Short-term effects of a perinatal exposure to the HBCDD α-isomer in rats: Assessment of early motor and sensory development, spontaneous locomotor activity and anxiety in pups

Maurice, Nicolas; Olry, Jean-Charles; Cariou, Ronan; Bizec, Bruno Le; Travel, Angélique; Jondreville, Catherine; Schroeder, Henri

doi:10.1016/j.ntt.2015.08.005

Cited by 23 publications

(27 citation statements)

References 68 publications

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“…Most of the new studies published since the previous EFSA assessment were based on repeated exposures to HBCDDs performed by exposing dams or neonatal rodents at different developmental stages, i.e. GD0‐PND21 (Maurice et al., 2015), GD1‐PND0 (Miller‐Rhodes et al., 2014) and PND10‐PND70 (Zhang et al., 2017a), followed by behavioural analyses of the offspring at different ages. One study exposed adult animals for 6 weeks (Pham‐Lake et al., 2017) (see Table 10 ).…”

Section: Assessmentmentioning

confidence: 99%

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Update of the risk assessment of hexabromocyclododecanes (HBCDDs) in food

Schrenk

Bignami

Bodin³

et al. 2021

EFS2

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The European Commission asked EFSA to update its 2011 risk assessment on hexabromocyclododecanes ( HBCDD s) in food. HBCDD s, predominantly mixtures of the stereoisomers α‐, β‐ and γ‐ HBCDD , were widely used additive flame retardants. Concern has been raised because of the occurrence of HBCDD s in the environment, food and in humans. Main targets for toxicity are neurodevelopment, the liver, thyroid hormone homeostasis and the reproductive and immune systems. The CONTAM Panel concluded that the neurodevelopmental effects on behaviour in mice can be considered the critical effects. Based on effects on spontaneous behaviour in mice, the Panel identified a lowest observed adverse effect level ( LOAEL ) of 0.9 mg/kg body weight (bw) as the Reference Point, corresponding to a body burden of 0.75 mg/kg bw. The chronic intake that would lead to the same body burden in humans was calculated to be 2.35 μg/kg bw per day. The derivation of a health‐based guidance value ( HBGV ) was not considered appropriate. Instead, the margin of exposure ( MOE ) approach was applied to assess possible health concerns. Over 6,000 analytical results for HBCDD s 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 LB exposure to HBCDD s were fish meat, eggs, livestock meat and poultry. The CONTAM Panel concluded that the resulting MOE values support the conclusion that current dietary exposure to HBCDD s across European countries does not raise a health concern. An exception is breastfed infants with high milk consumption, for which the lowest MOE values may raise a health concern.

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Section: Assessmentmentioning

confidence: 99%

“…Maurice et al. (2015) found impaired motor activity and reduced anxiety, associated with decreased pup weight, at 22 ng/kg bw per day in offspring of female rats dosed with hens’ egg contaminated with α‐HBCDD by gavage from GD0 to PND21. No effects were reported at a three‐fold higher dose of 66 ng/kg bw per day.…”

Section: Assessmentmentioning

confidence: 99%

Update of the risk assessment of hexabromocyclododecanes (HBCDDs) in food

Schrenk

Bignami

Bodin³

et al. 2021

EFS2

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“…Furthermore, early life adversity, such as psychosocial stress, infections or exposure to pollutants, has shown to play a major role in the development of certain disease phenotypes, and DNA methylation is believed to be the link between these events ( Murphy et al, 2015 ; Mitchell et al, 2016 ; Duca et al, 2018 ; Elwenspoek et al, 2019 ; Vonderwalde, 2019 ). Exposures of rodents to Persistent Organic Pollutants (POPs) through the diet of the dams, such as Brominated flame retardants [e.g., HexaBromoCycloDoDecane (HBCDD) or Polycyclic aromatic Hydrocarbons (PAHs)], during development was shown to induce significant behavioral changes (increased anxious-like behavior, hyperactivity, and altered social behavior) in their offspring ( Crepeaux et al, 2014 ; Maurice et al, 2015 ). These results underline the existence of a critical window of exposure for brain and behavior development and suggest that epigenetic modifications could be involved in these behavioral impairments ( Ibhazehiebo et al, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

N6-Methyladenine in Eukaryotic DNA: Tissue Distribution, Early Embryo Development, and Neuronal Toxicity

et al. 2021

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DNA methylation is one of the most important epigenetic modifications and is closely related with several biological processes such as regulation of gene transcription and the development of non-malignant diseases. The prevailing dogma states that DNA methylation in eukaryotes occurs essentially through 5-methylcytosine (5mC) but recently adenine methylation was also found to be present in eukaryotes. In mouse embryonic stem cells, 6-methyladenine (6mA) was associated with the repression and silencing of genes, particularly in the X-chromosome, known to play an important role in cell fate determination. Here, we have demonstrated that 6mA is a ubiquitous eukaryotic epigenetic modification that is put in place during epigenetically sensitive periods such as embryogenesis and fetal development. In somatic cells there are clear tissue specificity in 6mA levels, with the highest 6mA levels being observed in the brain. In zebrafish, during the first 120 h of embryo development, from a single pluripotent cell to an almost fully formed individual, 6mA levels steadily increase. An identical pattern was observed over embryonic days 7–21 in the mouse. Furthermore, exposure to a neurotoxic environmental pollutant during the same early life period may led to a decrease in the levels of this modification in female rats. The identification of the periods during which 6mA epigenetic marks are put in place increases our understanding of this mammalian epigenetic modification, and raises the possibility that it may be associated with developmental processes.

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“…7 Ultimately the higher water solubility (49 µg/L), bioavailability and resistance to biological and thermal reactions renders the α-isomer more persistent in the environment and more bioaccumulative in biota, including humans. [8][9][10] Recent studies have shown HBCDD concentrations in humans can be as high as 36 ng/g lipid weight. 11 This is of concern because the toxicity of HBCDD is indiscriminate to both aquatic and terrestrial organism, with adverse impacts on the liver, thyroid gland, increased genetic recombination and neurotoxic effects being recorded as a result of exposure.…”

Section: Introductionmentioning

confidence: 99%