Brominated and phosphate flame retardants from interior and surface dust of personal computers: insights into sources for human dermal exposure

Yu, Lehuan; Ru, Shuling; Zheng, Xiaobo; Chen, She-Jun; Guo, Huiying; Gao, Guijuan; Zeng, Yuan; Tang, Yanbin; Mai, Bi-Xian

doi:10.1007/s11356-020-11132-0

Cited by 12 publications

(5 citation statements)

References 41 publications

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“…As expected, DBDPE has entered various organisms including humans 15,18 . Moreover, it was found that DBDPE was one of the most abundant flame retardants in both environmental matrices (dust, groundwater, indoor air) and biological matrices (human milk, human serum, hair) 8,19–23 . With the extensive use of DBDPE, its accumulation in organisms will gradually increase because DBDPE undergoes bioaccumulation 24 .…”

Section: Introductionmentioning

confidence: 79%

“…15,18 Moreover, it was found that DBDPE was one of the most abundant flame retardants in both environmental matrices (dust, groundwater, indoor air) and biological matrices (human milk, human serum, hair). 8,[19][20][21][22][23] With the extensive use of DBDPE, its accumulation in organisms will gradually increase because DBDPE undergoes bioaccumulation. 24 The widespread use and presence of DBDPE in organisms underscore the importance of understanding how it affects reproductive health and whether it affects the health of offspring.…”

Section: Introductionmentioning

confidence: 99%

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Decabromodiphenyl ethane affects embryonic development by interfering with nuclear F‐actin in zygotes and leads to cognitive and social disorders in offspring mice

Shi

Zhang

et al. 2022

The FASEB Journal

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Decabromodiphenyl ethane (DBDPE) is a novel retardant. DBDPE is used in various flammable consumer products such as electronics, building materials, textiles, and children's toys. The presence of DBDPE in humans makes it extremely urgent to assess the health effects of DBDPE exposure. Here, we used female mice as an animal model to investigate the effects of DBDPE on embryonic development and offspring health. The results showed that 50 μg/kg bw/day of DBDPE exposure did not affect spindle rotation in oocytes after fertilization, but led to a decrease of pronuclei (PN) in zygotes. Further investigation found that DBDPE interferes with the self‐assembly of F‐actin in PN, resulting in PN reduction, DNA damage, and reduced expression of zygotic genome activating genes, and finally leading to abnormal embryonic development. More importantly, we found that maternal DBDPE exposure did not affect the growth and development of the first generation of offspring (F1) mice, but resulted in behavioral defects in F1 mice. Female F1 mice from DBDPE‐exposed mothers exhibited increased motor activity and deficits in social behavior. Both female and male F1 mice from DBDPE‐exposed mothers exhibited cognitive memory impairment. These results suggest that DBDPE has developmental toxicity on embryos and has a cross‐generational interference effect. It is suggested that people should pay attention to the reproductive toxicity of DBDPE. In addition, it also provides a reference for studying the origin of neurological diseases and indicates that adult diseases caused by environmental pollutants may have begun in the embryonic stage.

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Section: Introductionmentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Decabromodiphenyl ethane affects embryonic development by interfering with nuclear F‐actin in zygotes and leads to cognitive and social disorders in offspring mice

Shi

Zhang

et al. 2022

The FASEB Journal

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“…Watkins et al (2011) measured PBDEs in handwipes and in office dust and found a weak association, but did not estimate dermal exposure as a result of using the wipes. Yu, Ru, et al (2021) investigated brominated and phosphate flame retardants from interior and surface dust of personal computers as potential sources for human dermal exposure, and found no significant correlation between interior dust and PC surfaces except for BDE-183. Exposure assessment results demonstrated a minor contribution from PC dermal contact, compared with hand-to-mouth uptake, to total exposure, meaning that uptake from inhalation of dust is still considered the largest contributor to non-dietary exposure for most of the population.…”

