Kembra L. Howdeshell
- Kembra L. Howdeshell, Ph.D.
Kembra Howdeshell, Ph.D., is a health scientist with the Office of Health Assessment and Translation in the National Toxicology Program at NIEHS. She provides NTP with expertise in endocrinology, reproductive biology and toxicology. She has served as lead scientist at OHAT on projects relating to the Pregnancy Outcomes Associated with Cancer Chemotherapy Use during Pregnancy. She is also pursuing laboratory studies assessing the potential for cumulative effects of estrogenic isoflavones in soy infant formula and the onset of daizen metabolism during development in rodents.
Howdeshell completed her undergraduate studies in Biology and Spanish at Friends University in Wichita, Kansas (1991) and her M.S. degree in Biological Sciences from Emporia State University in Emporia, Kansas (1996). She earned her Ph.D. in Biology from the University of Missouri-Columbia (2002). Her doctoral research focused on the effects of estrogen-mimicking chemicals on reproductive tract development and function in mice. Howdeshell also served as a research fellow at World Wildlife Fund (2001-2002) in Washington DC, where she published a detailed literature review on the influence of the thyroid hormone system on brain development in humans and rodents, and the effects of thyroid hormone disrupting chemicals on this process. As a postdoctoral scientist, she studied the molecular mechanisms of thyroid hormone-directed brain development working on the African clawed frog in the Environmental Toxicology Program at the School of Public Health at the University of Michigan (2002-2004). Howdeshell also worked as a postdoctoral researcher in the Reproductive and Developmental Toxicology Division, National Human and Environmental Effects Laboratory of the US Environmental Protection Agency (US EPA) (2004-2009), where she focused on the effects of antiandrogenic chemicals on male reproductive development. Her postdoctoral research on the dose additive effects of reproductive toxicant phthalate esters has been highlighted in special editorials in Toxicological Sciences and used by the National Academy of Sciences in their 2008 review of the Cumulative Effects of Phthalate Esters in Risk Assessment.
- Howdeshell KL , Rider CV, Wilson VS, Furr J, Lambright CR, Gray, LE. 2015. Dose Addition Models Based on Biologically Relevant Reductions in Fetal Testosterone Accurately Predict Postnatal Reproductive Tract Alterations by a Phthalate Mixture in Rats. Toxicological sciences: an official journal of the Society of Toxicology 148(2):488-502. [Abstract]
- Hannas BR, Howdeshell KL, Furr J, Earl Gray L Jr. 2013. In utero phthalate effects in the female rat: A model for MRKH syndrome. Toxicology Letters 223(3):315-21. [Abstract]
- Hannas BR, Lambright CS, Furr J, Howdeshell KL, Wilson VS, Gray LE Jr. 2011. Dose-response assessment of fetal testosterone production and gene expression levels in rat testes following in utero exposure to diethylhexyl phthalate, diisobutyl phthalate, and diisononyl phthalate. Toxicological Sciences 123:206-16. [Abstract]
- Noriega N, Howdeshell KL, Furr JR, Lambright CR, Wilson VS and Gray LE, Jr. 2009. Pubertal administration of DEHP delays puberty, suppresses testosterone production and inhibits reproductive tract development in male Sprague-Dawley and Long-Evans Rats. Toxicological Sciences 111:163-178. [Abstract]
- Howdeshell, KL, Rider CV, Wilson VS and Gray LE Jr. 2008. Mechanisms of action of phthalate esters, individually and in combination, to induce abnormal reproductive development in male laboratory rats. Environmental Research 108 (2):168-76. [Abstract]
- Howdeshell, KL, Wilson VS, Furr J, Lambright CR, Rider CV, Blystone CR, Hotchkiss AK and Gray LE Jr. 2008. A mixture of five phthalate esters inhibits fetal testicular testosterone production in the Sprague Dawley rat in a cumulative, dose additive manner. Toxicological Sciences 105 (1):153-165. [Abstract]
- Howdeshell KL, Furr J, Lambright CR, Wilson VS, Ryan BC, and Gray LE Jr. 2007. Gestational and lactational exposure to ethinyl estradiol, but not bisphenol A decreases androgen-dependent reproductive organ weights and epididymal sperm abundance in the male Long Evans Hooded rat. Toxicological Sciences 102(2):371-382. [Abstract]
- Bagamasbad P, Howdeshell KL, Sachs LM, Demeneix BA and Denver RJ. 2007. A role for basic transcription element binding protein 1 (BTEB1) in the autoinduction of thyroid hormone receptor beta. Journal of Biological Chemistry 283(4):2275-85. [Abstract]
- Howdeshell KL, Furr J, Lambright CR, Rider CV, Wilson VS, Gray LE Jr. 2007. Cumulative effects of dibutyl phthalate and diethylhexyl phthalate on male rat reproductive tract development: altered fetal steroid hormones and genes. Toxicological Sciences 99(1):190-202. [Abstract]
- Howdeshell KL, Peterman PH, Judy BM, Taylor JA, Orazio CE, Ruhlen RL, vom Saal FS and Welshons WV. 2003. Bisphenol A is released from used polycarbonate animal cages into water at room temperature. Environmental Health Perspectives 111(9):1180-1187. [Full Text]
- Howdeshell KL. 2002. A model of the development of the brain as a construct of the thyroid system. Environmental Health Perspectives 110 (Suppl 3):337-348. [Full Text]
- Howdeshell KL and vom Saal FS. 2000. Developmental exposure to bisphenol A: Interaction with endogenous estradiol during pregnancy in mice. American Zoologist 40:429-437.
- Howdeshell KL, Hotchkiss AK, Thayer KA, Vandenbergh JG and vom Saal FS. 1999. Exposure to bisphenol A advances puberty. Nature 401:763-763. [Abstract]