Assessments of the effects of tris(1,3-dichloro-2-propyl) phosphate (TDCPP) on human intestinal health from the aspects of intestinal flora changes and cytotoxicity to human cells

• Published in: The Science of the total environment Vol. 894; p. 164823
• Main Authors: Huang, Wantang, Jin, Lizhu, Yin, Hua, Tang, Shaoyu, Yu, Yuanyuan, Yang, Yuanyu
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 10.10.2023
• Subjects: Caco-2 Cells; Cytotoxicity; Flame Retardants - metabolism; Flame Retardants - toxicity; Gastrointestinal Microbiome; Human health; Humans; Intestinal flora; Intestines; Organophosphates - metabolism; Organophosphates - toxicity; Organophosphorus Compounds - toxicity; Organophosphorus flame retardants; Phosphates - toxicity; TDCPP; Cytotoxicity; Human health; Intestinal flora; TDCPP; Organophosphorus flame retardants
• ISSN: 0048-9697; 1879-1026
• DOI: 10.1016/j.scitotenv.2023.164823

Organophosphorus flame retardants (OPFRs) are now drawing the public's attention due to their potential toxicity. Given that contaminated food may result in the ingestion of OPFRs to the human intestine, further investigation is required to determine the potential adverse effects of these compounds on human intestinal health. The present study aimed to comprehensively assess the effect of tris(1,3-dichloro-2-propyl) phosphate (TDCPP), a typical OPFR, on human intestinal health by evaluating both intestinal flora and human cell Caco-2. Based on the results, TDCPP exposure altered the composition of intestinal flora and increased the proportion of pathogenic bacteria. PICRUSt2 analysis revealed that certain pathways were affected by TDCPP, and the resulting metabolic disorders might cause health problems. Orthologous genes of glutathione S-transferase and multidrug efflux system were up-regulated, demonstrating that the bacteria resisted TDCPP to maintain their vitality. Compared to the other two OPFRs, TDCPP induced greater cytotoxicity, and the results were consistent with the dose-effect relationship. Three OPFRs, especially TDCPP, caused the release of lactate dehydrogenase, accumulation of ROS, decline in mitochondrial membrane potential and increase in intracellular Ca2+, which could consequently induce cell death. The simultaneous effects of TDCPP on both intestinal cells and intestinal flora are likely to engender more severe intestinal health issues. [Display omitted] •TDCPP caused dysbiosis of intestinal flora by altering its community structure.•Multiple metabolic pathways of intestinal flora were influenced by TDCPP.•Intestinal flora resisted TDCPP by GST and multidrug efflux system.•TDCPP showed the stronger cytotoxicity to Caco-2 cell than TCEP and TCPP.•ROS accumulation induced by OPFRs was the main reason that attributed to cell death.