Section: Non-dietary Sources Of Exposurementioning

confidence: 99%

Update of the risk assessment of polybrominated diphenyl ethers (PBDEs) in food

Schrenk,

Bignami,

Bodin

et al. 2024

EFS2

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The European Commission asked EFSA to update its 2011 risk assessment on polybrominated diphenyl ethers (PBDEs) in food, focusing on 10 congeners: BDE‐28, ‐47, ‐49, ‐99, ‐100, ‐138, ‐153, ‐154, ‐183 and ‑209. The CONTAM Panel concluded that the neurodevelopmental effects on behaviour and reproductive/developmental effects are the critical effects in rodent studies. For four congeners (BDE‐47, ‐99, ‐153, ‐209) the Panel derived Reference Points, i.e. benchmark doses and corresponding lower 95% confidence limits (BMDLs), for endpoint‐specific benchmark responses. Since repeated exposure to PBDEs results in accumulation of these chemicals in the body, the Panel estimated the body burden at the BMDL in rodents, and the chronic intake that would lead to the same body burden in humans. For the remaining six congeners no studies were available to identify Reference Points. The Panel concluded that there is scientific basis for inclusion of all 10 congeners in a common assessment group and performed a combined risk assessment. The Panel concluded that the combined margin of exposure (MOET) approach was the most appropriate risk metric and applied a tiered approach to the risk characterisation. Over 84,000 analytical results for the 10 congeners in food were used to estimate the exposure across dietary surveys and age groups of the European population. The most important contributors to the chronic dietary Lower Bound exposure to PBDEs were meat and meat products and fish and seafood. Taking into account the uncertainties affecting the assessment, the Panel concluded that it is likely that current dietary exposure to PBDEs in the European population raises a health concern.

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“…OPEs and their metabolites are now routinely found in human urine (He et al 2018;Ospina et al 2018;Hou et al 2020), blood (Hou et al 2020;Ma et al 2017b), placental tissue (Ding et al 2016), and breast milk (Chen et al 2021;Ma et al 2019;Hammel et al 2020b) across the globe, with one study documenting high urinary levels in Australian infants and children (He et al 2018). Air, dust, and food are three known pathways of exposure (Xu et al 2016;Yu et al 2021). The semivolatile properties of OPEs ensure their widespread distribution from sources to surfaces and materials indoors with which we come into contact, including dust and clothing, which would allow for dermal uptake (Saini et al 2016;Yang et al 2019b;Yu et al 2021).…”

Section: Uses and Exposurementioning

confidence: 99%

“…Air, dust, and food are three known pathways of exposure (Xu et al 2016;Yu et al 2021). The semivolatile properties of OPEs ensure their widespread distribution from sources to surfaces and materials indoors with which we come into contact, including dust and clothing, which would allow for dermal uptake (Saini et al 2016;Yang et al 2019b;Yu et al 2021). Household dust is an important exposure pathway (Stapleton et al 2009;Hoffman et al 2015a;Larsson, et al 2018;Khairy and Lohmann 2019;Yang et al 2019b;Xu et al 2016), particularly for children, who have higher concentrations than adults owing to hand-to-mouth contact and high levels of OPEs in baby products (Butt et al 2014(Butt et al , 2016Hoffman et al 2015b;Gibson et al 2019).…”

Section: Uses and Exposurementioning

confidence: 99%

Beyond Cholinesterase Inhibition: Developmental Neurotoxicity of Organophosphate Ester Flame Retardants and Plasticizers

Patisaul

Behl

Birnbaum

et al. 2021

Environ Health Perspect

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Background: To date, the toxicity of organophosphate esters has primarily been studied regarding their use as pesticides and their effects on the neurotransmitter acetylcholinesterase (AChE). Currently, flame retardants and plasticizers are the two largest market segments for organophosphate esters and they are found in a wide variety of products, including electronics, building materials, vehicles, furniture, car seats, plastics, and textiles. As a result, organophosphate esters and their metabolites are routinely found in human urine, blood, placental tissue, and breast milk across the globe. It has been asserted that their neurological effects are minimal given that they do not act on AChE in precisely the same way as organophosphate ester pesticides. Objectives: This commentary describes research on the non-AChE neurodevelopmental toxicity of organophosphate esters used as flame retardants and plasticizers (OPEs). Studies in humans, mammalian, nonmammalian, and in vitro models are presented, and relevant neurodevelopmental pathways, including adverse outcome pathways, are described. By highlighting this scientific evidence, we hope to elevate the level of concern for widespread human exposure to these OPEs and to provide recommendations for how to better protect public health. Discussion: Collectively, the findings presented demonstrate that OPEs can alter neurodevelopmental processes by interfering with noncholinergic pathways at environmentally relevant doses. Application of a pathways framework indicates several specific mechanisms of action, including perturbation of glutamate and gamma-aminobutyric acid and disruption of the endocrine system. The effects may have implications for the development of cognitive and social skills in children. Our conclusion is that concern is warranted for the developmental neurotoxicity of OPE exposure. We thus describe important considerations for reducing harm and to provide recommendations for government and industry decision makers. https://doi.org/10.1289/EHP9285

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Brominated and phosphate flame retardants from interior and surface dust of personal computers: insights into sources for human dermal exposure

Cited by 12 publications

References 41 publications

Decabromodiphenyl ethane affects embryonic development by interfering with nuclear F‐actin in zygotes and leads to cognitive and social disorders in offspring mice

Decabromodiphenyl ethane affects embryonic development by interfering with nuclear F‐actin in zygotes and leads to cognitive and social disorders in offspring mice

Update of the risk assessment of polybrominated diphenyl ethers (PBDEs) in food

Beyond Cholinesterase Inhibition: Developmental Neurotoxicity of Organophosphate Ester Flame Retardants and Plasticizers

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