Skip header and navigation

Refine By

21 records – page 1 of 2.

Caffeine N3-demethylation (CYP1A2) in a population with an increased exposure to polychlorinated biphenyls.

https://arctichealth.org/en/permalink/ahliterature166669
Source
Eur J Clin Pharmacol. 2006 Dec;62(12):1041-8
Publication Type
Article
Date
Dec-2006
Author
Maria Skaalum Petersen
Jónrit Halling
Per Damkier
Flemming Nielsen
Philippe Grandjean
Pál Weihe
Kim Brøsen
Author Affiliation
Institute of Public Health, Department of Environmental Medicine, University of Southern Denmark, Winslovparken 17, 5000 Odense C, Denmark. mskaalum@health.sdu.dk
Source
Eur J Clin Pharmacol. 2006 Dec;62(12):1041-8
Date
Dec-2006
Language
English
Publication Type
Article
Keywords
Administration, Oral
Adolescent
Adult
Biometry
Caffeine - administration & dosage - metabolism
Cohort Studies
Cytochrome P-450 CYP1A2 - genetics - metabolism
Environmental Pollutants - chemistry - metabolism - poisoning
Female
Genotype
Humans
Male
Methylation
Middle Aged
Polychlorinated Biphenyls - chemistry - metabolism - poisoning
Sex Factors
Smoking - metabolism
Uracil - analogs & derivatives - metabolism
Uric Acid - analogs & derivatives - metabolism
Xanthines - metabolism
Abstract
To investigate the CYP1A2 phenotype distribution in a population with an increased exposure to polychlorinated biphenyls (PCBs) that would likely induce an increased activity of this enzyme. Further, to investigate the effect of sex, smoking, and oral contraceptive use on the CYP1A2 activity.
In 305 randomly selected Faroese residents aged 18-60 years, the CYP1A2 activity was determined following oral intake of a caffeine dose and subsequent determination of the urinary metabolites and calculation of the caffeine metabolic ratio (CMR). PCB exposure was assessed by measuring the serum concentration of major congeners.
The CYP1A2 phenotype distribution was unimodal. The CMR was significantly higher both in smoking men and in smoking women, independent of oral contraceptive use, as compared with non-smokers. Among non-smokers, the CMR was significantly higher in women not using oral contraceptives than in those using oral contraceptives; a similar difference could not be established among smokers. The CMR appeared higher in men than in women, but stratified analyses confirmed a significant sex-related difference only among smokers not using oral contraceptives. Overall, the mean CMR in Faroese was significantly higher compared with the mean CMR in Danish historical controls. No association was found with PCB exposure and individual PCB congeners, except for one of three dioxin-like congeners, in confounder-adjusted multiple regression analyses.
The CYP1A2 phenotype in Faroese residents was unimodally distributed and showed the inducing effect of smoking and the inhibiting effect of use of oral contraceptives, but a sex-related difference was not apparent after confounder adjustment. There was no statistically significant association between CMR and PCB exposure.
PubMed ID
17089110 View in PubMed
Less detail

Autoantibodies associated with prenatal and childhood exposure to environmental chemicals in Faroese children.

https://arctichealth.org/en/permalink/ahliterature264893
Source
Toxicol Sci. 2014 Nov;142(1):158-66
Publication Type
Article
Date
Nov-2014
Author
Christa E Osuna
Philippe Grandjean
Pál Weihe
Hassan A N El-Fawal
Source
Toxicol Sci. 2014 Nov;142(1):158-66
Date
Nov-2014
Language
English
Publication Type
Article
Keywords
Autoantibodies - blood
Autoantigens - immunology
Child
Denmark
Environmental monitoring
Environmental Pollutants - blood - toxicity
Female
Fetal Blood - chemistry
Fluorocarbons - blood - toxicity
Hair - chemistry
Humans
Infant, Newborn
Male
Methylmercury Compounds - blood - toxicity
Pilot Projects
Polychlorinated Biphenyls - blood - toxicity
Pregnancy
Prenatal Exposure Delayed Effects - blood - chemically induced - immunology
Abstract
Methylmercury, polychlorinated biphenyls (PCBs), and perfluorinated compounds (PFCs) are ubiquitous and persistent environmental chemicals with known or suspected toxic effects on the nervous system and the immune system. Animal studies have shown that tissue damage can elicit production of autoantibodies. However, it is not known if autoantibodies similarly will be generated and detectable in humans following toxicant exposures. Therefore, we conducted a pilot study to investigate if autoantibodies specific for neural and non-neural antigens could be detected in children at age 7 years who have been exposed to environmental chemicals. Both prenatal and age-7 exposures to mercury, PCBs, and PFCs were measured in 38 children in the Faroe Islands who were exposed to widely different levels of these chemicals due to their seafood-based diet. Concentrations of IgM and IgG autoantibodies specific to both neural (neurofilaments, cholineacetyltransferase, astrocyte glial fibrillary acidic protein, and myelin basic protein) and non-neural (actin, desmin, and keratin) antigens were measured and the associations of these autoantibody concentrations with chemical exposures were assessed using linear regression. Age-7 blood-mercury concentrations were positively associated with titers of multiple neural- and non-neural-specific antibodies, mostly of the IgM isotype. Additionally, prenatal blood-mercury and -PCBs were negatively associated with anti-keratin IgG and prenatal PFOS was negatively associated with anti-actin IgG. These exploratory findings demonstrate that autoantibodies can be detected in the peripheral blood following exposure to environmental chemicals. The unexpected association of exposures with antibodies specific for non-neural antigens suggests that these chemicals may have toxicities that have not yet been recognized.
Notes
Cites: Exp Cell Res. 2004 Nov 15;301(1):1-715501438
Cites: J Toxicol Environ Health A. 2007 Nov;70(21):1873-717934961
Cites: Bull Exp Biol Med. 2007 Aug;144(2):241-518399291
Cites: Nature. 2008 May 1;453(7191):65-7118362915
Cites: Neurotoxicol Teratol. 2008 May-Jun;30(3):161-618353611
Cites: Environ Health Perspect. 2008 Jun;116(6):716-2218560525
Cites: Lab Invest. 2008 Aug;88(8):796-80718521063
Cites: J Chromatogr A. 2009 Jan 16;1216(3):385-9319026423
Cites: Nat Rev Immunol. 2009 Mar;9(3):185-9419240757
Cites: J Immunol. 2009 Apr 1;182(7):4479-8719299749
Cites: Horm Metab Res. 2009 Jun;41(6):471-419530273
Cites: Endocr Regul. 2009 Apr;43(2):75-8119856712
Cites: Environ Health Perspect. 2010 Oct;118(10):1429-3320562055
Cites: Neurotoxicology. 2008 Jan;29(1):109-1518001836
Cites: Altern Med Rev. 2011 Mar;16(1):5-1321438643
Cites: Environ Sci Technol. 2011 Oct 1;45(19):8037-4521469664
Cites: Environ Sci Technol. 2011 Oct 1;45(19):8151-921682250
Cites: Environ Sci Technol. 2011 Oct 1;45(19):7954-6121866930
Cites: Toxicol Sci. 2011 Nov;124(1):1-2221908767
Cites: JAMA. 2012 Jan 25;307(4):391-722274686
Cites: Am J Epidemiol. 2012 Mar 1;175(5):451-6522287639
Cites: Toxicol Pathol. 2012;40(2):300-1122109712
Cites: Environ Res. 2012 Jul;116:93-11722560884
Cites: Arch Toxicol. 2012 Sep;86(9):1349-6722456834
Cites: Neurotoxicology. 2012 Dec;33(6):1491-823137609
Cites: J Prev Med Public Health. 2012 Nov;45(6):353-6323230465
Cites: PLoS One. 2013;8(3):e5680523483891
Cites: Annu Rev Immunol. 2013;31:345-8523516983
Cites: Environ Health Perspect. 2013 Apr;121(4):507-1323309686
Cites: J Toxicol Environ Health A. 2013;76(6):363-8023557235
Cites: PLoS One. 2013;8(4):e6072623589757
Cites: Int J Hyg Environ Health. 2013 Nov;216(6):721-723419585
Cites: J Immunotoxicol. 2013 Oct-Dec;10(4):373-923350954
Cites: Endocr J. 1999 Dec;46(6):765-7210724351
Cites: Neurology. 2001 Feb 27;56(4):529-3011222800
Cites: Proc Natl Acad Sci U S A. 2002 Apr 16;99(8):5545-5011960012
Cites: Cold Spring Harb Perspect Biol. 2010 Nov;2(11):a00399620961976
Cites: Arch Toxicol. 2010 Nov;84(11):891-620386881
Cites: Proc Natl Acad Sci U S A. 1982 Dec;79(23):7590-46760199
Cites: Mol Pharmacol. 1984 Jul;26(1):90-86087120
Cites: Brain Res. 1988 Oct 11;462(1):31-93179736
Cites: Environ Res. 1993 Apr;61(1):176-838472672
Cites: Arch Toxicol. 1994;68(5):317-218085943
Cites: Eur J Gastroenterol Hepatol. 1995 Jul;7(7):615-218590155
Cites: Clin Chem. 1995 Dec;41(12 Pt 2):1874-817497648
Cites: Environ Res. 1995 Oct;71(1):29-388757236
Cites: Acta Neuropathol. 1996;91(1):72-78773149
Cites: Neurotoxicology. 1996 Summer;17(2):531-98856747
Cites: Toxicol Lett. 1998 Feb;94(3):227-329609326
Cites: FASEB J. 1998 Nov;12(14):1559-699806765
Cites: Environ Health Perspect. 1999 Oct;107 Suppl 5:767-7510502543
Cites: MMWR Morb Mortal Wkly Rep. 2004 Nov 5;53(43):1018-2015525900
Cites: Toxicol Sci. 2006 Aug;92(2):476-8916731579
Cites: J Clin Invest. 2007 Mar;117(3):712-817332892
Cites: Immunol Res. 2006;36(1-3):3-1217337761
Cites: Toxicol Sci. 2007 Oct;99(2):366-9417519394
Cites: Eur J Biochem. 1982 Mar;123(1):209-156279396
PubMed ID
25124724 View in PubMed
Less detail

Can profiles of poly- and Perfluoroalkyl substances (PFASs) in human serum provide information on major exposure sources?

