New Insights in the Endocrine Disrupting Effects of Three Primary Metabolites of Organophosphate Flame Retardants

Zhang, Quan; Chang, Yu; Fu, Lili; Gu, Sijia; Wang, Cui

doi:10.1021/acs.est.9b07874

Cited by 85 publications

(45 citation statements)

References 54 publications

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“…The level of OPEs was significantly associated with treatment capacity, processing volume, and the population served of sewage treatment plants [57]. Sludge samples from municipal and industrial STPs contain high levels of nonchlorinated OPEs [58]. For instance, the sludge from STPs in Beijing was contaminated by Tri(2-ethylhexyl) phosphate) (TEHP) and Tricresyl phosphate (TCrP), with an average concentration of 233 and 137 ng/g, respectively, which was attributed to their strong absorption tendency and the use pattern of different OPE [56].…”

Section: Water and Sedimentmentioning

confidence: 99%

Organophosphate Esters in China: Fate, Occurrence, and Human Exposure

Zhi-hui

Yin

Wen

et al. 2021

Toxics

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Organophosphate esters (OPEs) are widely used as flame retardants and plasticizers. OPEs have been released into various environments (e.g., water, sediments, dust and air, and soil). To investigate the occurrence and distribution of OPEs in various environments in China, this review collects and discusses the published scientific studies in this field. Chlorinated OPEs, as flame retardants, are the predominant OPEs found in the environment. The analysis of data revealed large concentration variations among microenvironments, including inflowing river water (range: 0.69–10.62 µgL−1), sediments (range: 0.0197–0.234 µg/g), dust (range: 8.706–34.872 µg/g), and open recycling sites’ soil (range: 0.122–2.1 µg/g). Moreover, OPEs can be detected in the air and biota. We highlight the overall view regarding environmental levels of OPEs in different matrices as a starting point to monitor trends for China. The levels of OPEs in the water, sediment, dust, and air of China are still low. However, dust samples from electronic waste workshop sites were more contaminated. Human activities, pesticides, electronics, furniture, paint, plastics and textiles, and wastewater plants are the dominant sources of OPEs. Human exposure routes to OPEs mainly include dermal contact, dust ingestion, inhalation, and dietary intake. The low level of ecological risk and risk to human health indicated a limited threat from OPEs. Furthermore, current challenges and perspectives for future studies are prospected. A criteria inventory of OPEs reflecting the levels of OPEs contamination association among different microenvironments, emerging OPEs, and potential impact of OPEs on human health, particularly for children are needed in China for better investigation.

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Section: Water and Sedimentmentioning

confidence: 99%

Organophosphate Esters in China: Fate, Occurrence, and Human Exposure

Zhi-hui

Yin

Wen

et al. 2021

Toxics

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“…11 Significantly greater mortality of embryos and lesser rates of hatching were observed in zebrafish after exposure to 10 μM (2.5 mg/L) DPhP from 4 to 96 hpf. 20 Recently, cardiotoxicity after acute exposure to high concentrations of DPhP (250 mg/L) have been observed, resulting in significantly greater distance between the sinus venosus and bulbus arteriosis (SV-BA) in zebrafish embryos. 21 However, exposure to DPhP less than 30 μM (7.5 mg/L) did not induce circulatory failure in zebrafish embryos.…”

Section: Resultsmentioning

confidence: 99%

“…21 Exposure to DPhP increased mortality of zebrafish larvae but only at a concentration greater than 10 −6 M (250 μg/L). 20 Currently, potential adverse effects of chronic exposure to DPhP at environmentally relevant concentrations is poorly characterized.…”

Section: Introductionmentioning

confidence: 99%

“…DPhP caused no significant effects to chicken embryonic hepatocytes at concentrations up to 1000 μM (250 mg/L) but altered more transcripts than its precursor TPhP . In addition, exposure to DPhP could result in developmental toxicity, endocrine disruption, and cardiotoxicity. ,− Recently, it was reported that chronic exposure to 10 mg/L DPhP through drinking water significantly disrupted the fatty acid catabolic processes and reduced the body mass in mice . To date, most of the studies on toxicity of DPhP have only focused on acute toxicity/short-term effects upon exposure to DPhP at concentrations that are far greater than those found in environmental matrices, which are generally at in the range of μg/L. ,, For example, DPhP-caused cardiac defects in zebrafish embryo were only observed at concentrations greater than 500 μM (125 mg/L) .…”

Section: Introductionmentioning

confidence: 99%

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Life Cycle Exposure to Environmentally Relevant Concentrations of Diphenyl Phosphate (DPhP) Inhibits Growth and Energy Metabolism of Zebrafish in a Sex-Specific Manner

Chen

Lian

et al. 2021

Environ. Sci. Technol.

