Alcohols, C8-14, γ-ω-perfluoro

Endpoint summary

Additional information

MITI :

Published Result:

Chemical substance determined to be persistent but not highly bio-accumulative

Judgement: Non-biodegradability

Remarks: None reported

Test Method: Bio-concentration test

Acute Toxicity Test

LC50 (96 hr): > 125 mg/L

LC50 (48 hr): Not Reported

Species: Rice fish (Oryzias latipes)

Flow-through Test

Test Equipment: Improved type for a volatile substance

Test period. 60 days

Species: Carp (Cyprinus carpio)

Lipid Content (%): Not Reported

Lipid Content (%) - start of testing: 4.2

Lipid Content (%) - end of testing: 3.97

Test Concentration - 1st Concentration: 10 microg/L

BCF– 1st Concentration: 200 - 1100

Test Concentration - 2nd Concentration: 1 microg/L

BCF– 2nd Concentration 87 - 310

Partition coefficient(noctanol/ water): not reported

Minimum (log Pow)

Maximum (log Pow)

Average (log Pow)

Brandsma:

The present study did not allow the detection of FTOHs because no validated method was available at the time. Therefore, this study should be regarded as a preliminary range finding investigation, which focused on the non-volatile transformation products in the fish. Exposure to 8:2 and 10:2 FTOHs via food resulted in a series of perfluoroalkyl metabolites (FTCAs and FTUCAs) as shown in Fig. 1. This figure shows the growth-corrected concentrations of FTCAs and FTUCAs in rainbow trout muscle samples over a 30-d dietary exposure to 6.7 lg g1 wet wt 8:2 FTOH and 5.0 lg g1 wet wt 10:2 FTOH, following by a 30-d depuration phase. The predominant metabolites are 10:2 FTCA and 10:2 FTUCA, followed by 8:2 FTCA and 8:2 FTUCA. This is consistent with earlier studies, which observed similar metabolites during exposure of 8:2 FTOH to rats and mice (Hagen et al., 1981; Kudo et al., 2005; Martin et al., 2005; Fasano et al., 2006). The same metabolites were also found in the 8:2 FTOH in vitro metabolism study with trout hepatocytes and the 8:2 FTAc in vivo metabolism study with rainbow trout (Nabb et al., 2007; Butt et al., in press). Butt et al. (in press) found that only low concentrations of 8:2 FTOH were accumulated in rainbow trout tissues following dietary exposure to 8:2FTAc. In addition, Butt et al. (in press) measured an 8:2 FTOH-glucuronide conjugate at relatively high concentrations in the bile and feces of the FTAc exposed trout. Conjugate metabolites (e.g. glucuronide and glutathione) and 7:3 FTCA reported in earlier studies were not measured in this study. The fish extract were only measured for the compounds shown in Table 1. Small quantities of PFOA and PFDA were also detected in rainbow trout exposed to 8:2 and 10:2 FTOH. This indicates that rainbow trout can metabolize FTOH to the more stable PFCAs. The concentrations appear to be very low, just above the detection limit (1 ng g1). Therefore, no calculation could be done concerning uptake and depuration parameters. This biotransformation observed in rainbow trout is consistent with previous animal studies which have shown that small quantities of PFOA and PFNA can be formed after exposure to 8:2 FTOH (24–28). PFNA was not detected in this study. Biotransformation of 8:2 FTAc and 8:2 FTOH to PFOA was also observed in exposed trout and trout hepatocytes, respectively (Nabb et al., 2007; Butt et al., in press) and Butt et al. (2010b) showed FTCAs and FTUCAs formed PFCAs. Butt et al. (in press) found that PFNA was formed in much lower concentrations than PFOA (1%), thus given that PFOA levels were just above the detection limit, the lack of detection of PFNA is not surprising. The concentrations found after 30 d for 10:2 FTCA are significantly higher than those of 8:2 FTCA (Fig. 1). The assimilation and the metabolism of the FTOHs was a relatively fast process detectable after 1 d of exposure. This is consistent with the trout exposure study of Butt et al. (in press) which observed 8:2 FTCA within 1 h after 8:2 FTAc dosing. Nabb et al., 2007 reported halflives after in vitro metabolism of 8:2 FTOH in rat, mouse, trout and human hepatocytes of 9.9, 13, 36 and 103 min, respectively. The fact that 8:2 FTCA and 8:2 FTUCA are almost at steady-state throughout the uptake (Fig. 1) seems consistent with a fast biotransformation of both the 8:2 FTOH, 8:2 FTCA and 8:2 FTUCA. After 10 d the 8:2 FTCA and 8:2 FTUCA decreased to concentrations below the LOD, while this took 20 and 30 d, respectively for the 10:2 FTCA and 10:2 FTUCA; 10:2 FTCA showed the longest half-life (3.7 ± 0.4 d). The others showed half-lives ranging from 1.3 to 3.3 d. Interpretations of the half-lives of 8:2 FTCA and 8:2 FTUCA should be done with care, because the calculations were only possible by linear regression through two growth-corrected concentration points, and no standard error could be calculated. The longer half-lives of the long-chain FTCAs are consistent with the results of Martin et al. (2003a,b). Half-lives reported in the literature for PFOA and PFDA, 5.2 and 14 d, respectively, show that the halflives of the FTCAs are comparable with that of PFOA, and, consequently, lower than that of PFDA. The differences in half-lives between chain-lengths may also explain why the 10:2 FTCA and 10:2 FTUCA were accumulated in greater quantities as compared to the 8:2 FTCA and 8:2 FTUCA.