https://arctichealth.org/en/permalink/ahliterature296906
Source
Environ Health. 2018 02 01; 17(1):11
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Date
02-01-2018
Author
Xindi C Hu
Clifton Dassuncao
Xianming Zhang
Philippe Grandjean
Pál Weihe
Glenys M Webster
Flemming Nielsen
Elsie M Sunderland
Author Affiliation
Harvard T.H. Chan School of Public Health, Boston, MA, 02215, USA. xhu@mail.harvard.edu.
Source
Environ Health. 2018 02 01; 17(1):11
Date
02-01-2018
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Keywords
Adolescent
Adult
Aged
Alkanesulfonic Acids - blood
Child
Denmark
Environmental Exposure
Environmental monitoring
Environmental pollutants - blood
Female
Fluorocarbons - blood
Humans
Male
Middle Aged
Nutrition Surveys
Prospective Studies
United States
Young Adult
Abstract
Humans are exposed to poly- and perfluoroalkyl substances (PFASs) from diverse sources and this has been associated with negative health impacts. Advances in analytical methods have enabled routine detection of more than 15 PFASs in human sera, allowing better profiling of PFAS exposures. The composition of PFASs in human sera reflects the complexity of exposure sources but source identification can be confounded by differences in toxicokinetics affecting uptake, distribution, and elimination. Common PFASs, such as perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS) and their precursors are ubiquitous in multiple exposure sources. However, their composition varies among sources, which may impact associated adverse health effects.
We use available PFAS concentrations from several demographic groups in a North Atlantic seafood consuming population (Faroe Islands) to explore whether chemical fingerprints in human sera provide insights into predominant exposure sources. We compare serum PFAS profiles from Faroese individuals to other North American populations to investigate commonalities in potential exposure sources. We compare individuals with similar demographic and physiological characteristics and samples from the same years to reduce confounding by toxicokinetic differences and changing environmental releases.
Using principal components analysis (PCA) confirmed by hierarchical clustering, we assess variability in serum PFAS concentrations across three Faroese groups. The first principal component (PC)/cluster consists of C9-C12 perfluoroalkyl carboxylates (PFCAs) and is consistent with measured PFAS profiles in consumed seafood. The second PC/cluster includes perfluorohexanesulfonic acid (PFHxS) and the PFOS precursor N-ethyl perfluorooctane sulfonamidoacetate (N-EtFOSAA), which are directly used or metabolized from fluorochemicals in consumer products such as carpet and food packaging. We find that the same compounds are associated with the same exposure sources in two North American populations, suggesting generalizability of results from the Faroese population.
We conclude that PFAS homologue profiles in serum provide valuable information on major exposure sources. It is essential to compare samples collected at similar time periods and to correct for demographic groups that are highly affected by differences in physiological processes (e.g., pregnancy). Information on PFAS homologue profiles is crucial for attributing adverse health effects to the proper mixtures or individual PFASs.
PubMed ID
29391068 View in PubMed
Less detail

Polychlorinated biphenyl (PCB) induction of CYP3A4 enzyme activity in healthy Faroese adults.

https://arctichealth.org/en/permalink/ahliterature161939
Source
Toxicol Appl Pharmacol. 2007 Oct 15;224(2):202-6
Publication Type
Article
Date
Oct-15-2007
Author
Maria Skaalum Petersen
Jónrit Halling
Per Damkier
Flemming Nielsen
Philippe Grandjean
Pál Weihe
Kim Brøsen
Author Affiliation
Institute of Public Health, Environmental Medicine, University of Southern Denmark, Winsløvparken 17, 5000 Odense C, Denmark. mskaalum@health.sdu.dk
Source
Toxicol Appl Pharmacol. 2007 Oct 15;224(2):202-6
Date
Oct-15-2007
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Cytochrome P-450 CYP3A
Cytochrome P-450 Enzyme System - drug effects - metabolism
DDT - blood - pharmacology
Dichlorodiphenyl Dichloroethylene - blood - pharmacology
Environmental Exposure
Environmental Pollutants - blood - pharmacology
Enzyme Induction - drug effects
Female
Genetics, Population
Humans
Hydrocortisone - analogs & derivatives - metabolism - urine
Male
Middle Aged
Polychlorinated Biphenyls - blood - pharmacology
Polymorphism, Genetic
Regression Analysis
Sex Factors
Toxicogenetics
Abstract
The CYP3A4 enzyme is, along with other cytochrome P450 enzymes, involved in the metabolism of environmental pollutants and is highly inducible by these substances. A commercial polychlorinated biphenyl (PCB) mixture, 1,1,1,-trichloro-2-(o-chlorophenyl), 2-(p'-chlorophenyl)ethane (o,p'-DDT) and 1,1,-dichloro-2,2-bis (p-chlorophenyl)ethene (p,p'-DDE) are known to induce CYP3A4 activity through activation of nuclear receptors, such as the pregnane X receptor. However, this induction of CYP3A4 has not yet been investigated in humans. Thus, the aim of the study was to determine the variability of the CYP3A4 phenotype in regard to increased concentrations of PCBs and other persistent organohalogen pollutants (POPs) in healthy Faroese adults. In 310 randomly selected Faroese residents aged 18-60 years, the CYP3A4 activity was determined based on the urinary 6beta-hydroxycortisol/cortisol (6beta-OHC/FC) ratio. POP exposures were assessed by measuring their concentrations in serum lipid. The results showed a unimodal distribution of the 6beta-OHC/FC ratio with values ranging from 0.58 to 27.38. Women had a slightly higher 6beta-OHC/FC ratio than men (p=0.07). Confounder-adjusted multiple regression analysis showed significant associations between 6beta-OHC/FC ratios and summation PCB, PCB-TEQ and p,p'-DDE, o,p'-DDT and HCB, respectively, but the associations were statistically significant for men only.
PubMed ID
17692354 View in PubMed
Less detail

Genetic predisposition to Parkinson's disease: CYP2D6 and HFE in the Faroe Islands.

https://arctichealth.org/en/permalink/ahliterature158611
Source
Pharmacogenet Genomics. 2008 Mar;18(3):209-12
Publication Type
Article
Date
Mar-2008
Author
Jónrit Halling
Maria Skaalum Petersen
Philippe Grandjean
Pál Weihe
Kim Brosen
Author Affiliation
Clinical Pharmacology, Institute of Public Health, University of Southern Denmark, Winslowparken, Odense C, Denmark. jhalling@health.sdu.dk
Source
Pharmacogenet Genomics. 2008 Mar;18(3):209-12
Date
Mar-2008
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Alleles
Base Sequence
Case-Control Studies
Cytochrome P-450 CYP2D6 - genetics
DNA Primers - genetics
Denmark
Female
Gene Frequency
Genetic Predisposition to Disease
Genotype
Histocompatibility Antigens Class I - genetics
Humans
Male
Membrane Proteins - genetics
Middle Aged
Parkinson Disease - genetics
Pharmacogenetics
Abstract
To investigate whether the genetic variants of CYP2D6 and HFE are more frequent in Parkinson's disease (PD) patients compared with controls in a population where the prevalence of these variants and PD are increased.
Blood samples were collected from 79 PD patients and 154 controls in the Faroe Islands. Genotyping for the 'CYP2D6*3, *4, *6 and *9' alleles and for the C282Y and H63D mutations were performed by real-time polymerase chain reaction before Taqman assessment.
The frequency of CYP2D6 poor metabolizers among the patients was not higher compared with the frequency found in the control group (chi2 test, P=0.86). The odds ratio was 0.92 (95% confidence interval: 0.44-1.90). Neither was a difference in HFE genotype or allele frequencies found between the patients and the controls, and the C282Y and H63D mutation carrier frequencies did not reveal any difference (chi2 test, P=0.50 and 0.60, respectively).
This study does not support an association between PD and mutations of the CYP2D6 and HFE genes, although a weak association cannot be excluded. The high frequency of PD in the Faroes is most likely the result of interactions between multiple genetic and environmental factors, still to be identified.
PubMed ID
18300942 View in PubMed
Less detail

A State-of-the-Science Review of Mercury Biomarkers in Human Populations Worldwide between 2000 and 2018.

https://arctichealth.org/en/permalink/ahliterature295791
Source
Environ Health Perspect. 2018 Oct; 126(10):106001
Publication Type
Journal Article
Date
Oct-2018
Author
Niladri Basu
Milena Horvat
David C Evers
Irina Zastenskaya
Pál Weihe
Joanna Tempowski
Author Affiliation
1 Faculty of Agricultural and Environmental Sciences, McGill University , Montreal, Quebec, Canada.
Source
Environ Health Perspect. 2018 Oct; 126(10):106001
Date
Oct-2018
Language
English
Publication Type
Journal Article
Abstract
The Minamata Convention on Mercury provided a mandate for action against global mercury pollution. However, our knowledge of mercury exposures is limited because there are many regions and subpopulations with little or no data.
We aimed to increase worldwide understanding of human exposures to mercury by collecting, collating, and analyzing mercury concentrations in biomarker samples reported in the published scientific literature.
A systematic search of the peer-reviewed scientific literature was performed using three databases. A priori search strategy, eligibility criteria, and data extraction steps were used to identify relevant studies.
We collected 424,858 mercury biomarker measurements from 335,991 individuals represented in 312 articles from 75 countries. General background populations with insignificant exposures have blood, hair, and urine mercury levels that generally fall under [Formula: see text], [Formula: see text], and [Formula: see text], respectively. We identified four populations of concern: a) Arctic populations who consume fish and marine mammals; b) tropical riverine communities (especially Amazonian) who consume fish and in some cases may be exposed to mining; c) coastal and/or small-island communities who substantially depend on seafood; and d) individuals who either work or reside among artisanal and small-scale gold mining sites.
This review suggests that all populations worldwide are exposed to some amount of mercury and that there is great variability in exposures within and across countries and regions. There remain many geographic regions and subpopulations with limited data, thus hindering evidence-based decision making. This type of information is critical in helping understand exposures, particularly in light of certain stipulations in the Minamata Convention on Mercury. https://doi.org/10.1289/EHP3904.
PubMed ID
30407086 View in PubMed
Less detail

Can profiles of poly- and Perfluoroalkyl substances (PFASs) in human serum provide information on major exposure sources?

