ArticleEnvironmental pollution (Barking, Essex : 1987)2024
A physiologically based pharmacokinetic model of diethyl phthalates in humans.
Article in Environmental pollution (Barking, Essex : 1987), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Potential association between endocrine disrupting chemicals (EDCs) and gynecomastia: a systematic review based on partial experimental evidenceendocrine-disrupting chemicals.Frontiers in endocrinology · 2026Pooled it
- High-concentration MEHP triggers mtDNA depletion in undifferentiated HepaRG and C2C12 cultures and disrupts mitochondrial homeostasis in both HepaRG culture states.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Unraveling diethyl phthalate-induced prostate carcinogenesis: core targets revealed by integrated network toxicology, machine learning, and structural validation.Human genomics · 2025Article
- Diethyl phthalate and dibutyl phthalate disrupt sirtuins expression in the HepG2 cells.Toxicology research · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Phthalates are a family of industrial and consumer product chemicals, among which diethyl phthalate (DEP) has been widely used. DEP is metabolized into the active metabolite monoethyl phthalate (MEP) and exposure to DEP may induce male reproductive toxicity, developmental toxicity and hepatotoxicity. To better assess the toxicity of DEP and MEP, it is important to understand and predict their internal concentrations, especially in reproductive organs. Here we present a human physiologically based pharmacokinetic (PBPK) model of DEP. Implemented in R, the PBPK model consists of seven tissue compartments, including blood, gut, liver, fat, skin, gonad, and rest of body (RB). In the blood both DEP and MEP partition into free and bound forms, and tissue distribution is considered as blood flow-limited. DEP is metabolized in the gut and liver into MEP which is further glucuronidated and cleared through the urine. The chemical-specific parameters of the model were predicted in silico or estimated based on published human urinary MEP data after exposure to DEP in the air at 250 or 300 μg/m
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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.