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1                                              PFOA and PFOS concentrations in plankton ranged from 0.1
2                                              PFOA removal kinetics followed using high-performance li
3                                              PFOA was detected in every surface water sample with con
4                                              PFOA was the predominant PFAS constituent in pine needle
5                                              PFOA, perfluorohexanesulfonate (PFHxS), and perfluorobut
6                                              PFOA, PFBS, PFHxS, and PFOS increased 1.2, 207, 7.4, and
7                                              PFOA, PFHxS, and linear PFOS isomers showed average half
8                                              PFOA, PFNA, perfluorodecanoate (PFDeA), and PFHxS were i
9 crease: PFOS RR = 0.87 (95% CI: 0.74, 1.02); PFOA RR = 0.98 (95% CI: 0.82, 1.16)] or autism [per natu
10 crease: PFOS RR = 0.92 (95% CI: 0.69, 1.22); PFOA RR = 0.98 (95% CI: 0.73, 1.31)].
11  PFCAs, PFHxS, and PFBS, trace amounts of 43 PFOA-related and 35 PFOS-related byproducts were also id
12  approximately 4000 (PFOS), 200 (PFHxS), 50 (PFOA), and 0.8 (PFBA) L kg dry weight(-1), suggesting th
13 eneration of perfluoroalkyl carboxylic acid (PFOA) at a yield of 30 mol % by day 180.
14 y due to perfluorooctatonic carboxylic acid (PFOA), with low relative concentrations of measured biot
15 oic acid (PFHxA), perfluoro-n-octanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), or 0.4% dime
16                      Perfluorooctanoic acid (PFOA or C8) has hepatotoxic effects in animals.
17 6.4 (5.6) ng/mL} and perfluorooctanoic acid (PFOA) [median (IQR): 4.4 (3.2) ng/mL].
18    Human exposure to perfluorooctanoic acid (PFOA) and other per- and polyfluoroalkyl substances (PFA
19            Tap water perfluorooctanoic acid (PFOA) and perfluorononanoic acid (PFNA) were statistical
20 ealth advisories for perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) in 2016.
21 ds (PFAAs) including perfluorooctanoic acid (PFOA) and perfluorooctanesulfonate (PFOS) at concentrati
22 oduced when treating perfluorooctanoic acid (PFOA) and perfluorooctanesulfonate (PFOS) in water using
23 rbent for removal of perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) in convent
24 sed model, described perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) interfacia
25 ed compounds, (i.e., perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS)) has resul
26                  For perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS), a meta-an
27 nd substances beyond perfluorooctanoic acid (PFOA) and PFOS.
28 anesulfonate (PFOS), perfluorooctanoic acid (PFOA) and their precursors.
29 sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are currently listed as priority substances under
30 ulfonate (PFBS), and perfluorooctanoic acid (PFOA) as high as 220 ng L(-1), 160 ng L(-1), and 120 ng
31 nd quantification of perfluorooctanoic acid (PFOA) by mass spectrometry.
32 onic acid (PFOS) and perfluorooctanoic acid (PFOA) concentrations was associated with higher homeosta
33                      Perfluorooctanoic acid (PFOA) concentrations were significantly higher in P. maj
34  sulfonic (PFOS) and perfluorooctanoic acid (PFOA) concentrations, using liquid chromatography-mass s
35                      Perfluorooctanoic acid (PFOA) dominated air and drinking water, while perfluorob
36              Modeled perfluorooctanoic acid (PFOA) exposure and liver function in a Mid-Ohio Valley c
37 onic acid (PFOS) and perfluorooctanoic acid (PFOA) exposure can cause pregnancy loss and infant death
38 um concentrations of perfluorooctanoic acid (PFOA) have been extensively used in epidemiologic studie
39 sulfonate (PFOS) and perfluorooctanoic acid (PFOA) in drinking water established by the U.S.
