Human fetuses undergo development while suspended in fluids that contain a complex mixture of environmental chemicals. This includes synthetic compounds prevalent in modern day foods, food packaging, personal care products, the indoor environment, air, and water. Even though most babies are born healthy and without birth defects; these exposures can cause changes at a molecular level.
Are these changes measurable and reproducible in human populations? Are they meaningful with respect to the exposure and the long-term health of the child and the mother? The work of our laboratory is to measure these molecular changes and understand their significance to the health of the future child.
This process is referred to as endocrine disruption, the theory that synthetic chemicals in our environment can cause chronic disease by mimicking biological molecules in our bodies. This can occur during key transitions over the lifespan (fetal development, puberty, reproduction, menopause). Mimicry in this case refers to a disruption in epigenetic regulation, and/or gene and protein expression. Some chronic health disorders studied as consequences of endocrine disruption are infertility, obesity, diabetes, asthma, and neurobehavioral disorders.
Because the fetus cannot be sampled or observed directly, we do this by measuring the response of the placenta. The placenta is a fetal endocrine organ that serves as a physical, physiologic, and statistical mediator of maternal exposures. It produces molecules in abundance that can be sampled at key developmental time points in maternal blood, urine, cord blood, and placental tissue. With careful selection of biomarkers, we can simultaneously measure a placental response to an exposure and early indication of risk of a future outcome in the child.
Our lab is funded by the National Institute of Environmental Health Sciences (NIEHS). We are affiliated with the Department of Epidemiology of the University of Pittsburgh School of Public Health.
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adibij [@] pitt.edu