https://arctichealth.org/en/permalink/ahliterature289389
Source
Environ Health. 2018 Feb 01; 17(1):11
Publication Type
Journal Article
Date
Feb-01-2018
Author
Xindi C Hu
Clifton Dassuncao
Xianming Zhang
Philippe Grandjean
Pál Weihe
Glenys M Webster
Flemming Nielsen
Elsie M Sunderland
Author Affiliation
Harvard T.H. Chan School of Public Health, Boston, MA, 02215, USA. xhu@mail.harvard.edu.
Source
Environ Health. 2018 Feb 01; 17(1):11
Date
Feb-01-2018
Language
English
Publication Type
Journal Article
Abstract
Humans are exposed to poly- and perfluoroalkyl substances (PFASs) from diverse sources and this has been associated with negative health impacts. Advances in analytical methods have enabled routine detection of more than 15 PFASs in human sera, allowing better profiling of PFAS exposures. The composition of PFASs in human sera reflects the complexity of exposure sources but source identification can be confounded by differences in toxicokinetics affecting uptake, distribution, and elimination. Common PFASs, such as perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS) and their precursors are ubiquitous in multiple exposure sources. However, their composition varies among sources, which may impact associated adverse health effects.
We use available PFAS concentrations from several demographic groups in a North Atlantic seafood consuming population (Faroe Islands) to explore whether chemical fingerprints in human sera provide insights into predominant exposure sources. We compare serum PFAS profiles from Faroese individuals to other North American populations to investigate commonalities in potential exposure sources. We compare individuals with similar demographic and physiological characteristics and samples from the same years to reduce confounding by toxicokinetic differences and changing environmental releases.
Using principal components analysis (PCA) confirmed by hierarchical clustering, we assess variability in serum PFAS concentrations across three Faroese groups. The first principal component (PC)/cluster consists of C9-C12 perfluoroalkyl carboxylates (PFCAs) and is consistent with measured PFAS profiles in consumed seafood. The second PC/cluster includes perfluorohexanesulfonic acid (PFHxS) and the PFOS precursor N-ethyl perfluorooctane sulfonamidoacetate (N-EtFOSAA), which are directly used or metabolized from fluorochemicals in consumer products such as carpet and food packaging. We find that the same compounds are associated with the same exposure sources in two North American populations, suggesting generalizability of results from the Faroese population.
We conclude that PFAS homologue profiles in serum provide valuable information on major exposure sources. It is essential to compare samples collected at similar time periods and to correct for demographic groups that are highly affected by differences in physiological processes (e.g., pregnancy). Information on PFAS homologue profiles is crucial for attributing adverse health effects to the proper mixtures or individual PFASs.
Notes
Cites: Environ Health Perspect. 2013 Nov-Dec;121(11-12):1313-8 PMID 24007715
Cites: Environ Health Perspect. 2014 Feb;122(2):187-92 PMID 24280536
Cites: Environ Sci Technol. 2011 Apr 15;45(8):3268-74 PMID 21413794
Cites: Environ Sci Technol. 2014 May 6;48(9):4637-48 PMID 24762048
Cites: Environ Int. 2013 Oct;60:242-8 PMID 24660230
Cites: Environ Sci Technol. 2005 Sep 1;39(17):6599-606 PMID 16190217
Cites: Environ Sci Technol. 2015 Dec 15;49(24):14503-11 PMID 26000882
Cites: Arch Environ Contam Toxicol. 2009 Oct;57(3):552-60 PMID 19152061
Cites: Environ Sci Technol. 2004 Jul 1;38(13):3698-704 PMID 15296323
Cites: Environ Int. 2016 Sep;94:315-324 PMID 27295048
Cites: Toxicol Appl Pharmacol. 2017 Sep 1;330:9-21 PMID 28684146
Cites: Environ Sci Technol. 2016 Sep 20;50(18):10216-25 PMID 27477586
Cites: Environ Sci Technol. 2008 Nov 1;42(21):8140-5 PMID 19031915
Cites: Environ Sci Technol Lett. 2016 Sep 13;3(9):316-321 PMID 28217711
Cites: Environ Sci Technol. 2013 Jul 16;47(14):7974-81 PMID 23777259
Cites: Environ Sci Technol. 2014 Apr 1;48(7):3864-74 PMID 24588690
Cites: Environ Sci Technol. 2011 Oct 1;45(19):8037-45 PMID 21469664
Cites: Environ Sci Technol. 2014;48(15):8807-14 PMID 24943117
Cites: Environ Sci Technol. 2009 Jun 1;43(11):4037-43 PMID 19569327
Cites: Environ Sci Technol. 2006 Feb 1;40(3):748-51 PMID 16509313
Cites: Environ Sci Technol. 2016 Jan 19;50(2):978-86 PMID 26691063
Cites: JAMA. 2012 Jan 25;307(4):391-7 PMID 22274686
Cites: Environ Res. 2014 Aug;133:338-47 PMID 25019470
Cites: Int J Hyg Environ Health. 2017 Jun;220(4):744-756 PMID 28372942
Cites: Environ Health Perspect. 2007 Sep;115(9):1298-305 PMID 17805419
Cites: Environ Res. 2014 Jul;132:407-12 PMID 24853977
Cites: Environ Sci Technol. 2017 Mar 7;51(5):2508-2518 PMID 28224793
Cites: Environ Int. 2010 Oct;36(7):772-8 PMID 20579735
Cites: J Environ Monit. 2010 Nov;12 (11):1979-2004 PMID 20944836
Cites: Environ Health. 2013 Apr 19;12 (1):35 PMID 23597293
Cites: Environ Sci Technol. 2008 Jul 15;42(14 ):5361-7 PMID 18754394
Cites: Environ Int. 2013 Apr;54:74-84 PMID 23419425
Cites: Environ Int. 2014 Oct;71:74-80 PMID 24980755
Cites: Environ Sci Technol. 2010 May 1;44(9):3572-9 PMID 20377175
Cites: Environ Sci Technol. 2004 Dec 15;38(24):6475-81 PMID 15669302
Cites: Environ Sci Technol. 2015 Oct 6;49(19):11622-30 PMID 26392038
Cites: Environ Sci Technol. 2011 Oct 1;45(19):7974-84 PMID 21630688
Cites: Environ Res. 2015 Jan;136:264-73 PMID 25460645
Cites: Chemosphere. 2010 Apr;79(3):314-9 PMID 20149408
Cites: J Chromatogr A. 2009 Jan 16;1216(3):385-93 PMID 19026423
Cites: Neurotoxicol Teratol. 2006 Sep-Oct;28(5):536-47 PMID 17067778
Cites: Environ Sci Technol. 2008 Aug 15;42(16):6291-5 PMID 18767701
Cites: Environ Sci Technol. 2009 Jun 1;43(11):4076-81 PMID 19569333
Cites: J Environ Health. 2014 Dec;77(5):14-9 PMID 25619022
Cites: Chemosphere. 2014 Nov;114:337-9 PMID 24938172
Cites: Chemosphere. 2017 Oct;184:687-693 PMID 28633063
Cites: Environ Int. 2014 Jun;67:43-53 PMID 24657493
Cites: Environ Health Perspect. 2011 Jan;119(1):92-7 PMID 20920951
Cites: New Solut. 2015 Aug;25(2):147-63 PMID 26084549
Cites: Environ Sci Technol. 2013 Sep 17;47(18):10619-27 PMID 23980546
Cites: Matern Child Health J. 2012 Feb;16(2):430-8 PMID 21210200
Cites: Toxicol Lett. 2014 Dec 1;231(2):233-8 PMID 25091270
Cites: Environ Sci Technol. 2017 May 2;51(9):5193-5204 PMID 28325044
Cites: Environ Sci Technol. 2008 May 15;42(10):3751-6 PMID 18546718
Cites: J Chromatogr A. 2007 Jun 22;1154(1-2):214-21 PMID 17416376
Cites: Environ Sci Technol. 2017 Apr 18;51(8):4512-4521 PMID 28350446
Cites: Environ Sci Technol. 2012 Jan 17;46(2):1209-15 PMID 22148395
Cites: Reprod Toxicol. 2017 Mar;68:164-170 PMID 27421579
Cites: Environ Sci Technol. 2015 Sep 1;49(17):10466-73 PMID 26291735
Cites: Environ Sci Technol. 2011 Oct 1;45(19):8006-14 PMID 21517063
Cites: Environ Res. 2017 Apr;154:145-151 PMID 28073048
Cites: J Agric Food Chem. 2007 Apr 18;55(8):3203-10 PMID 17381114
Cites: Food Chem Toxicol. 2009 Jul;47(7):1577-83 PMID 19362113
PubMed ID
29391068 View in PubMed
Less detail

Health effects associated with measured levels of contaminants in the Arctic.

