ReviewReproductive toxicology (Elmsford, N.Y.)2016
A systematic evaluation of the potential effects of trichloroethylene exposure on cardiac development.
Review in Reproductive toxicology (Elmsford, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 36 citations in OpenAlex.
- A case-control study of early-life residential exposure to tetrachloroethylene and risks of childhood cancer and birth defects.Environment international · 2025Article
- Gremlin1 repression-mediated mitochondrial network hyperfunction contributes to TCE-induced zebrafish cardiac defects.Cell communication and signaling : CCS · 2025Article
- Trichloroethylene: An Update on an Environmental Contaminant with Multiple Health Effects.Annual review of pharmacology and toxicology · 2025Review
- The trichloroethylene metabolite S-(1,2-dichlorovinyl)-l-cysteine inhibits lipopolysaccharide-induced inflammation transcriptomic pathways and cytokine secretion in a macrophage cell model.Toxicology in vitro : an international journal published in association with BIBRA · 2022Article
- Charting a Path Forward: Assessing the Science of Chemical Risk Evaluations under the Toxic Substances Control Act in the Context of Recent National Academies Recommendations.Environmental health perspectives · 2022Article
- The effects of temperature and relative humidity on trichloroethylene sorption capacities of building materials under conditions relevant to vapor intrusion.Journal of hazardous materials · 2021Article
- HNF4a transcription is a target of trichloroethylene toxicity in the embryonic mouse heart.Environmental science. Processes & impacts · 2020Article
- Complex epigenetic patterns in cerebellum generated after developmental exposure to trichloroethylene and/or high fat diet in autoimmune-prone mice.Environmental science. Processes & impacts · 2020Article
- Review
- Trichloroethylene in drinking water throughout gestation did not produce congenital heart defects in Sprague Dawley rats.Birth defects research · 2019Article
- Trichloroethylene perturbs HNF4a expression and activity in the developing chick heart.Toxicology letters · 2018Article
- Application of Adverse Outcome Pathways to U.S. EPA's Endocrine Disruptor Screening Program.Environmental health perspectives · 2017Review
- 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
13 authors at 3 institutions in 1 country.
Funding
Abstract
The 2011 EPA trichloroethylene (TCE) IRIS assessment, used developmental cardiac defects from a controversial drinking water study in rats (Johnson et al. [51]), along with several other studies/endpoints to derive reference values. An updated literature search of TCE-related developmental cardiac defects was conducted. Study quality, strengths, and limitations were assessed. A putative adverse outcome pathway (AOP) construct was developed to explore key events for the most commonly observed cardiac dysmorphologies, particularly those involved with epithelial-mesenchymal transition (EMT) of endothelial origin (EndMT); several candidate pathways were identified. A hypothesis-driven weight-of-evidence analysis of epidemiological, toxicological, in vitro, in ovo, and mechanistic/AOP data concluded that TCE has the potential to cause cardiac defects in humans when exposure occurs at sufficient doses during a sensitive window of fetal development. The study by Johnson et al. [51] was reaffirmed as suitable for hazard characterization and reference value derivation, though acknowledging study limitations and uncertainties.
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What OpenQuestion holds
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.