2,2',3,4,5,6-Hexabromobiphenyl

H350: May cause cancer [Danger Carcinogenicity]

P203, P280, P318, P405, and P501 (click each P-code to see the statement)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment.

INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.

INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital.

OTHER: Since this chemical is a known or suspected carcinogen you should contact a physician for advice regarding the possible long term health effects and potential recommendation for medical monitoring. Recommendations from the physician will depend upon the specific compound, its chemical, physical and toxicity properties, the exposure level, length of exposure, and the route of exposure. (NTP, 1992)

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)

Excerpt from ERG Guide 171 [Substances (Low to Moderate Hazard)]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

SMALL SPILLS AND LEAKAGE: If a spill of this chemical occurs, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with acetone and transfer the dampened material to a suitable container. Use absorbent paper dampened with acetone to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with acetone followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

STORAGE PRECAUTIONS: You should protect this material from exposure to light, and store it in a refrigerator. (NTP, 1992)

Acute Oral: 0.01 mg/kg/day (L134)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with a combination filter cartridge, i.e. organic vapor/acid gas/HEPA (specific for organic vapors, HCl, acid gas, SO2 and a high efficiency particulate filter). (NTP, 1992)

Hexabromobiphenyl appears as white solid or tan powder. (NTP, 1992)

White solid; [HSDB] White or tan solid; [CAMEO]

White solid

162 °F (NTP, 1992)

less than 1 mg/mL at 77 °F (NTP, 1992)

Soluble in acetone and benzene

In water, 0.011 mg/L at 25 °C

7.6e-05 mmHg at 194 °F (NTP, 1992)

0.00000005 [mmHg]

5.2X10-8 mm Hg at 25 °C

log Kow = 6.39

When heated to decomposition it emits toxic fumes of /hydrogen bromide/.

Other Classes -> Halogenated Polyaromatics

Insoluble in water.

Aryl Halides

Simple aromatic halogenated organic compounds, such as HEXABROMOBIPHENYL, are very unreactive. Halogenated organics generally become less reactive as more of their hydrogen atoms are replaced with halogen atoms. Materials in this group may be incompatible with strong oxidizing and reducing agents. Also, they may be incompatible with many amines, nitrides, azo/diazo compounds, alkali metals, and epoxides.

FireMaster BP-6 hydrolyzed when refluxed with 2% potassium hydroxide in ethanol, but the possible rate of PBB hydrolysis under much milder environmental conditions remains unknown. /FireMaster BP-6/

The exact mechanism of toxicty of PBBs varies depending on the specific congener. The predominant interaction is believed to involve the aryl hydrocarbon receptor (AhR). PBBs bind to and activate the AhR, which in turn initiates the transcriptional upregulation of a number of genes, affecting biochemical and endocrine pathways, cell cycle regulation, morphogenesis, oxidative stress response, and various other processes. This results in the numerous toxic responses characteristic of PBBs. Some of the known induced genes include the cytochrome P-450-dependent monooxygenases CYP1A1 and CYP1A2. (L628)

2A, probably carcinogenic to humans. (L135)

PBB exposure may cause weight loss, skin disorders (such as acne), nervous and immune systems effects, and effects on the liver, kidneys, and thyroid gland. (L628)

Oral (L628) ; inhalation (L628) ; dermal (L628)

Symptoms of PBB exposure may include nausea, abdominal pain, loss of appetite, joint pain, fatigue, and weakness. (L629)

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.

Reproductive Toxin - A chemical that is toxic to the reproductive system, including defects in the progeny and injury to male or female reproductive function. Reproductive toxicity includes developmental effects. See Guidelines for Reproductive Toxicity Risk Assessment.

Dermatotoxin - Chloracne.

LD50 Rabbit dermal 5 g/kg bw /FireMaster BP-6/ /from table/

LD50 Rat oral 21.5 g/kg /FireMaster BP-6/

LD50 Rat (Fischer-344 N, female) oral 1.43 g/kg bw /FireMaster FF-1/ /from table/

LD50 Rat (Fischer-344 N, male) oral 3.28 g/kg bw /FireMaster FF-1/ /from table/

LD50 Mouse oral >15 g/kg

EYES: irrigate opened eyes for several minutes under running water.

INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice.

SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention.

INHALATION: supply fresh air. If required provide artificial respiration.

Mice fed diet containing Firemaster BP-6 were more susceptible to chlorinated hydrocarbon solvent-induced renal and hepatic damage and to lethal effects of chloroform and carbon tetrachloride than mice that received control diet. /Firemaster BP-6/

...Female Sprague-Dawley rats were initiated on day 1 by ip administration of diethylnitrosamine. On day 7 after initiation, the rats were fed a vitamin A-deficient basal diet that was supplemented with either 2000 IU (low-vitamin A) or 200,000 IU (high-vitamin A) retinyl acetate/kg feed. From day 30 after initiation until the end of the study the following PBBs were added to the diets: Firemaster BP-6 (10 ppm), 2,4,5,2',4',5'-hexabromobiphenyl (10 ppm) or 3,4,5,3',4',5'-hexabromobiphenyl (1 ppm). The control animals received low- or high-vitamin A diets containing no PBBs. On day 180, ... numbers of gamma-glutamyl transpeptidase-positive foci/cu cm liver and the mean volumes of these foci were lower in the high-vitamin A groups than those in the corresponding low-vitamin A groups, but these differences were not significant. The percentage of the liver volume occupied by foci was significantly greater in the low-vitamin A with 345-HBB group than in the corresponding high-vitamin A group. Thus, high dietary levels of vitamin A had some inhibitory effect on the promotion of hepatic-altered foci by 345-HBB in initiated rats.

