Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/
Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/
Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/
/EPIDEMIOLOGY STUDIES/ In a longitudinal cohort initiated after 11 September 2001, including 329 mothers who delivered in one of three hospitals in lower Manhattan, New York, ... prenatal PBDE exposure and neurodevelopment /were examined/ when their children were 12-48 and 72 months of age ... 210 cord blood specimens /were tested/ for selected PBDE congeners and assessed neurodevelopmental effects in the children at 12-48 and 72 months of age; 118, 117, 114, 104, and 96 children with available cord PBDE measurements were assessed at 12, 24, 36, 48, and 72 months, respectively. ... Multivariate regression analyses /was used/ to evaluate the associations between concentrations of individual PBDE congeners and neurodevelopmental indices. Median cord blood concentrations of PBDE congeners 47 /2,2',4,4'-tetrabromodiphenyl ether/, 99 /2,2',4,4',5-pentabromodiphenyl ether/, and 100 /2,2',4,4',6-pentabromodiphenyl ether/ were 11.2, 3.2, and 1.4 ng/g lipid, respectively. After adjustment for potential confounders, children with higher concentrations of BDEs 47, 99, or 100 scored lower on tests of mental and physical development at 12-48 and 72 months. Associations were significant for 12-month Psychomotor Development Index (BDE-47), 24-month Mental Development Index (MDI) (BDE-47, 99, and 100), 36-month MDI (BDE-100), 48-month full-scale and verbal IQ (BDE-47, 99, and 100) and performance IQ (BDE-100), and 72-month performance IQ (BDE-100). This epidemiologic study demonstrates neurodevelopmental effects in relation to cord blood PBDE concentrations.
/EPIDEMIOLOGY STUDIES/ Epidemiological studies ... have revealed only limited information about associations between PBDE exposure and menstruation characteristics. /The goal of this study/ was to examine whether high breast milk PBDE levels in reproductive-age females lead to interference with menstruation characteristics. Fifteen PBDE congeners in 46 breast milk samples /were analyzed/. (BDE-15 /4,4'-dibromodiphenyl ether/, 28 /4,4'-dibromodiphenyl ether/, 47 /2,2',4,4'-tetrabromodiphenyl ether/, 49 /2,2',4,5'-tetrabromodiphenyl ether/, 99 /2,2',4,4',5-pentabromodiphenyl ether//, 100 /2,2',4,4',6-pentabromodiphenyl ether/, 153 /2,2',4,4',5,5'-hexabromodiphenyl ether/, 154 /2,2',4,4',5,6'-hexabromodiphenyl ether/, 183 /2,2',3,4,4',5',6-heptabromodiphenyl ether/, 196 /2,2',3,3',4,4',5,6'-octabromodiphenyl ether/, 197 /2,2',3,3',4,4',6,6'-octabromodiphenyl ether/, 203 /2,2',3,4,4',5,5',6-octabromodiphenyl ether/, 207 /2,2',3,3',4,4',5,6,6'-nonabromodiphenyl ether/, 208 /2,2',3,3',4,5,5',6,6'-nonabromodiphenyl ether/, and 209 /decabromodiphenyl ether/). The mean sum of PBDEs (SigmaPBDEs) in breast milk was 3.42 ng/g lipid. Women's age at menarche was not correlated with breast milk PBDE levels. Increased BDE-208 and 209 levels were significantly associated with the prolonged length of average and the longest menstrual cycle independent of age, pre-pregnant BMI, and parity. Higher concentrations of SigmaPBDEs and the higher brominated PBDEs from BDE-183 to 209, except 197, were significantly linked to women whose menstruation periods were still coming irregularly at the sampling time. Age-adjusted odds ratios (ORs) of BDE-153, 183, 207, 208, and SigmaPBDEs were significantly higher in women with length of average menstrual cycle >32 days, compared to the control. Women whose menstruation periods still came irregularly when they were 18 years old had higher age-adjusted ORs of BDE-207, 208, 209, and SigmaPBDEs than those whose periods came regularly at the same age. Although SigmaPBDEs and certain higher brominated PBDEs appear to have potential to prolong length of average menstrual cycle and delay the age when menstruation periods begin coming regularly, these findings are not conclusive ...
Significant absorption of tetrabromodiphenyl ether (TBDPE) in the gastro-intestinal tract of rats and mice occurs after oral administration. The main excretory pathway for rats is via feces, whereas excretion in the mouse is equally distributed in feces and urine. Although a number of TBDPE metabolites were detected in different tissues, the majority of the administered dose was retained in adipose tissue, mainly as the parent compound, for five days following administration. In the rat, the lung had the second highest concentration of TBDPE and its metabolites. The authors postulated that similarities between these metabolites and thyroxine may be biologically and toxicologically relevant, whereby structural similarities may enable them to compete for binding sites on transport proteins.
... Tetrabromodiphenyl ether (TeBDE) is one congener in a mixture of polybrominated diphenyl ethers that makes up a flame-retardant commercial product called pentabromodiphenyl ether (PeBDE). ... This study was designed to assess the rate and extent of absorption of (14C)-tetrabromodiphenyl ether ([14C]-TeBDE) through human and rat skin in vitro. (14C)-TeBDE was applied to human and rat split thickness skin membranes in vitro in a single test preparation: (14C)-TeBDE in acetone (ca. 20%, w/v). Dermal delivery and absorbed dose of TeBDE applied to human skin was 3.13% (313 ug equiv/sq cm) and 1.94% (194 ug equiv/sq cm) of the applied dose, respectively. Dermal delivery and absorbed dose of TeBDE applied to rat skin was 17.94% (1804 ug equiv/sq cm) and 14.81% (1489 ug equiv/sq cm) of the applied dose, respectively. These results confirm that the risk of systemic exposure due to external dermal exposure of the PeBDE product is low in the human. ... The results also confirm that the rat is a conservative model overpredicting human absorption about eight fold.
... 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. /PBDE congeners/
