Polybrominated biphenyls can be absorbed through oral, inhalation, and dermal routes. Once in the body they distribute throughout and bioaccumulate in the blood, breast milk, and adipose tissue. The extent of PBDE metabolism depends on the degree of bromination. Metabolism is believed to involve debromination and methylation, resulting in phenolic metabolites. Metabolized and unmetabolized PDBE compounds are excreted mainly in the faeces. (L628, L881)
Animal data show an absorption of Octabromodiphenyl ether (OBDPE) by oral or inhalation route with an accumulation of the parent compound or its metabolites in the liver and also in the adipose tissue and the lung following inhalation administration. The extent of absorption and elimination cannot be assessed from the data available. No information on the metabolism of OBDPE is available. Following oral administration, OBDPE is an inducer of xenobiotic metabolism. There are no measured data on OBDPE dermal absorption. However based on OBDPE physicochemical properties and analogy with PCBs, a dermal absorption of 4.5% may be estimated. Evidence from humans indicates that OBDPE, HxBDPE, HpBDPE and NonaBDPE which are components of commercial OBDPE can be absorbed into the body and distributed into the blood. Distribution to the adipose tissue was evidenced at least for OBDPE and HxBDPE. There are no data available on the rate of elimination or on bioaccumulation of OBDPE from human adipose tissue neither for PeBDPO but given the high lipophilicity of these compounds and the adipose tissue accumulation observed in rats following oral or inhalation routes, it can be assumed that in humans OBDPE might bioaccumulate in these tissues as well. Following pregnancy HxBDPE and others PBDPEs such as TeBDPE and PeBDPEs are excreted in the breast milk. Unfortunately, such measurements were not carried out on OBDPE. However, based on the high lipophilicity of OBDPE, its potential to bioaccumulate in adipose tissues and the breast milk measured data with HxBDPE (one component of commercial OBDPE), excretion of OBDPE in the breast milk may be anticipated OBDPE has a low acute toxicity in animals. Acute oral toxicity data indicate a rat LD50 greater than 28,000 mg/kg. No deaths, no weight changes or necropsy lesions were reported up to 5,000 mg/kg. At 10,000 mg/kg and 28,000 mg/kg, no deaths were observed but no more information on these studies are available. A dermal LD50 greater than 2,000 mg/kg has been demonstrated in rabbits using DBDPE applied neat under occlusive wraps for 24 hours. No deaths were observed up to 2,000 mg/kg. Local and general signs of toxicity were not reported and necropsies were not performed in this dermal toxicity study. An inhalation LC50 greater than 60 mg/l has been demonstrated in rats exposed with OBDPE during one hour. No deaths and no clinical signs of toxicity were observed up to 60 mg/l. OBDPE is not a dermal or an ocular irritant. There is no indication of skin sensitization in animals. The only information concerning the effects of repeated oral and inhalation exposure to OBDPE comes from studies in rats involving administration of commercial OBDPE. These studies consistently indicate that the liver is the key target organ within 4 and 13 weeks of repeated oral dosing and within 14 days and 90 days of inhalation exposure. The changes in thyroid status are apparent within 4 and 13 weeks of repeated oral dosing from 1,000 ppm and within 13 weeks of repeated inhalation dosing from 16 mg/m3 (analytical concentration). The LOAEL is considered to be 100 ppm . 7.2 mg/kg/day in the 90 day dietary study based on the liver changes (increase of liver weight and granular cytoplasmic changes) observed from 100 ppm . 7.2 mg/kg/day. The NOAEC for systemic toxicity is considered to be 1.1 mg/cu m in the 90 day rat study by inhalation route based on the liver and thyroid status changes observed at the concentration just above: 16 mg/cu m . Alterations in thyroid homeostasis were reported with organochlorine compounds for many species, including humans and a thyroid hormone like affinity for the serum transport protein transthyretin was shown for hydroxylated PCBs as well as for PBDPE congeners such as DiBDPE and TeBDPE. To our knowledge, no studies on transthyretin-T4 competition have been carried out on OBDPE neither on DBDPE. Following inhalation exposure, local toxicity was demonstrated with hyperplasia/hypertrophy of the goblet cells within 2 weeks of exposure and with chronic active lung inflammation and alveolar histiocytosis within 13 weeks of exposure. It is obvious that the observed effect at 1.1 mg/cu m is minimal and reveals only a trend to a chronic inflammation however this value has been taken to set up the LOAEC for local toxicity. Regarding mutagenicity no in vivo data are available. However based on the available in vitro data, OBDPE is considered as non-genotoxic in vitro and no concern for mutagenicity is assumed. No chronic or carcinogenicity studies in animals are available. No specific fertility study is available. A recent rat inhalation sub-chronic study, well conducted and specifically designed to investigate reproductive organs, did not demonstrate adverse effects on male reproductive organs. Therefore no concern is assumed for male fertility. Regarding female reproductive