A single oral dose of HBB (3,3',4,4',5,5',-hexabromobiphenyl), a congener of the polybrominated biphenyls (PBBs), and a dioxin-type cytochrome P-450 enzyme inducer rapidly and dramatically altered the steady-state metabolism of vitamin A and caused an abnormal two-fold enhancement in the metabolic output of degraded vitamin A in urine and feces of rats. The effects are most likely explained by an increased metabolism of vitamin A in kidney and deregulation of vitamin A metabolism in liver; this may lead to an increased dietary vitamin A requirement. /3,3',4,4',5,5'-hexabromobiphenyl/

Preliminary studies with FireMaster BP-6 indicated that iron overload may enhance the hepatocarcinogenicity of PBBs in C57BL/10 ScSn male mice. /FireMaster BP-6/

Japanese quail /administered/ FM BP-6 (single dose of 100 mg/kg bw) /by/ gavage .../caused/ increased mortality during anesthesia when the pentobarbital /(single im dose of 50 (male) or 60 (female) mg/kg bw)/ was administered 2 hr after PBB dosing; reduction in pentobarbital sleeping times 48 hr after PBB dosing. 300 mg/kg feed for 3 days in diet /caused/ reduction in pentobarbital sleeping times. /FireMaster BP-6/ /from table/

/EPIDEMIOLOGY STUDIES/ A field biochemical epidemiology study was conducted using the Michigan cohort consisting of 51 rural residents exposed to polybrominated biphenyls (PBB). ...PBB serum levels were detected in 36 of the 51 PBB-exposed subjects. The serum half-life of /the major PBB congener, hexabromobiphenyl/ HBB was determined by comparing the current serum HBB values to the subject's previous serum values obtained 5 to 8 years earlier...The /caffeine breath test/ CBT and caffeine urinary metabolite ratio/ CMR were elevated in the subjects exposed to PBBs as compared to the values obtained from urban nonsmokers and were similar to those found in adults who smoke. A gender effect was seen in the PBB-exposed subjects, the median CBT and CMR values of the females being lower than the values of males. There was a correlation between the CBT and the HBB serum values (r2= 0.2, p=0.01) but not between CMR and HBB serum values. The CBT and CMR were easily conducted in the field and appear to be useful metabolic probes of cytochrome P-450I activity in human environmental toxicology.

/LABORATORY ANIMALS: Acute Exposure/ Firemaster BP-6 induced...cytochrome P-450 and P-448 in liver of rats 192 hr after treatment with single ip injections of 25 mg/kg; major component, 2,2',4,4',5,5'-hexabromobiphenyl /63%/, induced only cytochrome P-450. /Firemaster BP-6/

/LABORATORY ANIMALS: Acute Exposure/ 20 male and 20 female 2.5 month old Sherman rats...given single...1000 mg/kg... Firemaster FF-1 by gavage as 5% solution in peanut oil. ...Killed...at 2, 6, 10 and 14 month after treatment... hepatocytes in center of liver lobules...enlarged, vacuolated or had foamy cytoplasm.../6 or more months after treatment/. /Firemaster FF-1/

/LABORATORY ANIMALS: Acute Exposure/ Toxic effects in rats and mice exposed to Firemaster FF-1 including body weight decrease, liver hypertrophy and fatty infiltration, hepatocyte swelling, cytoplasmic vacuoles and microscopic abscesses. Chloracne-like lesions occurred in rabbit ears exposed to total dose of 60 mg Firemaster FF-1 per ear. /Firemaster FF-1/

/LABORATORY ANIMALS: Acute Exposure/ Some ...effects of 2,4,5,2',5'-penta- (congener 1), 2,3,4,2',4',5'-hexa- (congener 5), 2,4,5,3',4',5'-hexa- (congener 6), 2,3,4,5,3',4',-hexa- (congener 7), and 2,3,4,5,2',3',4'-heptabromobiphenyl (congener 9) were evaluated in male rats given a single 90 mg/kg ip injection and killed 7 days later. Only congener 7 depressed body weight gain, spleen and thymus weights, and caused severe histopathological changes in the thymus. Congener 7 caused the largest incr in liver weight and the most changes in liver pathology while congener 1 failed to enlarge this organ and caused the mildest ultrastructural changes. Liver microsomes were isolated and evaluated for enzyme induction from all treated rats except those administered congener 6... . All congeners increased the liver microsomal cytochrome P-450 content, but only congener 7 shifted the carbon monoxide difference spectrum absorption maximum to 448.0 nm. The microsomal ethyl isocyanide difference spectrum 455/430 nm ratio was increased the most by congener 7 (3 fold). All congeners increased cytochrome P-450 reductase and microsomal epoxide hydrase activities by nearly 1.5-3 fold. Congener 7 failed to induce aminopyrine-N-demethylase activity but the remaining congeners increased it by 2 fold. Congener 7 was the most effective inducer of benzo(a)pyrene hydroxylase and p-nitrophenol UDP-glucuronyl transferase. These results add to the suggestion that the presence of an ortho halogen on a polyhalogenated biphenyl does not completely abolish toxicity or 3-methylcholanthrene-type microsomal enzyme induction. /Firemaster/

For more Non-Human Toxicity Excerpts (Complete) data for HEXABROMOBIPHENYL (61 total), please visit the HSDB record page.

