| Perfluorononanoic acid, or PFNA, is a synthetic perfluorinated carboxylic acid and fluorosurfactant that is also an environmental contaminant found in people and wildlife along with PFOS and PFOA. |
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InChI=1S/C9HF17O2/c10- 2(11,1(27)28)3(12,13)4(14,15)5(16,17)6(18,19)7(20,21)8(22,23)9(24,25)26/h(H,27,28) |
| UZUFPBIDKMEQEQ-UHFFFAOYSA-N |
| OC(=O)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)F |
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surfactant
A substance which lowers the surface tension of the medium in which it is dissolved, and/or the interfacial tension with other phases, and, accordingly, is positively adsorbed at the liquid/vapour and/or at other interfaces.
persistent organic pollutant
Any environmental contaminant that is resistant to environmental degradation through photolytic, biological or chemical processes. Such substances can have significant impact on health and the environment, as they persist in the environment, bioaccumulate in animal tissue and so biomagnify in food chains.
Bronsted acid
A molecular entity capable of donating a hydron to an acceptor (Bronsted base).
(via oxoacid )
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xenobiotic
A xenobiotic (Greek, xenos "foreign"; bios "life") is a compound that is foreign to a living organism. Principal xenobiotics include: drugs, carcinogens and various compounds that have been introduced into the environment by artificial means.
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View more via ChEBI Ontology
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heptadecafluorononanoic acid
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2,2,3,3,4,4,5,5,6,6,7,7,8,8,9,9,9-heptadecafluorononanoic acid
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NIST Chemistry WebBook
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Heptadecafluornonansäure
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ChEBI
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Heptadekafluornonansäure
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ChEBI
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Perfluornonansäure
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ChEBI
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perfluoro-n-nonanoic acid
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ChemIDplus
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perfluorononan-1-oic acid
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ChemIDplus
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perfluorononanoic acid
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NIST Chemistry WebBook
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PFNA
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ChEBI
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1897287
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Reaxys Registry Number
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Reaxys
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317302
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Gmelin Registry Number
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Gmelin
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375-95-1
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CAS Registry Number
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ChemIDplus
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375-95-1
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CAS Registry Number
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NIST Chemistry WebBook
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Yang S, Liu S, Ren Z, Jiao X, Qin S (2014)
Induction of oxidative stress and related transcriptional effects of perfluorononanoic acid using an in vivo assessment.
Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 160, 60-65 [PubMed:24295853]
[show Abstract]
Perfluorononanoic acid (PFNA) is an organic pollutant ubiquitous in the environment. However, the potential toxicity of PFNA remains largely unknown in teleost fish. This study defined the oxidative stress and related transcriptional effects of PFNA at various concentrations on zebrafish larvae. Activities of superoxide dismutase were induced in PFNA-treated groups but attenuated with exposure to higher concentration. Catalase activity and lipid peroxidation were significantly inhibited or increased at the highest concentration, respectively. To test the apoptotic pathway, several genes related to cell apoptosis were examined using real-time PCR. The expression of p53, apoptosis-inducing factor (AIF) and c-Jun NH (2)-terminal kinase (JNK) was partially increased, while Bcl-2, an anti-apoptotic gene, was reduced, with no significant effects on Bax and caspase-3 during the exposure period. The effect of PFNA on lipid β-oxidation system was investigated by examining the activity of peroxisome fatty acyl-COA oxidase (ACOX) and the expression of peroxisome proliferating activating receptors (PPARs). ACOX activity was moderately elevated with marginal significance and was not a significant consequence of PPARα and PPARγ expression. The overall results suggest that turbulence of oxidative stress and apoptotic pathway is involved in PFNA-induced toxicity in zebrafish larvae, and the gene expression patterns are able to reveal some potential mechanisms of developmental toxicity. | Hardell E, Kärrman A, van Bavel B, Bao J, Carlberg M, Hardell L (2014)
Case-control study on perfluorinated alkyl acids (PFAAs) and the risk of prostate cancer.
Environment international 63, 35-39 [PubMed:24246240]
[show Abstract]
Perfluorinated alkyl acids (PFAAs) are emerging environmental contaminants. Possible health effects for humans include increased risk for cancer but the knowledge is limited. In this study serum concentrations of certain perfluorinated sulfonates (PFHxS and PFOS) and carboxylates (PFOA, PFNA, PFDA, PFUnDA) were analyzed among 201 cases with prostate cancer and 186 population based control subjects. All blood samples were collected during 2007-2011 and no case had been treated with radio- or chemotherapy before enrolment in the study. The blood concentrations did not differ statistically significant between cases and controls except for PFDA with higher concentration among the cases (p=0.03). Analyses based on Gleason score and prostate specific antigen (PSA) level did not change the results. Heredity was a risk factor for prostate cancer yielding odds ratio (OR)=1.8, 95% confidence interval (CI)=1.01-3.1. The analyzed PFAAs yielded statistically significant higher ORs in cases with a first degree relative reporting prostate cancer, e.g., PFOA gave OR=2.6, 95% CI=1.2-6.0 and PFOS gave OR=2.7, 95% CI=1.04-6.8. The results showed a higher risk for prostate cancer in cases with heredity as a risk factor. In further studies interaction between gene and environment should be considered. | Jain RB (2014)
Contribution of diet and other factors to the levels of selected polyfluorinated compounds: data from NHANES 2003-2008.
