Environmental Profiles of Chemical Flame-Retardant Alternatives for

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NEUROTOXICITY Conclusion: The available neurotoxicity data were judged inadequate to meet the endpoint. Basis for Conclusion: Available acute and 28-day studies indicate that there is a risk of delayed neurotoxicity from exposure to Proprietary G. Most studies either were conducted on undefined substances or were not described in sufficient detail. A summary of a study on purified components of [Formulated] flame retardants suggests that [Chemical 4] or [Chemical 2] are the neurotoxic components of these mixtures; however, details of the in vivo study in hens were not located. The neurotoxicity of Proprietary G preparations would be dependent on the relative content of [Formulation 11] isomers. No data are available for the full battery of tests for functional neurotoxicity or for developmental neurotoxicity. Delayed Neurotoxicity Conclusion: The available delayed neurotoxicity data were judged adequate to meet the endpoint. Basis for Conclusion: The acute study (experiment A) on a defined Proprietary G mixture departed from guideline in that enzyme inhibition was assayed 24 hours after dosing rather than 48 hours, but reported significant suppression of both brain neurotoxic esterase and plasma cholinesterase levels. The longer study did not conduct a complete battery of neurobehavioral tests as stipulated under the guideline, but reported adverse effects on motor coordination at all doses on the day of treatment. The highest dose (11,700 mg/kg) exceeded that recommended under the guideline, but that deviation does not affect the conclusion of the study. Studies on purified components of [Formulated] flame retardants identified the neurotoxic components, but were not adequately described. The majority of studies suggest that delayed neurotoxicity may result from exposure to oral doses in excess of 1,000 mg//kg. • Acute and 28-Day Delayed Neurotoxicity of Organophosphorus Substances (OPPTS Harmonized Guideline 870.6100; OECD Guideline 418, 419) Critical Studies Type: Acute oral delayed neurotoxicity Species, strain, sex, number: Hen, 12-14 months old, White Leghorn, 4/dose for experiment A; 10-12/dose for experiment B. Purity: Proprietary G with the composition as in the following table. 10-11
Composition of Proprietary G assayed by Ref. 37 Component Percent Total Proprietary G
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Volume 2 Chemical Hazard Reviews Fu
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LIST OF TABLES Page 1-1 Summary of
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Flame Retardant Alternatives Triphe
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Triphenyl Phosphate: Existing Data
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Type: Acute oral LD50 Species, stra
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concentration was much higher, but
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Vehicle: Not reported, but acute or
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• 90-Day Oral Toxicity in Rodents
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Subchronic Inhalation Toxicity: 90-
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hydroureter, enlarged ureter proxim
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NEUROTOXICITY Conclusion: The avail
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Critical Studies Type: Delayed neur
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Neurotoxicity (Adult) Conclusion: T
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Species, strain, sex, number: Rat,
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Type: Mitotic Gene Conversion Speci
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Study Reference Ahrens et al., 1978
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Study Reference Geiger et al., 1986
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Study Reference Mayer et al., 1981
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Study Reference Sasaki et al., 1981
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those reported in the publicly avai
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Algal Toxicity (OPPTS Harmonized Gu
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Study Reference Millington et al.,
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Chronic Toxicity to Fish (OPPT Harm
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Chronic Toxicity to Aquatic Inverte
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Log K ow Reference 4.63 Saeger, 197
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Oxidation/Reduction: No data Oxidat
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Bioconcentration Environmental Fate
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Fish Metabolism: Conclusion: The me
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Study Type/ Method Innoculum Acclim
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Sediment/Water Biodegradation: Conc
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References Ahrens, V; Henion, J; Ma
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Dorby, A; Keller, R. 1957. Vapor pr
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Johnson, MK. 1975. Organophosphorus
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Perry, R; Green, D. 1984. Vapor pre
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Flame Retardant Alternatives Tribro
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Tribromoneopentyl alcohol: Existing
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Results: Male mortality was 2/5 at
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Additional Study: An acute inhalati
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application, four rabbits displayed
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Bladder effects were seen in some o
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• Combined Repeated Dose Toxicity
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• Immunotoxicity (OPPTS Harmonize
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tissue, one with rabbit tissue) sug
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Acute Toxicity to Aquatic Organisms
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1-Propanol, 2,2-dimethyl-, tribromo
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Environmental Fate Bioconcentration
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References AmeriBrom, Inc. 1982a. A
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Flame Retardant Alternatives Tris(1
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Tris(1,3-dichloro-2-propyl) phospha
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Species, strain, sex, number: Rat,
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Results: No mortality after 14 days
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Additional Studies: Another study,
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occurred in treated groups compared
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high enough to induce significant r
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Doses: 0, 25, 100, and 400 mg/kg/da
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mid-dose of 20 mg/kg/day as a LOAEL
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Critical Studies Type: Acute oral d
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English summary and therefore could
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Basis for Conclusion: TDCPP has bee
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Gene Mutation in Vivo: C Sex-linked
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TDCPP administered as 2,000 mg/kg b
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Another study showed that the 96-ho
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Study Reference Akzo- Nobel, Inc.,
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Study Reference Sasaki et al., 1981
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Table 3-2. Summary of available acu
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hours (Unpublished study conducted
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Terrestrial Organism Toxicity Acute
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Oxidation/Reduction: No data Meltin
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pH: This chemical does not contain
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Species Rate Comment Reference Kill
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Pyrolysis Products Reference When h
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Brusick, D; Matheson, D; Jagannath,
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Majeska, JB; Matheson, DW. 1983. Qu
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Thomas, MB; Collier, TA. 1985. Tolg
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Proprietary A: Chloroalkyl phosphat
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Proprietary A: Chloroalkyl phosphat
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Basis for Conclusion: The available
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Additional Studies and Information:
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Conclusion: The available subchroni
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Basis for Conclusion: No repeated-e
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Prenatal Developmental Toxicity Stu
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Combined Chronic Toxicity/Carcinoge
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Basis for Conclusion: The delayed n
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histopathological effects in the ne
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Immunotoxicity (OPPTS Harmonized Gu
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C In vitro Mammalian Cell Gene Muta
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Chromosomal Aberration in Vivo: C M
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Aquatic Organism Toxicity Ecotoxici
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Study Reference Species Tested Ref.