Chronic toxicity and carcinogenicity studies of polybrominated biphenyls (Firemaster FF-1 ®) were conducted in F344/N rats and B6C3F1 micce of each sex. The studies were designed to determine: a) the effects of polybrominated biphenyls in rats and mice receiving adult (F0 exposure only (a typical carcinogenicity study), b) the toxic and carcinogenic effects of polybrominated biphenyls in rats and mice receiving perinatal (F0) exposure only (dietary exposure of dams prior to breeding and throughout gestation and lactation), and c) the effects of combined perinatal and adult exposure to polybrominated biphenyls. ... Studies in F344/N Rats: The exposure levels selected for F1 exposure, based on studies of polybrominated biphenyls in the literature, were 3, 10, and 30 ppm. In a preliminary study to determine the pcrinatal dietary concentrations for the 2-year study, female rats were administered 1 to 30 ppm polybrominatcd biphenyls in the feed beginning 60 days prior to breeding and continuing throughout gestation, lactation, and up to 4 weeks postwcaning. The mean prcwcaning litter weight of the 30 ppm group was less than 80% of the mean litter weight of the control group at days 0, 4, and 12. At weaning, the mean weight of litters in this group was 80% of the control group mean. The final mean body weights (28 days after weaning) of males and females receiving 30 ppm were 13% to 19% lower than the final mean body weights of the controls. Therefore, dietary concentrations of 0, 1, 3, and 10 ppm wcrc selected for the F0 exposure levels in the 2-year study. ... The major organ affected by toxicity of polybrominated biphenyls was the liver. Rats evaluated at 9 months had decreased body weights, hepatomegaly, nonneoplastic histopathologic changes in the liver, mild anemia, increases in serum cholesterol concentrations, and decreases in serum triglyceride concentrations (males only). In rats receiving adult-only exposure (F0:F1 concentrations of 0:10 or 0:30 ppm), there were no significant effects on survival. Mean body weights were significantly reduced in 0:10 and 0:30 ppm male rats and in 0:30 ppm female rats. Males and females exposed to 0:10 or 0:30 ppm had increased incidences of hepatocellular neoplasms (males: 0:0 ppm, 1/50; 0:10 ppm, 12/49; 0:30 ppm, 41/50; females: 0/50, 12/50, 39/50). Increased incidences of the following nonneoplastic lesions were associated with the administration of polybrominated biphenyls: eosinophilic foci, cytoplasmic vacuolization, oval cell hyperplasia, and hypertrophy in the liver of males and females; acanthosis, inflammation, and ulceration of the forestomach in exposed males; and cystic endometrial hyperplasia of the uterus in 0:30 ppm females. ... For rats receiving only perinatal exposure (10:0 ppm), there were no changes in survival or body weights compared to the 0:0 ppm control groups. In female rats, there were no effects on neoplasm incidences, but perinatal exposure was associated with a marginally increased incidence of hepatocellular adenoma in male rats (0:0 ppm, 1/50; 10:0 ppm, 5/50). The incidences of nonneoplastic lesions in the liver were increased in exposed males (eosinophilic foci and cytoplasmic vacuolization) and females (eosinophilic foci). ... Combined perinatal and adult exposure resulted in marginally reduced survival compared to the 0:0 ppm control group for male rats in the 3:10, 10:10, and 10:30 ppm groups. No significant survival differences were observed in female rats. The final mean body weights of male and female rats receiving 3:10, 10:10, or 10:30 ppm were lower than those of the 0:0 ppm controls. In male rats, there were no enhancing effects of combined perinatal and adult exposure on the incidence of hepatocellular neoplasms. However, perinatal exposure enhanced the development of liver neoplasms in female rats receiving 10 or 30 ppm adult exposure. A combined analysis of all male and female exposure groups also revealed increased incidences of mononuclear cell leukemia that were considered related to polybrominated biphenyls exposure. ... Studies in B6C3F1 Mice: The exposure levels selected for the F1 exposure, based on studies of polybrominated biphenyls in the literature, were 3, 10, and 30 ppm. In a preliminary study to determine the perinatal dietary concentrations for the 2-year study, female C57BL/6N mice were exposed to 1 to 30 ppm polybrominated biphenyls in the feed beginning 60 days before breeding to C3H/HeN males, continuing throughout gestation and lactation and up to 4 weeks postweaning. There were no clear chemical-related effects on survival or growth at any phase of the study; therefore, 0, 3, 10, and 30 ppm dietary concentrations were selected for the F0 exposure levels in the 2-year study. ... The major organ affected by toxicity of polybrominated biphenyls was the liver. Animals evaluated at 9 months had lower body weights than the controls, hepatomegaly, and histopathologic changes in the liver. In mice receiving adult-only exposure, no males or females in the 0:30 ppm group survived to the end of the study. Neither survival nor body weights were affected in the 0:10 ppm groups. Males and females receiving 0:10 or 0:30 ppm had markedly increased incidences of hepatocellular neoplasms (males: 0:0 ppm, 16/50; 0:10 ppm, 48/49; 0:30 ppm, 48/50; females: 5/50, 42/50, 47/48). Increased incidences of nonneoplastic liver lesions including cytomegaly (hypertrophy), fatty change (cytoplasmic vacuolization), bile duct hyperplasia, eosinophilic and clear ccell loci, and necrosis of individual hepatocytes were related to treatment with polybrominated biphenyls. Increased incidences and severity of chronic nephropathy in the kidney and excessive hematopoiesis in the spleen of 0:30 ppm males and females were also considered to be related to exposure to polybrominated biphenyls. ... There were no survival or body weight differences in mice receiving only perinatal exposure (30:0 ppm). Perinatal exposure resulted in significantly increased incidences of hepatocellular neoplasms in males and females. The incidences of nonneoplastic lesions (cytomegaly, eosinophilic foci, clear cell foci) were increased in males and females. ... Combined perinatal and adult exposure resulted in markedly reduced survival for females in the 30:10 ppm group; no mice receiving 30:30 ppm survived to the end of the study. In those groups receiving adult exposure of 30 ppm, mean body weights were not affected. The incidence of hepatocellular neoplasms in male and female mice was significantly increased. At the 9-month interim evaluation the incidence of hepatocellular adenomas was significantly increased in males (0:30 ppm, 1/10; 30:30 ppm, 7/10). The incidence of hepatocellular adenomas in 30:30 ppm females was similar to that of 0:30 ppm females (0:30 ppm, 0/10; 30:30 ppm, 3/10). At the end of the study the incidence of hepatocellular adenomas in males was statistically increased (0:30 ppm, 42/50; 30:30 ppm, 48/50). The incidence of hepatocellular adenomas in 30:30 ppm females was statistically decreased compared to that of 0:30 ppm females (0:30 ppm, 46/48; 30:30 ppm, 41/47). It was not possible to assess the potential enhancing effect of combined perinatal and adult exposure on hepatocellular neoplasms because adult-only exposure resulted in such high (84% to 98%) liver neoplasm incidences.

