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Ecotoxicological information

Toxicity to birds

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Description of key information

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.

Key value for chemical safety assessment

Long-term EC10, LC10 or NOEC for birds:
1 000 mg/kg food

Additional information

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) - 1 weeks.

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 weeks.

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.

Halldin 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 low.

Sashihara 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.

Considering 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.