Health Scientist

Brandy Beverly, Ph.D.
Brandy Beverly, Ph.D.
Health Scientist
Tel 984-287-3112
[email protected]
P.O. Box 12233
Mail Drop K2-04
Durham, NC 27709

Brandy Beverly, Ph.D., is a health scientist with the Office of Health Assessment and Translation (OHAT) in the National Toxicology Program at NIEHS. Beverly is co-leading evaluations about the effects of traffic-related air pollution on selected health outcomes, including high blood pressure during pregnancy. Her expertise and areas of interest include disease outcomes and underlying molecular mechanisms related to reproduction and development.

Beverly earned her Ph.D. in molecular medicine from the University of Maryland, Baltimore, where she investigated changes in hormonal function and blood flow during pregnancy. She received her postdoctoral training in reproductive and developmental toxicology at the U.S. Environmental Protection Agency (EPA) National Health and Environmental Effects Research Laboratory, where she examined the effects of environmental toxicants and pharmaceutical agents on reproductive and developmental outcomes. Before joining OHAT, Beverly worked in the Integrated Risk and Information Systems (IRIS) Program within the National Center of Environmental Assessment at EPA, using her reproductive and developmental toxicology expertise to draft IRIS assessments.

Selected Publications

  1. Boyles AL, Beverly BE, Fenton SE, Jackson CL, Jukic AMZ, Sutherland VL, Baird DD, Collman GW, Dixon D, Ferguson KK, Hall JE, Martin EM, Schug TT, White AJ, Chandler KJ. 2020. Environmental Factors Involved in Maternal Morbidity and Mortality. J Womens Health (Larchmt); doi: 10.1089/jwh.2020.8855 [Online 18 November 2020]. [Abstract Boyles AL, Beverly BE, Fenton SE, Jackson CL, Jukic AMZ, Sutherland VL, Baird DD, Collman GW, Dixon D, Ferguson KK, Hall JE, Martin EM, Schug TT, White AJ, Chandler KJ. 2020. Environmental Factors Involved in Maternal Morbidity and Mortality. J Womens Health (Larchmt); doi: 10.1089/jwh.2020.8855 [Online 18 November 2020].]
  2. Beverly BEJ, Lambright CS, Furr JR, Sampson H, Wilson VS, McIntyre BS, Foster PMD, Travlos G, Gray, LE. 2014. Simvastatin and dipentyl phthalate lower ex vivo testosterone production and exhibit additive effects on testicular testosterone and gene expression via distinct mechanistic pathways in the fetal rat. Toxicol Sci 141(2):524-537. [Abstract Beverly BEJ, Lambright CS, Furr JR, Sampson H, Wilson VS, McIntyre BS, Foster PMD, Travlos G, Gray, LE. 2014. Simvastatin and dipentyl phthalate lower ex vivo testosterone production and exhibit additive effects on testicular testosterone and gene expression via distinct mechanistic pathways in the fetal rat. Toxicol Sci 141(2):524-537.]
  3. *Jacobs BE, Liu Y, Pulina MV, Golovina VA, Hamlyn JM. 2012. Normal pregnancy: mechanisms underlying the paradox of a ouabain-resistant state with elevated endogenous ouabain, suppressed arterial sodium calcium exchange, and low blood pressure. Am J Physiol Heart Circ Physiol 302(6):H1317-1329. [Abstract *Jacobs BE, Liu Y, Pulina MV, Golovina VA, Hamlyn JM. 2012. Normal pregnancy: mechanisms underlying the paradox of a ouabain-resistant state with elevated endogenous ouabain, suppressed arterial sodium calcium exchange, and low blood pressure. Am J Physiol Heart Circ Physiol 302(6):H1317-1329.]
  4. Mason AK, *Jacobs BE, Welling PA. 2008. AP-2-dependent internalization of potassium channel Kir2.3 is driven by a novel di-hydrophobic signal. J Biol Chem 283(10):5973-5984. [Abstract Mason AK, *Jacobs BE, Welling PA. 2008. AP-2-dependent internalization of potassium channel Kir2.3 is driven by a novel di-hydrophobic signal. J Biol Chem 283(10):5973-5984.]

*Denotes maiden name