LC50 Colinus virginianus (Bobwhite quail) dietary 428 mg/kg/8 days /FireMaster/ /from table/

LC50 Mustela vison (Mink) dietary 3.95 ppm/313 days /FireMaster FF-1/

/BIRDS and MAMMALS/ Observations of intoxicated Bobwhite quails, prior to death, included asthenia, low carriage, an unkempt appearance, wing droop, diarrhea, limited ataxia, and general lethargy. /Birds were given a dietary concentration of 100-700 mg/kg feed for 5 days of an 8 day observation period. Feed intake was also reduced./ /FireMaster/

/BIRDS and MAMMALS/ The sensitivity of three genetic lines of Japanese quail to polybrominated biphenyls (PBBs) was evaluated using criteria of egg production, reproduction, and induction of the hepatic microsomal mixed-function oxidase (MFO) system. Two genetic lines of quail, developed to diverge in their plasma cholesterol response to exogenous adrenocorticotropin (ACTH) (a "Low" line and a "High" line), were compared to a random-bred line ("Random"). ACTH administration caused increases in plasma cholesterol in the Low line that were 15 and 39% below the Random-line values in males and females, respectively, while High-line values were 31% higher in males and 36% higher in females when compared to the respective Random-line values. Hepatic activities of aryl hydrocarbon hydroxylase (AHH) and hexobarbital hydroxylase (HxH) were not significantly influenced by ACTH administration or by genetic line in either sex. PBBs fed at 40 or 80 mg/kg diet for 5 wk resulted in significant increases in hepatic AHH and aminopyrine N-demethylase (APND) activities and cytochrome P-450 concentrations. The induction of AHH, APND, and cytochrome P-450 was significantly less in Low-line males in comparison to Random- and High-line males, while the induction of AHH was less in Low-line females when compared to females from the other two lines, based on covariance analysis. In terms of reproductive parameters, there was a greater adverse effect on egg production at 80 ppm PBBs in Low-line females when compared to the Random and High lines. These data indicate an example in which the biological toxicity of a compound and the induction of a 3-methylcholanthrene-type hepatic enzyme are not directly correlated.

5.00e+02

Volatile

Hexabromobiphenyl's former production and use as an additive in flame retardants primarily in thermoplastics that were ultimately used in electrical housing equipment, may have resulted in its release to the environment through various waste streams. Hexabromobiphenyl consists of 42 possible congeners, the 2,2',4,4',5,5' isomer was the key component in flame retardants such as Firemaster BP-6 and Firemaster FF-1. The sole US producer of hexabromobiphenyl ceased production in November 1974 due to a 1973 incident in which Firemaster BP-6 was mistaken for a nutrient additive and 450-1,000 kg was added to animal feed in Michigan, thereby resulting in the contamination of livestock and subsequent contamination of meat, milk, and other diary products that were consumed by humans. If released to air, a vapor pressure of 5.2X10-8 mm Hg at 25 °C indicates hexabromobiphenyl will exist solely in the particulate phase in the ambient atmosphere. Particulate-phase hexabromobiphenyl will be removed from the atmosphere by wet and dry deposition. Hexabromobiphenyl has been shown to undergo direct photolysis in solutions of cyclohexane, resulting in lower brominated biphenyls as photodegradation products; however, it is unclear whether direct photolysis will occur for particulate phase hexabromobiphenyl in the atmosphere. If released to soil, hexabromobiphenyl is expected to have slight or no mobility based upon Koc values in the range of 2138-7413. Volatilization from moist soil surfaces is expected to be an important fate process based upon an estimated Henry's Law constant of 4.3X10-6 atm-cu m/mole; however, the strong adsorption of hexabromobiphenyl to soils should attenuate volatilization. Volatilization from dry soil surfaces is not expected to be an important environmental fate process based on the vapor pressure. Hexabromobiphenyl is persistent in the environment, with little or no biodegradation observed in soils or sediment under aerobic conditions; however debromination at the meta and para positions have been observed under anaerobic conditions. If released into water, hexabromobiphenyl is expected to adsorb to suspended solids and sediment based upon the range of Koc values. Volatilization from water surfaces is expected to be an important fate process based upon this compound's estimated Henry's Law constant. However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. Estimated volatilization half-lives for a model river and model lake are 14 and 165 days, respectively when adsorption is neglected. The estimated volatilization half-life from a model pond is 160 days when adsorption is considered. A BCF value of 18,100 measured in fish suggests bioconcentration in aquatic organisms is very high. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. The photolysis half-life of hexabromobiphenyl is approximately 9 hours following 12 hours of irradiation in cyclohexane solution, suggesting that there is potential for direct photolysis in sunlit surface waters. Since hexabromobiphenyl is no longer produced or used in the United States, the potential for occupational exposure and exposure to the general population is low. One of the significant sources of environmental contamination occurred as a result of the 1973 accidental mixup of FireMaster BP-6 and cattle feed in a number of farms in the lower peninsula of Michigan with 412 farms quarantined in June, 1975. Disposal of contaminated feed, animal carcasses and animal products contributed to environmental contamination. Therefore, exposure to PBBs for people residing in the lower peninsula of Michigan especially in the immediate vicinity of the FireMaster BP-6 contaminated areas, may still be occurring. However, environmental levels have likely decreased since the 1970s and current exposure, if any, will be at low levels. (SRC)

