ライフサイエンスコーパス: PFOA

1 PFOA and PFOS concentrations in plankton ranged from 0.1

2 PFOA consistently increased over time reaching 1.7 +/- 0

3 PFOA exposure was associated with kidney and testicular

4 PFOA was far less toxic than these triazoles: EC50(PFOA)

5 PFOA was the predominant PFAS constituent in pine needle

6 PFOA, beta-hexachlorocyclohexane, PCB-178, PBDE-28, PBDE

7 PFOA, PFNA, perfluorodecanoate (PFDeA), and PFHxS were i

8 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

9 crease: PFOS RR = 0.92 (95% CI: 0.69, 1.22); PFOA RR = 0.98 (95% CI: 0.73, 1.31)].

10 H, geocoded addresses were integrated with a PFOA exposure model to examine the relationship between

11 eneration of perfluoroalkyl carboxylic acid (PFOA) at a yield of 30 mol % by day 180.

12 y due to perfluorooctatonic carboxylic acid (PFOA), with low relative concentrations of measured biot

13 s, even for perfluorooctane carboxylic acid (PFOA, 6%).

14 Perfluorooctanoic acid (PFOA or C8) has hepatotoxic effects in animals.

15 opmental exposure to perfluorooctanoic acid (PFOA) affect fetal growth in humans?" METHODS: We develo

16 opmental exposure to perfluorooctanoic acid (PFOA) affects fetal growth in humans.

17 associations between perfluorooctanoic acid (PFOA) and high cholesterol levels, but studies of hypert

18 Human exposure to perfluorooctanoic acid (PFOA) and other per- and polyfluoroalkyl substances (PFA

19 ealth advisories for perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) in 2016.

20 Serum perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) levels have b

21 us research suggests perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) may be associ

22 Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS) were prev

23 ds (PFAAs) including perfluorooctanoic acid (PFOA) and perfluorooctanesulfonate (PFOS) at concentrati

24 nd substances beyond perfluorooctanoic acid (PFOA) and PFOS.

25 anesulfonate (PFOS), perfluorooctanoic acid (PFOA) and their precursors.

26 Toxicity of perfluorooctanoic acid (PFOA) and triazoles, that is, paclobutrazol (PBZ) and tr

27 sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are currently listed as priority substances under

28 ulfonate (PFBS), and perfluorooctanoic acid (PFOA) as high as 220 ng L(-1), 160 ng L(-1), and 120 ng

29 onic acid (PFOS) and perfluorooctanoic acid (PFOA) concentrations was associated with higher homeosta

30 sulfonic (PFOS) and perfluorooctanoic acid (PFOA) concentrations, using liquid chromatography-mass s

31 Modeled perfluorooctanoic acid (PFOA) exposure and liver function in a Mid-Ohio Valley c

32 ion with substantial perfluorooctanoic acid (PFOA) exposure due to releases from a chemical plant.

33 Perfluorooctanoic acid (PFOA) has been linked to cancer in occupational mortalit

34 Serum levels of perfluorooctanoic acid (PFOA) have been associated with decreased renal function

35 um concentrations of perfluorooctanoic acid (PFOA) have been extensively used in epidemiologic studie

36 PFAM derivatives of perfluorooctanoic acid (PFOA) in a wide range of compounds, experimental materia

37 had been exposed to perfluorooctanoic acid (PFOA) in drinking water contaminated by industrial waste

38 ic acid (PFOS) or to perfluorooctanoic acid (PFOA) increases mouse and human peroxisome proliferator-

39 Perfluorooctanoic acid (PFOA) is a persistent environmental contaminant that has

40 Perfluorooctanoic acid (PFOA) is a potential cause of adverse pregnancy outcomes

41 Perfluorooctanoic acid (PFOA) is a synthetic chemical ubiquitous in the serum of

42 ect (i.e., uptake of perfluorooctanoic acid (PFOA) itself) and indirect (i.e., uptake of 8:2 fluorote

43 opmental exposure to perfluorooctanoic acid (PFOA) or its salts affect fetal growth in animals ?" and

44 were associated with perfluorooctanoic acid (PFOA) serum levels in previous cross-sectional studies.