https://arctichealth.org/en/permalink/ahliterature289272
Source
Int J Circumpolar Health. 2016; 75:33805
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
2016
Author
Pál Weihe
Fróði Debes
Jónrit Halling
Maria Skaalum Petersen
Gina Muckle
Jon Øyvind Odland
Alexey Dudarev
Pierre Ayotte
Éric Dewailly
Philippe Grandjean
Eva Bonefeld-Jørgensen
Author Affiliation
Department of Occupational Medicine and Public Health, The Faroese Hospital System, Torshavn, Faroe Islands; pal@health.fo.
Source
Int J Circumpolar Health. 2016; 75:33805
Date
2016
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Arctic Regions
Environmental Exposure - statistics & numerical data
Environmental Monitoring - statistics & numerical data
Environmental Pollutants - adverse effects
Health status
Humans
Pesticides - adverse effects
Abstract
The Human Health Assessment Group has over the past decade recommended that effect studies be conducted in the circumpolar area. Such studies examine the association between contaminant exposure in the Arctic populations and health effects. Because foetuses and young children are the most vulnerable, effect studies are often prospective child cohort studies. The emphasis in this article is on a description of the effects associated with contaminant exposure in the Arctic. The main topics addressed are neurobehavioural, immunological, reproductive, cardiovascular, endocrine and carcinogenic effect. For each topic, the association between exposure and effects is described, and some results are reported for similar studies outside the Arctic.
Notes
Cites: Environ Int. 2010 Nov;36(8):980-6 PMID 19735942
Cites: Reprod Toxicol. 2011 Nov;32(3):293-7 PMID 21729750
Cites: Alaska Med. 2008 Jan-Mar;49(4):120-5 PMID 18491804
Cites: Environ Sci Pollut Res Int. 2013 Nov;20(11):8045-56 PMID 23539207
Cites: Arctic Med Res. 1988;47 Suppl 1:659-65 PMID 3078512
Cites: Mutat Res. 2012 May 1;733(1-2):69-77 PMID 21945723
Cites: J Nutr. 2014 Apr;144(4):425-30 PMID 24477300
Cites: Environ Int. 2013 Apr;54:85-91 PMID 23422685
Cites: Int J Circumpolar Health. 2002 Feb;61(1):41-9 PMID 12002946
Cites: PLoS One. 2010 May 20;5(5):e10746 PMID 20505766
Cites: Mutat Res. 2010 Jul 19;700(1-2):39-43 PMID 20451658
Cites: Neurotoxicol Teratol. 2014 Mar-Apr;42:85-92 PMID 24561639
Cites: N Engl J Med. 1996 Sep 12;335(11):783-9 PMID 8703183
Cites: Environ Toxicol Pharmacol. 2008 Mar;25(2):273-6 PMID 21783863
Cites: Environ Health Perspect. 2009 Mar;117(3):367-72 PMID 19337510
Cites: Dan Med Bull. 2000 Apr;47(2):132-7 PMID 10822803
Cites: Asian J Androl. 2013 Jan;15(1):97-104 PMID 23223027
Cites: Epidemiology. 2011 May;22(3):410-7 PMID 21364465
Cites: Neurotoxicology. 2012 Oct;33(5):1067-74 PMID 23227484
Cites: Environ Health Perspect. 2011 May;119(5):607-14 PMID 21220222
Cites: Reprod Toxicol. 2012 Dec;34(4):498-503 PMID 22841741
Cites: Hum Reprod. 2012 Aug;27(8):2532-40 PMID 22647447
Cites: Mol Cell Endocrinol. 2013 May 6;370(1-2):163-71 PMID 23510718
Cites: J Biol Chem. 2003 Feb 28;278(9):7294-9 PMID 12466278
Cites: Environ Health. 2013 Jul 02;12(1):54 PMID 23816203
Cites: Environ Health Perspect. 2008 Mar;116(3):269-77 PMID 18335090
Cites: Environ Health Perspect. 2000 Mar;108(3):205-11 PMID 10706525
Cites: Fam Cancer. 2009;8(4):413-9 PMID 19504351
Cites: Environ Health Perspect. 2009 Jun;117(6):1014-20 PMID 19590699
Cites: Lancet Oncol. 2013 Apr;14(4):287-8 PMID 23499544
Cites: Arch Environ Health. 1992 May-Jun;47(3):185-95 PMID 1596101
Cites: Chemosphere. 2010 Jun;80(2):75-82 PMID 20435334
Cites: Hypertension. 2012 Sep;60(3):645-52 PMID 22868395
Cites: Front Genet. 2013 Dec 13;4:278 PMID 24379825
Cites: Environ Sci Pollut Res Int. 2013 Nov;20(11):8031-44 PMID 23764977
Cites: Environ Health Perspect. 2015 Aug;123(8):827-33 PMID 25757069
Cites: Environ Health Perspect. 2009 Sep;117(9):1380-6 PMID 19750101
Cites: PLoS One. 2012;7(7):e41046 PMID 22815906
Cites: Int J Circumpolar Health. 2012 May 22;71:18368 PMID 22663941
Cites: Int J Circumpolar Health. 2013;72:20471 PMID 23519821
Cites: J Toxicol Environ Health B Crit Rev. 2006 Nov-Dec;9(6):485-99 PMID 17090484
Cites: Int J Circumpolar Health. 2013 May 29;72 :null PMID 23730628
Cites: Lancet Oncol. 2008 Sep;9(9):892-900 PMID 18760245
Cites: Neurotoxicology. 2006 Jul;27(4):567-78 PMID 16620993
Cites: Toxicol Sci. 2007 Jul;98 (1):87-98 PMID 17420220
Cites: PLoS Med. 2006 Aug;3(8):e311 PMID 16942395
Cites: Reprod Toxicol. 2011 Nov;32(3):261-7 PMID 21736938
Cites: Environ Health Perspect. 2002 Sep;110(9):917-21 PMID 12204827
Cites: Am J Epidemiol. 2001 Jan 1;153(1):53-63 PMID 11159147
Cites: Mol Cell Endocrinol. 2012 May 22;355(2):240-8 PMID 21939731
Cites: Environ Toxicol. 2015 Feb;30(2):168-76 PMID 23913582
Cites: Ecohealth. 2011 Jun;8(2):210-22 PMID 22160443
Cites: Biomarkers. 2012 Dec;17(8):692-705 PMID 23030067
Cites: Environ Health Perspect. 2006 Jan;114(1):100-5 PMID 16393665
Cites: J Steroid Biochem Mol Biol. 2004 Feb;88(2):157-66 PMID 15084347
Cites: Int J Circumpolar Health. 2012 Aug 16;71:19155 PMID 22901290
Cites: Environ Health Perspect. 2005 Oct;113(10):1376-80 PMID 16203250
Cites: Environ Health. 2014 Mar 16;13(1):19 PMID 24629213
Cites: Chemosphere. 2009 Mar;74(11):1413-9 PMID 19108870
Cites: Environ Res. 2008 Nov;108(3):387-92 PMID 18814871
Cites: Am J Clin Nutr. 2011 May;93(5):1025-37 PMID 21389181
Cites: Environ Health Perspect. 1997 Nov;105(11):1228-32 PMID 9370524
Cites: Basic Clin Pharmacol Toxicol. 2014 Jul;115(1):118-28 PMID 24797035
Cites: Int J Circumpolar Health. 2006 Feb;65(1):8-17 PMID 16544643
Cites: Int J Androl. 2002 Aug;25(4):243-52 PMID 12121574
Cites: Chemosphere. 2015 Jun;129:239-45 PMID 25455676
Cites: Environ Sci Technol. 2013 Nov 19;47(22):13086-92 PMID 24160776
Cites: N Engl J Med. 2011 Mar 24;364(12):1116-25 PMID 21428767
Cites: Vis Neurosci. 2004 May-Jun;21(3):421-9 PMID 15518224
Cites: Hum Reprod. 2014 Feb;29(2):359-67 PMID 24163265
Cites: Chemosphere. 2012 Jan;86(1):65-9 PMID 21962538
Cites: Int J Circumpolar Health. 2010 Apr;69(2):181-94 PMID 20356465
Cites: Neurotoxicology. 2009 Nov;30(6):1070-7 PMID 19576242
Cites: Neurotoxicology. 2009 Jul;30(4):564-71 PMID 19635390
Cites: Toxicol Appl Pharmacol. 2013 Jan 1;266(1):132-42 PMID 23142464
Cites: Int J Circumpolar Health. 2012 May 15;71:18581 PMID 22663938
Cites: JAMA. 2012 Jan 25;307(4):391-7 PMID 22274686
Cites: Rev Environ Health. 2002 Oct-Dec;17(4):263-77 PMID 12611469
Cites: Acta Oncol. 1996;35(5):571-6 PMID 8813063
Cites: Hypertension. 2009 Nov;54(5):981-6 PMID 19805642
Cites: Neurotoxicol Teratol. 2011 Mar-Apr;33(2):205-11 PMID 20868742
Cites: Environ Health Perspect. 2012 Oct;120(10):1456-61 PMID 23008274
Cites: Cortex. 2016 Jan;74:358-69 PMID 26109549
Cites: Rev Environ Health. 2008 Jan-Mar;23(1):59-74 PMID 18557598
Cites: J Pediatr. 2004 Feb;144(2):177-83 PMID 14760257
Cites: Environ Health Perspect. 2008 Oct;116(10):1416-22 PMID 18941588
Cites: Environ Health. 2012 Jul 02;11:44 PMID 22747793
Cites: Environ Health Perspect. 2000 Oct;108(10):961-6 PMID 11049816
Cites: Pediatrics. 2011 Jan;127(1):e59-68 PMID 21187307
Cites: Neurotoxicology. 2008 Sep;29(5):776-82 PMID 18590765
Cites: Environ Health Perspect. 2007 Sep;115(9):1298-305 PMID 17805419
Cites: Crit Rev Toxicol. 2005 Jan;35(1):61-88 PMID 15742903
Cites: Environ Health. 2011 Oct 06;10:88 PMID 21978366
Cites: Toxicol Sci. 2007 Mar;96(1):133-44 PMID 17132714
Cites: Toxicol Lett. 1995 May;77(1-3):351-6 PMID 7618161
Cites: Exp Toxicol Pathol. 1996 Feb;48(2-3):189-95 PMID 8672874
Cites: Environ Health Perspect. 2012 Dec;120(12):A452; author reply A452 PMID 23211440
Cites: Chem Res Toxicol. 2010 Feb 15;23(2):432-42 PMID 20092276
Cites: Environ Health Perspect. 2010 Dec;118(12):1654-67 PMID 20829149
Cites: Reprod Toxicol. 2006 Nov;22(4):765-73 PMID 17008049
Cites: J Pediatr. 2002 Jan;140(1):33-9 PMID 11815761
Cites: Int J Circumpolar Health. 2010 Feb;69(1):72-86 PMID 20167158
Cites: Environ Health Perspect. 2006 Aug;114(8):1301-5 PMID 16882544
Cites: Reprod Toxicol. 2014 Jan;43:1-7 PMID 24513925
Cites: Carcinogenesis. 2005 Nov;26(11):1835-45 PMID 15975961
Cites: Pediatrics. 1997 Nov;100(5):856-62 PMID 9346987
Cites: Arch Toxicol. 2008 Aug;82(8):493-512 PMID 18496671
Cites: Environ Health Perspect. 2008 Nov;116(11):1547-52 PMID 19057709
Cites: Pediatr Res. 1995 Sep;38(3):404-10 PMID 7494667
Cites: Neurotoxicol Teratol. 2009 Sep-Oct;31(5):267-74 PMID 19595760
Cites: Clin Biochem. 2000 Mar;33(2):131-8 PMID 10751591
Cites: J Toxicol Environ Health A. 2014;77(9-11):516-34 PMID 24754389
Cites: Environ Health Perspect. 2001 Apr;109(4):391-7 PMID 11335188
Cites: Int J Circumpolar Health. 2004;63 Suppl 2:174-8 PMID 15736646
Cites: Environ Health Perspect. 2003 Apr;111(4):409-13 PMID 12676591
Cites: Diabetes Care. 2008 Aug;31(8):1574-9 PMID 18487481
Cites: Ann Oncol. 2007 Jun;18 Suppl 6:vi93-8 PMID 17591843
Cites: Neurotoxicology. 2007 Sep;28(5):924-30 PMID 17659343
Cites: Environ Health Perspect. 2000 Dec;108(12):1203-7 PMID 11133402
Cites: Fertil Steril. 2010 Nov;94(6):2128-34 PMID 20149358
Cites: Toxicol Lett. 2007 Jun 15;171(1-2):19-28 PMID 17509781
Cites: Neurotoxicol Teratol. 2006 May-Jun;28(3):363-75 PMID 16647838
Cites: Met Ions Life Sci. 2013;11:491-507 PMID 23430782
Cites: Arch Toxicol. 2009 Sep;83(9):851-61 PMID 19468714
Cites: Neurotoxicol Teratol. 1999 Jul-Aug;21(4):471-2 PMID 10440491
Cites: Environ Health Perspect. 2008 Aug;116(8):1085-91 PMID 18709170
Cites: Environ Health. 2008 Jun 06;7:29 PMID 18538022
Cites: Proc Natl Acad Sci U S A. 2014 Oct 21;111(42):15273-8 PMID 25288728
Cites: Environ Health Perspect. 2002 Mar;110(3):229-33 PMID 11882472
Cites: J Natl Cancer Inst. 1995 Nov 15;87(22):1681-5 PMID 7473816
Cites: Int J Circumpolar Health. 2013 Jun 17;72:21113 PMID 23785672
Cites: Rural Remote Health. 2010 Apr-Jun;10(2):1362 PMID 20572746
Cites: Front Biosci (Elite Ed). 2011 Jan 01;3:690-700 PMID 21196344
Cites: J Viral Hepat. 2013 Feb;20(2):122-30 PMID 23301547
Cites: J Pediatr. 2004 Feb;144(2):169-76 PMID 14760255
Cites: Sci Total Environ. 2010 Nov 1;408(23):5744-9 PMID 20825977
Cites: Environ Res. 2013 Jan;120:102-8 PMID 22959488
Cites: Toxicology. 2001 Feb 14;158(3):141-53 PMID 11275356
Cites: Diabetologia. 2007 Sep;50(9):1841-51 PMID 17624515
Cites: Lancet Oncol. 2008 Dec;9(12):1124 PMID 19038761
Cites: Neurotoxicol Teratol. 2012 Jul;34(4):466-72 PMID 22705177
Cites: Int J Cancer. 2003 Dec 20;107(6):1017-22 PMID 14601064
Cites: Hum Reprod. 2002 Sep;17(9):2468-73 PMID 12202443
Cites: Chemosphere. 2013 Jul;92(5):583-91 PMID 23648332
Cites: Arch Environ Health. 1997 Jul-Aug;52(4):257-62 PMID 9210724
Cites: Environ Res. 2009 Jan;109(1):86-92 PMID 18995849
Cites: Chemosphere. 2012 Nov;89(8):919-28 PMID 22858370
Cites: Environ Health Perspect. 2010 Oct;118(10):1434-8 PMID 20562056
Cites: Am J Epidemiol. 2002 Apr 1;155(7):629-35 PMID 11914190
Cites: Environ Health Perspect. 2003 Sep;111(12):1519-23 PMID 12948893
Cites: Int J Hyg Environ Health. 2014 Apr-May;217(4-5):473-82 PMID 24138783
Cites: Environ Res. 2011 Nov;111(8):1265-70 PMID 21962568
Cites: Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):155-61 PMID 18226069
Cites: Environ Health Perspect. 2007 Mar;115(3):323-7 PMID 17431478
Cites: Environ Health Perspect. 2010 Apr;118(4):465-71 PMID 20064776
Cites: Environ Res. 2010 May;110(4):388-95 PMID 20378105
Cites: Environ Health Perspect. 2002 Feb;110 Suppl 1:25-42 PMID 11834461
Cites: Carcinogenesis. 2013 Jan;34(1):93-101 PMID 23027621
Cites: Environ Res. 2016 Nov;151:71-79 PMID 27451001
Cites: Reprod Toxicol. 2012 Jul;33(4):577-83 PMID 22449571
Cites: Diabetes Care. 2011 Jun;34(6):1284-8 PMID 21515843
Cites: Int J Audiol. 2012 Jun;51(6):433-6 PMID 22369226
Cites: Mol Cell Biochem. 2004 Jan;255(1-2):67-78 PMID 14971647
Cites: Hum Reprod. 2002 Aug;17(8):2199-208 PMID 12151459
Cites: Int J Environ Res Public Health. 2012 Dec 06;9(12):4486-97 PMID 23222182
Cites: Cancer Res. 2010 Nov 1;70(21):8927-36 PMID 20959477
Cites: Arch Environ Health. 2002 Sep-Oct;57(5):482-8 PMID 12641193
Cites: Environ Int. 2010 May;36(4):398-401 PMID 20299099
Cites: Epidemiology. 1999 Jul;10(4):370-5 PMID 10401870
Cites: Environ Health Perspect. 2006 Sep;114(9):1348-53 PMID 16966087
Cites: Environ Health Perspect. 2004 Oct;112(14):1359-65 PMID 15471725
Cites: Neurotoxicol Teratol. 1997 Nov-Dec;19(6):417-28 PMID 9392777
Cites: Toxicol Appl Pharmacol. 2009 Aug 1;238(3):266-71 PMID 19362102
Cites: Nat Med. 2003 Aug;9(8):1081-4 PMID 12858169
Cites: Neurotoxicol Teratol. 1991 Jul-Aug;13(4):417-27 PMID 1921921
Cites: Neurotoxicology. 2010 Aug;31(4):373-84 PMID 20403381
Cites: Am J Epidemiol. 2009 Nov 1;170(9):1156-64 PMID 19700501
Cites: BMJ Open. 2013 Mar 01;3(3):null PMID 23457323
Cites: Environ Health Perspect. 2012 Apr;120(4):608-15 PMID 22142904
Cites: Sci Rep. 2015 Jul 23;5:11713 PMID 26203819
PubMed ID
27974137 View in PubMed
Less detail

