucocorticoid negative feedback following maternal Pb, prenatal stress and the combination: a potential biological unifying mechanism for their corresponding disease profiles. Toxicol Appl Pharmacol. 2009 Jan 1;234(1):117-127.

Weiss B, Cory-Slechta D, Gilbert SG, Mergler D, Miller E, Miller C, Newland MC, Rice D, Schettler T. The new tapestry of risk assessment. Neurotoxicology. 2008 Sep;29(5):883-1890

Virgolini MB, Rossi-George A, Lisek R, Weston DD, Thiruchelvam M, Cory-Slechta DA. CNS effects of developmental Pb exposure are enhanced by combined maternal and offspring stress. Neurotoxicology. 2008 Sep;29(5):812-827

Lanphear BP, Hornung RW, Khoury J, Dietrich KN, Cory-Slechta DA, Canfield RL. The conundrum of unmeasured confounding: Comment on: “Can some of the detrimental neurodevelopmental effects attributed to lead be due to pesticides? by Brian Gulson”. Sci Total Environ. 2008 Jun 25;396(2-3):196-200.

Jusko TA, Henderson CR, Lanphear BP, Cory-Slechta DA, Parsons PJ, Canfield RL. Blood lead concentrations < 10 microg/dL and child intelligence at 6 years of age. Environ Health Perspect. 2008 Feb;116(2):243-248.

Cory-Slechta DA, Virgolini MB, Rossi-George A, Thiruchelvam M, Lisek R, Weston D. Lifetime consequences of combined maternal lead and stress. Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):218-227. Review.

White LD, Cory-Slechta DA, Gilbert ME, Tiffany-Castiglioni E, Zawia NH, Virgolini M, Rossi-George A, Lasley SM, Qian YC, Basha MR. New and evolving concepts in the neurotoxicology of lead. Toxicol Appl Pharmacol. 2007 Nov 15;225(1):1-27.

Barlow BK, Cory-Slechta DA, Richfield EK, Thiruchelvam M. The gestational environment and Parkinson's disease: evidence for neurodevelopmental origins of a neurodegenerative disorder. Reprod Toxicol. 2007 Apr-May;23(3):457-470.

Froehlich TE, Lanphear BP, Dietrich KN, Cory-Slechta DA, Wang N, and Kahn RS. Interactive effects of a DRD4 polymorphism, lead, and sex on executive functions in children. Biol Psychiatry. 2007 Aug 1;62(3):243-249.

Gray JP, Heck DE, Mishin V, Smith PJ, Hong JY, Thiruchelvam M, Cory-Slechta DA, Laskin DL, and Laskin JD. Paraquat increases cyanide-insensitive respiration in murine lung epithelial cells by activating an NAD(P)H:paraquat oxidoreductase: identification of the enzyme as thioredoxin reductase. J Biol Chem. 2007 Mar 16;282(11):7939-7949.

Vahter M, Gochfeld M, Casati B, Thiruchelvam M, Falk-Filippson A, Kavlock R, Marafante E, and Cory-Slechta D. Implications of gender differences for human health risk assessment and toxicology. Environ Res. 2007 May;104(1):70-84.

Davidson PW, Weiss B, Beck C, Cory-Slechta DA, Orlando M, Loiselle D, Young EC, Sloane-Reeves J, and Myers GJ. Development and validation of a test battery to assess subtle neurodevelopmental differences in children. Neurotoxicology. 2006 Dec;27(6):951-969.

Cory-Slechta DA, Thiruchelvam M, Barlow BK, and Richfield EK. Developmental pesticide models of the Parkinson disease phenotype. Environ Health Perspect. 2005 Sep;113(9):1263-1270.

Virgolini MB, Bauter MR, Weston DD, and Cory-Slechta DA. Permanent alterations in stress responsivity in female offspring subjected to combined maternal lead exposure and/or stress. Neurotoxicology. 2006 Jan;27(1):11-21.