Associations of Prenatal Urinary Bisphenol A Concentrations with Child Cognition and Behavior

2016 ◽  
Vol 2016 (1) ◽  
Author(s):  
Joseph Braun* ◽  
Bruce Lanphear ◽  
Tye Arbuckle ◽  
William Fraser ◽  
Youssef Oulhote ◽  
...  
2011 ◽  
Vol 59 (3) ◽  
pp. 296-305 ◽  
Author(s):  
Jennifer T. Wolstenholme ◽  
Emilie F. Rissman ◽  
Jessica J. Connelly
Keyword(s):  

2019 ◽  
Vol 209 ◽  
pp. 112614
Author(s):  
Justin Dillard ◽  
Amanda Wilson Carter ◽  
Geoff D. Ower ◽  
Ryan T. Paitz ◽  
Rachel M. Bowden

1998 ◽  
Vol 14 (1-2) ◽  
pp. 239-260 ◽  
Author(s):  
Frederick S. Vom Saal ◽  
Paul S. Cooke ◽  
David L. Buchanan ◽  
Paola Palanza ◽  
Kristina A. Thayer ◽  
...  

Two chemicals previously shown to have estrogenic activity, bisphenol A and octylphenol, were examined for their effects on accessory reproductive organs and daily sperm production in male offspring of mice fed these chemicals during pregnancy. These chemicals are used in the manufacture of plastics and other products, and have been detected in food and water consumed by animals and people. From gestation day 11-17 female mice were fed an average concentration (dissolved in oil) of bisphenol A or octylphenol of 2 ng/g body weight (2 ppb) and 20 ng/g (20 ppb). The 2 ppb dose of bisphenol A is lower than the amount reported to be swallowed during the first hour after application of a plastic dental sealant (up to 931 μg; 13.3 ppb in a 70 kg adult). We found that the 2 ng/g dose of bisphenol A permanently increased the size of the preputial glands, but reduced the size of the epididymides; these organs develop from different embryonic tissues. At 20 ng/g, bisphenol A significantly decreased efficiency of sperm production (daily sperm production per g testis) by 20% relative to control males. The only significant effect of octylphenol was a reduction in daily sperm production and efficiency of sperm production at the 2 ng/g dose. A new approach to studying physiologically relevant doses of environmental endocrine disruptors is discussed, particularly with regard to the development of the reproductive organs, the brain, and behavior.


PEDIATRICS ◽  
2010 ◽  
Vol 127 (1) ◽  
pp. e202-e211 ◽  
Author(s):  
M.-J. Brion ◽  
M. Zeegers ◽  
V. Jaddoe ◽  
F. Verhulst ◽  
H. Tiemeier ◽  
...  
Keyword(s):  

2013 ◽  
Vol 126 ◽  
pp. 43-50 ◽  
Author(s):  
Kim G. Harley ◽  
Robert B. Gunier ◽  
Katherine Kogut ◽  
Caroline Johnson ◽  
Asa Bradman ◽  
...  

Endocrinology ◽  
2012 ◽  
Vol 153 (8) ◽  
pp. 3828-3838 ◽  
Author(s):  
Jennifer T. Wolstenholme ◽  
Michelle Edwards ◽  
Savera R. J. Shetty ◽  
Jessica D. Gatewood ◽  
Julia A. Taylor ◽  
...  

Bisphenol A (BPA) is a plasticizer and an endocrine-disrupting chemical. It is present in a variety of products used daily including food containers, paper, and dental sealants and is now widely detected in human urine and blood. Exposure to BPA during development may affect brain organization and behavior, perhaps as a consequence of its actions as a steroid hormone agonist/antagonist and/or an epigenetic modifier. Here we show that BPA produces transgenerational alterations in genes and behavior. Female mice received phytoestrogen-free chow with or without BPA before mating and throughout gestation. Plasma levels of BPA in supplemented dams were in a range similar to those measured in humans. Juveniles in the first generation exposed to BPA in utero displayed fewer social interactions as compared with control mice, whereas in later generations (F2 and F4), the effect of BPA was to increase these social interactions. Brains from embryos (embryonic d 18.5) exposed to BPA had lower gene transcript levels for several estrogen receptors, oxytocin, and vasopressin as compared with controls; decreased vasopressin mRNA persisted into the F4 generation, at which time oxytocin was also reduced but only in males. Thus, exposure to a low dose of BPA, only during gestation, has immediate and long-lasting, transgenerational effects on mRNA in brain and social behaviors. Heritable effects of an endocrine-disrupting chemical have implications for complex neurological diseases and highlight the importance of considering gene-environment interactions in the etiology of complex disease.


2016 ◽  
Vol 53 ◽  
pp. 12-19 ◽  
Author(s):  
R. Perez-Lobato ◽  
V. Mustieles ◽  
I. Calvente ◽  
I. Jimenez-Diaz ◽  
R. Ramos ◽  
...  

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