This review describes the sources, fate, and transport of perfluorocarboxylates (PFCAs) in the environment, with a specific focus on perfluorooctanoate (PFO). The global historical industry-wide ...emissions of total PFCAs from direct (manufacture, use, consumer products) and indirect (PFCA impurities and/or precursors) sources were estimated to be 3200−7300 tonnes. It was estimated that the majority (∼80%) of PFCAs have been released to the environment from fluoropolymer manufacture and use. Although indirect sources were estimated to be much less important than direct sources, there were larger uncertainties associated with the calculations for indirect sources. The physical−chemical properties of PFO (negligible vapor pressure, high solubility in water, and moderate sorption to solids) suggested that PFO would accumulate in surface waters. Estimated mass inventories of PFO in various environmental compartments confirmed that surface waters, especially oceans, contain the majority of PFO. The only environmental sinks for PFO were identified to be sediment burial and transport to the deep oceans, implying a long environmental residence time. Transport pathways for PFCAs in the environment were reviewed, and it was concluded that, in addition to atmospheric transport/degradation of precursors, atmospheric and ocean water transport of the PFCAs themselves could significantly contribute to their long-range transport. It was estimated that 2−12 tonnes/year of PFO are transported to the Artic by oceanic transport, which is greater than the amount estimated to result from atmospheric transport/degradation of precursors.
The aerobic biotransformation of 6:2 FTS salt F(CF
2)
6CH
2CH
2
SO
3
-
K
+ was determined in closed bottles for 90
d in diluted activated sludge from three waste water treatment plants (WWTPs) to ...compare its biotransformation potential with that of 6:2 FTOH F(CF
2)
6CH
2CH
2OH. The 6:2 FTS biotransformation was relatively slow, with 63.7% remaining at day 90 and all observed transformation products together accounting for 6.3% of the initial 6:2 FTS applied. The overall mass balance (6:2 FTS plus observed transformation products) at day 90 in live and sterile treatments averaged 70% and 94%, respectively. At day 90, the stable transformation products observed were 5:3 acid F(CF
2)
5CH
2CH
2COOH, 0.12%, PFBA F(CF
2)
3COOH, 0.14%, PFPeA F(CF
2)
4COOH, 1.5%, and PFHxA F(CF
2)
5COOH 1.1%. In addition, 5:2 ketone F(CF
2)
5C(O)CH
3 and 5:2 sFTOH F(CF
2)
5CH(OH)CH
3 together accounted for 3.4% at day 90. The yield of all the stable transformation products noted above (2.9%) was 19 times lower than that of 6:2 FTOH in aerobic soil. Thus 6:2 FTS is not likely to be a major source of PFCAs and polyfluorinated acids in WWTPs. 6:2 FTOH, 6:2 FTA F(CF
2)
6CH
2COOH, and PFHpA F(CF
2)
6COOH were not observed during the 90-d incubation. 6:2 FTS primary biotransformation bypassed 6:2 FTOH to form 6:2 FTUA F(CF
2)
5CF
=
CHCOOH, which was subsequently degraded via pathways similar to 6:2 FTOH biotransformation. A substantial fraction of initially dosed 6:2 FTS (24%) may be irreversibly bound to diluted activated sludge catalyzed by microbial enzymes. The relatively slow 6:2 FTS degradation in activated sludge may be due to microbial aerobic de-sulfonation of 6:2 FTS, required for 6:2 FTS further biotransformation, being a rate-limiting step in microorganisms of activated sludge in WWTPs.
•6:2 FTSA is a principal degradation product of short-chain fluorotelomer surfactants.•6:2 FTSA is not classified for aquatic hazard and presents little risk to aquatic organisms.•6:2 FTSA BCFs were ...<40 and the dietary BMF was 0.295.•6:2 FTSA is unlikely to bioaccumulate or biomagnify in aquatic systems.•Studies are needed of the fate/effects of commercial AFFF surfactants.
This study assessed the aquatic toxicity and bioaccumulation potential of 6:2 fluorotelomer sulfonate (6:2 FTSA). Acute and chronic aquatic hazard endpoints indicate 6:2 FTSA is not classified for aquatic hazard according to GHS or European CLP legislation. The aqueous bioconcentration factors for 6:2 FTSA were <40 and the dietary assimilation efficiency, growth corrected half-life and dietary biomagnification factor (BMF) were 0.435, 23.1d and 0.295, respectively. These data indicate that 6:2 FTSA is not bioaccumulative in aquatic organisms. Comparison of PNECs with the reported surface water concentrations (non-spill situations) suggests low risk to aquatic organisms from 6:2 FTSA. Future studies are needed to elucidate the biotic and abiotic fate of commercial AFFF surfactants in the environment.
The long-term (1950−2050) global fate of perfluorooctanoate (PFO) is investigated using the global distribution model, GloboPOP. The model is used to test the hypotheses that direct PFO emissions can ...account for levels observed in the global oceans and that ocean water transport to the Arctic is an important global distribution pathway. The model emission scenarios are derived from historical and projected PFO emissions solely from direct sources. Modeled ocean water concentrations compare favorably to observed PFO concentrations in the world's oceans and thus ocean inventories can be accounted for by direct sources. The model results support the hypothesis that long-range ocean transport of PFO to the Arctic is important and estimate a net PFO influx of approximately 8−23 tons per year flowing into the model's Northern Polar zone in 2005, an amount at least 1 order of magnitude greater than estimated PFO flux to the Arctic from potential indirect sources such as atmospheric transport and degradation of fluorotelomer alcohols. Modeled doubling times of ocean water concentrations in the Arctic between 1975 and 2005 of approximately 7.5−10 years are in good agreement with doubling times of PFO in Arctic biota estimated from monitoring data. The model is further applied to predict future trends in PFO contamination levels using forecasted (2005−2050) direct emissions, including substantial reductions committed to by industry. Modeled ocean water concentrations in zones near to sources decline markedly after 2005, whereas modeled concentrations in the Arctic are predicted to continue to increase until approximately 2030 and show no significant decrease for the remaining 20 years of the model simulation. Since water is the primary exposure medium for Arctic biota, these model results suggest that concentrations in Arctic biota may continue to rise long after direct emissions have been substantially reduced or eliminated.