Hexabromobiphenyl's former production and use as an additive in flame retardants primarily in thermoplastics that were used in electrical housing equipment(1), may have resulted in its release to the environment through various waste streams(SRC). Although there are 42 possible congeners of hexabromobiphenyl, the 2,2',4,4',5,5' isomer was the key component in fire retardants such as Firemaster BP-6 and Firemaster FF-1(1,2). The production of hexabromobiphenyl was voluntarily discontinued in 1974(2).

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values in the range of 2138-7413(2), indicate that hexabromobiphenyl will have little or no mobility in soil(SRC). Volatilization of hexabromobiphenyl from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 4.3X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 5.2X10-8 mm Hg(3), and water solubility, 0.011 mg/L(4); however, adsorption is expected to attenuate volatilization(SRC). Hexabromobiphenyl is not expected to volatilize from dry soil surfaces(SRC) based on its vapor pressure(3). Hexabromobiphenyl is highly persistent under aerobic conditions, but may biodegrade slowly under anaerobic conditions(2). Hexabromobiphenyl was not degraded when incubated in a Brookston Loam (58% sand, 27.9% silt, 14.1% clay, 3.14% organic carbon, pH 7) and a Spinks loamy sand (81.1% sand, 14.5% silt, 4.4% clay, 1.1% organic carbon, pH 5.8) for 24 weeks maintained under aerobic conditions(3).

AQUATIC FATE: Based on a classification scheme(1), Koc values in the range of 2138-7413(2), indicate that hexabromobiphenyl is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 4.3X10-6 atm-cu m/mole(SRC),derived from its vapor pressure, 5.2X10-8 mm Hg(4), and water solubility, 0.011 mg/L(5); however, adsorption to suspended solids and sediment is expected to attenuate volatilization(SRC). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 14 and 165 days, respectively, if adsorption is ignored(SRC). The estimated volatilization half-life from a model pond is about 160 days when adsorption is considered(6). According to a classification scheme(7), a BCF of 18,100 measured in fathead minnows (8), suggests bioconcentration in aquatic organisms is very high(SRC). Hexabromobiphenyl is resistant to degradation under aerobic conditions, but may slowly undergo debromination at the meta and para positions under anaerobic conditions(2). Hexabromobiphenyl is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(2,9). The photolysis half-life of hexabromobiphenyl (calculated using the degradation rates of 6 isomers) is approximately 9 hours following 12 hours of irradiation in cyclohexane solution(10), suggesting that there is potential for direct photolysis in sunlit surface waters(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), hexabromobiphenyl, which has a vapor pressure of 5.2X10-8 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase hexabromobiphenyl may be removed from the air by wet and dry deposition(SRC). In solution, hexabromobiphenyl has been shown to undergo direct photolysis resulting in lower brominated biphenyls as photodegradation products(3,4); however, it is unclear whether direct photolysis will occur for particulate phase hexabromobiphenyl in the atmosphere.

AEROBIC: Higher brominated biphenyls such as hexabromobiphenyl are resistant to biodegradation under aerobic conditions(1). 2,2',4,4',5,5'-Hexabromobiphenyl was slowly degraded to lower brominated biphenyls over the course of several years in soil samples contaminated with polybrominated biphenyls from a former manufacturing site(2). Hexabromobiphenyl was not degraded when incubated in a Brookston Loam (58% sand, 27.9% silt, 14.1% clay, 3.14% organic carbon, pH 7) and a Spinks loamy sand (81.1% sand, 14.5% silt, 4.4% clay, 1.1% organic carbon, pH 5.8) for 24 weeks(3). Hexabromobiphenyl added at 0.4 and 0.8 ppm to 25 grams of a Brookston Loam (58% sand, 27.9% silt, 14.1% clay, 3.14% organic carbon, pH 7), showed little or no biodegradation after a one year incubation period(4).

ANAEROBIC: Anaerobic microorganisms have been shown to degrade the higher brominated biphenyls(1). Anaerobic biodegradation involves the debromination at the meta and para positions, with no reactions observed at the ortho position(2). 2,2',4,4',5,5'-Hexabromobiphenyl, present in the fire retardant Firemaster, had approximately 32% debromination at the meta and para positions when incubated in anaerobic microcosms prepared from Hudson River sediment over a 32 week incubation period(2).

Hexabromobiphenyl is subject to direct photolysis in the environment with the subsequent formation of lower brominated biphenyls as degradation products(1). In the atmosphere, hexabromobiphenyl will exist primarily in the particulate-phase, thus reaction with photochemically produced hydroxyl radicals is expected to be a slow abiotic degradation process(1). Irradiation of Firemaster BP-6, a fire retardant agent consisting of several brominated biphenyls including 8 isomers of hexabromobiphenyl, was carried out in cyclohexane with a UV light source having peak energy output at 300 nm(2). Following 12 hours of irradiation approximately 47%, 25%, 62%, 85%, 68%, and 80% photodegradation was observed for 2,2',3,4,4'5-, 2,2',3,4',5',6-, 2,2',4,4',5,5'-, 2,3,3',4,4'5-, 2,3,3',4,4',5'- and 2,3',4,4',5,5'-hexabromobiphenyl isomers, respectively(2). Using the degradation losses of all six isomers over the 12 hour irradiation period, a direct photolysis half-life of approximately 9 hours is calculated for hexabromobiphenyl in cyclohexane(SRC). Hexabromobiphenyl is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(1).

