A systematic evaluation of the potential effects of trichloroethylene exposure on cardiac development
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- 作者：Susan L. Makrisa ; makris.susan@epa.gov" class="auth_mail" title="E-mail the corresponding author ; Cheryl Siegel Scotta ; John Foxa ; Thomas B. Knudsend ; Andrew K. Hotchkissb ; Xabier Arzuagaa ; Susan Y. Eulinga ; Christina M. Powerse ; 1 ; Jennifer Jinota ; Karen A. Hogana ; Barbara D. Abbottc ; E. Sidney Hunter IIIc ; Michael G. Narotskyc
- 关键词：AOP ; adverse outcome pathway ; BMD ; benchmark dose ; BMDS ; Benchmark Dose Software ; BMDL ; 95% lower confidence limit on the benchmark dose ; BMR ; benchmark response ; CHD ; congenital heart defects ; CI ; confidence interval ; DCA ; dichloroacetic acid ; IRIS ; Integrated Risk Information System ; EPA ; U.S. Environmental Protection Agency ; MGI ; Mouse Genome Informatics ; NTP ; National Toxicology Program ; POD ; point of departure ; TCA ; trichloroacetic acid ; TCE ; trichloroethylene ; WOE ; weight of evidence (evid
- 刊名：Reproductive Toxicology
- 出版年：2016
- 出版时间：October 2016
- 年：2016
- 卷：65
- 期：Complete
- 页码：321-358
- 全文大小：1559 K
文摘
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The evaluation of developmental cardiac defects was updated for trichloroethylene.
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Evidence integration suggests prenatal TCE exposures can cause human cardiac defects.
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EndMT disruption is likely a potential key event in TCE-induced valvulo-septal defects.
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Johnson et al. [51] remains a valid choice for hazard/dose-response assessment.