45 .40, -2.04), and for perfluorooctanoic acid (PFOA) was 7.13 g (95% CI: -8.46, -5.80); results based o

46 revealed that (13)C8-perfluorooctanoic acid (PFOA) was suitable for the calculation of site-specific

47 sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were detected in all samples; four other PFASs wer

48 uorophenol (PFP) and perfluorooctanoic acid (PFOA)) from the solution state (after a spill) through t

49 sulfonate (PFOS) and perfluorooctanoic acid (PFOA), analysed by HPLC-ESI-MS, in human milk and food s

50 ulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and 2,2',4,4'-tetrahydroxybenzophenone (BP2).

51 ulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) in maternal pla

52 ces (PFASs), notably perfluorooctanoic acid (PFOA), contaminate many ground and surface waters and ar

53 substances, such as perfluorooctanoic acid (PFOA), in organisms.

54 ic compounds such as perfluorooctanoic acid (PFOA), is ill-defined.

55 xanoic acid (PFHxA), perfluorooctanoic acid (PFOA), perfluorodecanoic acid (PFDA), and perfluorooctan

56 s (PFAAs), including perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorooctan

57 um concentrations of perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorononano

58 s (PFASs), including perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS), perfluorohe

59 ight PFCs, including perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS), perfluorono

60 ostnatal exposure to perfluorooctanoic acid (PFOA), perfluorooctanesulfonate (PFOS), and perfluorohex

61 score, dominated by perfluorooctanoic acid (PFOA), was inversely associated with current wheeze (OR

62 level of exposure to perfluorooctanoic acid (PFOA), which was introduced in the late 1940s and is now

63 e been suggested for perfluorooctanoic acid (PFOA).

64 he transformation of perfluorooctanoic acid (PFOA).

65 onic acid (PFOS) and perfluorooctanoic acid (PFOA).

66 ding PFOS, PFDS, and perfluorooctanoic acid (PFOA); no trend in two analytes; and increases in two an

67 ulfonate (PFOS), and perfluorooctanoic acid (PFOA)] were associated with 17 semen quality end points

68 PFCAs include perfluorooctanoic acid (PFOA; C8) and long-chain PFCAs (C9-C20).

69 y gland development (perfluorooctanoic acid; PFOA) and suppression of immune response (perfluorooctan

70 her than requiring in vivo data fitting, all PFOA-related parameters were obtained from in vitro assa

71 Although PFOA was the most commonly detected PFC (57% of samples)

72 In cross-sectional analyses, we analyzed PFOA in relation to self-reported menopause among women

73 m at delivery of PFOS [8.50 (7.01-9.58)] and PFOA [3.43 (3.01-3.90)] were significantly lower than at

74 184 ng/g of lipid), PFOS (GM 3369 ng/L), and PFOA (GM 1617 ng/L) were detected in all samples.

75 hnicity were associated with higher PFOS and PFOA concentrations in colostrum.

76 Maternal PFOS and PFOA concentrations were overall inversely but nonsignif

77 chanisms underlying isomer-specific PFOS and PFOA disposition have not previously been studied.

78 me category had significantly lower PFOS and PFOA GM concentrations than other women.

79 er, unclear if exposure to prenatal PFOS and PFOA has a lasting influence on growth.

80 In conclusion, plasma levels of PFOS and PFOA in pregnant women did not seem to have any apprecia

81 iation constants (Kd) of individual PFOS and PFOA isomers with human serum albumin (HSA) and (ii) rel

82 ies and renal clearance of branched PFOS and PFOA isomers, compared to the respective linear isomer.

83 t each 1-ng/mL increase in prenatal PFOS and PFOA levels was associated with 5.00 g (95% CI: -21.66,

84 PFOS and PFOA predictors were identified by optimizing multiple l

85 higher binding affinities of linear PFOS and PFOA to total serum protein were confirmed when both cal

86 PFOS and PFOA were the most abundant PFAS (geometric mean: 5.80 a

87 ion byproducts, chromium(VI), strontium, and PFOA/PFOS.

