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Environmental Health Perspectives Volume 116, Number 2, February 2008 Open Access
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Low-Level Prenatal and Postnatal Blood Lead Exposure and Adrenocortical Responses to Acute Stress in Children

Brooks B. Gump,1 Paul Stewart,1 Jacki Reihman,1 Ed Lonky,1 Tom Darvill,1 Patrick J. Parsons,2,3 and Douglas A. Granger4

1Department of Psychology, State University of New York College at Oswego, Oswego, New York, USA; 2Trace Elements Laboratory, Wadsworth Center, New York State Department of Health, Albany, New York, USA; 3Department of Environmental Health Sciences, School of Public Health, The University at Albany, Albany, New York, USA; 4Behavioral Endocrinology Laboratory, Department of Biobehavioral Health, Pennsylvania State University, State College, Pennsylvania, USA

Abstract
Background: A few recent studies have demonstrated heightened hypothalamic–pituitary–adrenal (HPA) axis reactivity to acute stress in animals exposed to heavy metal contaminants, particularly lead. However, Pb-induced dysregulation of the HPA axis has not yet been studied in humans.

Objective: In this study, we examined children's cortisol response to acute stress (the glucocorticoid product of HPA activation) in relation to low-level prenatal and postnatal Pb exposure.

Methods: Children's prenatal blood Pb levels were determined from cord blood specimens, and postnatal lead levels were abstracted from pediatrician and state records. Children's adrenocortical responses to an acute stressor were measured using assays of salivary cortisol before and after administration of a standard cold pressor task.

Results: Pb exposure was not associated with initial salivary cortisol levels. After an acute stressor, however, increasing prenatal and postnatal blood Pb levels were independently associated with significantly heightened salivary cortisol responses.

Conclusions: Our results suggest that relatively low prenatal and postnatal blood lead levels—notably those below the 10 µg/dL blood lead level identified by the Centers for Disease Control and Prevention for public health purposes—can alter children's adrenocortical responses to acute stress. The behavioral and health consequences of this Pb-induced HPA dysregulation in children have yet to be determined.

Key words: , , , , , , , . Environ Health Perspect 116:249–255 (2008) . doi:10.1289/ehp.10391 available via http://dx.doi.org/ [Online 17 November 2007]


Address correspondence to B.B. Gump, 414 Mahar Hall, Department of Psychology, SUNY Oswego, Oswego, NY 13126 USA. Telephone: (315) 312-4150. Fax: (315) 342-2558. E-mail: gump@oswego.edu

We are grateful to S. Fitzgerald, C. Hosley, P. West, C. Smith, W. Morgan, K. Cahill, K. Foley, A. Quad, and J. Casey for their assistance in data collection.

This work was supported by grants ES-10190 and ES09815 from the National Institutes of Health, Grant 875-ATH298326-10 from the Agency for Toxic Substances and Disease Registry, the Great Lakes Protection Fund, and a Faculty Enhancement Grant from SUNY Oswego.

The authors declare they have no competing financial interests.

Received 23 April 2007 ; accepted 15 November 2007.


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