organs, absence of corpora lutea was shown in this study in 3/10 females at 202 mg/m3 versus 0/10 in the control group. Since the absence of corpora lutea is considered to be an unusual finding in rats at 20 weeks of age, the 30% incidence in this group was considered treatment-related and therefore a NOAEC for female fertility of 16 mg/m3 was considered. Developmental effects are observed in rats in two studies (decrease of fetal body weight from 10 mg/kg/day, increase of post-implantation loss with late resorptions, increase in dead or resorbed conceptuses per litter at 25 mg/kg/day (33.2% versus 4.3%); decrease in the average number of live fetuses per litter (8.9 versus 14.6) and fetal malformation/variation and delayed skeletal ossification at 25 mg/kg/day. Those developmental effects do not seem to be related to maternal toxicity. However, these developmental effects are not confirmed in a third assay in rats conducted with a test article containing a lower percentage of the OBDPE component. In rabbits, the substance produces only slight foetotoxicity from 5 mg/kg/day (slight decrease of the fetal body weight and increase in delayed ossification). The lowest identified NOAEL is considered i.e. 2 mg/kg/day from the rabbit study. Since some of these results are indicative of developmental effects which are most likely unrelated to maternal toxicity, OBDPE is considered as a developmental toxicant. With regard to neurotoxicity, recently behavioural disturbances have been reported when mice (10 day old) were exposed to a single oral dose of hexabromo-diphenyl ether (0.45, 0.9 and 9 mg/kg bw). Those effects are observed at 2, 4 but also 6 months of age. Nicotinic receptors were also affected in adult mouse in the previous conditions of exposure. The study has certain limitations compared with regulatory guidelines and thus uncertainty as regards interpretation of the results remains. Moreover only an abstract of this study is available with very few details. Therefore, no firm conclusion can be drawn from these data.
Like other halogenated aromatic hydrocarbons, polybrominated diphenyl ethers bind to the cellular aryl hydrocarbon receptor (AhR), which regulates the synthesis of a variety of proteins. Activation of the AhR induces a number of enzymes, including cytochrome P-450-dependent monooxygenases of the CYP1A and CYP2B families, UDP-glucuronosyltransferase, and ethoxyresorufin-o-deethylase. PBDEs are also believed to disrupt the production, transport, and disposition of thyroid hormones. One mechanism of this involves metabolites ot PDBEs competing with thyroxine to bind to transthyretin, decreasing serum thyroid hormone levels. This change in thyroid hormone levels has been linked to both thyroid toxicity and neurobehavioral alterations. Certain PDBEs and their metabolites are also endocrine disruptors and may act as agonists at the estrogen receptors or antagonists at the androgen and progesterone receptors. (L628, A262)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌物分类
对人类不具有致癌性(未被国际癌症研究机构IARC列名)。
No indication of carcinogenicity to humans (not listed by IARC).
来源:Toxin and Toxin Target Database (T3DB)
毒理性
健康影响
多溴联苯醚可能影响甲状腺和肝脏。动物研究也表明,多溴联苯醚可以导致神经行为改变并影响免疫系统。
Polybrominated diphenyl ethers may affect the thyroid gland and liver. Animals studies have also shown that PDBEs can cause neurobehavioral alterations and affect the immune system. (L628)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
暴露途径
这种物质可以通过吸入和摄入被身体吸收。
The substance can be absorbed into the body by inhalation and by ingestion.
来源:ILO-WHO International Chemical Safety Cards (ICSCs)
Animal data show an absorption of octabromodiphenyl ether (OBDPE) by oral or inhalation route with an accumulation of the parent compound or its metabolites in the liver and also in the adipose tissue and the lung following inhalation administration. The extent of absorption and elimination cannot be assessed from the data available ... There are no measured data on OBDPE dermal absorption. However based on OBDPE physicochemical properties and analogy with PCBs, a dermal absorption of 4.5% may be estimated.
Evidence from humans indicates that octabromodiphenyl ether (OBDPE), HxBDPE(/hexabromodiphenyl ethe)/, HpBDPE (heptabromodiphenyl ether), and NonaBDPE (nonabromodiphenyl ether), which are components of commercial OBDPE, can be absorbed into the body and distributed into the blood. Distribution to the adipose tissue was evidenced at least for OBDPE and HxBDPE. There are no data available on the rate of elimination or on bioaccumulation of OBDPE from human adipose tissue, neither for PeBDPO /Pentabromodiphenyl oxide/, but given the high lipophilicity of these compounds and the adipose tissue accumulation observed in rats following oral or inhalation routes, it can be assumed that in humans OBDPE might bioaccumulate in these tissues as well. Following pregnancy HxBDPE and others PBDPEs such as TeBDPE /tetrabromodiphenyl ether/ and PeBDPEs /pentabromodiphenyl ethers/ are excreted in the breast milk. Unfortunately, such measurements were not carried out on OBDPE. However, based on the high lipophilicity of OBDPE, its potential to bioaccumulate in adipose tissues, and the breast milk measured data with HxBDPE (one component of commercial OBDPE), excretion of OBDPE in the breast milk may be anticipated.