88 imate formation of terminal products such as PFOA.

89 ectional studies showing association between PFOA and ALT, a marker of hepatocellular damage.

90 s on the epidemiological association between PFOA and preeclampsia.

91 There was no apparent association between PFOA exposure and hypertension or coronary artery diseas

92 tudinal cohort study of associations between PFOA exposure and adult chronic diseases.

93 s being used to examine associations between PFOA exposure and multiple adult chronic diseases.

94 c studies that examined associations between PFOA exposures and adverse health outcomes among residen

95 Assuming no interactions between PFOA and the triazoles, the toxicity of PFOA in mixtures

96 We investigated the relationship between PFOA exposure and cancer among residents living near the

97 In boys, PFOA concentrations were significantly associated with t

98 The relative abundance of branched PFOA in the northern hemisphere was correlated with dist

99 have contributed to the presence of branched PFOA isomers in blood by serving as an indirect source.

100 e strongly bound to HSA compared to branched PFOA isomers (Kd range from 4(+/-2)x10(-4) M to 3(+/-2)x

101 nd that pregnant women had lower circulating PFOA and PFOS concentrations in peripheral blood than no

102 as also used to treat groundwater containing PFOA and several cocontaminants including perfluorooctan

103 er (a) from direct emissions of contemporary PFOA via manufacturing or use in Asia, or (b) from atmos

104 eric transport and oxidation of contemporary PFOA-precursors.

105 We measured serum creatinine, PFOA, perfluorooctane sulfonate (PFOS), perfluorononanoi

106 he association between cancer and cumulative PFOA serum concentration using proportional hazards mode

107 cidence increased with increasing cumulative PFOA exposure (sum of yearly serum concentration estimat

108 he first to the fifth quintile of cumulative PFOA exposure was associated with a 6% increase in ALT l

109 associations between quartiles of cumulative PFOA serum levels and the incidence of autoimmune diseas

110 om error in the yearly public water district PFOA concentrations, systematic error specific to each w

111 biomonitoring, and suggest that the dominant PFOA source(s) to the Pacific and Canadian Arctic Archip

112 as far less toxic than these triazoles: EC50(PFOA) = 0.20-0.24 mM.

113 certainty can substantially change estimated PFOA serum concentrations, but results in only minor imp

114 evaluate impact of uncertainty in estimated PFOA drinking-water concentrations on estimated serum co

115 ween cancer odds and categories of estimated PFOA serum.

116 For PFOA, we derived a pKa of 0.5 from fitting the experimen

117 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.

118 contribution to riverine discharge (21% for PFOA, 6% for PFOS), while atmospheric deposition to the

119 62 (95% confidence interval: 1.10, 2.37) for PFOA and 1.65 (95% confidence interval: 1.10, 2.49) for

120 sed polymer network with higher affinity for PFOA compared to powdered activated carbon, along with c

121 m was 35.3 pg/mL for PFOS and 32.8 pg/mL for PFOA.

122 d with those in the lowest quartiles (OR for PFOA = 1.98; 95% CI: 1.24, 3.19 and OR for PFOS = 1.73;

123 in the lowest quartile [odds ratio (OR) for PFOA = 1.55; 95% CI: 0.99, 2.43; OR for PFOS = 1.77; 95%

124 Women provided serum for PFOA and PFOS measurement in 2005-2006 and reported repr

125 Calculated population halving time for PFOA varied between 8.2-14.5 years, which contrasts to t

126 o Valley (USA) with local contamination from PFOA.

127 OMA-IR was more pronounced in females [e.g., PFOA: -15.6% (95% CI: -25.4, -4.6) vs. -6.1% (95% CI: -1

128 Both achieved remarkably high PFOA removal and defluorination efficiencies compared to

129 Higher PFOA exposure was associated with incident hypercholeste

130 Our results suggest that higher PFOA serum levels may be associated with testicular, kid

131 ated associations between modeled historical PFOA exposures and liver injury biomarkers and medically

132 r elevated direct bilirubin or GGT; however, PFOA was associated with decreased direct bilirubin.

