Environmental Profiles of Chemical Flame-Retardant Alternatives for

Type: Acute oral LD50
Species, strain, sex, number: Rat, Sprague-Dawley, male and female, number not specified
Dose: Up to 15,800 mg/kg
Purity: GC-verified, but not specifically reported
Vehicle: Corn oil
Observation period: 14 days post dosing
Method: LD50 calculated according to DeBeer (1945); not specified whether fed or fasted at
time of dosing; 14-day post-exposure observation period; mortality only
Results: LD50 = 10,800 mg/kg; actual mortality data not reported
Reference: Johannsen et al., 1977
Type: Acute oral limit test
Species, strain, sex, number: Mouse, strain not specified, male and female, 5 total/dose
Doses: 2,500 and 5,000 mg/kg
Purity: Not specified
Vehicle: Emulsion in aqueous gum acacia
Method: Similar to limit test; not specified whether fed or fasted at time of dosing; 8-day
observation period; observations limited to mortality and overt signs
Results: No deaths at either dose; therefore, LD50 >5,000 mg/kg; slight stupor
Reference: Ciba-Geigy Ltd., 1954
Type: Acute oral limit test
Species, strain, sex, number: Rabbit, strain and sex not specified, 1/dose
Purity: Technical grade TPP
Doses: 3,000 and 5,000 mg/kg
Vehicle: Suspended in aqueous gum acacia
Method: Preliminary limit test, observation was for “several days”, observations limited to
clinical signs and mortality
Results: Neither rabbit died, indicating LD >5,000 mg/kg; both had diarrhea
Reference: Dow Biochemical Research, 1934
Additional Studies and Information:
Other studies that were of lesser quality or were reported in less detail are generally consistent
with the above studies (Houghton EF & Company, no date; Kettering Lab, 1945; Smith et al.,
1932; Sutton et al., 1960).
Specific organ toxicity was generally not observed in the studies that include gross pathological
examinations. Some signs possibly indicative of neurotoxicity (lassitude incoordination,
tremors, or weakness) were observed in a few studies (Ciba-Geigy Ltd. 1954; Kettering Lab,
1945; Smith et al., 1932). It has been suggested that at the very high doses employed in these
acute toxicity studies, even small amounts of impurities could be responsible for the apparent
neurotoxicity, which has not been seen with purified TPP (see section on neurological effects),
or that the signs may have been secondary to other effects.
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