40 ic acid (PFOS) or to perfluorooctanoic acid (PFOA) increases mouse and human peroxisome proliferator-
41                      Perfluorooctanoic acid (PFOA) is a persistent environmental contaminant that has
42                      Perfluorooctanoic acid (PFOA) is a poly- and perfluoroalkyl substance (PFAS) ass
43       The surfactant perfluorooctanoic acid (PFOA) is particularly commonly found in contaminated sit
44 ect (i.e., uptake of perfluorooctanoic acid (PFOA) itself) and indirect (i.e., uptake of 8:2 fluorote
45  three PFAAs, namely perfluorooctanoic acid (PFOA) perfluorohexanoic acid (PFHxA) and perfluorobutane
46 ulfonate (PFOS) plus perfluorooctanoic acid (PFOA) ranged between 365 and 73700 ng/L.
47 were associated with perfluorooctanoic acid (PFOA) serum levels in previous cross-sectional studies.
48 .40, -2.04), and for perfluorooctanoic acid (PFOA) was 7.13 g (95% CI: -8.46, -5.80); results based o
49      However, linear perfluorooctanoic acid (PFOA) was enriched, suggesting fluorotelomer precursor t
50                      Perfluorooctanoic acid (PFOA) was used as a fluoropolymer manufacturing aid at a
51 sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were detected in all samples; four other PFASs wer
52 uorophenol (PFP) and perfluorooctanoic acid (PFOA)) from the solution state (after a spill) through t
53 ulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and 2,2',4,4'-tetrahydroxybenzophenone (BP2).
54 sulfonate (PFOS) and perfluorooctanoic acid (PFOA), and ADHD in a collaborative study including nine
55 hloride, humic acid, perfluorooctanoic acid (PFOA), and perfluorobutanesulfonate (PFBS) was also inve
56 ulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) in maternal pla
57  Arsenic, sucralose, perfluorooctanoic acid (PFOA), atrazine-2-hydroxy, benzotriazole, acesulfame, an
58 sulfonate (PFOS) and perfluorooctanoic acid (PFOA), but impacts of regulations on PFAS releases to th
59 sulfonate (PFOS) and perfluorooctanoic acid (PFOA), but seen as the result of higher oral doses.
60 ces (PFASs), notably perfluorooctanoic acid (PFOA), contaminate many ground and surface waters and ar
61  substances, such as perfluorooctanoic acid (PFOA), in organisms.
62 ne sulfonate (PFOS), perfluorooctanoic acid (PFOA), perfluorohexane sulfonate (PFHxS), and perfluoroh
63 ulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorohexane sulfonate, perfluorononanoic acid
64 ulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorodecan
65 s (PFAAs), including perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorooctan
66  and serum levels of perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic
67 s (PFASs), including perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS), perfluorohe
68 ostnatal exposure to perfluorooctanoic acid (PFOA), perfluorooctanesulfonate (PFOS), and perfluorohex
69 oundwater containing perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorooct
70 acement compound for perfluorooctanoic acid (PFOA), was detected in Arctic seawater for the first tim
71  score, dominated by perfluorooctanoic acid (PFOA), was inversely associated with current wheeze (OR
72  situ remediation of perfluorooctanoic acid (PFOA), yet a comprehensive understanding of the degradat
73 es (PFAS), including perfluorooctanoic acid (PFOA).
74 he transformation of perfluorooctanoic acid (PFOA).
75 onic acid (PFOS) and perfluorooctanoic acid (PFOA).
76 ulfonate (PFOS), and perfluorooctanoic acid (PFOA)] were associated with 17 semen quality end points
77        PFCAs include perfluorooctanoic acid (PFOA; C8) and long-chain PFCAs (C9-C20).
78 y gland development (perfluorooctanoic acid; PFOA) and suppression of immune response (perfluorooctan
79 her than requiring in vivo data fitting, all PFOA-related parameters were obtained from in vitro assa
80                        Overall, 10 analytes, PFOA, PFNA, 8:2 FTS, PFOSA, N-MeFOSA, NEtFOSA, N-MeFOSAA
81     In cross-sectional analyses, we analyzed PFOA in relation to self-reported menopause among women
82 nt suggested that metals (i.e., arsenic) and PFOA were the top ranked pollutants that have the potent
83 ond pulses, the detection limit for DMMP and PFOA in human blood plasma can be lowered by more than a
84 hnicity were associated with higher PFOS and PFOA concentrations in colostrum.