133 experiments monitoring each phase illustrate PFOA rapidly transfers from solution to the solid phase

134 The decline in PFOA concentrations in human blood is consistent with a

135 = 1.18; 95% CI: 1.01, 1.39 for a doubling in PFOA], whereas for PFOS there were inverse relationships

136 d odds ratios (ORs) per log unit increase in PFOA and PFOS of 1.27 (95% CI: 1.05, 1.55) and 1.47 (95%

137 , -2.3) per interquartile range increment in PFOA].

138 Uncertainty in PFOA water concentrations could cause major changes in e

139 The infant PFOA and PFOS serum concentrations were 6% (95% CI: 1, 1

140 Similarly, linear PFOA (Kd=1(+/-0.9)x10(-4) M) was more strongly bound to

141 n measured serum PFOA concentrations [IQR ln(PFOA) = 1.63] was associated with a decrease in eGFR of

142 wer PFOS (95% CI: -56 to -17%) and 40% lower PFOA (95% CI: -54 to -23%) concentrations compared with

143 Measured PFOA levels increased for the first 7 years after menopa

144 We also analyzed measured PFOA (dependent variable) in relation to the number of y

145 at the observed association between measured PFOA and menopause is subject to reverse causation for t

146 mates were modeled independently of measured PFOA based on residential history and plant emissions.

147 -59% ( approximately 11-19 pg/L) of measured PFOA concentrations in the PML (mean 32 +/- 15 pg/L).

148 mothers and their term infants, we measured PFOA and four long-chain PFCAs (ng/mL) in third-trimeste

149 The median PFOA intakes from residential indoor air (5.7 pg kg bw(-

150 According to the extended IA model, PFOA had nonsignificant effects on the toxicity of PBZ w

151 Using measured and modeled PFOA in 2005 or 2006 (predictor variables), cross-sectio

152 we examined the association between modeled PFOA exposure and incident hypertension, hypercholestero

153 Historically modeled PFOA exposure, estimated using environmental fate and tr

154 In multivariable-adjusted models, PFOA was associated with higher odds of ever having rece

155 f other PFCs were at sites with little or no PFOA.

156 the byproducts showed that only about 10% of PFOA and PFOS is converted into shorter-chain perfluoroa

157 ith indirect exposure contributing to 45% of PFOA serum concentrations.

158 Open application of PFOA in industry and products has been banned in Norway

159 ately 10% lower in the highest categories of PFOA, PFNA, and perfluorohexane sulfonate (PFHxS) compar

160 olism yield and the initial concentration of PFOA in serum was mainly contributing to the uncertainty

161 with lower maternal serum concentrations of PFOA (-3%; 95% CI: -5, -2%), PFOS (-3%; 95% CI: -3, -2%)

162 in daughters with prenatal concentrations of PFOA (beta = 0.24; 95% CI: 0.05, 0.43) and PFHxS (beta =

163 hnicians with high initial concentrations of PFOA in serum (250-1050 ng/mL), the ongoing occupational

164 regnant mice to increasing concentrations of PFOA was associated with a change in mean pup birth weig

165 ts after starting or stopping consumption of PFOA-contaminated water.

166 nd perhaps contribute to the slow decline of PFOA.

167 as of minor importance and net depuration of PFOA was observed throughout the ski season.

168 he toxicokinetics and tissue distribution of PFOA in male rats.

169 he toxicokinetics and tissue distribution of PFOA in rats following exposure via both IV and oral rou

170 rgest study to date of the health effects of PFOA.

171 considers the cellular uptake and efflux of PFOA via both passive diffusion and transport facilitate

172 e input parameters quantifying the intake of PFOA were mainly responsible for the uncertainty of the

173 variety of epidemiological investigations of PFOA have been published, mostly using measured or model

174 trast was performed to compare the levels of PFOA and perfluorooctanesulfonic acid (PFOS) in pregnant

175 We found that serum levels of PFOA and PFOS were positively associated with hyperurice

176 o Valley community exposed to high levels of PFOA through drinking-water contamination.

