The effect of adverse maternal exposures during pregnancy on offspring health outcomes has gained particular interest in recent years, based on the popularity of the “fetal origins of disease” hypothesis. Dr. Papandonatos and his collaborators have employed between-within decomposition of maternal effects to deal with unobserved familial confounding in studies of adverse maternal exposures during pregnancy, in datasets where multiple births are available from the same mother. They have also been using shrinkage approaches to estimate effects of chemical mixtures on child outcomes, where mixture components tend to be highly correlated. Of particular interest are big data approaches to shrinkage and selection in longitudinal trajectory models, seeking to identify antecedents and sequelae of methylation and metabolomic profiles on children's health.
The U.S. National Toxicological Program (NTP) recently recommended further research on the relationship between environmental exposures and type 2 diabetes (T2D) and recent data linking heavy metals to T2D risk, while tantalizing, is far from establishing causality. Utilizing the resources collected from an on-going prospective cohort study, we propose to conduct a nested case-control study to comprehensively investigate if heavy metal exposures increase T2D risk and to determine if the diabetic effects of toxic metals can be mitigated by essential metals, and the optimal body levels of essential metals that could reduce T2D risk from toxic metals. The results from the study will help to establish appropriate interventions to prevent T2D.
|George Papandonatos||Staff 1||Research Assistant i|
Chromium (Cr) exposure through the drinking water and in occupational settings is a serious public health concern, inducing carcinogenesis in lung-derived cells and exposed populations. We propose an approach to investigate Chromium-gene interactions that is anchored in a major nuclear organelle (the nucleolus) and rDNA loci. The proposed work focuses on a novel pathway, an important exposure, and advances the NIH mission by generating knowledge, resources, and technologies that will advance both basic and public health studies of environmental triggers of human diseases.
|Jean Wu||Staff 1||Research Assistant i|