85                                     PFOS and PFOA concentrations were greater in Lake Ontario precipi
86         At lower and field-relevant PFOS and PFOA concentrations, the Langmuir-based model underpredi
87 chanisms underlying isomer-specific PFOS and PFOA disposition have not previously been studied.
88 me category had significantly lower PFOS and PFOA GM concentrations than other women.
89 ation to estimate concentrations of PFOS and PFOA in children at birth and at 3, 6, 12, and 24 months
90 iation constants (Kd) of individual PFOS and PFOA isomers with human serum albumin (HSA) and (ii) rel
91 ies and renal clearance of branched PFOS and PFOA isomers, compared to the respective linear isomer.
92 t each 1-ng/mL increase in prenatal PFOS and PFOA levels was associated with 5.00 g (95% CI: -21.66,
93                                     PFOS and PFOA predictors were identified by optimizing multiple l
94 tment can be effective for treating PFOS and PFOA to meet health advisory levels, remediation of the
95 higher binding affinities of linear PFOS and PFOA to total serum protein were confirmed when both cal
96  The Irish population's exposure to PFOS and PFOA via non-dietary sources is well below estimates of
97                   Concentrations of PFOS and PFOA were measured in maternal serum/plasma during pregn
98    In 9 of the 13 IDW samples, both PFOS and PFOA were removed to below United States Environmental P
99                                     PFOS and PFOA were the most abundant PFAS (geometric mean: 5.80 a
100             For legacy PFAS such as PFOS and PFOA, a comparison of inland and offshore measurements f
101 sional tolerable weekly intakes for PFOS and PFOA.
102 ciation with early life exposure to PFOS and PFOA.
103 tions of perfluorooctanesulfonate (PFOS) and PFOA in P. major feathers and plasma were significantly
104  with low to moderate PFBS, PFHxS, PFOS, and PFOA contamination is an important source of exposure fo
105 that PFOA removal by the capsules was pH and PFOA concentration dependent, with adsorption efficienci
106 ion byproducts, chromium(VI), strontium, and PFOA/PFOS.
107 (*-) and showed that the reaction of anionic PFOA with HSO(4)(*) was most favorable with a DeltaG(*)
108 ectional studies showing association between PFOA and ALT, a marker of hepatocellular damage.
109 s on the epidemiological association between PFOA and preeclampsia.
110 c studies that examined associations between PFOA exposures and adverse health outcomes among residen
111   We observed nonlinear associations between PFOA in pregnancy and some measures of adiposity.
112 to C7) were identified as byproducts of both PFOA and PFOS treatment.
113                                     In boys, PFOA concentrations were significantly associated with t
114           The relative abundance of branched PFOA in the northern hemisphere was correlated with dist
115 e strongly bound to HSA compared to branched PFOA isomers (Kd range from 4(+/-2)x10(-4) M to 3(+/-2)x
116 as also used to treat groundwater containing PFOA and several cocontaminants including perfluorooctan
117 he first to the fifth quintile of cumulative PFOA exposure was associated with a 6% increase in ALT l
118 nificantly lower after exposure to 5 mg/kg/d PFOA (9.4% decrease relative to controls).
119 zes were similar for higher doses (5 mg/kg/d PFOA and 10 mg/kg/d GenX) and lower doses (1 mg/kg/d PFO
120  10 mg/kg/d GenX) and lower doses (1 mg/kg/d PFOA and 2 mg/kg/d GenX), including higher maternal live
121        Results show that A6 can defluorinate PFOA/PFOS while reducing iron, using ammonium or hydroge
122 ytical performance of each MOF for detecting PFOA was correlated with both the calculated binding ene
123 om error in the yearly public water district PFOA concentrations, systematic error specific to each w
124 ort-chain PFAS along with legacy PFAS (i.e., PFOA, PFHxS, and PFOS) through drinking water.
125 P. major feathers cannot be used to estimate PFOA and PFOS concentrations in blood plasma, except whe
126 certainty can substantially change estimated PFOA serum concentrations, but results in only minor imp
127  evaluate impact of uncertainty in estimated PFOA drinking-water concentrations on estimated serum co
128 ng fluxes were 0.8 +/- 1.3 ng m(-2)d(-1) for PFOA, and 1.1 +/- 2.1 ng m(-2)d(-1) for PFOS.