Using rats as a model, ... tissue distribution of polybromodiphenyl ethers (PBDEs) /was investigated/ after oral administration and ... a suitable matrix /was evaluated/ for body burden estimation. Male rats were administered dust or corn oil containing 8 or 6 ug PBDEs/kg bw, respectively, in the diet for 21 days (N=4 rats per treatment), and the concentration of 15 PBDEs were measured in various tissues, plasma, and feces. PBDEs were found in all tissues, including the brain, and showed no difference in distribution patterns between treatments for most PBDEs. Tri- to hexa-BDEs comprised >80% of the total PBDEs in the adipose, brain, kidney, lung, and residual carcass, but <40% in the liver and plasma. The ratio of the lipid-weight concentration of tri- to hexa-BDEs in adipose tissue, residual carcass, and plasma was 1:1:2. For the hepta- to nona-BDEs, lipid-weight concentrations increased from adipose tissue to residual carcass to plasma in the ratio 0.3:1:>4. BDE-209 was the dominant congener in the liver and plasma, but was not detected in the adipose tissue or carcass. In summary, the lower brominated congeners tended to distribute equally into lipids implying both adipose tissue and plasma would be suitable matrices for biomonitoring. Plasma was the best matrix for detection of the higher brominated congeners (especially BDE-209), although on a lipid-weight basis tended to overestimate the total body burdens.
significant difference between the Pd–TiO2 and pristine TiO2 systems, and much less position selectivity for the debromination on Pd–TiO2 was observed than that on the pristine TiO2 surface. For another polybrominateddiphenylether (BDE15), pristine TiO2 was incapable of its photocatalytic reduction, whereas the loading of Pd enabled its debromination to diphenylether within 20 min. In addition, an evident
to develop methods for the synthesis of authentic octaBDE congeners in order to make them available as standards for analytical, toxicological, and stability studies, as well as studies concerning physical-chemical properties. The syntheses of six octaBDEs, 2,2',3,3',4,4',5,5'-octabromodiphenyl ether (BDE-194), 2,2',3,3',4,4',5,6'-octabromodiphenyl ether (BDE-196), 2,2',3,3',4,5,5',6-octabromodiphenyl
Epoxy resin composition and molded articles obtained therefrom
申请人:HITACHI, LTD.
公开号:EP0103804A2
公开(公告)日:1984-03-28
An epoxy resin composition comprising (a) an epoxy resin, (b) an alkenylphenol polymer, (c) a curing promoter, (d) halogen compounds (compound) represented by the formula:
and/or the formula:
wherein X1 to X10 each represents a hydrogen, chlorine or bromine atom, at least three of X1 to X5 and at least three of X6 to X10 being chlorine or bromine atoms, and R represents an alkylene group or a hydroxyl-substituted alkylene group, and (e) a filler can give molded articles excellent in properties, particularly in heat resistance and flame retardancy, even if metal inserts are contained therein.
Compositions and methods for reducing fire hazard of flammable refrigerants
申请人:E. I. du Pont de Nemours and Company
公开号:EP2455438A2
公开(公告)日:2012-05-23
The present invention relates to compositions comprising flammable refrigerant, fire hazard-reducing agent, and optionally a lubricant suitable for use in a refrigeration or air conditioning apparatus. Further, the present invention relates to compositions comprising lubricant and fire hazard-reducing agent and methods for reducing flammability of flammable refrigerant, for delivering a fire hazard-reducing agent to a refrigeration or air conditioning apparatus, and for replacing a non-flammable refrigerant with a flammable refrigerant.
SCORCH RETARDANT HALOGENATED FLAME RETARDANT COMPOUNDS AND ARTICLES MADE THEREFROM
申请人:PolyOne Corporation
公开号:EP3699224A1
公开(公告)日:2020-08-26
A halogenated flame retardant polyethylene compound is disclosed containing at least one organic additive which presents in its molecular structure at least one nitrogen atom to serve as a scorch retardant to forestall premature crosslinking during manufacture of wire and cable insulation and/or jacketing, in order to obtain a flame retardant crosslinked polyethylene (XLPE), and especially when the XLPE material is obtained via an alkoxysilane condensation-hydrolysis step.