ArticleToxicological sciences : an official journal of the Society of Toxicology2010
Altered cardiac function and ventricular septal defect in avian embryos exposed to low-dose trichloroethylene.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 44 citations in OpenAlex.
- The Chorioallantoic Membrane Assay in Nanotoxicological Research-An Alternative forNanomaterials (Basel, Switzerland) · 2020Review
- HNF4a transcription is a target of trichloroethylene toxicity in the embryonic mouse heart.Environmental science. Processes & impacts · 2020Article
- Placenta as a target of trichloroethylene toxicity.Environmental science. Processes & impacts · 2020Article
- Protecting Children from Toxic Waste: Data-Usability Evaluation Can Deter Flawed Cleanup.International journal of environmental research and public health · 2020Article
- Trichloroethylene perturbs HNF4a expression and activity in the developing chick heart.Toxicology letters · 2018Article
- Trichloroethylene metabolite S-(1,2-dichlorovinyl)-l-cysteine induces lipid peroxidation-associated apoptosis via the intrinsic and extrinsic apoptosis pathways in a first-trimester placental cell line.Toxicology and applied pharmacology · 2018Article
- Target Organ Metabolism, Toxicity, and Mechanisms of Trichloroethylene and Perchloroethylene: Key Similarities, Differences, and Data Gaps.The Journal of pharmacology and experimental therapeutics · 2016Review
- A systematic evaluation of the potential effects of trichloroethylene exposure on cardiac development.Reproductive toxicology (Elmsford, N.Y.) · 2016Review
- Birth defects in infants born to employees of a microelectronics and business machine manufacturing facility.Birth defects research. Part A, Clinical and molecular teratology · 2016Article
- Air toxics and birth defects: a Bayesian hierarchical approach to evaluate multiple pollutants and spina bifida.Environmental health : a global access science source · 2015Article
- Lipophilic chemical exposure as a cause of cardiovascular disease.Interdisciplinary toxicology · 2013Review
- Human health effects of trichloroethylene: key findings and scientific issues.Environmental health perspectives · 2013Review
- Low-dose trichloroethylene alters cytochrome P450-2C subfamily expression in the developing chick heart.Cardiovascular toxicology · 2013Article
- Avian models in teratology and developmental toxicology.Methods in molecular biology (Clifton, N.J.) · 2012Review
- Role of Risk of Bias in Systematic Review for Chemical Risk Assessment: A Case Study in Understanding the Relationship Between Congenital Heart Defects and Exposures to Trichloroethylene.International journal of toxicologyArticle
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Trichloroethylene (TCE) is the most frequently reported organic groundwater contaminant in the United States. It is controversial whether gestational TCE exposure causes congenital heart defects. The basis for TCE's proposed cardiac teratogenicity is not well understood. We previously showed that chick embryos exposed to 8 ppb TCE during cardiac morphogenesis have reduced cardiac output and increased mortality. To further investigate TCE's cardioteratogenic potential, we exposed in ovo chick embryos to TCE and evaluated the heart thereafter. Significant mortality was observed following TCE exposures of 8-400 ppb during a narrow developmental period (Hamburger-Hamilton [HH] stages 15-20, embryo day ED2.3-3.5) that is characterized by myocardial expansion, secondary heart looping, and endocardial cushion formation. Of the embryos that died, most did so between ED5.5 and ED6.5. Echocardiography of embryos at ED5.5 found that TCE-exposed hearts displayed significant functional and morphological heterogeneity affecting heart rate, left ventricular mass, and wall thickness. Individual embryos were identified with cardiac hypertrophy as well as with hypoplasia. Chick embryos exposed to 8 ppb TCE at HH17 that survived to hatch exhibited a high incidence (38%, p < 0.01, n = 16) of muscular ventricular septal defects (VSDs) as detected by echocardiography and confirmed by gross dissection; no VSDs were found in controls (n = 14). The TCE-induced VSDs may be secondary to functional impairments that alter cardiac hemodynamics and subsequent ventricular foramen closure, an interpretation consistent with recent demonstrations that TCE impairs calcium handling in cardiomyocytes. These data demonstrate that TCE is a cardiac teratogen for chick.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.