Shorter duration of breastfeeding at elevated exposures to perfluoroalkyl substances.

https://arctichealth.org/en/permalink/ahliterature289307
Source
Reprod Toxicol. 2017 03; 68:164-170
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Date
03-2017
Author
Clara Amalie Gade Timmermann
Esben Budtz-Jørgensen
Maria Skaalum Petersen
Pál Weihe
Ulrike Steuerwald
Flemming Nielsen
Tina Kold Jensen
Philippe Grandjean
Author Affiliation
Department of Environmental Medicine, University of Southern Denmark, J.B. Winsløws Vej 17A, 5000 Odense C, Denmark. Electronic address: atimmermann@health.sdu.dk.
Source
Reprod Toxicol. 2017 03; 68:164-170
Date
03-2017
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Keywords
Alkanesulfonic Acids - adverse effects - blood
Breast Feeding - trends
Cohort Studies
Denmark
Environmental Pollutants - adverse effects - blood
Female
Fluorocarbons - adverse effects - blood
Humans
Infant, Newborn
Maternal Exposure - adverse effects
Time Factors
Abstract
The aim of this study was to determine whether maternal exposure to persistent perfluoroalkyl substances (PFASs) affect the capability to breastfeed. In two Faroese birth cohorts (N=1130), concentrations of five PFASs were measured in maternal serum during pregnancy or two weeks after term. Duration of breastfeeding was assessed by questionnaire and clinical interview. In adjusted linear regression models, a doubling of maternal serum PFASs was associated with a reduction in duration of both total and exclusive breastfeeding, most pronounced for perfluorooctane sulfonic acid (PFOS) where a doubling was associated with a reduction in total breastfeeding of 1.4 (95% CI: 0.6; 2.1) months and perfluorooctanoic acid (PFOA) where a doubling was associated with a reduction in exclusive breastfeeding of 0.5 (0.3; 0.7) months. The associations were evident among both primiparous and multiparous women, and thus cannot be explained by confounding from previous breastfeeding.
Notes
Cites: Environ Sci Technol. 2012 Aug 21;46(16):9071-9 PMID 22770559
Cites: Am J Public Health. 2003 Dec;93(12):2000-10 PMID 14652321
Cites: Environ Sci Technol. 2006 Jun 1;40(11):3463-73 PMID 16786681
Cites: Pediatrics. 2005 Dec;116(6):1408-12 PMID 16322165
Cites: Pediatr Allergy Immunol. 2015 Dec;26(8):742-9 PMID 25845848
Cites: J Hum Lact. 2005 Aug;21(3):245-58 PMID 16113013
Cites: Environ Health Perspect. 2011 Aug;119(8):1070-6 PMID 21501981
Cites: Environ Sci Pollut Res Int. 2013 Nov;20(11):7940-8 PMID 23589272
Cites: Environ Int. 2014 Aug;69:58-66 PMID 24815340
Cites: Mol Cell Endocrinol. 2015 Feb 5;401:165-72 PMID 25449418
Cites: Am J Public Health. 1987 Oct;77(10):1294-7 PMID 3115123
Cites: JAMA. 2012 Jan 25;307(4):391-7 PMID 22274686
Cites: Obesity (Silver Spring). 2016 Jan;24(1):231-7 PMID 26554535
Cites: Lancet. 2016 Jan 30;387(10017):475-90 PMID 26869575
Cites: Environ Res. 2014 Jul;132:407-12 PMID 24853977
Cites: Toxicol Sci. 2007 Mar;96(1):133-44 PMID 17132714
Cites: Am J Public Health. 1995 Apr;85(4):504-8 PMID 7702113
Cites: Reprod Toxicol. 2009 Jun;27(3-4):299-306 PMID 19013232
Cites: J Obstet Gynecol Neonatal Nurs. 2009 May-Jun;38(3):259-68 PMID 19538614
Cites: Reprod Toxicol. 2009 Jun;27(3-4):289-98 PMID 19095057
Cites: Environ Int. 2013 Apr;54:74-84 PMID 23419425
Cites: Int J Hyg Environ Health. 2014 Jan;217(1):52-61 PMID 23601780
Cites: Am J Epidemiol. 2002 Jan 15;155(2):176-84 PMID 11790682
Cites: PLoS One. 2015 Apr 07;10(4):e0123496 PMID 25848775
Cites: PLoS One. 2015 Sep 10;10 (9):e0137768 PMID 26356420
Cites: J Perinat Med. 2014 Jan;42(1):9-18 PMID 24057589
Cites: J Womens Health (Larchmt). 2014 May;23(5):404-12 PMID 24655291
Cites: Scand J Work Environ Health. 2010 Sep;36(5):413-21 PMID 20200757
Cites: Environ Health Perspect. 2010 Oct;118(10):1429-33 PMID 20562055
Cites: Environ Health Perspect. 2010 Oct;118(10):1434-8 PMID 20562056
Cites: New Solut. 2015 Aug;25(2):147-63 PMID 26084549
Cites: Environ Sci Technol. 2015 Oct 6;49(19):11849-58 PMID 26333069
Cites: Environ Sci Technol. 2014 Aug 19;48(16):9600-8 PMID 25026485
Cites: Int J Hyg Environ Health. 2009 May;212(3):239-70 PMID 18565792
Cites: FASEB J. 2003 Apr;17(6):699-701 PMID 12586743
Cites: Environ Int. 2013 Sep;59:354-62 PMID 23892228
Cites: Environ Res. 2016 Aug;149:239-46 PMID 27179585
Cites: Environ Sci Technol. 2015 Sep 1;49(17):10466-73 PMID 26291735
Cites: Pediatrics. 2008 Oct;122 Suppl 2:S69-76 PMID 18829834
PubMed ID
27421579 View in PubMed
Less detail