129 sed polymer network with higher affinity for PFOA compared to powdered activated carbon, along with c
130 m was 35.3 pg/mL for PFOS and 32.8 pg/mL for PFOA.
131 the calculated binding energy of the MOF for PFOA and the relative change in the surface area of the
132 uth and dermal contacts (for hands only) for PFOA were 0.83 and 0.50 pg.kg bw(-1).day(-1), respective
133 pear to decrease over time, particularly for PFOA and PFOS.
134            For the electron abstraction from PFOA, we investigated reactions using protonated and dep
135 step was the first electron abstraction from PFOA, yet the generation of SO(4)(*-) from the decomposi
136 o Valley (USA) with local contamination from PFOA.
137 OMA-IR was more pronounced in females [e.g., PFOA: -15.6% (95% CI: -25.4, -4.6) vs. -6.1% (95% CI: -1
138  modest positive associations of gestational PFOA and PFHxS concentrations with central adiposity and
139 e sample site, 28 km north of the plant, had PFOA at 143 ng/L and HFPO-DA at 42 ng/L.
140 andfills containing fluorochemical waste had PFOA concentrations ranging up to >1000 ng/L.
141                Both achieved remarkably high PFOA removal and defluorination efficiencies compared to
142                The ORs comparing the highest PFOA or PFHpS quartile to the lowest were 2.2 (95% CI: 1
143 ated associations between modeled historical PFOA exposures and liver injury biomarkers and medically
144                                     However, PFOA, which is the carboxylate analog of PFOS, revealed
145 r elevated direct bilirubin or GGT; however, PFOA was associated with decreased direct bilirubin.
146                              To determine if PFOA/PFOS or some of their degradation products were met
147 experiments monitoring each phase illustrate PFOA rapidly transfers from solution to the solid phase
148 , -2.3) per interquartile range increment in PFOA].
149                               Uncertainty in PFOA water concentrations could cause major changes in e
150 s for miscarriage associated with increasing PFOA and PFHpS levels.
151                                   The infant PFOA and PFOS serum concentrations were 6% (95% CI: 1, 1
152               At concentrations of 100 mg/L, PFOA/PFOS were the main contributors to DOC, which remai
153                            Similarly, linear PFOA (Kd=1(+/-0.9)x10(-4) M) was more strongly bound to
154 rotelomer precursor transformation to linear PFOA.
155 wer PFOS (95% CI: -56 to -17%) and 40% lower PFOA (95% CI: -54 to -23%) concentrations compared with
156                                     Measured PFOA levels increased for the first 7 years after menopa
157                    We also analyzed measured PFOA (dependent variable) in relation to the number of y
158 at the observed association between measured PFOA and menopause is subject to reverse causation for t
159 mates were modeled independently of measured PFOA based on residential history and plant emissions.
160 -59% ( approximately 11-19 pg/L) of measured PFOA concentrations in the PML (mean 32 +/- 15 pg/L).
161  mothers and their term infants, we measured PFOA and four long-chain PFCAs (ng/mL) in third-trimeste
162                                   The median PFOA intakes from residential indoor air (5.7 pg kg bw(-
163                   Using measured and modeled PFOA in 2005 or 2006 (predictor variables), cross-sectio
164                         Historically modeled PFOA exposure, estimated using environmental fate and tr
165  charged outer corona that attracts negative PFOA molecules.
166 the byproducts showed that only about 10% of PFOA and PFOS is converted into shorter-chain perfluoroa
167 ith indirect exposure contributing to 45% of PFOA serum concentrations.
168                      Removal of up to 60% of PFOA and PFOS was observed during 100 day incubations, w
169 udies demonstrated substantial adsorption of PFOA and PFOS by polyDADMAC-stabilized PAC, which yielde
170                          Open application of PFOA in industry and products has been banned in Norway
171 phy-mass spectrometry showed that capture of PFOA by the capsules reached a maximum of >99.9% in 2-3
172 ately 10% lower in the highest categories of PFOA, PFNA, and perfluorohexane sulfonate (PFHxS) compar
173 olism yield and the initial concentration of PFOA in serum was mainly contributing to the uncertainty
174 in daughters with prenatal concentrations of PFOA (beta = 0.24; 95% CI: 0.05, 0.43) and PFHxS (beta =
175 hnicians with high initial concentrations of PFOA in serum (250-1050 ng/mL), the ongoing occupational
176                Atmospheric concentrations of PFOA, PFNA, and methyl perfluorooctane sulfonamido ethan
177 ion measurements show that concentrations of PFOA, PFOS, and FOSA at the air-water interface were fro
178 hildren with higher plasma concentrations of PFOA, PFOS, and perfluorodecanoate (PFDA) had lower aBMD
179 ts after starting or stopping consumption of PFOA-contaminated water.