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Acute Toxicity to Freshwater Invert
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Chronic Toxicity to Freshwater and
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CAS MF MW SMILES Physical/Chemical
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Vapor Pressure (torr//C) Reference
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Study type/ Method Innoculum Acclim
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Flame Retardant Alternatives Propri
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Proprietary B: Aryl phosphate Exist
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ACUTE TOXICITY Human Health Endpoin
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Additional Studies and Information:
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were elevated in all treated groups
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Basis for Conclusion: No pertinent
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Experiment B. Doses were chosen bas
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These studies may be indicated, for
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• Mammalian Bone Marrow Chromosom
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• Algal Toxicity (OPPTS Harmonize
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Bioconcentration Fish: No data Daph
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Flame Retardant Alternatives Propri
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Proprietary C: Chloroalkyl phosphat
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Basis for Conclusion: Acute oral to
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Acute Eye Irritation (OPPTS Harmoni
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Critical Studies: Type: Dermal sens
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C Reproduction/Developmental Toxici
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• Combined Chronic Toxicity/Carci
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Gene Mutation in Vitro: • Bacteri
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Acute Toxicity to Aquatic Organisms
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• Acute Oral Toxicity in Birds (O
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Corrosion Characteristics: No data
Page 243 and 244: determined at 50°C and it was foun
Page 245 and 246: Proprietary D: Reactive brominated
Page 247 and 248: Chemical Identity Proprietary D: Re
Page 249 and 250: Acute Dermal Irritation (OPPTS Harm
Page 251 and 252: • Prenatal Developmental Toxicity
Page 253 and 254: Gene Mutation in vitro C Bacterial
Page 255 and 256: • Chronic Toxicity to Freshwater
Page 257 and 258: Bioconcentration Fish: No data Daph
Page 259 and 260: Proprietary E: Tetrabromophthalate
Page 261 and 262: Proprietary E: Tetrabromophthalate
Page 263 and 264: • Reproduction and Fertility Effe
Page 265 and 266: GENOTOXICITY Conclusion: No availab
Page 267 and 268: Acute and Subchronic Toxicity to Te
Page 269 and 270: Bioconcentration Fish: No data Daph
Page 271 and 272: Proprietary F: Halogenated aryl est
Page 273 and 274: Proprietary F: Halogenated aryl est
Page 275 and 276: REPRODUCTIVE TOXICITY Conclusion: N
Page 277 and 278: • Neurotoxicity Screening Battery
Page 279 and 280: Basis for Conclusion: No pertinent
Page 281 and 282: Henry’s Law Constant: No data 9-1
Page 283 and 284: Anaerobic Biodegradation: No data P
Page 285 and 286: Proprietary G: Triaryl phosphate, i
Page 289 and 290: Acute Inhalation Toxicity (OPPTS Ha
Page 291 and 292: SUBCHRONIC TOXICITY Subchronic Oral
Page 293: • Prenatal Developmental Toxicity
Page 297 and 298: Several components of the [Formulat
Page 299 and 300: As described in unvalidated robust
Page 301 and 302: Acute Toxicity to Aquatic Organisms
Page 305 and 306: Sediment/Water Biodegradation: No d
Page 307 and 308: Proprietary H: Halogenated aryl est
Page 309 and 310: Proprietary H: Halogenated aryl est
Page 311 and 312: REPRODUCTIVE TOXICITY Conclusion: N
Page 313 and 314: IMMUNOTOXICITY Conclusion: No avail
Page 317 and 318: Henry’s Law Constant: No data 11-
Page 321 and 322: Proprietary I: Organic phosphate es
Page 323 and 324: Proprietary I: Organic phosphate es
Page 327 and 328: CARCINOGENICITY Conclusion: No avai
Page 329 and 330: No studies were located that were r
Page 331 and 332: • Chronic Toxicity to Freshwater
Page 333 and 334: Explosivity: No data Corrosion Char
Page 337 and 338: Proprietary J: Aryl phosphate Exist
Page 339 and 340: Proprietary J: Aryl phosphate Synon
Page 341 and 342: Results: No deaths. Clinical signs
Page 343 and 344: As described in a robust summary, m
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third animal on days 2 and 3 only.
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however, identify target organs tha
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Basis for Conclusion: The only avai
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Basis for Conclusion: The available
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EPA proposed guidelines (Ref. 58).
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[Formulation 2] (typically 43% Prop
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No additional, pertinent acute toxi
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Proprietary J: Aryl phosphate CAS M
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Odor: No data Oxidation/Reduction C
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Degradation and Transport Photolysi
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Sediment Temp. T 1/2 Comments Refer
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Proprietary K: Aryl phosphate Exist
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Proprietary K: Aryl phosphate CAS M
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• Reproduction and Fertility Effe
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GENOTOXICITY Conclusion: No availab
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Acute and Subchronic Toxicity to Te
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Proprietary L: Aryl phosphate Exist
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Proprietary L: Aryl phosphate Synon
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• Reproduction and Fertility Effe
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GENOTOXICITY Conclusion: No availab
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Acute and Subchronic Toxicity to Te
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United States Environmental Protect
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