LC50 Colinus virginianus (Bobwhite quail) dietary 428 mg/kg/8 days /FireMaster/ /from table/

LC50 Mustela vison (Mink) dietary 3.95 ppm/313 days /FireMaster FF-1/

/BIRDS and MAMMALS/ Observations of intoxicated Bobwhite quails, prior to death, included asthenia, low carriage, an unkempt appearance, wing droop, diarrhea, limited ataxia, and general lethargy. /Birds were given a dietary concentration of 100-700 mg/kg feed for 5 days of an 8 day observation period. Feed intake was also reduced./ /FireMaster/

/BIRDS and MAMMALS/ The sensitivity of three genetic lines of Japanese quail to polybrominated biphenyls (PBBs) was evaluated using criteria of egg production, reproduction, and induction of the hepatic microsomal mixed-function oxidase (MFO) system. Two genetic lines of quail, developed to diverge in their plasma cholesterol response to exogenous adrenocorticotropin (ACTH) (a "Low" line and a "High" line), were compared to a random-bred line ("Random"). ACTH administration caused increases in plasma cholesterol in the Low line that were 15 and 39% below the Random-line values in males and females, respectively, while High-line values were 31% higher in males and 36% higher in females when compared to the respective Random-line values. Hepatic activities of aryl hydrocarbon hydroxylase (AHH) and hexobarbital hydroxylase (HxH) were not significantly influenced by ACTH administration or by genetic line in either sex. PBBs fed at 40 or 80 mg/kg diet for 5 wk resulted in significant increases in hepatic AHH and aminopyrine N-demethylase (APND) activities and cytochrome P-450 concentrations. The induction of AHH, APND, and cytochrome P-450 was significantly less in Low-line males in comparison to Random- and High-line males, while the induction of AHH was less in Low-line females when compared to females from the other two lines, based on covariance analysis. In terms of reproductive parameters, there was a greater adverse effect on egg production at 80 ppm PBBs in Low-line females when compared to the Random and High lines. These data indicate an example in which the biological toxicity of a compound and the induction of a 3-methylcholanthrene-type hepatic enzyme are not directly correlated.

5.00e+02

Volatile

Hexabromobiphenyl's former production and use as an additive in flame retardants primarily in thermoplastics that were ultimately used in electrical housing equipment, may have resulted in its release to the environment through various waste streams. Hexabromobiphenyl consists of 42 possible congeners, the 2,2',4,4',5,5' isomer was the key component in flame retardants such as Firemaster BP-6 and Firemaster FF-1. The sole US producer of hexabromobiphenyl ceased production in November 1974 due to a 1973 incident in which Firemaster BP-6 was mistaken for a nutrient additive and 450-1,000 kg was added to animal feed in Michigan, thereby resulting in the contamination of livestock and subsequent contamination of meat, milk, and other diary products that were consumed by humans. If released to air, a vapor pressure of 5.2X10-8 mm Hg at 25 °C indicates hexabromobiphenyl will exist solely in the particulate phase in the ambient atmosphere. Particulate-phase hexabromobiphenyl will be removed from the atmosphere by wet and dry deposition. Hexabromobiphenyl has been shown to undergo direct photolysis in solutions of cyclohexane, resulting in lower brominated biphenyls as photodegradation products; however, it is unclear whether direct photolysis will occur for particulate phase hexabromobiphenyl in the atmosphere. If released to soil, hexabromobiphenyl is expected to have slight or no mobility based upon Koc values in the range of 2138-7413. Volatilization from moist soil surfaces is expected to be an important fate process based upon an estimated Henry's Law constant of 4.3X10-6 atm-cu m/mole; however, the strong adsorption of hexabromobiphenyl to soils should attenuate volatilization. Volatilization from dry soil surfaces is not expected to be an important environmental fate process based on the vapor pressure. Hexabromobiphenyl is persistent in the environment, with little or no biodegradation observed in soils or sediment under aerobic conditions; however debromination at the meta and para positions have been observed under anaerobic conditions. If released into water, hexabromobiphenyl is expected to adsorb to suspended solids and sediment based upon the range of Koc values. Volatilization from water surfaces is expected to be an important fate process based upon this compound's estimated Henry's Law constant. However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. Estimated volatilization half-lives for a model river and model lake are 14 and 165 days, respectively when adsorption is neglected. The estimated volatilization half-life from a model pond is 160 days when adsorption is considered. A BCF value of 18,100 measured in fish suggests bioconcentration in aquatic organisms is very high. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. The photolysis half-life of hexabromobiphenyl is approximately 9 hours following 12 hours of irradiation in cyclohexane solution, suggesting that there is potential for direct photolysis in sunlit surface waters. Since hexabromobiphenyl is no longer produced or used in the United States, the potential for occupational exposure and exposure to the general population is low. One of the significant sources of environmental contamination occurred as a result of the 1973 accidental mixup of FireMaster BP-6 and cattle feed in a number of farms in the lower peninsula of Michigan with 412 farms quarantined in June, 1975. Disposal of contaminated feed, animal carcasses and animal products contributed to environmental contamination. Therefore, exposure to PBBs for people residing in the lower peninsula of Michigan especially in the immediate vicinity of the FireMaster BP-6 contaminated areas, may still be occurring. However, environmental levels have likely decreased since the 1970s and current exposure, if any, will be at low levels. (SRC)

Hexabromobiphenyl's former production and use as an additive in flame retardants primarily in thermoplastics that were used in electrical housing equipment(1), may have resulted in its release to the environment through various waste streams(SRC). Although there are 42 possible congeners of hexabromobiphenyl, the 2,2',4,4',5,5' isomer was the key component in fire retardants such as Firemaster BP-6 and Firemaster FF-1(1,2). The production of hexabromobiphenyl was voluntarily discontinued in 1974(2).

