Perfluorooctanoate (PFOA) and Perfluorooctane sulfonate (PFOS) are two environmentally persistent perfluorinated compounds widely used for many industrial and consumer products due to their high thermal, oxidative resistance and surface repellence to water and oil. Their reproductive and developmental toxicity in lab animals and their persistence in environment have raised a serious concern for humans and animals. Trace amounts of these compounds have been found in water bodies, human blood, and wildlife samples. PFOA and PFOS are currently listed in Environmental Protection Agency's drinking water Contaminant Candidate List and in the list of Persistent Organic Pollutants in the Stockholm Convention. The strong covalent bond between carbon and fluorine present in PFOA and PFOS makes them stable and resistant to conventional treatment processes. Several advanced chemical processes can degrade PFOA and PFOS under high temperatures and pressures or other extreme conditions. However, the potential of biodegradation as a treatment technology for these compounds hasn't been developed successfully. This thesis focuses on evaluating the biodegradation potential of PFOA and PFOS. Fluoroacetate dehalogenase is an enzyme capable of defluorinating fluorinated aliphatic compounds. In this study, the potential of fluoroacetate dehalogenaseexpressing microorganisms to biodegrade PFOA and PFOS is examined. Two known fluoroacetate dehalogenase-expressing strains and fluoroacetate-degrading mixed cultures were used. The effect of ammonia in the enzyme activity was extended to study its effect on the biodegradation of PFOA and PFOS. Fluoride ions released during the mineralization of the PFOA and PFOS was used as a proof of biodegradation. The experiments with fluoroacetate dehalogenase-expressing strains and mixed culture consortia enriched from soil showed an increase in fluoride concentration in the solution thus indicating the possibility of successful biodegradation of PFOA and PFOS. Based on the fluoride ion content, it was also concluded that ammonia inhibits the enzyme activity in one of the two pure strains.

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Perfluorinated acids (PFAs) are widespread global and human blood organohalogen contaminants. These monomer decomposition products used in surface treatment products and in fluoropolymer manufacturing and fire fighting may disrupt maternal thyroid hormone homeostasis given that animal studies demonstrate an apparent hypothyroxinemic condition upon PFA exposure. Firstly, we developed a method for properly quantifying perfluorohexane sulfonate (PFHxS), a PFA suspected of overreporting in past literature. We then investigated whether perfluorooctanoate (PFOA), PFHxS and perfluorooctane sulfonate (PFOS) were determinants of maternal hypothyroxinemia in a pregnant women population from Edmonton using a case-control design. Free thyroxine (fT4) and thyroid stimulating hormone (TSH) were screened in 974 women collected during 15-20 weeks of pregnancy. Cases (n=96, hypothyroxinemic: normal TSH and fT4: lowest 10th percentile) and controls (n=175, fT4: 50th and 90th percentile) were matched based on age and physician. Conditional logistic regression indicated that these PFAs are not associated with maternal hypothyroxinemia. / Environmental Health Sciences

Humans are exposed to chemicals every day in our indoor environment. Chemicals have contributed to increased prosperity but also caused negative health effects. Children are vulnerable to chemicals because of their development and they breathe and drink more in relation to their body weight. That is why it’s important to reduce chemical exposure in environment for children. Preschools have a central role when it comes to materials and products that may pose a risk for exposure. The municipality has an important role to achieve a nontoxic environment which is based on a Swedish environmental quality goal (Non-toxic environment). This study is a part of the prioritized local environmental work in the municipal of Nordmaling. An inventory has been done to find out what type of chemicals that may expose children to harmful effects in preschools of Nordmaling. Electronic as a toy, soft and smelling toys, plastic around food and drinks, foam play pads were common products found during the inventory. This materials containing phthalates, brominated flame retardants, perfluorinated compounds, bisphenol A, lead and cadmium that can expose children through leaching into the indoor environment. A guidance have been constructed to achieve a non-toxic environment based on the results from the inventory in a cost effective way. The conclusion of the report is clear, identified problem areas can quickly be accomplished with small measures and low costs. Increased awareness of harmful substances and good routines for purchases and cleaning can further reduce the exposure to chemicals in the preschools.

