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Children Exposed to Metals Mixtures Demonstrate Dysregulation of Infectious Disease Response
Citation:
Edwards, S., J. Gruber, R. Patel, J. Rager1, A. Sanders, AND R. Fry. Children Exposed to Metals Mixtures Demonstrate Dysregulation of Infectious Disease Response. Presented at Environmetal Mutagen Society, September 08 - 12, 2012.
Impact/Purpose:
presentation at EMS conference. Prelimanry analysis suggests that multiple biological pathways are impacted by summing the concentrations of mutliple essential and toxic metals as detected in fingernails from children
Description:
Exposure to toxic metals can have harmful health effects, particularly in children. Although studies have investigated the individual effects toxic metals have on gene expression and health outcomes, there are no studies assessing the effect of metal mixtures on gene expression profiles. Here, we assessed the mixture effect of six toxic metals (arsenic, beryllium, cadmium, chromium, mercury, and lead) on gene expression profiles in children in Detroit, Michigan. As part of the Mechanistic Indicators of Childhood Asthma (MICA) cross sectional study, we assessed metal exposure in 131 children in Detroit using fingernail metals levels by inductively coupled plasma optical emission spectrometry. A metals mixture score was calculated and compared to gene expression profiles across the population. There were 46 unique genes that were significantly differentially expressed when comparing children assigned to either high or low levels of the metals mixture. Of the genes differentially expressed, 41 (89%) had increased expression while 5 (11%) had decreased expression. The main network functions associated with multiple metals were infectious disease, inflammatory disease, and respiratory disease (P = 10-33); cellular development, cell-mediated immune response, cellular function and maintenance (P = 10-20); inflammatory disease, respiratory disease, and cellular movement (P = 10-17). Taken together, these data demonstrate that exposure to metals mixtures may activate gene networks related to respiratory and infectious disease response pathways. This abstract does not necessarily reflect the views or policies of the EPA.