Abstract Sodium perfluorohexanoate NaPFHx, F(CF2 )5 CO2 Na, CAS#2923-26-4 was evaluated in acute, 90-day subchronic, one-generation reproduction, developmental and in vitro genetic toxicity studies. ...In the subchronic/one-generation reproduction study, four groups of young adult male and female Crl:CD(SD) rats were administered NaPFHx daily for approximately 90 days by gavage at dosages of 0, 20, 100, or 500 mg/kg. Selected groups of rats were evaluated after 1- and 3-month recovery periods. Rats selected for reproductive evaluations were dosed for approximately 70 days prior to cohabitation, through gestation and lactation, for a total of about 4 months. The subchronic toxicity no observed adverse effect level (NOAEL) was 20 mg/(kg day), based on nasal lesions observed at 100 and 500 mg/(kg day). No effects were observed for neurobehavioral endpoints. NaPFHx was a moderate inducer of hepatic peroxisomal β-oxidation with a no observed effect level (NOEL) of 20 (male rats) and 100 mg/(kg day) (female rats). Elevated hepatic β-oxidation levels were observed following 1-month recovery in male and female rats at 500 mg/(kg day). No NaPFHx-related effects were observed on any reproductive parameters. The P1 adult rat NOAEL was 20 mg/(kg day), based on reduced body weight parameters, whereas the NOAEL for reproductive toxicity was 100 mg/(kg day), based on effects limited to reduced F1 pup weights. In the developmental study, female rats were dosed via gavage on gestation day (GD) 6–20 with the same doses of NaPFHx administered in the subchronic study. The maternal and developmental toxicity NOAEL was 100 mg/(kg day), based on maternal and fetal body weight effects at 500 mg/(kg day). NaPFHx is therefore concluded not to present a reproductive or developmental hazard. NaPFHx genotoxicity studies showed no mutations in the bacterial reverse mutation (Ames) assay or chromosome aberrations in human lymphocytes treated with NaPFHx in vitro . The lowest NOAEL from all of the studies was 20 mg/(kg day) in the subchronic study based on nasal lesions. Benchmark doses (BMDL10) for nasal lesions were 13 and 21 mg/(kg day) for male and female rats, respectively. The relevance of the nasal lesions to humans is not known.
The absorption, distribution, metabolism, and elimination of 3-14C 8-2 fluorotelomer alcohol (8-2 FTOH, C7F1514CF2CH2CH2OH) following a single oral dose at 5 and 125 mg/kg in male and female rats ...have been determined. Following oral dosing, the maximum concentration of 8-2 FTOH in plasma occurred by 1 h postdose and cleared rapidly with a half-life of less than 5 h. The internal dose to 8-2 FTOH, as measured by area under the concentration-time curve to infinity, was similar for male and female rats and was observed to increase in a dose-dependent fashion. The majority of the 14C 8-2 FTOH (> 70%) was excreted in feces, and 37–55% was identified as parent. Less than 4% of the administered dose was excreted in urine, which contained low concentrations of perfluorooctanoate (∼ 1% of total 14C). Metabolites identified in bile were principally composed of glucuronide and glutathione conjugates, and perfluorohexanoate was identified in excreta and plasma, demonstrating the metabolism of the parent FTOH by sequential removal of multiple CF2 groups. At 7 days postdose, 4–7% of the administered radioactivity was present in tissues, and for the majority, 14C concentrations were greater than whole blood with the highest concentration in fat, liver, thyroid, and adrenals. Distribution and excretion of a single 125-mg/kg 3-14C 8-2 FTOH dermal dose following a 6-h exposure in rats was also determined. The majority of the dermal dose either volatilized from the skin (37%) or was removed by washing (29%). Following a 6-h dermal exposure and a 7-day collection period, excretion of total radioactivity via urine (< 0.1%) and feces (< 0.2%) was minor, and radioactivity concentrations in most tissues were below the limit of detection. Systemic availability of 8-2 FTOH following dermal exposure was negligible.
A high spatial and temporal resolution atmospheric model is used to evaluate the potential contribution of fluorotelomer alcohol (FTOH) and perfluorocarboxylate (PFCA) emissions associated with the ...manufacture, use, and disposal of DuPont fluorotelomer-based products in North America to air concentrations of FTOH, perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) in North America and the Canadian Arctic. A bottom-up emission inventory for PFCAs and FTOHs was developed from sales and product composition data. A detailed FTOH atmospheric degradation mechanism was developed to simulate FTOH degradation to PFCAs and model atmospheric transport of PFCAs and FTOHs. Modeled PFCA yields from FTOH degradation agree with experimental smog-chamber results supporting the degradation mechanism used. Estimated PFCA and FTOH air concentrations and PFCA deposition fluxes are compared to monitoring data and previous global modeling. Predicted FTOH air concentrations are generally in agreement with available monitoring data. Overall emissions from the global fluorotelomer industry are estimated to contribute approximately 1−2% of the PFCAs in North American rainfall, consistent with previous global emissions estimates. Emission calculations and modeling results indicate that atmospheric inputs of PFCAs in North America from fluorotelomer-based products will decline by an order of magnitude in the near future as a result of current industry commitments to reduce manufacturing emissions and lower the residual fluorotelomer alcohol raw material and trace PFCA product content.
PDF