Hydroxylated PCB metabolites and PCBs in serum from pregnant Faroese women.

https://arctichealth.org/en/permalink/ahliterature4494
Source
Environ Health Perspect. 2002 Sep;110(9):895-9
Publication Type
Article
Date
Sep-2002
Author
Britta Fängström
Maria Athanasiadou
Philippe Grandjean
Pál Weihe
Ake Bergman
Author Affiliation
Department of Environmental Chemistry, Stockholm University, Stockholm, Sweden. britta.fangstrom@mk.su.se
Source
Environ Health Perspect. 2002 Sep;110(9):895-9
Date
Sep-2002
Language
English
Publication Type
Article
Keywords
Adult
Animals
Arctic Regions
Diet
Environmental Exposure
Environmental Pollutants - blood - metabolism - pharmacokinetics
Female
Fishes
Food Contamination
Humans
Hydroxylation
Infant, Newborn
Milk, human - chemistry
Polychlorinated Biphenyls - blood - metabolism - pharmacokinetics
Pregnancy
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Whales
Abstract
In the Faroe Islands in the North Atlantic, the traditional diet includes pilot whale meat and blubber and other marine food. Fatty fish and blubber of mammals may contain high concentrations of organohalogen substances (OHSs). Elevated levels of OHSs have been reported from the Faroe Islands, first documented in breast milk samples obtained in 1987. The aim of this study was to determine the concentrations of hydroxylated polychlorinated biphenyls (OH-PCBs) and polychlorinated biphenyls (PCBs) in serum samples from pregnant Faroese women known to differ in their dietary habits. High concentrations of OH-PCBs and PCBs were found in part of the human serum samples analyzed, and the relative OH-PCB and PCB congener distributions were similar to those observed elsewhere. There was a wide span between the lowest and highest OH-PCB and PCB concentrations in the serum samples analyzed, with ranges of 19-1,800 ng/g lipid weight (lw) and 150-22,000 ng/g lw, respectively. The ratio of sigmaOH-PCB/sigmaPCB averaged about 10% and varied little. 4-Hydroxy-2,2,3,4,5,5,6-heptachlorobiphenyl was the most abundant OH-PCB metabolite in all samples analyzed, with four other OH-PCB congeners as dominating metabolites in the serum. More than 25 additional OH-PCBs were indicated. This study confirms the presence of high concentrations of organohalogen substances in populations or areas far removed from their sources.
PubMed ID
12204824 View in PubMed
Less detail

Assessing sources of human methylmercury exposure using stable mercury isotopes.

https://arctichealth.org/en/permalink/ahliterature268003
Source
Environ Sci Technol. 2014;48(15):8800-6
Publication Type
Article
Date
2014
Author
Miling Li
Laura S Sherman
Joel D Blum
Philippe Grandjean
Bjarni Mikkelsen
Pál Weihe
Elsie M Sunderland
James P Shine
Source
Environ Sci Technol. 2014;48(15):8800-6
Date
2014
Language
English
Publication Type
Article
Keywords
Animals
Chemical Fractionation
Denmark
Environmental monitoring
Fishes
Gulf of Mexico
Hair - chemistry
Humans
Mercury - analysis
Mercury Isotopes - analysis
Methylmercury compounds - analysis
Seafood - analysis
Whales, Pilot
Abstract
Seafood consumption is the primary route of methylmercury (MeHg) exposure for most populations. Inherent uncertainties in dietary survey data point to the need for an empirical tool to confirm exposure sources. We therefore explore the utility of Hg stable isotope ratios in human hair as a new method for discerning MeHg exposure sources. We characterized Hg isotope fractionation between humans and their diets using hair samples from Faroese whalers exposed to MeHg predominantly from pilot whales. We observed an increase of 1.75‰ in d(202)Hg values between pilot whale muscle tissue and Faroese whalers' hair but no mass-independent fractionation. We found a similar offset in d(202)Hg between consumed seafood and hair samples from Gulf of Mexico recreational anglers who are exposed to lower levels of MeHg from a variety of seafood sources. An isotope mixing model was used to estimate individual MeHg exposure sources and confirmed that both ?(199)Hg and d(202)Hg values in human hair can help identify dietary MeHg sources. Variability in isotopic signatures among coastal fish consumers in the Gulf of Mexico likely reflects both differences in environmental sources of MeHg to coastal fish and uncertainty in dietary recall data. Additional data are needed to fully refine this approach for individuals with complex seafood consumption patterns.
Notes
Cites: Anal Bioanal Chem. 2007 May;388(2):353-917375289
Cites: Ambio. 2007 Feb;36(1):3-1117408186
Cites: Environ Health Perspect. 2007 Feb;115(2):235-4217384771
Cites: Environ Res. 2005 May;98(1):133-4215721894
Cites: Risk Anal. 1999 Aug;19(4):547-5810765421
Cites: Sci Total Environ. 1998 Jul 11;218(1):19-319718742
Cites: Environ Health. 2003 Jun 4;2(1):812844364
Cites: Neurotoxicology. 2005 Mar;26(2):149-5715713336
Cites: Environ Sci Technol. 2009 Dec 1;43(23):8985-9019943677
Cites: Environ Health Perspect. 2009 Mar;117(3):367-7219337510
Cites: Am J Epidemiol. 2008 May 15;167(10):1171-8118353804
Cites: Environ Sci Technol. 2009 Dec 15;43(24):9148-5420000504
Cites: Environ Sci Technol. 2010 Mar 1;44(5):1630-720104887
Cites: Environ Sci Technol. 2010 Mar 1;44(5):1698-70420121085
Cites: J Phys Chem A. 2010 Apr 1;114(12):4246-5320218588
Cites: Environ Health Perspect. 2011 Feb;119(2):245-5120980220
Cites: Environ Sci Technol. 2011 Dec 1;45(23):9910-622003970
Cites: Environ Sci Technol. 2012 Jun 5;46(11):5902-1122545798
Cites: Environ Sci Technol. 2012 Jul 17;46(14):7527-3422681311
Cites: Environ Sci Technol. 2012 Oct 16;46(20):10957-6423033864
Cites: Environ Health Perspect. 2012 Nov;120(11):1512-922732656
Cites: Environ Res. 2012 Nov;119:101-1722559948
Cites: Environ Res. 2012 Nov;119:27-4122572623
Cites: Environ Res. 2012 Nov;119:42-5223098613
Cites: Sci Total Environ. 2013 Mar 15;448:163-7523062970
Cites: Environ Sci Technol. 2011 Feb 15;45(4):1264-7021250676
Cites: Environ Sci Technol. 2013 Apr 2;47(7):3403-923463943
Cites: Environ Toxicol Chem. 2013 Oct;32(10):2322-3023787815
Cites: Environ Sci Technol. 2004 Mar 1;38(5):1487-9515046351
Cites: Sci Total Environ. 2000 Oct 16;261(1-3):21-3211036974
Cites: Sci Total Environ. 1987 Sep;65:53-623685941
Cites: Sci Total Environ. 1996 Jul 16;186(1-2):95-1048685711
Cites: Arch Environ Health. 1992 May-Jun;47(3):185-951596101
PubMed ID
24967674 View in PubMed
Less detail

Attenuated growth of breast-fed children exposed to increased concentrations of methylmercury and polychlorinated biphenyls.

https://arctichealth.org/en/permalink/ahliterature186651
Source
FASEB J. 2003 Apr;17(6):699-701
Publication Type
Article
Date
Apr-2003
Author
Philippe Grandjean
Esben Budtz-Jørgensen
Ulrike Steuerwald
Birger Heinzow
Larry L Needham
Poul J Jørgensen
Pál Weihe
Author Affiliation
Department of Environmental Health, Boston University Schools of Medicine and Public Health, Boston, Massachusetts, USA. pgrand@health.sdu.dk
Source
FASEB J. 2003 Apr;17(6):699-701
Date
Apr-2003
Language
English
Publication Type
Article
Keywords
Body Height - drug effects
Body Weight - drug effects
Breast Feeding
Child, Preschool
Cohort Studies
Environmental Exposure - adverse effects
Environmental Pollutants - adverse effects
Female
Growth - drug effects
Humans
Infant
Infant, Newborn
Male
Methylmercury Compounds - adverse effects
Polychlorinated biphenyls - adverse effects - blood
Predictive value of tests
Pregnancy
Prenatal Exposure Delayed Effects
Prospective Studies
Abstract
Breast-feeding has been linked to slowed postnatal growth. Although the basis for this "weanling's dilemma" is unclear, environmental contaminants in human milk may be of relevance. We studied a Faroese birth cohort of 182 singleton children, born at term in 1994-95. Concentrations of mercury in cord blood and of polychlorinated biphenyls in maternal milk were measured, and duration of breast-feeding was recorded. At 18 months, children who had been exclusively breast-fed for at least 6 months weighed 0.59 kg less [95% confidence interval (CI) = 0.03, 1.16 kg] and were 1.50 cm [95% CI = 0.52, 2.47 cm] shorter than those not breast-fed. However, calculated transfer of contaminants from human milk fully explained the attenuated growth. Irrespective of duration of breast-feeding, a doubling of the mercury concentration in cord blood was associated with a decrease in weight at 18 months by 0.19 kg (95% CI = 0.03, 0.35 kg) and in height by 0.26 cm (95% CI = -0.02, 0.55 cm). Weight and height at 42 months showed the same tendencies, but the main effect occurred before 18 months of age. Thus, in communities with increased contaminant exposures, risks associated with lactational transfer of toxicants to the infant must be considered when judging the benefits of prolonged breast-feeding.
PubMed ID
12586743 View in PubMed
Less detail

Sperm Aneuploidy in Faroese Men with Lifetime Exposure to Dichlorodiphenyldichloroethylene (DDE) and Polychlorinated Biphenyl (PCB) Pollutants.

