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Lead Exposure and Cardiovascular Dysregulation in Children
Author(s) -
MacKenzie James A.,
Gump Brooks B.,
Roosa Kristen,
Bendinskas Kestas,
Dumas Amy,
Morgan Robert,
Parsons Patrick
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.786.13
Subject(s) - aldosterone , medicine , endocrinology , vascular resistance , blood pressure , sympathetic nervous system , reactivity (psychology) , peripheral , peripheral blood , psychology , pathology , alternative medicine
Increasing lead (Pb) exposure is associated with increased blood pressure in humans and animal studies suggest this is due to increased vascular resistance. We looked at cardiovascular reactions to acute stress (AS) in 9‐11 year old children ( N = 134) with low blood Pb levels (≤3.76 μg/dL). Pb levels were significantly associated with increased total peripheral resistance (TPR) responses and diminished stroke volume and cardiac output responses to AS. This vascular pattern of response to AS tasks may predict future hypertension. Pb was also associated with sympathetic nervous system (SNS) withdrawal during AS and SNS activation at rest, and the Pb‐SNS relationship during AS was not significant when baseline SNS was included as a covariate. In addition, serum aldosterone was negatively associated with blood Pb and positively associated with SNS reactivity to AS. Inclusion of aldosterone as a covariate also eliminated the Pb‐SNS reactivity relationship. Our data suggests two independent mediational pathways underlying the Pb‐TPR association. One involves SNS activation at rest and the other involves decreased circulating aldosterone levels, and both ultimately decrease the capacity to elicit a SNS response to AS. The effects described here were significant for Pb levels considered well below the 10 μg/dL threshold set by the CDC for deleterious effects. Supported by grants ES10190 and ES09815 (NIH).