The overall aim of this thesis was to investigate the fate of perfluorinated alkyl compounds (PFCs) in biological systems. During the past several years, it has been shown that wildlife are ubiquitously contaminated with two classes of PFCs, the perfluoroalkyl carboxylates (CxF2x+1C(O)OH, PFCAs) and sulfonates (CxF2x+1SO3H, PFSAs). However, there is still considerable uncertainty regarding how wildlife are accumulating these PFCs, particularly in remote areas such as the Canadian arctic. The potential for fluorotelomer acrylate monomers (CxF2x+1CH2CH2OC(O)CH=CH2, FTAcs) to act as precursors to PFCAs through atmospheric oxidation was investigated using smog chamber experiments. FTAc atmospheric fate is determined by OH radical reaction with a lifetime of approximately 1 day. The sole primary product of this reaction was the 4:2 fluorotelomer glyoxylate which is expected to undergo further atmospheric oxidation or photolysis to ultimately yield PFCAs. Temporal and spatial trends of PFCs in arctic ringed seals and seabirds were investigated to assist in understanding PFC transport mechanisms to remote regions. In ringed seals, perfluorooctane sulfonate (PFOS) levels decreased rapidly, coinciding with the phase out by the major manufacturer. These findings are consistent with volatile precursors as the dominant source of PFCs to arctic wildlife. The bioaccumulation and biotransformation of the 8:2 FTAc was investigated in two complimentary studies with rainbow trout. During the in vivo dietary exposure study, fish rapidly accumulated and biotransformed the 8:2 FTAc, with intermediate metabolites observed within 1 hour of dosing. Perfluorooctanoate (PFOA), perfluorononanoate (PFNA) and perfluoroheptanoate (PFHpA) were formed and accumulated in low yields. The carboxylesterase activity in the trout liver and stomach was investigated using in vivo sub-cellular (S9) incubations. Very high esterase activities were shown with approximately equal efficiency in the stomach and liver. The metabolic pathway of the 8:2 fluorotelomer alcohol (8:2 FTOH) was investigated by separately dosing whole rainbow trout with three intermediate metabolites that represented important branching points. The 7:3 fluorotelomer saturated carboxylate (FTCA) did not form PFOA, but formed PFHpA and the 7:3 fluorotelomer unsaturated carboxylate (FTUCA). The 8:2 FTCA and 8:2 FTUCA did form PFOA, confirming a “beta-like-oxidation” mechanism.

The overall aim of this thesis was to investigate the fate of perfluorinated alkyl compounds (PFCs) in biological systems. During the past several years, it has been shown that wildlife are ubiquitously contaminated with two classes of PFCs, the perfluoroalkyl carboxylates (CxF2x+1C(O)OH, PFCAs) and sulfonates (CxF2x+1SO3H, PFSAs). However, there is still considerable uncertainty regarding how wildlife are accumulating these PFCs, particularly in remote areas such as the Canadian arctic. The potential for fluorotelomer acrylate monomers (CxF2x+1CH2CH2OC(O)CH=CH2, FTAcs) to act as precursors to PFCAs through atmospheric oxidation was investigated using smog chamber experiments. FTAc atmospheric fate is determined by OH radical reaction with a lifetime of approximately 1 day. The sole primary product of this reaction was the 4:2 fluorotelomer glyoxylate which is expected to undergo further atmospheric oxidation or photolysis to ultimately yield PFCAs. Temporal and spatial trends of PFCs in arctic ringed seals and seabirds were investigated to assist in understanding PFC transport mechanisms to remote regions. In ringed seals, perfluorooctane sulfonate (PFOS) levels decreased rapidly, coinciding with the phase out by the major manufacturer. These findings are consistent with volatile precursors as the dominant source of PFCs to arctic wildlife. The bioaccumulation and biotransformation of the 8:2 FTAc was investigated in two complimentary studies with rainbow trout. During the in vivo dietary exposure study, fish rapidly accumulated and biotransformed the 8:2 FTAc, with intermediate metabolites observed within 1 hour of dosing. Perfluorooctanoate (PFOA), perfluorononanoate (PFNA) and perfluoroheptanoate (PFHpA) were formed and accumulated in low yields. The carboxylesterase activity in the trout liver and stomach was investigated using in vivo sub-cellular (S9) incubations. Very high esterase activities were shown with approximately equal efficiency in the stomach and liver. The metabolic pathway of the 8:2 fluorotelomer alcohol (8:2 FTOH) was investigated by separately dosing whole rainbow trout with three intermediate metabolites that represented important branching points. The 7:3 fluorotelomer saturated carboxylate (FTCA) did not form PFOA, but formed PFHpA and the 7:3 fluorotelomer unsaturated carboxylate (FTUCA). The 8:2 FTCA and 8:2 FTUCA did form PFOA, confirming a “beta-like-oxidation” mechanism.

A complete, sensitive and selective procedure was developed for gas chromatographic determination of perfluoroalkyl carboxylic acids (PFCAs, C5 - C12) in river water samples. A rapid and simple derivatization procedure was developed and optimized at first, using isobutyl chloroformate (IBCF) to convert the acids into the more volatile isobutyl esters. The second task was to find the most suitable stationary phase for separation of perfluoroalkyl carboxylic acids by GC. The retention characteristics of PFCA isobutyl esters were measured and compared on 9 different stationary phases. The physical-chemical parameters of analyte interactions with stationary phase were monitored on selected column Rtx-200MS, and these parameters were compared with a non-fluorinated homologue - octanoic acid. A sensitive GC-MS system was used with negative chemical ionization, which is suitable for the selected type of fluorinated analytes. The developed method exhibits very low limits of detection and determination of PFCA isobutyl esters: 0.05 - 9.7 ng mL-1 (LOD) and 0.16 - 32.2 ng mL-1 (LOQ). An optimum pre-concentration technique was found for real water samples, where SPE SupelTM-Select HLB cartridges were used. In these cartridges, PFCAs were captured as ion- pairs with enrichment factor of 400. The recoveries of...

