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EC number: 201-245-8
CAS number: 80-05-7
Bisphenol A; BPA
There were no treatment-related mortalities, overt signs of toxicity or treatment-related effects upon body weight or feed consumption at any of the concentrations tested. Additionally, there were no treatment-related effects upon any of the reproductive parameters measured at the 1, 30, 300 or 1000 ppm a.i. test concentrations. The no-observed-effect concentration for Japanese quail exposed to bisphenol A in the diet during the study was 1000 ppm a.i. (168 mg a.i./kg/day), the highest concentration tested.
The key study from Frey et al., 2010, was
conducted according at the method OECD guideline 206 "Avian Reproduction
Test". The objective of this study was to evaluate the effects upon the
adult Japanese quail (Coturnix japonica) of dietary exposure to
Bisphenol A over a period of nine weeks. Effects on adult health, body
weight, and feed consumption were evaluated. In addition, the effects of
adult exposure to Bisphenol A on the number of eggs laid, fertility,
embryo viability, hatchability, offspring survival, and egg shell
thickness were evaluated.
The primary phases of the study and their
approximate durations were:
1. Acclimation - 4 weeks.
2. Pre-egg laying (with photostimulation) -
3. Egg laying - Approximately 8 weeks.
4. Post-adult termination (final incubation,
hatching, and 14-day offspring rearing period) – 5 weeks.
The total duration of the study were14
There were no treatment-related mortalities,
overt signs of toxicity or treatment-related effects upon body weight or
feed consumption at any of the concentrations tested. Additionally,
there were no treatment-related effects upon any of the reproductive
parameters measured at the 1, 30, 300 or 1000 ppm a.i. test
concentrations. The no-observed-effect concentration for Japanese quail
exposed to Bisphenol A in the diet during the study was 1000 ppm a.i.
(168 mg a.i./kg/day), the highest concentration tested.
et al., 2001 performed three different studies with quail embryos or
adults after in ovo exposure to 67 µg/egg (uptake study), 67 µg/egg and
200 µg/g egg (male and female behavioural and reproduction study), or
105 µg/bird (female distribution study). The most relevant studies for
the assessment of reproductive effects are the male and female
reproductive variable assessment studies. For the male reproductive
variable assessment, 7-week old males were individually placed in metal
cages. Sexual behaviour tests were performed in the 8th week after
hatching. Neck grab and mount attempt were assessed upon placement with
a female. Blood for testosterone analysis was collected and testis
weight and gonadosomatic index were assessed. Female reproductive
variables assessed were egg laying and oviduct pathology. No significant
oestrogen-like effects were observed in males or females treated with
Bisphenol A. There was a tendency for females exposed to the 200 µg/g
egg to retain the right oviduct. Bisphenol A was readily excreted by the
laying female as well as the growing embryo. In view of the data on
distribution, maternal transfer, embryonic uptake and oestrogenic
potency, it was concluded that the risk for adverse reproductive
toxicity in avian wildlife resulting from embryonic exposure is probably
et al., 2003 reported that hatchability was not significantly affected
by Bisphenol A exposure to embryos after egg injection. There was no
indication that Bisphenol A exposure significantly damaged chick embryos
as determined by the stage of development at death. The phenotypic ratio
of male chicks in the 10 and 100 ng/µL treatment groups was slightly
higher than the 50% ratio found in controls. When compared, the genotype
and phenotype ratios completely matched. The results of this study
indicate that low doses of Bisphenol A do not affect the hatchability or
embryonic development of chickens.
a supporting study to the two weight of evidence studies described
above, Berg et al., 2001 assessed embryo development just prior to hatch
in eggs that were treated by injection on day 3 of incubation. There was
a statistically significant increase in mortality in chickens at both
doses but no impact on quail. In quail embryos treated with 200 µg/g
Bisphenol A, malformations of the mullerian ducts occurred in 6 of the
14 females. No impact was seen in males or in either sex in chickens. In
quail embryos, Bisphenol A did not cause an increased ovotestis
frequency compared to controls. In chicken embryos, the ovotestis
frequency was 55% following exposure to 200 µg/g Bisphenol A, but none
were found in the 67 µg/g dose group. The risk for reproductive impacts
in avian wildlife, as predicted by this study, are probably low as the
doses required for effects in this study were fairly high.
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