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values in the range of 2138-7413(2), indicate that hexabromobiphenyl will have little or no mobility in soil(SRC). Volatilization of hexabromobiphenyl from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 4.3X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 5.2X10-8 mm Hg(3), and water solubility, 0.011 mg/L(4); however, adsorption is expected to attenuate volatilization(SRC). Hexabromobiphenyl is not expected to volatilize from dry soil surfaces(SRC) based on its vapor pressure(3). Hexabromobiphenyl is highly persistent under aerobic conditions, but may biodegrade slowly under anaerobic conditions(2). Hexabromobiphenyl was not degraded when incubated in a Brookston Loam (58% sand, 27.9% silt, 14.1% clay, 3.14% organic carbon, pH 7) and a Spinks loamy sand (81.1% sand, 14.5% silt, 4.4% clay, 1.1% organic carbon, pH 5.8) for 24 weeks maintained under aerobic conditions(3).

AQUATIC FATE: Based on a classification scheme(1), Koc values in the range of 2138-7413(2), indicate that hexabromobiphenyl is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 4.3X10-6 atm-cu m/mole(SRC),derived from its vapor pressure, 5.2X10-8 mm Hg(4), and water solubility, 0.011 mg/L(5); however, adsorption to suspended solids and sediment is expected to attenuate volatilization(SRC). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 14 and 165 days, respectively, if adsorption is ignored(SRC). The estimated volatilization half-life from a model pond is about 160 days when adsorption is considered(6). According to a classification scheme(7), a BCF of 18,100 measured in fathead minnows (8), suggests bioconcentration in aquatic organisms is very high(SRC). Hexabromobiphenyl is resistant to degradation under aerobic conditions, but may slowly undergo debromination at the meta and para positions under anaerobic conditions(2). Hexabromobiphenyl is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(2,9). The photolysis half-life of hexabromobiphenyl (calculated using the degradation rates of 6 isomers) is approximately 9 hours following 12 hours of irradiation in cyclohexane solution(10), suggesting that there is potential for direct photolysis in sunlit surface waters(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), hexabromobiphenyl, which has a vapor pressure of 5.2X10-8 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase hexabromobiphenyl may be removed from the air by wet and dry deposition(SRC). In solution, hexabromobiphenyl has been shown to undergo direct photolysis resulting in lower brominated biphenyls as photodegradation products(3,4); however, it is unclear whether direct photolysis will occur for particulate phase hexabromobiphenyl in the atmosphere.

AEROBIC: Higher brominated biphenyls such as hexabromobiphenyl are resistant to biodegradation under aerobic conditions(1). 2,2',4,4',5,5'-Hexabromobiphenyl was slowly degraded to lower brominated biphenyls over the course of several years in soil samples contaminated with polybrominated biphenyls from a former manufacturing site(2). Hexabromobiphenyl was not degraded when incubated in a Brookston Loam (58% sand, 27.9% silt, 14.1% clay, 3.14% organic carbon, pH 7) and a Spinks loamy sand (81.1% sand, 14.5% silt, 4.4% clay, 1.1% organic carbon, pH 5.8) for 24 weeks(3). Hexabromobiphenyl added at 0.4 and 0.8 ppm to 25 grams of a Brookston Loam (58% sand, 27.9% silt, 14.1% clay, 3.14% organic carbon, pH 7), showed little or no biodegradation after a one year incubation period(4).

ANAEROBIC: Anaerobic microorganisms have been shown to degrade the higher brominated biphenyls(1). Anaerobic biodegradation involves the debromination at the meta and para positions, with no reactions observed at the ortho position(2). 2,2',4,4',5,5'-Hexabromobiphenyl, present in the fire retardant Firemaster, had approximately 32% debromination at the meta and para positions when incubated in anaerobic microcosms prepared from Hudson River sediment over a 32 week incubation period(2).

Hexabromobiphenyl is subject to direct photolysis in the environment with the subsequent formation of lower brominated biphenyls as degradation products(1). In the atmosphere, hexabromobiphenyl will exist primarily in the particulate-phase, thus reaction with photochemically produced hydroxyl radicals is expected to be a slow abiotic degradation process(1). Irradiation of Firemaster BP-6, a fire retardant agent consisting of several brominated biphenyls including 8 isomers of hexabromobiphenyl, was carried out in cyclohexane with a UV light source having peak energy output at 300 nm(2). Following 12 hours of irradiation approximately 47%, 25%, 62%, 85%, 68%, and 80% photodegradation was observed for 2,2',3,4,4'5-, 2,2',3,4',5',6-, 2,2',4,4',5,5'-, 2,3,3',4,4'5-, 2,3,3',4,4',5'- and 2,3',4,4',5,5'-hexabromobiphenyl isomers, respectively(2). Using the degradation losses of all six isomers over the 12 hour irradiation period, a direct photolysis half-life of approximately 9 hours is calculated for hexabromobiphenyl in cyclohexane(SRC). Hexabromobiphenyl is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(1).

A BCF value of 18,100 was measured in fathead minnow exposed to hexabromobiphenyl for 32 days(1). According to a classification scheme(2), this measured BCF value suggests that bioconcentration in aquatic organisms is very high(SRC).

