Relative rate methods were used to measure the gas-phase reaction of N-methyl perfluorobutane sulfonamidoethanol (NMeFBSE) with OH radicals, giving k(OH + NMeFBSE) = (5.8 +/- 0.8) x 10(-12) cm3 molecule(-1) s(-1) in 750 Torr of air diluent at 296 K. The atmospheric lifetime of NMeFBSE is determined by reaction with OH radicals and is approximately 2 days. Degradation products were identified by in situ FTIR spectroscopy and offline GC-MS and LC-MS/MS analysis. The primary carbonyl product C4F9SO2N(CH3)CH2CHO, N-methyl perfluorobutane sulfonamide (C4F9SO2NH(CH3)), perfluorobutanoic acid (C3F7C(O)OH), perfluoropropanoic acid (C2F5C(O)OH), trifluoroacetic acid (CF3C(O)OH), carbonyl fluoride (COF2), and perfluorobutane sulfonic acid (C4F9SO3H) were identified as products. A mechanism involving the addition of OH to the sulfone double bond was proposed to explain the production of perfluorobutane sulfonic acid and perfluorinated carboxylic acids in yields of 1 and 10%, respectively. The gas-phase N-dealkylation product, N-methyl perfluorobutane sulfonamide (NMeFBSA), has an atmospheric lifetime (>20 days) which is much longer than that of the parent compound, NMeFBSE. Accordingly,the production of NMeFBSA exposes a mechanism by which NMeFBSE may contribute to the burden of perfluorinated contamination in remote locations despite its relatively short atmospheric lifetime. Using the atmospheric fate of NMeFBSE as a guide, it appears that anthropogenic production of N-methyl perfluorooctane sulfonamidoethanol (NMeFOSE) contributes to the ubiquity of perfluoroalkyl sulfonate and carboxylate compounds in the environment.

Perfluorinated acids are detected in human blood world-wide, with increased levels observed in industrialized areas. The origin of this contamination is not well understood. A possible route of exposure, which has received little attention experimentally, is indirect exposure to perfluorinated acids through ingestion of chemicals applied to food contact paper packaging. The current investigation quantified the load of perfluorinated acids to Sprague-Dawley rats upon exposure to polyfluoroalkyl phosphate surfactants (PAPS), nonpolymeric fluorinated surfactants approved for application to food contact paper products. The animals were administered a single dose at 200 mg/kg by oral gavage of 8:2 fluorotelomer alcohol (8:2 FTOH) mono-phosphate (8:2 monoPAPS), or the corresponding di-phosphate (8:2 diPAPS), with blood taken over 15 days post-dosing to monitor uptake, biotransformation, and elimination. Upon completion of the time-course study the animals were redosed using an identical dosing procedure, with sacrifice and necropsy 24 h after the second dosing. Increased levels of perfluorooctanoic acid (PFOA), along with both 8:2 PAPS congeners, were observed in the blood of the dosed animals. In the 8:2 monoPAPS-dosed animals, 8:2 monoPAPS and PFOA blood concentrations peaked at 7900 +/- 1200 ng/g and 34 +/- 4 ng/g respectively. In the 8:2 diPAPS-dosed animals, 8:2 diPAPS peaked in concentration at 32 +/- 6 ng/g, and 8:2 monoPAPS and PFOA peaked at 900 +/- 200 ng/g and 3.8 +/- 0.3 ng/g, respectively. Several established polyfluorinated metabolites previously identified in 8:2 FTOH metabolism studies were also observed in the dosed animals. Consistent with other fluorinated contaminants, the tissue distributions showed increased levels of both PFOA and the 8:2 PAPS congeners in the liver relative to the other tissues measured. Previous investigations have found that PAPS can migrate into food from paper packaging. Here we link ingestion of PAPS with in vivo production of perfluorinated acids.

Wastewater treatment plants (WWTPs) have been identified as a major source of perfluorocarboxylates (PFCAs) to aqueous environments. The observed increase in PFCA mass flows from WWTP influent to effluent suggests the biodegradation of commercial fluorinated materials within the WWTP. Commercial fluorinated surfactants are used as greaseproofing agents in food-contact paper products as well as leveling and wetting agents. As WWTPs are likely the major fate of these surfactants, their biodegradation may be a source of PFCA production. One class of commercial surfactants, the polyfluoroalkyl phosphates (PAPs), have been observed in WWTP sludge. While PAPs have been shown to degrade into PFCAs in a rat model, the present study investigates their microbial fate to determine whether the biodegradation of PAPs within a WWTP-simulated system will contribute to the load of PFCAs released. PAPs are applied commercially in mixed formulations of different chain lengths and substitution at the phosphate center. The effect of chain length and phosphate substitution on the biodegradation of PAPs was investigated by incubating mixtures of 4:2, 6:2, 8:2, and 10:2 monosubstituted PAPs (monoPAPs) in an aerobic microbial system and by separately incubating the 6:2 monoPAP and 6:2 disubstituted PAP (diPAP) for 92 days. Headspace sampling revealed production of the fluorotelomer alcohols (FTOHs) from the hydrolysis of the PAP phosphate ester linkages. Analysis of the aqueous phase revealed microbial transformation of the PAPs to the final PFCA products was possible. The majority of the oxidation products observed were consistent with previous investigations that have suggested fluorotelomer precursor compounds degrade predominantly via a beta-oxidation-like mechanism. However, in this study, the detection of odd-chain PFCAs suggests that other pathways may be important. The present study demonstrated microbially mediated biodegradation of PAPs to PFCAs. This observation, together with the diPAP concentrations observed in WWTP sludge, suggest PAPs-containing commercial products may be a significant contributor to the increased PFCA mass flows observed in WWTP effluents.

BackgroundPerfluorinated carboxylic acids (PFCAs) are ubiquitous in human sera worldwide. Biotransformation of the polyfluoroalkyl phosphate esters (PAPs) is a possible source of PFCA exposure, because PAPs are used in food-contact paper packaging and have been observed in human sera.ObjectivesWe determined pharmacokinetic parameters for the PAP monoesters (monoPAPs) and PAP diesters (diPAPs), as well as biotransformation yields to the PFCAs, using a rat model.MethodsThe animals were dosed intravenously or by oral gavage with a mixture of 4:2, 6:2, 8:2, and 10:2 monoPAP or diPAP chain lengths. Concentrations of the PAPs and PFCAs, as well as metabolic intermediates and phase II metabolites, were monitored over time in blood, urine, and feces.ResultsThe diPAPs were bioavailable, with bioavailability decreasing as the chain length increased from 4 to 10 perfluorinated carbons. The monoPAPs were not absorbed from the gut; however, we found evidence to suggest phosphate-ester cleavage within the gut contents. We observed biotransformation to the PFCAs for both monoPAP and diPAP congeners.ConclusionsUsing experimentally derived biotransformation yields, perfluorooctanoic acid (PFOA) sera concentrations were predicted from the biotransformation of 8:2 diPAP at concentrations observed in human serum. Because of the long human serum half-life of PFOA, biotransformation of diPAP even with low-level exposure could over time result in significant exposure to PFOA. Although humans are exposed directly to PFCAs in food and dust, the pharmacokinetic parameters determined here suggest that PAP exposure should be considered a significant indirect source of human PFCA contamination.