How the Environmental influences on Child Health Outcome (ECHO) Cohort can spur discoveries in environmental epidemiology.

NIH's Environmental influences on Child Health Outcome (ECHO) program is an innovative, large, collaborative research initiative whose mission is to enhance the health of children for generations to come. The goal of the ECHO Cohort is to examine effects of a broad array of early environmental exposures on child health and development. It includes longitudinal data and biospecimens from over 100,000 children and family members from diverse settings across the U.S. ECHO investigators have published collaborative analyses showing associations of environmental exposures--primarily in the developmentally sensitive pre-, peri-, and post-natal periods--with preterm birth and childhood asthma, obesity, neurodevelopment, and positive health. Investigators have addressed health disparities, joint effects of environmental and social determinants, and effects of mixtures of chemicals. The ECHO Cohort is now entering its second 7-year cycle (2023-2030), which will add the preconception period to its current focus on prenatal through adolescence. Through a controlled access public use database, ECHO makes its deidentified data available to the general scientific community. ECHO Cohort data provide opportunities to fill major knowledge gaps in in environmental epidemiology, and to inform policies, practices, and programs to enhance child health.

Safety assessment of biotechnology products for potential risk of food allergy: implications of new research.

Food allergy is a potential risk associated with use of transgenic proteins in crops. Currently, safety assessment involves consideration of the source of the introduced protein, in silico amino acid sequence homology comparisons to known allergens, physicochemical properties, protein abundance in the crop, and, when appropriate, specific immunoglobulin E binding studies. Recently conducted research presented at an International Life Sciences Institute/Health and Environmental Sciences Institute-hosted workshop adds to the scientific foundation for safety assessment of transgenic proteins in five areas: structure/activity, serum screening, animal models, quantitative proteomics, and basic mechanisms. A web-based tool is now available that integrates a database of allergenic proteins with a variety of computational tools which could be used to improve our ability to predict allergenicity based on structural analysis. A comprehensive strategy and model protocols have been developed for conducting meaningful serum screening, an extremely challenging process. Several animal models using oral sensitization with adjuvant and one dermal sensitization model have been developed and appear to distinguish allergenic from non-allergenic food extracts. Data presented using a mouse model suggest that pepsin resistance is indicative of allergenicity. Certain questions remain to be addressed before considering animal model validation. Gel-free mass spectrometry is a viable alternative to more labor-intensive approaches to quantitative proteomics. Proteomic data presented on four nontransgenic varieties of soy suggested that if known allergen expression in genetically modified crops falls within the range of natural variability among commercial varieties, there appears to be no need to test further. Finally, basic research continues to elucidate the etiology of food allergy.

Effects of prenatal chlordecone on sexually differentiated behavior in adult rats.

In rodents, exposure to estrogens during early development masculinizes the structure and function of the brain. The effects of early exposure to estrogens or estrogenic compounds can be evaluated by neurobehavioral testing after puberty. In this study, the effect of developmental exposure to the chlorinated pesticide, chlordecone (CD) on sexually differentiated behaviors in adults was investigated because CD binds to estrogen receptors and causes estrogenic effects in the reproductive tract of humans and rodents at relatively high doses. Pregnant Sprague-Dawley rats were exposed to 5 mg/kg CD by intraperitoneal injection on gestation day 16 (GD 16). Offspring were gonadectomized on postnatal day 50 (PN 50) to remove the effects of circulating hormones and were sequentially tested for sex-typic spontaneous behaviors in an open field and elevated plus maze, and for male and female mating behavior following the appropriate steroid regimen. Female rats exposed in utero to CD showed an increased ratio of inner to total crossings in the open field and significantly increased lordosis and male mounting as compared to female control rats. Male rats exposed in utero to CD showed significantly increased lordosis as compared to male control rats and no change in male mating behaviors. Permanent changes in adult behavior were consistent with both estrogenic and anti-estrogenic actions following developmental exposure to CD at the dose tested.