180 ire reaction pathways for the degradation of PFOA by persulfate, with specific considerations on the
181 ine qua non condition for the degradation of PFOA by persulfate.
182 as of minor importance and net depuration of PFOA was observed throughout the ski season.
183                    The limit of detection of PFOA in ultrapure water was 11.0 ng L(-1).
184 he toxicokinetics and tissue distribution of PFOA in male rats.
185 he toxicokinetics and tissue distribution of PFOA in rats following exposure via both IV and oral rou
186 e text], [Formula: see text] per doubling of PFOA].
187 enX recapitulated many documented effects of PFOA in CD-1 mice, regardless of its much shorter report
188  considers the cellular uptake and efflux of PFOA via both passive diffusion and transport facilitate
189         We demonstrate here the formation of PFOA and PFOS in earthworms (Lumbricus terrestris) from
190 e input parameters quantifying the intake of PFOA were mainly responsible for the uncertainty of the
191 variety of epidemiological investigations of PFOA have been published, mostly using measured or model
192 cted water that meets the current 70 ng/L of PFOA and PFOS U.S. Environmental Protection Agency's lif
193       Maternal exposures to higher levels of PFOA, PFHpS, and PFAS mixtures were associated with the
194 ed with significantly higher serum levels of PFOA, PFNA, PFDA, and PFOS, based on 24-h and 12-month r
195 tion was not reported or if the half-life of PFOA was mis-specified.
196 rric iron, were conducted in the presence of PFOA or PFOS at 0.1 mg/L and 100 mg/L.
197 pid (<5 min) and sensitive quantification of PFOA molecules at low ng L(-1) levels in environmental w
198 n the highest versus the lowest quartiles of PFOA, PFHxS, and PFNA, with aORs of 2.59 (95% CI: 1.01,
199                       Historical releases of PFOA and related epidemiological work in this area has b
200                           The replacement of PFOA with short-chain substitutes is thus considered the
201                  This is the first report of PFOA, perfluorooctane sulfonate (PFOS), perfluorohexane
202 at airborne PFAA precursors were a source of PFOA, PFNA, and PFOS exposure in this population.
203 roject investigating the indirect sources of PFOA/PFOS in the environment and engineered systems, thi
204 using protonated and deprotonated species of PFOA and SO(4)(*-) and showed that the reaction of anion
205                  We compared the toxicity of PFOA and GenX in pregnant mice and their developing embr
206 ergy requirement (EE/O) for the treatment of PFOA and PFOS from SBs ranged from 380 to 830 kWh/m(3).
207  the diverging individual temporal trends of PFOA in serum with correlation coefficients of 0.82-0.94
208                          Exposure to GenX or PFOA resulted in increased GWG, with increase in weight
209                            ADONA, PFESA1, or PFOA exposure resulted in detectable levels of parent co
210               Early life exposure to PFOS or PFOA was not associated with ADHD during childhood [odds
211 % of the fluorine associated with the parent PFOA and 58% of the fluorine associated with the parent
212 nyl, mirex, PBDEs, PCBs, PCDDs, PCDFs, PeCB, PFOA, and PFOS) monitored in 9 countries (Congo, Ghana,
213                          Perfluorononanoate (PFOA) and perfluorooctanesulfonate (PFOS) dominated in c
214                          Perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS) are two enviro
215 tanesulfonate (PFOS) and perfluorooctanoate (PFOA) are among the most prominent contaminants in human
216 ane sulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations generally decreased in precipitatio
217 ane sulfonate (PFOS) and perfluorooctanoate (PFOA) have been associated with early menopause.