International journal of hygiene and environmental health 217, 52-61 [PubMed:23601780]
[show Abstract]
Contribution of diet and selected risk factors to the levels of four polyfluorinated compounds was evaluated. Data from National Health and Nutrition Examination Survey for the years 2003-2008 were used. Dietary factors accounted for 10.4% to 21.2% of the explained variation. Amount of milk consumed was found to be positively associated (p<0.01) with perfluorononanoic acid (PFNA) but negatively associated with perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) (p<0.01). Amount of meat and fish consumed was positively associated (p<0.01) with PFNA and PFOS. Amount of non-alcoholic beverages consumed was positively associated (p<0.01) with PFNA and PFOA. Levels of PFOS increased (p<0.01) with increase in the amount of alcoholic beverages consumed. Total amount of alcohol consumed was positively associated (p<0.01) with PFNA. Levels of both PFOA and PFOS decreased with increase in total amount of caffeine consumed. Total amount of fat consumed was negatively associated with PFNA and positively associated with PFOS. Total calories consumed were negatively associated with perfluorohexane sulfonate (PFHxS) and PFOS but positively associated with PFNA. New to this study, positive correlations (p<0.01) between serum cholesterol and PFNA, PFOA, and PFOS were found. Serum albumin levels were negatively correlated with PFHxS but positively correlated with PFOA and PFOS. Males had statistically significantly higher levels of all four PFCs as compared to females and Mexican Americans had the lowest levels of all four PFCs than other race/ethnic groups. Levels of all four PFCs increased with increase in family income. Body mass index was negatively correlated with PFNA but positively associated with PFOA. There was a statistically significant decrease in the levels of PFOS over survey years 2003-2008. | Henderson WM, Smith MA (2007)
Perfluorooctanoic acid and perfluorononanoic acid in fetal and neonatal mice following in utero exposure to 8-2 fluorotelomer alcohol.
Toxicological sciences : an official journal of the Society of Toxicology 95, 452-461 [PubMed:17093205]
[show Abstract]
8-2 Fluorotelomer alcohol (FTOH) and its metabolites, perfluorooctanoic acid (PFOA) and perfluorononanoic acid (PFNA), are developmental toxicants but metabolism and distribution during pregnancy are not known. To examine this, timed-pregnant mice received a single gavage dose (30 mg 8-2 FTOH/kg body weight) on gestational day (GD) 8. Maternal and neonatal serum and liver as well as fetal and neonatal homogenate extracts were analyzed using gas chromatography coupled with mass spectrometry. During gestation (GD9 to GD18), maternal serum and liver concentrations of PFOA decreased from 789 +/- 41 to 668 +/- 23 ng/ml and from 673 +/- 23 to 587 +/- 55 ng/g, respectively. PFOA was transferred to the developing fetuses as early as 24-h posttreatment with concentrations increasing from 45 +/- 9 ng/g (GD10) to 140 +/- 32 ng/g (GD18), while PFNA was quantifiable only at GD18 (31 +/- 4 ng/g). Post-partum, maternal serum PFOA concentrations decreased from 451 +/- 21 ng/ml postnatal day (PND) 1 to 52 +/- 19 ng/ml (PND15) and PFNA concentrations, although fivefold less, exhibited a similar trend. Immediately after birth, pups were cross-fostered with dams that had been treated during gestation with 8-2 FTOH (T) or vehicle (C) resulting in four treatment groups in which the first letter represents in utero (fetal) exposure and the second represents lactational (neonatal) exposure: C/C, T/C, C/T, T/T. On PND1, neonatal whole-body homogenate concentrations of PFOA from T/T and T/C groups averaged 200 +/- 26 ng/g, decreased to 149 +/- 19 ng/g at PND3 and this decreasing trend was seen in both neonatal liver and serum from PND3 to PND15. Based on detectible amounts of PFOA in neonatal serum in the C/T group on PND3 (57 +/- 11 ng/ml) and on PND15 (58 +/- 3 ng/ml), we suggest that the neonates were exposed through lactation. In conclusion, exposure of neonates to PFOA and PFNA occurs both pre- and postnatally following maternal 8-2 FTOH exposure on GD8. |
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2014-10-29