https://arctichealth.org/en/permalink/ahliterature267484
Source
Environ Health Perspect. 2015 Nov 4;
Publication Type
Article
Date
Nov-4-2015
Author
Melissa J Perry
Heather A Young
Philippe Grandjean
Jónrit Halling
Maria S Petersen
Sheena E Martenies
Parisa Karimi
Pál Weihe
Source
Environ Health Perspect. 2015 Nov 4;
Date
Nov-4-2015
Language
English
Publication Type
Article
Abstract
While it is known that sperm aneuploidy contributes to early pregnancy losses and congenital abnormalities, causes are unknown and environmental contaminants are suspected.
Our goal was to evaluate associations between lifetime exposure to organochlorines, specifically dichlorodiphenyldicholorethylene (p,p'-DDE) and polychlorinated biphenyls (PCBs) and sperm aneuploidy in men from the general population of the Faroe Islands, a population with a known history of organochlorine exposures.
Serum and semen samples from men (n=90) ages 22-44 participating in Faroe Islands health studies were analyzed for p,p'-DDE and PCB (118, 138, 153, and 180) and adjusted for total lipids. Cord blood and age 14 serum were available for a subgroup (n=40) and also analyzed for p,p'-DDE and PCBs. Sperm fluorescence in situ hybridization (FISH) for chromosome X, Y, and 18 was used to determine rates of XX18, XY18, YY18 and total disomy. Multivariable adjusted Poisson models were used to estimate the relation between organochlorine exposure and sperm disomy outcomes.
Adult p,p'-DDE and total PCB serum concentrations were each associated with significantly increased rates of XX18, XY18 and total disomy. Age 14 p,p'-DDE and PCB concentrations were each associated with significantly increased rates of XX, XY and total disomy at adult age. Associations between cord blood concentrations of p,p'-DDE and PCBs and sperm disomy at adult age were not consistently significant.
Organochlorine exposures measured at age 14 and in adulthood were associated with sperm disomy in this sample of high exposure men, suggesting the impacts of persistent pollutants on testicular maturation and function need deeper investigation.
PubMed ID
26535963 View in PubMed
Less detail

A retrospective study of PBDEs and PCBs in human milk from the Faroe Islands.

https://arctichealth.org/en/permalink/ahliterature173878
Source
Environ Health. 2005;4:12
Publication Type
Article
Date
2005
Author
Britta Fängström
Anna Strid
Philippe Grandjean
Pál Weihe
Ake Bergman
Author Affiliation
Department of Environmental Chemistry, Stockholm University, SE-106 91 Stockholm, Sweden. britta.fangstrom@mk.su.se
Source
Environ Health. 2005;4:12
Date
2005
Language
English
Publication Type
Article
Keywords
Animals
Arctic Regions
DDT - analysis
Denmark
Dichlorodiphenyl Dichloroethylene - analysis - metabolism
Environmental Exposure - analysis
Environmental Pollutants - analysis - metabolism
Female
Food Contamination
Gas Chromatography-Mass Spectrometry
Geography
Halogenated Diphenyl Ethers
Humans
Milk, human - chemistry
Phenyl Ethers - analysis - metabolism
Polybrominated Biphenyls - analysis - metabolism
Polychlorinated Biphenyls - analysis - metabolism
Retrospective Studies
Whales
Abstract
Persistent organic pollutants (POPs) in wildlife and humans remain a cause of global concern, both in regard to traditional POPs, such as the polychlorinated biphenyls (PCBs), and emerging POPs, such as the polybrominated diphenyl ethers (PBDEs). To determine the time related concentrations, we analyzed human milk for these substances at three time points between 1987 and 1999. Polychlorobiphenylols (OH-PCBs), the dominating class of PCB metabolites, some of which are known to be strongly retained in human blood, were also included in the assessment.
We obtained milk from the Faroe Islands, where the population is exposed to POPs from their traditional diet (which may include pilot whale blubber). In addition to three pools, nine individual samples from the last time point were also analyzed. After cleanup, partitioning of neutral and acidic compounds, and separation of chemical classes, the analyses were carried out by gas chromatography and/or gas chromatography/mass spectrometry.
Compared to other European populations, the human milk had high PCB concentrations, with pool concentrations of 2300 ng/g fat 1987, 1600 ng/g fat in 1994, and 1800 ng/g fat in 1999 (based on the sum of eleven major PCB congeners). The nine individual samples showed great variation in PCB concentrations. The OH-PCBs were present in trace amounts only, at levels of approximately 1% of the PCB concentrations. The PBDE concentrations showed a clear increase over time, and their concentrations in human milk from 1999 are among the highest reported so far from Europe, with results of individual samples ranging from 4.7 to 13 ng/g fat
Although remote from pollution sources, the Faroe Islands show high concentrations of POPs in human milk, particularly PCBs, but also PBDEs. The PBDEs show increasing concentrations over time. The OH-PCB metabolites are poorly transferred to human milk, which likely is related to their acidic character.
Notes
Cites: Chemosphere. 2005 Aug;60(7):836-4315992590
Cites: Environ Sci Technol. 2005 Jul 15;39(14):5177-8216082945
Cites: Environ Health Perspect. 2004 Aug;112(11):1208-1215289169
Cites: Environ Health Perspect. 1993 Dec;101(7):618-208143594
Cites: J Toxicol Environ Health A. 1999 Nov 26;58(6):329-4110580757
Cites: Environ Health Perspect. 2000 Feb;108(2):167-7210656858
Cites: Chemosphere. 2000 May-Jun;40(9-11):1111-2310739053
Cites: Environ Health Perspect. 2000 Nov;108(11):1035-4111102293
Cites: J Anal Toxicol. 2000 Nov-Dec;24(8):696-70311110024
Cites: J Toxicol Environ Health A. 2001 Jan 26;62(2):69-8111209822
Cites: Environ Sci Technol. 2001 Feb 1;35(3):435-4011351711
Cites: Int J Epidemiol. 2001 Dec;30(6):1272-811821327
Cites: Environ Sci Technol. 2002 May 1;36(9):1886-9212026966
Cites: Environ Health Perspect. 2002 Sep;110(9):895-912204824
Cites: J Toxicol Environ Health A. 2002 Nov 22;65(22):1893-90812470493
Cites: Acta Paediatr. 2003 Apr;92(4):467-7212801115
Cites: Environ Health Perspect. 2003 Jul;111(9):1235-4112842779
Cites: Environ Int. 2003 Sep;29(6):757-7012850094
Cites: Environ Int. 2003 Sep;29(6):829-3912850099
Cites: Chemosphere. 2003 Nov;53(6):645-5412962714
Cites: Environ Res. 2003 Oct;93(2):186-9412963403
Cites: Environ Health Perspect. 2003 Oct;111(13):1660-414527847
Cites: Environ Health Perspect. 2003 Nov;111(14):1723-914594622
Cites: Chemosphere. 2004 Mar;54(10):1509-2014659953
Cites: Environ Sci Technol. 2004 Feb 15;38(4):945-5614998004
Cites: Environ Health Perspect. 2004 Jul;112(10):1085-9115238282
Cites: J Toxicol Environ Health. 1994 Jun;42(2):157-718207752
Cites: Chemosphere. 1995 Jun;30(11):2143-537620848
Cites: Chemosphere. 1996 Aug;33(3):559-658680832
Cites: Environ Res. 1995 Oct;71(1):29-388757236
Cites: Arch Environ Contam Toxicol. 1997 Apr;32(3):329-369096084
Cites: Sci Total Environ. 1998 Apr 23;215(1-2):31-99599454
Cites: Arch Environ Contam Toxicol. 1999 Apr;36(3):355-6310047605
Cites: Environ Sci Technol. 2005 Apr 1;39(7):1980-615871227
PubMed ID
16014177 View in PubMed
Less detail

Reproductive Function in a Population of Young Faroese Men with Elevated Exposure to Polychlorinated Biphenyls (PCBs) and Perfluorinated Alkylate Substances (PFAS).

