OCTABROMODIPHENYL ETHER
Flammability | 1 | |
Toxicity | 2 | |
Body Contact | 2 | |
Reactivity | 1 | |
Chronic | 3 | |
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4 |
Fire retardant for high impact polystyrene, ABS polymers, adhesives, polyethylene,
thermoset applications of epoxy resins and unsaturated polymers and synthetic fibers.
C12-H2-Br8-O, "benzene, 1, 1'-oxybis-, octabromo-", "benzene, 1, 1'-oxybis-,
octabromo-", "1, 1'-oxybisoctabromobenzene", "1, 1'-oxybisoctabromobenzene",
"octabromobiphenyl oxide", "octabromophenyl ether", OBDPE, "Bromkal 79-8DE", "Bromkal 79-
8DE", CD-79, D-79, D-79, EB-8, FR-143, FR-1208, fire-retardant
May cause harm to the unborn child.
Possible risk of impaired fertility.
May cause long- term adverse effects in the environment.
Toxic to aquatic organisms, may cause long- term adverse effects in the aquatic
environment.
Accidental ingestion of the material may be damaging to the health of the individual. Digestion of PCBs and related substances can lead to nausea and vomiting, abdominal pain, loss of appetite, jaundice, liver damage, coma and death. Headache, dizziness, lethargy, depression, nervousness, loss of libido and muscle and joint pain may also occur. Symptoms and death may be delayed for months; the substance occurs in the breastmilk of women and is toxic to babies.
There is some evidence to suggest that this material can causeeye irritation and damage in some persons. Vapors of PCBs may be irritating and may be absorbed by the eye.
Skin contact with the material may damage the health of the individual; systemic effects may result following absorption. Skin contact is not thought to have harmful health effects, however the material may still produce health damage following entry through wounds, lesions or abrasions. There is some evidence to suggest that this material can cause inflammation of the skin on contact in some persons. Direct contact of the skin with liquid PCBs may result in irritation and defatting leading to dermatitis. PCBs may be absorbed by skin and as a result may be retained in body tissues. Open cuts, abraded or irritated skin should not be exposed to this material. Entry into the blood-stream, through, for example, cuts, abrasions or lesions, may produce systemic injury with harmful effects. Examine the skin prior to the use of the material and ensure that any external damage is suitably protected. Chlorinated diphenyl ethers may produced skin irritation; systemic toxicitymay occur following absorption.
Inhalation may produce health damage*. Inhalation of dusts, generated by the material during the course of normal handling, may be damaging to the health of the individual. There is some evidence to suggest that the material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage. Persons with impaired respiratory function, airway diseases and conditions such as emphysema or chronic bronchitis, may incur further disability if excessive concentrations of particulate are inhaled. Inhalation of vapors containing PCBs may cause respiratoryirritation, eczema and skin burns.
Ample evidence exists, from results in experimentation, that developmental disorders are directly caused by human exposure to the material. Ample evidence from experiments exists that there is a suspicionthis material directly reduces fertility. Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems. There has been some concern that this material can cause cancer or mutations but there is not enough data to make an assessment. Prolonged contact with chlorinated diphenyl ethers may cause skin irritation, weight loss and liver injury. Repeated absorption has produced liver damage in animals. The congener, decabromodiphenyl oxide, showed some evidence of carcinogenicity in a lifelong feeding study in male and female rats based on an increased incidence of benign- tumour like changes in the liver produced at high dose rates. No data were available on kinetics and metabolism of OBDPE. Following oral treatment, total bromine increased in the liver during the study period, but decreased slowly following suspension of treatment, but remained higher than the controls after one year of withdrawal. Similarly, total bromine concentrations in the lung, liver and fat were higher in treated animals than incontrols following 14 day inhalation exposure . OBDPE is of low acute oral and dermal toxicity with LD50 > 28 g/kg in rats and >2 g/kg in rabbits, respectively. Inhalation exposure caused similar effects to those observed with DBDPE. The LC50 in rats is > 50 mg/L. Tachypnea was also noted in animals exposed to 60 mg/L of OBDPE. OBDPE was not a skin irritant and only transient eye irritation was observed in rabbits. Inhalation of up to 1200 mg/m3 of OBDPE over 14 days caused a non-persistent increase in breathing pattern. Significant dose-related increases in relative liver weights accompanied with histopathological lesions were also observed. Short-term feeding studies over 4 and 13 weeks showed more pronounced effects on animals treated with OBDPE than was observed with decabromodiphenyl ether (DBDPE). Increased liver weights and microscopic changes in liver tissue were identified and found to be dose-related and reversible. Hyperplasia of the thyroid was also observed in the treated animals. Changes in absolute and relative liver and thyroid weights were also reported in rats administered commercial preparations of OBDPE over 90 days. The NOAELs for orally administered OBDPE were not determined from the available studies, however, the LOAEL in rats was determined to be 100 ppm (28 and 90 day studies). OBDPE was reported to be non-mutagenic in the microbial and eukaryotic cell systems tested. No study reports investigating the potential for carcinogenicity of OBDPE are available. Three developmental toxicity studies have been performed using commercial OBDPE. In one rat study, malformations and foetal variations were observed at 50 mg/kg, which were considered secondary to maternal toxicity. No compound related effects were observed in the 15 mg/kg or lower dose groups . In a second rat study, the test substance was found to be more toxic to the conceptus than the dam, with malformations and/or foetal variations seen at and above 10 mg/kg. The NOEL for developmental effects was determined to be 2.5 mg/kg. In a study in rabbits, no evidence of teratogenic activity was reported but slight foetotoxicity was observed at a maternally toxic dose of 15 mg/kg.