Environmental Profiles of Chemical Flame-Retardant Alternatives for

neurotoxicity in 4/4 hens treated with 300 mg/kg/day for 5 days (cumulative dose of 1,500 mg/kg).
The acute oral LD50 in hens exceeded 10,000 mg/kg (no mortality data reported).
Reference: Ref. 34
Type: Acute oral delayed neurotoxicity
Species, strain, sex, number: Hen, female, older than 14 months, 4 control and 8 test birds
Purity: Not reported; [Formulation 3] is >99% Proprietary J and 99% purity
and tested at doses as high as 1,000 mg/kg in mature hens for neurotoxicity and suppression of
neurotoxic esterase (Ref. 24). Details of these studies were not located. [Chemical 2], [Chemical
1], and Proprietary J elicited no signs of neurotoxicity and no suppression of NTE levels. [Chemical
7] was also judged to be non-neurotoxic, eliciting no ataxia or other signs of neurotoxicity and
insignificant suppression of NTE (-4% or -15%) in two tests. However, [Chemical 8] was
neurotoxic, eliciting ataxia and neurotoxicity, as well as suppression of NTE levels (by -71% and
-57 to -62% in two tests) at 1 mL/kg. The author suggested that neurotoxicity was associated with
[Chemical Class 1] with an oxidizable alpha-hydrogen.
Hens given [Formulation 4] (100% [Chemical Class 1]; 30-35% Proprietary J, see Table 1) at a dose
of 5,000 mg/kg/day on five consecutive days by oral gavage lost weight and developed paralysis
(4/4) and 3/4 died before the end of the test (Ref. 14). The study authors suggested that residual
[Chemical Class 4] chemicals may have been responsible for the observed neurotoxicity.
Hens treated with 2,000 mg/kg of [Formulation 10] did not elicit clinical signs of neurotoxicity,
lesions of the nervous system, or depression in NTE, whereas hens treated with TOCP at 500 mg/kg
showed all of these effects (Ref. 35 abstract as described in Ref. 61).
There was no effect on survival or walking behavior among a group of 15 hens (12-14 months old)
given oral doses of 11, 679 mg/kg [Formulation 5] (see Note e in Table 1) on days 1 and 21 under
13-17