177 tion was not reported or if the half-life of PFOA was mis-specified.

178 report on a 2009 study of the occurrence of PFOA, PFOS, and eight other perfluorinated compounds (PF

179 Women in the highest quartiles of PFOA and PFOS exposure had higher odds of osteoarthritis

180 n the highest versus the lowest quartiles of PFOA, PFHxS, and PFNA, with aORs of 2.59 (95% CI: 1.01,

181 The replacement of PFOA with short-chain substitutes is thus considered the

182 at airborne PFAA precursors were a source of PFOA, PFNA, and PFOS exposure in this population.

183 We conducted a population-based study of PFOA and PFOS and birth outcomes from 2005 through 2010

184 ween PFOA and the triazoles, the toxicity of PFOA in mixtures with the triazoles estimated by the con

185 lleviation of PBZ and TDF on the toxicity of PFOA was found by the extended CA model only.

186 the diverging individual temporal trends of PFOA in serum with correlation coefficients of 0.82-0.94

187 between the maternal plasma level of PFOS or PFOA and the children's body mass index, waist circumfer

188 Perfluorononanoate (PFOA) and perfluorooctanesulfonate (PFOS) dominated in c

189 Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) are persisten

190 tanesulfonate (PFOS) and perfluorooctanoate (PFOA) are among the most prominent contaminants in human

191 ane sulfonate (PFOS) and perfluorooctanoate (PFOA) have been associated with early menopause.

192 tanesulfonate (PFOS) and perfluorooctanoate (PFOA), are not placed into the context of total fluorine

193 tanesulfonate (PFOS) and perfluorooctanoate (PFOA), has been associated with lower birth weight and l

194 tanesulfonate (PFOS) and perfluorooctanoate (PFOA).

195 8:2 FTOH-dosed animals, perfluorooctanoate (PFOA) was produced as the primary PFCA, at 623.13 +/- 59

196 te (PFDA) at 7 y and for perfluorooctanoate (PFOA) at 13 y, both suggesting a decrease by approximate

197 osolids were highest for perfluorooctanoate (PFOA; 67 ng/g) in radish root, perfluorobutanoate (PFBA;

198 her FTPs degrade to form perfluorooctanoate (PFOA) and perfluorocarboxylate (PFCA) homologues has bee

199 acids (PFAAs), including perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), and perfluorono

200 nizable PFASs, including perfluorooctanoate (PFOA), perfluorooctanesulfonate (PFOS) and their respect

201 Increasing perfluorooctanoate (PFOA) concentrations were also associated with fewer aut

202 l to estimate individual perfluorooctanoate (PFOA) serum concentrations and assess the association wi

203 Maternal perfluorooctanoate (PFOA) and perfluorononanoate (PFNA) concentrations were

204 holds, levels of neither perfluorooctanoate (PFOA) nor PFOS in seabird eggs from the Canadian Arctic

205 A was similar to that of perfluorooctanoate (PFOA, log Koc = 1.89).

206 concentrations of PFASs [perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), perfluorononano

207 luoroheptanoate (PFHpA), perfluorooctanoate (PFOA), perfluorononanoate (PFNA), perfluorodecanoate (PF

208 exane sulfonate (PFHxS), perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), and perfluorono

209 ooctanesulfonate (PFOS), perfluorooctanoate (PFOA), and six additional PFASs in maternal serum at app

210 ooctanesulfonate (PFOS), perfluorooctanoate (PFOA), perfluorohexanesulfonate (PFHxS) and perfluoronon

211 ooctanesulfonate (PFOS), perfluorooctanoate (PFOA), perfluorohexanesulfonate (PFHxS), and 2-(N-methyl

212 entiles) prenatal plasma perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), perfluorohexane

213 egraded predominantly to perfluorooctanoate (PFOA) in soils and at a significantly higher rate in the

214 t pathways contribute to perfluorooctanoate (PFOA) in the world's oceans, particularly in remote loca

215 , respectively], whereas perfluorooctanoate (PFOA) was positively associated with total cholesterol [

216 were found in personal air for PFHxA, PFHpA, PFOA, PFNA, PFDA, PFUnDA, and PFOS, respectively.