Polyfluorinated compounds (PFCs) are a class of anthropogenic chemicals that have been found in groundwater and wastewater around the world. Perfluoroctane sulfonate (PFOS) and perfluoroctanoic acid (PFOA) are primarily used for industrial surfactants, and aqueous film forming foams (AFFFs). These PFCs and many of their constituents have been found to be carcinogenic to humans and other animals. A simple method for defluorination of these compounds is needed. Advanced oxidation of PFOS, PFHxS, and PFBS-k was carried out using activated sodium persulfate through ultrasonic irradiation with the following condition; [PFC] = 20 millimolar (mM), [Na2S2O8] = 25 mM, pH = 7, and 25°C. Fluoride concentrations were quantified by ion chromatography (IC). In laboratory experiments, batch reactions of PFBS solutions were conducted in purified water at different pH conditions and N2S¬2O8: PFBS molar ratios of 1:1, 2:1, 10:1, and 100:1 respectively. Solution pH was maintained at 7 using HNO3. Of the three compounds, PFHxS had the greatest defluorination (11%) after 120 minutes reaction time. However, PFBS-K had the greatest increase in defluorination (115%) between the control ultrasound (US) experiment and the combination experiment. When Na2S2O8 was increased, the defluorination ratio of PFBS decreased. This decrease was partly attributed to scavenging reactions between SO4¯• and S2O8²¯. These results show a synergism between ultrasonic irradiation and activated sodium persulfate as a form of advanced oxidation. Recommendations for further research into defluorination of PFOS and its constituents by ultrasonic degradation include: the use of high performance liquid chromatograph with accompanying mass spectrometry (HPLC/MS), the use of an ultrasonic probe with alternate frequencies, and the effects of surface tension on defluorination.

Perfluorinated compounds, non-degradable xenobiotics in many consumer products, can cause developmental toxicity in animals, and human exposure is associated with asthma symptoms. We tested the hypothesis that sustained chronic exposure to perfluorooctanoic acid (PFOA), fluorotelomer alcohol (FTOH) or perfluorooctanesulfonic acid (PFOS) induces lung dysfunction that exacerbates allergen-induced airway hyperresponsiveness (AHR) and inflammation. Mice were exposed to the chemicals from early gestation day to adulthood. Some pups were sensitized and challenged with ovalbumin. Serum PFOA was analyzed by liquid chromatograph-tandem mass spectrometry. Lung function was measured using a small animal ventilator. We assayed inflammatory cells in the lung, performed PCR for lung cytokines, and examined bronchial goblet cell hyperplasia by histology. Here we show that either PFOA or FTOH exposure can induce AHR, but neither one predisposes for exaggerated allergic lung inflammation or AHR. FTOH or PFOS exposure appears to suppress allergic lung inflammation, but does not affect allergic lung dysfunction.

Perfluorinated carboxylates (PFCAs) are persistent and ubiquitous in the environment. Humans are exposed to PFCAs through direct and indirect sources, although the relative importance of each is uncertain. Direct sources of PFCAs have been attributed to two primary fluorochemical manufacturing processes: electrochemical fluorination (ECF) and telomerization. A focus of this thesis was to elucidate an additional direct source of PFCAs resulting from the direct fluorination of polyolefin materials. High density polyethylene bottles with varying levels of fluorination were observed to contain significant amounts of PFCAs, particularly those with carbon chain-lengths ≤ C6, marking an unexplored source of PFCA exposure. PFCAs are also produced indirectly from the biotransformation of fluorotelomer-based compounds, such as polyfluoroalkyl phosphate esters (PAPs) and fluorotelomer alcohols (FTOHs). During this transformation process, two predominant classes of metabolic intermediates are formed: the fluorotelomer unsaturated aldehydes (FTUALs) and the fluorotelomer unsaturated carboxylic acids (FTUCAs). Another focus of this thesis was to examine the reactivity of FTUALs and FTUCAs with endogenous nucleophiles such as glutathione (GSH), select amino acids, and model proteins. FTUALs formed adducts with all nucleophiles examined, where those having shorter carbon chain lengths (i.e. 6:2 and 8:2 FTUAL) were more reactive than longer carbon chains (i.e. 10:2 FTUAL). By contrast, FTUCAs had comparably limited reactivity; although FTUCAs showed mild reactivity with GSH, they did not react with any other nucleophiles. In vitro and in vivo experiments were carried out to determine the extent of protein binding formed from the biotransformation of fluorotelomer-based compounds, including the 8:2 FTOH and the 6:2 PAP diester. A significant portion of these biotransformations yielded covalent protein binding at nmol/mg protein concentrations. Protein adducts were observed predominantly in rat liver and also in plasma and kidney. The formation of reactive intermediates may be toxicologically important through protein deactivation. Cellular toxicity of FTUALs was significantly higher compared to PFCAs and the acid metabolic intermediates (i.e. FTUCAs). The EC50 values calculated from dose-response incubations were dependant on chain length and functional group. The work in this thesis examined an unexplored consequence of indirect exposure to PFCAs, potentially impacting the relative importance of PFCA exposure sources.