The Koc of hexabomobiphenyl was reported to range from 2138-7413(1). According to a classification scheme(2), this range of Koc values indicates that hexabromobiphenyl should possess slight mobility or be totally immobile in soils(SRC). The leaching potential of hexabromobiphenyl was assessed using four soils from Michigan(3). Leaching studies using 100 ppm of hexabromobiphenyl applied to the surface of the soils and leached with 20 times the average annual rainfall in Michigan indicated that less than 0.6% of the initially applied amount leached through the soil columns and it was concluded that hexabromobiphenyl should not leach below its incorporation depth(3).

The Henry's Law constant for hexabromobiphenyl is estimated as 4.3X10-6 atm-cu m/mole(SRC) derived from its vapor pressure, 5.2X10-8 mm Hg(1), and water solubility, 0.011 mg/L(2). This Henry's Law constant indicates that hexabromobiphenyl is expected to volatilize from water surfaces(3); however, adsorption to suspended solids and sediment should attenuate the potential for volatilization(SRC). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(3) is estimated as 14 days if adsorption is neglected(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(3) is estimated as 165 days if adsorption is neglected (SRC). The estimated volatilization half-life from a model pond is about 160 days if adsorption is considered(4). Hexabromobiphenyl is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1). 14C labeled hexabromobiphenyl was incubated in soils from Michigan and stored in the dark for 1 year(5). Less than 0.2% of the originally applied hexabromobiphenyl was shown to volatilize(5).

SURFACE WATER: Hexabromobiphenyl was identified, not quantified, in Lake Ontario and Lake Huron(1).

A major source of environmental contamination of hexabromobiphenyl occurred in the lower peninsula of Michigan where Firemaster BP-6 was accidentally substituted for a cattle nutrient in feed sent to a number of farms in 1973(1). The disposal of contaminated feed, animal carcasses (poultry, dairy cattle, swine) and animal products such as meat, eggs, and diary products was a major source of hexabromobiphenyl emitted to the environment(1).

Hexabromobiphenyl was detected in soil and sludge samples at 30 and 3800 ppb, respectively in NJ(1). Soil at three sites from a farm contaminated with Firemaster BP-6 contained levels of 4.1, 5.7 and 4.4 ppb of 2,2',4,4',5,5'-hexabromobiphenyl(2). Soil samples from 30 farms located in Michigan heavily contaminated with Firemaster BP-6 contained polybrominated biphenyl (PBBs) at levels of 0.1 to 224 ppb(3). Although levels of hexabromobiphenyl were not quantified in these samples, 2,2',4,4',5,5'-hexabromobiphenyl is the main constituent of Firemaster BP-6 and is likely to be the primary contaminant in the soils.

SOURCE DOMINATED: Hexabromobiphenyl was detected at 0.06 ng/cu m in the air 900 meters downwind from the White Chemical Company in Bayonne, NJ(1).

3,3',4,4',5,5'-Hexabromobiphenyl was detected at a max concn of 36 mg/kg fat in samples from fish obtained from the Baltic Sea and concns of 2,2',4,4',5,5'-hexabromobiphenyl ranged from 0.2-4.2 mg/kg(1).

The concentration of hexabromobiphenyl ranged from 13-61 ug/kg wet weight from harbor seals collected from the North Sea(1). In whitebeaked dolphins from the North Sea, the concentration of hexabromobiphenyl was 13 ug/kg wet weight(1).

Hexabromobiphenyl is no longer produced or used in the United States(1,2); therefore, the potential for occupational exposure and exposure to the general public is low. Hexabromobiphenyl was a major constituent in Firemaster BP-6 and Firemaster FF-1, which were used in thermoplastics incorporated into electronic products such as televisions and computers which are eventually landfilled or incinerated(1). Farms or other sites located in Michigan that were heavily contaminated with Firemaster BP-6 may also contain residual quantities of hexabromobiphenyl since this compound is recalcitrant in the environment. Persons living near landfills or contaminated sites in Michigan may potentially be exposed to hexabromobiphenyl(SRC).

Polybrominated biphenyls (PBB) were detected in blood and adipose tissue of 1788 persons in Michigan(1). The source of the PBBs was thought to be from the accidental substitution of Firemaster (a flame retardant largely composed of 2,2',4,4',5,5'-hexabromobiphenyl) for cattle feed in the summer of 1973. Resulting in contaminated meat, butter, milk and other diary products that were eventually consumed by humans. Of the 1681 serum samples tested, 70% were positive for PBBs and of the 844 adipose tissues tested, over 97% were positive(1). Levels were highest in that part of the state where meat and diary products were most contaminated, and levels were lowest in the upper peninsula, furthest from the source. Hexabromobiphenyl was identified, not quantified, in 8%, 41%, 18%, 57%, 13% and 44% of adipose tissue from autopsy bodies in six Ontario Canada municipalities(2).

Hexabromobiphenyl was detected (detection limit, 6.6 ug/kg) at a frequency of 8-57% in human adipose tissue samples from six Canadian Great Lakes municipalities in 1984(1). The concn of 2,2',4,4',5,5'-hexabromobiphenyl in adipose tissue samples pooled from tissues of the general population of the conterminous United States ranged from 1 to 2 ug/kg(2). In the fall of 1993, the serum levels of BB-167 (2,2',4,4',5,5'-hexabromobiphenyl) in 32 subjects, approx 10 of whom consumed sport fish from the Great Lakes, were measured(3). The Lake Huron fish consumers had the highest levels of PBBs (avg, 0.6 ppb) and Lake Erie fish consumers had the lowest (avg, 0.2 ppb)(3).

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.