217 Median concentrations of PFHxS, PFOA, PFOS, and PFNA were 8, 35, 22, and 1.7 ng/mL in bo

218 PFDeA, PFNA, PFOA, and PFOS were associated with a lower percentage o

219 e investigated the association between PFOS, PFOA, perfluorononanoate (PFNA), and perfluorohexane sul

220 We explored if maternal levels of PFOS, PFOA, and PFNA during the early nursing period are repre

221 ge 15 years with prenatal exposures to PFOS, PFOA, perfluorohexane sulfonic acid (PFHxS), and perfluo

222 d that a 1-ng/mL increase in serum or plasma PFOA was associated with a -18.9 g (95% CI: -29.8, -7.9)

223 nd well-characterized contrasts in predicted PFOA serum levels from six contaminated water supplies.

224 ch interquartile range increment of prenatal PFOA concentrations was associated with 0.21 kg/m(2) (95

225 The beta-CD polymer reduces PFOA concentrations from 1 mug L(-1) to <10 ng L(-1), at

226 Serum PFOA and PFOS were both positively associated with pregn

227 covered between airborne 10:2 FTOH and serum PFOA and PFNA and between airborne MeFOSE and serum PFOS

228 eGFR, a marker of kidney function) and serum PFOA concentration were measured in blood samples collec

229 sectional association between eGFR and serum PFOA observed in this and prior studies may be a consequ

230 ssion to estimate associations between serum PFOA and PFOS concentrations and self-reported diagnosis

231 he cross-sectional association between serum PFOA and PFOS concentrations with markers of liver funct

232 efore examined the association between serum PFOA and PFOS levels and hyperuricemia in a representati

233 eled (unaffected by reverse causation) serum PFOA in association with these outcomes to examine the p

234 Estimated cumulative serum PFOA concentrations were positively associated with kidn

235 Modeled cumulative serum PFOA was positively associated with ALT levels (p for tr

236 r at the federal limit, and decreasing serum PFOA after carbon filtration began in a contaminated wat

237 could cause major changes in estimated serum PFOA concentrations among participants.

238 culator that easily plots the expected serum PFOA concentration over time and at steady state for adu

239 terviewed 32,254 U.S. adults with high serum PFOA serum levels (median, 28 ng/mL) associated with dri

240 We predicted concurrent and historical serum PFOA concentrations using a validated environmental, exp

241 ge (IQR) contrast of 13 to 68 ng/mL in serum PFOA measured in 2005-2006.

242 However, an IQR shift in serum PFOA was not associated with TSH or TT4 levels in all ch

243 With one log unit increase in serum PFOA, PFHxS, and PFNA, osteoporosis prevalence in women

244 tion, whereby health outcomes increase serum PFOA, may underlie these associations.

245 age are provided, including increasing serum PFOA after ongoing consumption of contaminated water at

246 idence of association between maternal serum PFOA or PFOS and preterm birth (n = 158) or low birth we

247 derived from estimates of annual mean serum PFOA levels during follow-up, which were based on plant

248 terquartile range increase in measured serum PFOA concentrations [IQR ln(PFOA) = 1.63] was associated

249 mographic characteristics and measured serum PFOA concentrations in 2005-2006.

250 Using measured serum PFOA levels in 2005-2006, we applied two calibration met

251 than the results of increased measured serum PFOA.

252 in a highly exposed population (median serum PFOA, 28.3 ng/mL).

253 05, respectively) but not with modeled serum PFOA (p = 0.50, p = 0.76, respectively).

254 shed, mostly using measured or modeled serum PFOA concentrations as the exposure metric.