218 anesulfonate (PFOS), and perfluorooctanoate (PFOA) in hand wipes.
219 tanesulfonate (PFOS) and perfluorooctanoate (PFOA), are not placed into the context of total fluorine
220 tanesulfonate (PFOS) and perfluorooctanoate (PFOA).
221 oheptanoate (PFHpA), and perfluorooctanoate (PFOA).
222 /L (median 180 ng/L) for perfluorooctanoate (PFOA) and 140 ng/L (median 850 ng/L) for perfluorooctane
223 te (PFDA) at 7 y and for perfluorooctanoate (PFOA) at 13 y, both suggesting a decrease by approximate
224 her FTPs degrade to form perfluorooctanoate (PFOA) and perfluorocarboxylate (PFCA) homologues has bee
225 nizable PFASs, including perfluorooctanoate (PFOA), perfluorooctanesulfonate (PFOS) and their respect
226 l to estimate individual perfluorooctanoate (PFOA) serum concentrations and assess the association wi
227                 Maternal perfluorooctanoate (PFOA) and perfluorononanoate (PFNA) concentrations were
228  blood concentrations of perfluorooctanoate (PFOA) (median of 120 pg/mL of ww in males and 150 pg/mL
229 concentrations of PFASs [perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), perfluorononano
230 luoroheptanoate (PFHpA), perfluorooctanoate (PFOA), perfluorononanoate (PFNA), perfluorodecanoate (PF
231 exane sulfonate (PFHxS), perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), and perfluorono
232 exane sulfonate (PFHxS), perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), and perfluoroun
233 ooctanesulfonate (PFOS), perfluorooctanoate (PFOA), perfluorohexanesulfonate (PFHxS) and perfluoronon
234 ooctanesulfonate (PFOS), perfluorooctanoate (PFOA), perfluorohexanesulfonate (PFHxS), and 2-(N-methyl
235 entiles) prenatal plasma perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), perfluorohexane
236                    Serum perfluorooctanoate (PFOA) and perfluorohexane sulfonate (PFHxS) concentratio
237 , respectively], whereas perfluorooctanoate (PFOA) was positively associated with total cholesterol [
238 AP1, was associated with perfluorooctanoate (PFOA) at FDR < 0.05.
239 were found in personal air for PFHxA, PFHpA, PFOA, PFNA, PFDA, PFUnDA, and PFOS, respectively.
240              Median concentrations of PFHxS, PFOA, PFOS, and PFNA were 8, 35, 22, and 1.7 ng/mL in bo
241                     Four legacy PFAS (PFHxS, PFOA, PFOS, PFNA) were detected in most ( >= 97%) partic
242 We studied the TK of four PFAA (PFOS, PFHxS, PFOA, and PFBA) with different chain lengths (4-8 carbon
243 e-firefighters and officers had higher PFNA, PFOA, PFDA, and PFUnDA levels compared to drivers.
244                                 PFDeA, PFNA, PFOA, and PFOS were associated with a lower percentage o
245  four perfluorinated compounds (PFHxS, PFNA, PFOA, PFOS) were measured.
246 e used to prepare a PAH mixture, while PFNA, PFOA, PFOS, and PFTrA were used to prepare a PFAS mixtur
247                                        PFOS, PFOA, PFBS, and PFHxS were all detected frequently in dr
248 d house dust samples were observed for PFOS, PFOA, and 6:2diPAP.
249 d with 30-50% higher concentrations of PFOS, PFOA, and 8:2diPAP in hand wipes.
250         Levels of seven types of PFAS [PFOS, PFOA, perfluorohexane sulfonate (PFHxS), perfluoroheptan
251 ge 15 years with prenatal exposures to PFOS, PFOA, perfluorohexane sulfonic acid (PFHxS), and perfluo
252 e, indicating that as defluorination of PFOS/PFOA occurred, some of the products were being metaboliz
253 l needles and used to rapidly preconcentrate PFOA from water for direct analysis by nanoelectrospray
254 ch interquartile range increment of prenatal PFOA concentrations was associated with 0.21 kg/m(2) (95
255                  The beta-CD polymer reduces PFOA concentrations from 1 mug L(-1) to <10 ng L(-1), at
256 s a novel technology to adsorb and sequester PFOA contamination in water.