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Due to commercial uses and environmental degradation of aryl phosphate esters, diphenyl phosphate (DPhP) is frequently detected in environmental matrices and is thus of growing concern worldwide. However, information on potential adverse effects of chronic exposure to DPhP at environmentally realistic concentrations was lacking. Here, we investigated the effects of life cycle exposure to DPhP on zebrafish at environmentally relevant concentrations of 0.8, 3.9, or 35.6 μg/L and employed a dual-omics approach (metabolomics and transcriptomics) to characterize potential modes of action. Exposure to DPhP at 35.6 μg/L for 120 days resulted in significant reductions in body mass and length of male zebrafish, but did not cause those same effects to females. Predominant toxicological mechanisms, including inhibition of oxidative phosphorylation, down-regulation of fatty acid oxidation, and up-regulation of phosphatidylcholine degradation, were revealed by integrated dual-omics analysis and successfully linked to adverse outcomes. Activity of succinate dehydrogenase and protein content of carnitine O-palmitoyltransferase 1 were significantly decreased in livers of male fish exposed to DPhP, which further confirmed the proposed toxicological mechanisms. This study is the first to demonstrate that chronic, low-level exposure to DPhP can retard growth via inhibiting energy output in male zebrafish.

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“…OPFRs added to materials are not chemically linked, making it easy for them to leach into the environment, increasing their presence in various environmental systems . OPFRs have been detected in air, soil, dust, sewage, surface waters, ground waters, drinking waters, and biota. − …”

Section: Introductionmentioning

confidence: 99%

Dose-Dependent Molecular Responses of Labeo rohita to Triphenyl Phosphate

Umamaheswari

Karthika

Suvenitha

et al. 2021

Chem. Res. Toxicol.

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Triphenyl phosphate (TPhP) is a broad-spectrum organophosphate compound widely used as an additive in several products to prevent ignition. However, its utilization produces a hazardous impact on various organisms. So far, very few studies have investigated the acute toxicity of TPhP at environmentally relevant concentrations in nontarget aquatic species. This study aimed to assess whether the short-term exposure of TPhP (4, 20, and 100 μg L −1 ) affects the oxidative stress, antioxidant activity, biomolecule metabolism, DNA stability, chromosomal integrity, apoptosis, and pathological changes in various organs of Labeo rohita fingerlings. The results illustrated that the reactive oxygen species (ROS) production and lipid peroxidation (LPO) rates were significantly higher in tissues (brain, liver, and kidney) of TPhP-treated groups. Interestingly, superoxide dismutase (SOD) and catalase (CAT) activities were remarkably decreased in tissues following TPhP exposure. The levels of protein, glucose, total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) in various tissues were also found to be significantly altered in TPhPexposed fish fingerlings. These significant alterations in the antioxidant system and biochemical profile induced genotoxic responses such as DNA and chromosomal damage in the fish fingerlings. Furthermore, the incidence of the observed genotoxic responses was also found to be dose-dependent. Likewise, the apoptotic responses were also significantly altered following TPhP acute exposure in L. rohita fingerlings. The subsequent effects on oxidative stress, antioxidant inhibition, dysregulated biomolecule metabolism, and genotoxicity might be the possible reason for the observed pathological changes in various tissues of L. rohita. Taken together, the present findings showed that the toxicity of TPhP is principally associated with exposure concentrations. Therefore, this study illustrates the toxicity risks of TPhP to vertebrate organisms at real-world concentrations.

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New Insights in the Endocrine Disrupting Effects of Three Primary Metabolites of Organophosphate Flame Retardants

Cited by 85 publications

References 54 publications

Organophosphate Esters in China: Fate, Occurrence, and Human Exposure

Organophosphate Esters in China: Fate, Occurrence, and Human Exposure

Life Cycle Exposure to Environmentally Relevant Concentrations of Diphenyl Phosphate (DPhP) Inhibits Growth and Energy Metabolism of Zebrafish in a Sex-Specific Manner

Dose-Dependent Molecular Responses of Labeo rohita to Triphenyl Phosphate

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