255 , and describe historical estimates of serum PFOA concentrations over time.

256 Higher concentrations of serum PFOA were associated with osteoarthritis in women, but n

257 In contrast, predicted serum PFOA concentrations at the time of enrollment were not a

258 iation of measured and model-predicted serum PFOA concentrations with estimated glomerular filtration

259 etween eGFR and measured and predicted serum PFOA concentrations.

260 Additionally, predicted serum PFOA levels at birth and during the first ten years of l

261 We hypothesized that predicted serum PFOA levels would be less susceptible to reverse causati

262 of age) as a function of retrospective serum PFOA concentration estimates (generated through fate, tr

263 Retrospective year-specific serum PFOA estimates were modeled independently of measured PF

264 for 1-unit increases in ln-transformed serum PFOA].

265 n a 2005-2006 baseline survey in which serum PFOA was measured.

266 ross-sectional epidemiologic studies suggest PFOA is associated with liver injury biomarkers.

267 lysis of birth records linked to the survey, PFOA was unrelated to pregnancy-induced hypertension or

268 pheral blood than nonpregnant women and that PFOA levels were consistently lower throughout all trime

269 Based on the assumption that PFOA may interact with the triazoles, different predicti

270 ating in which review authors concluded that PFOA is "known to be toxic" to human reproduction and de

271 We did not observe evidence that PFOA increases the risk of clinically diagnosed liver di

272 We found evidence that PFOA is associated with ulcerative colitis.

273 Interaction-based experiments reveal that PFOA enters the soil via its hydrophobic tails and selec

274 The PFOA replacement chemical GenX was detected at all downs

275 During a 30 min treatment, the PFOA concentration in 1.4 L of aqueous solutions was red

276 cal half-life of PFOS in humans, compared to PFOA, and for the higher transplacental transfer efficie

277 at pH 8.5 showed no degradation of EtFOA to PFOA after 8 days due to the stability of the amide bond

278 ence in Mid-Ohio Valley residents exposed to PFOA in drinking water due to chemical plant emissions.

279 We concluded that developmental exposure to PFOA adversely affects human health based on sufficient

280 uggests an ongoing or additional exposure to PFOA or one of its precursor compounds.

281 vidence that fetal developmental exposure to PFOA reduces fetal growth in animals.

282 uman evidence that developmental exposure to PFOA reduces fetal growth.

283 l (FTOH) and metabolism to PFOA) exposure to PFOA serum concentrations was investigated using a dynam

284 Cumulative exposure to PFOA was derived from estimates of annual mean serum PFO

285 as derived for transformation of 8:2 FTOH to PFOA.

286 uorotelomer alcohol (FTOH) and metabolism to PFOA) exposure to PFOA serum concentrations was investig

287 with TFBMD and FNBMD, and for ln-transformed PFOA exposure with TFBMD (p < 0.05).

288 These results are promising for treating PFOA-contaminated water and demonstrate the versatility

289 t a Mid-Ohio Valley chemical plant that used PFOA, and residents of the surrounding community.

290 Comparison of drinking water PFOA concentrations to those study findings or to typica

291 ith child's age, child's sex, drinking-water PFOA concentration, reported bottled water use, and moth

292 ntrations of PFNA, PFDA, and PFUnDA, whereas PFOA concentrations were decreasing.

293 We investigated whether PFOA and PFOS exposures are associated with prevalence o

294 reast milk samples (0.76+/-1.27 ng/g), while PFOA was detected in one sample (8.04 ng/g).

295 ver cancers, which have been associated with PFOA in animal or human studies.

296 significantly increased in association with PFOA exposure, with adjusted rate ratios by quartile of

297 itional NJ PWS known to be contaminated with PFOA were also each sampled 4-9 times in 2010-13 for nin

298 e species involved in primary reactions with PFOA showed that hydroxyl and superoxide radicals, which

299 e Carlo simulations to vary the year-by-year PFOA drinking-water concentration by randomly sampling f

300 Retrospective yearly PFOA serum concentrations were estimated for each partic