257 covered between airborne 10:2 FTOH and serum PFOA and PFNA and between airborne MeFOSE and serum PFOS
258 eGFR, a marker of kidney function) and serum PFOA concentration were measured in blood samples collec
259 eled (unaffected by reverse causation) serum PFOA in association with these outcomes to examine the p
260                Including all children, serum PFOA, PFHxS, and PFOS concentrations in children increas
261                     Modeled cumulative serum PFOA was positively associated with ALT levels (p for tr
262 r at the federal limit, and decreasing serum PFOA after carbon filtration began in a contaminated wat
263 could cause major changes in estimated serum PFOA concentrations among participants.
264 culator that easily plots the expected serum PFOA concentration over time and at steady state for adu
265          With one log unit increase in serum PFOA, PFHxS, and PFNA, osteoporosis prevalence in women
266 tion, whereby health outcomes increase serum PFOA, may underlie these associations.
267 age are provided, including increasing serum PFOA after ongoing consumption of contaminated water at
268                         Using measured serum PFOA levels in 2005-2006, we applied two calibration met
269 than the results of increased measured serum PFOA.
270 05, respectively) but not with modeled serum PFOA (p = 0.50, p = 0.76, respectively).
271 shed, mostly using measured or modeled serum PFOA concentrations as the exposure metric.
272            Retrospective year-specific serum PFOA estimates were modeled independently of measured PF
273  followed by PFHxS (1.6-5.0 ng g(-1) serum), PFOA (2.0-2.5 ng g(-1) serum), and perfluorononanoate (P
274  a sorptive region that increased subsequent PFOA and PFOS retention by 3 orders of magnitude relativ
275 ross-sectional epidemiologic studies suggest PFOA is associated with liver injury biomarkers.
276 ficient at lowering interfacial tension than PFOA, FPOS, or FOSA substances below 100 mg/L, while abo
277                        It was confirmed that PFOA removal by the capsules was pH and PFOA concentrati
278             We did not observe evidence that PFOA increases the risk of clinically diagnosed liver di
279    Interaction-based experiments reveal that PFOA enters the soil via its hydrophobic tails and selec
280  to perfluoroalkyl acids (PFAAs) showed that PFOA contributed the highest exposure to adults via hand
281 logical features in placentas suggested that PFOA and GenX may exhibit divergent mechanisms of toxici
282                                          The PFOA replacement chemical GenX was detected at all downs
283               During a 30 min treatment, the PFOA concentration in 1.4 L of aqueous solutions was red
284 cal half-life of PFOS in humans, compared to PFOA, and for the higher transplacental transfer efficie
285     Pregnant CD-1 mice were exposed daily to PFOA (0, 1, or 5 mg/kg) or GenX (0, 2, or 10 mg/kg) via
286 compounds were metabolized within 10 days to PFOA/PFOS at yields of 3.4-20.8 mol % by day 21 and seve
287 l (FTOH) and metabolism to PFOA) exposure to PFOA serum concentrations was investigated using a dynam
288 r results indeed show decreasing exposure to PFOA with distance to the airports.
289                       Early life exposure to PFOA, PFHxS, and PFOS is an important determinant of ser
290 the surface area of the MOF upon exposure to PFOA.
291 as derived for transformation of 8:2 FTOH to PFOA.
292 uorotelomer alcohol (FTOH) and metabolism to PFOA) exposure to PFOA serum concentrations was investig
293 with TFBMD and FNBMD, and for ln-transformed PFOA exposure with TFBMD (p < 0.05).
294     These results are promising for treating PFOA-contaminated water and demonstrate the versatility
295                 Comparison of drinking water PFOA concentrations to those study findings or to typica
296 ater to measured plasma concentrations were: PFOA 12% (95% probability interval 11%-14%), PFNA 13% (8
297 oxicity in the embryo-placenta unit, whereas PFOA- and GenX-exposed livers shared a similar constella
298                                        While PFOA and PFNA exposure did not follow a significant time
299 e species involved in primary reactions with PFOA showed that hydroxyl and superoxide radicals, which
300 e Carlo simulations to vary the year-by-year PFOA drinking-water concentration by randomly sampling f

 
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