https://arctichealth.org/en/permalink/ahliterature294876
Source
Int J Environ Res Public Health. 2018 Aug 30; 15(9):
Publication Type
Journal Article
Date
Aug-30-2018
Author
Maria Skaalum Petersen
Jónrit Halling
Niels Jørgensen
Flemming Nielsen
Philippe Grandjean
Tina Kold Jensen
Pál Weihe
Author Affiliation
Department of Occupational Medicine and Public Health, the Faroes Hospital System, FO-100 Tórshavn, Faroe Islands. maria@health.fo.
Source
Int J Environ Res Public Health. 2018 Aug 30; 15(9):
Date
Aug-30-2018
Language
English
Publication Type
Journal Article
Abstract
Semen quality may be adversely affected by exposure to environmental chemicals such as polychlorinated biphenyls (PCBs) and perfluorinated alkylate substances (PFASs) that are persistent and may act as endocrine disrupting compounds. The aim of this study was to explore whether PCBs or PFASs exposure were associated with abnormalities in semen quality or reproductive hormones in Faroese men. This population based cross-sectional study includes 263 Faroese men (24?26 years) who delivered a semen sample for assessment of sperm concentration, total sperm count, semen volume, morphology and motility. A blood sample was drawn and analyzed for reproductive hormones, PCBs and PFASs. Exposure to ?PCBs and perfluorooctane sulfonate (PFOS) was positively associated with sex hormone-binding globulin (SHBG) and luteinizing hormone (LH). In addition, total testosterone (T) was positively associated with ?PCB. Both PCBs and PFOS appear to lead to increased SHBG, perhaps mediated via the liver. The higher total T associated with PCB may represent a compensatory adaption to elevated SHBG levels to maintain an unchanged free testosterone concentration. The positive association to LH for both PCBs and PFOS may indicate a direct adverse effect on the testosterone producing Leydig cells.
Notes
Cites: Chemosphere. 2006 Feb;62(7):1167-82 PMID 16169054
Cites: Arch Environ Contam Toxicol. 1989 Jul-Aug;18(4):495-500 PMID 2505694
Cites: Int J Circumpolar Health. 2012 Jul 10;71:18594 PMID 22789518
Cites: Eur Urol. 1993;24(2):231-8 PMID 8104150
Cites: Hum Reprod. 2013 Mar;28(3):599-608 PMID 23250927
Cites: J Steroid Biochem Mol Biol. 1995 Jun;52(6):595-7 PMID 7779764
Cites: Reprod Toxicol. 2012 Dec;34(4):498-503 PMID 22841741
Cites: Hum Reprod. 2012 Aug;27(8):2532-40 PMID 22647447
Cites: Environ Health Perspect. 2008 Mar;116(3):269-77 PMID 18335090
Cites: Environ Res. 2015 Apr;138:345-51 PMID 25766940
Cites: Environ Sci Pollut Res Int. 2013 Nov;20(11):8031-44 PMID 23764977
Cites: Environ Int. 2015 Nov;84:154-60 PMID 26292060
Cites: PLoS Med. 2006 Aug;3(8):e311 PMID 16942395
Cites: Reprod Toxicol. 2011 Nov;32(3):261-7 PMID 21736938
Cites: Environ Health Perspect. 2003 Sep;111(12):1505-11 PMID 12948891
Cites: Environ Health Perspect. 2015 Jan;123(1):57-63 PMID 25127343
Cites: Tissue Cell. 2001 Apr;33(2):169-77 PMID 11392670
Cites: Rev Environ Health. 2006 Jan-Mar;21(1):1-23 PMID 16700427
Cites: Environ Health Perspect. 2003 Jan;111(1):65-70 PMID 12515680
Cites: Int J Androl. 2011 Aug;34(4 Pt 2):e68-84; discussion e84-5 PMID 21668838
Cites: Toxicol Ind Health. 2017 Aug;33(8):636-645 PMID 28502228
Cites: J Gen Intern Med. 2014 Jul;29(7):1060-4 PMID 24452418
Cites: Syst Biol Reprod Med. 2010 Apr;56(2):122-31 PMID 20377311
Cites: JAMA. 2012 Jan 25;307(4):391-7 PMID 22274686
Cites: Pure Appl Chem. 2010 Jan 25;82(2):383-391 PMID 20419070
Cites: Reprod Toxicol. 2004 Nov;19(1):5-26 PMID 15336708
Cites: J Endocrinol Invest. 2018 Jun;41(6):639-645 PMID 29147953
Cites: Asian J Androl. 2014 Jan-Feb;16(1):71-80 PMID 24369135
Cites: J Pediatr. 2000 May;136(5):599-605 PMID 10802490
Cites: Eur J Clin Pharmacol. 2006 Dec;62(12):1041-8 PMID 17089110
Cites: Reprod Toxicol. 2005 May-Jun;20(1):117-26 PMID 15808795
Cites: Reprod Toxicol. 2012 Jul;33(4):419-27 PMID 21736937
Cites: Crit Rev Toxicol. 2016 Oct;46(9):735-55 PMID 27268162
Cites: Environ Health Perspect. 2013 Apr;121(4):453-8 PMID 23360585
Cites: J Clin Endocrinol Metab. 1999 Oct;84(10):3666-72 PMID 10523012
Cites: Environ Health Perspect. 2003 Apr;111(4):409-13 PMID 12676591
Cites: J Occup Environ Med. 1998 Jul;40(7):614-22 PMID 9675720
Cites: Environ Health Perspect. 2009 Jun;117(6):923-7 PMID 19590684
Cites: J Chromatogr A. 2009 Jan 16;1216(3):385-93 PMID 19026423
Cites: Toxicology. 2001 Feb 14;158(3):141-53 PMID 11275356
Cites: Neurotoxicol Teratol. 2012 Jul;34(4):466-72 PMID 22705177
Cites: Int J Androl. 1997 Aug;20(4):201-8 PMID 9401822
Cites: Arch Environ Health. 2001 Mar-Apr;56(2):138-43 PMID 11339677
Cites: Environ Health Perspect. 2010 Oct;118(10):1434-8 PMID 20562056
Cites: Environ Res. 1995 Oct;71(1):29-38 PMID 8757236
Cites: Reproduction. 2014 Dec;148(6):635-46 PMID 25190505
Cites: BMJ Open. 2012 Jul 02;2(4):null PMID 22761286
Cites: Environ Res. 2014 Oct;134:251-6 PMID 25173059
Cites: Environ Health Perspect. 2006 Sep;114(9):1348-53 PMID 16966087
Cites: J Endocrinol. 2007 Feb;192(2):325-38 PMID 17283232
Cites: BMJ Open. 2013 Mar 01;3(3):null PMID 23457323
PubMed ID
30200252 View in PubMed
Less detail

Secondary sex ratio in relation to exposures to polychlorinated biphenyls, dichlorodiphenyl dichloroethylene and methylmercury.

https://arctichealth.org/en/permalink/ahliterature294700
Source
Int J Circumpolar Health. 2017; 76(1):1406234
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Date
2017
Author
Clara Amalie Gade Timmermann
Anna L Choi
Maria Skaalum Petersen
Flemming Nielsen
Esben Budtz-Jørgensen
Pál Weihe
Philippe Grandjean
Author Affiliation
a Department of Environmental Medicine , University of Southern Denmark , Odense C , Denmark.
Source
Int J Circumpolar Health. 2017; 76(1):1406234
Date
2017
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Keywords
Adult
Animals
Arctic Regions - epidemiology
Denmark - epidemiology
Dichlorodiphenyl Dichloroethylene - adverse effects - analysis
Female
Fetal Blood - chemistry
Food Contamination
Humans
Maternal Exposure - adverse effects
Methylmercury Compounds - adverse effects - analysis
Polychlorinated Biphenyls - adverse effects - analysis
Pregnancy
Prospective Studies
Sex ratio
Whales, Pilot
Young Adult
Abstract
This study was undertaken to assess the potential impact of maternal exposures to polychlorinated biphenyl (PCB), dichlorodiphenyl dichloroethylene (DDE) and methylmercury on the secondary sex ratios (the ratio of male to female live births) over a span of 23 years. The study includes prospective data from three Faroese birth cohorts, with a total of 2,152 healthy mother-child dyads recruited between 1986 and 2009. The Faroe Islands is a subarctic fishing community, where pilot whale meat and blubber are part of the traditional marine diet. Exposures were measured in maternal hair, serum or umbilical cord blood. Confounder adjusted logistic regression models were used to assess the associations between maternal exposures and the secondary sex ratio. A doubling in SPCB, p,p'-DDE and mercury concentrations were associated with increased odds by 8% (95% CI = 0-16%), 7% (95% CI = 0-14%) and 9% (95% CI = 2-17%), respectively, of giving birth to a boy. In conclusion, maternal exposure to SPCB, DDE and methylmercury was associated with a slightly increased secondary sex ratio. The impact of paternal exposures could not be taken into account and deserves attention.
Notes
Cites: Int J Circumpolar Health. 2012 Jul 10;71:18594 PMID 22789518
Cites: Environ Res. 2006 Jan;100(1):77-85 PMID 15922323
Cites: Ann Hum Genet. 1977 Oct;41(2):205-17 PMID 596828
Cites: Environ Int. 2013 Jan;51:88-96 PMID 23201820
Cites: Neurotoxicol Teratol. 2001 Jul-Aug;23(4):305-17 PMID 11485834
Cites: J Expo Sci Environ Epidemiol. 2007 Mar;17(2):191-5 PMID 16773124
Cites: Pediatr Allergy Immunol. 2015 Dec;26(8):742-9 PMID 25845848
Cites: Environ Health. 2008 Jul 15;7:37 PMID 18627595
Cites: Environ Health. 2009 Aug 15;8:35 PMID 19682390
Cites: Arch Environ Health. 1992 May-Jun;47(3):185-95 PMID 1596101
Cites: Soc Biol. 1999 Spring-Summer;46(1-2):33-46 PMID 10842500
Cites: J Toxicol Environ Health A. 2007 Nov;70(21):1873-7 PMID 17934961
Cites: Environ Health. 2003 Mar 12;2(1):2 PMID 12694628
Cites: Int J Hyg Environ Health. 2017 Mar;220(2 Pt A):201-208 PMID 27663635
Cites: Arch Pediatr Adolesc Med. 2012 Dec;166(12):1123-31 PMID 23044994
Cites: J Occup Environ Med. 2002 Jan;44(1):8-13 PMID 11802470
Cites: Arch Environ Health. 2004 Nov;59(11):559-65 PMID 16599003
Cites: Early Hum Dev. 2015 Dec;91(12):793-4 PMID 26527391
Cites: Int J Epidemiol. 2009 Dec;38(6):1674-80 PMID 19667054
Cites: Ambul Pediatr. 2003 Jan-Feb;3(1):18-23 PMID 12540249
Cites: Environ Res. 2014 Jul;132:407-12 PMID 24853977
Cites: Environ Int. 2014 Dec;73:359-64 PMID 25222300
Cites: Lancet. 2005 Aug 27-Sep 2;366(9487):763-73 PMID 16125595
Cites: Lancet. 2002 Jul 13;360(9327):143-4 PMID 12126828
Cites: Eur J Clin Pharmacol. 2006 Dec;62(12):1041-8 PMID 17089110
Cites: Lancet. 1996 Aug 10;348(9024):409 PMID 8709758
Cites: Environ Sci Technol. 2008 Sep 15;42(18):6991-6 PMID 18853821
Cites: Neurotoxicol Teratol. 2012 Jul;34(4):466-72 PMID 22705177
Cites: Environ Health Perspect. 2010 Oct;118(10):1429-33 PMID 20562055
Cites: Sci Total Environ. 1996 Jul 16;186(1-2):141-8 PMID 8685706
Cites: Paediatr Perinat Epidemiol. 2016 May;30(3):238-45 PMID 27038010
Cites: Environ Health Perspect. 2010 Oct;118(10):1434-8 PMID 20562056
Cites: Environ Res. 1995 Oct;71(1):29-38 PMID 8757236
Cites: J Expo Sci Environ Epidemiol. 2008 Nov;18(6):581-7 PMID 18285840
Cites: Am J Hum Biol. 2012 Mar-Apr;24(2):165-9 PMID 22287096
Cites: Rev Environ Contam Toxicol. 2009;201:137-58 PMID 19484591
Cites: Environ Sci Technol. 2010 Jul 15;44(14):5633-40 PMID 20578718
Cites: Int Arch Occup Environ Health. 2016 May;89(4):659-65 PMID 26497019
Cites: Chemosphere. 2013 Apr;91(2):131-8 PMID 23260246
Cites: Int Arch Occup Environ Health. 2004 Nov;77(8):571-9 PMID 15688249
Cites: Environ Sci Technol. 2011 Feb 1;45(3):1121-6 PMID 21166449
Cites: Reprod Toxicol. 2017 Mar;68:164-170 PMID 27421579
Cites: Environ Health Perspect. 2001 Jul;109(7):749-52 PMID 11485875
Cites: Early Hum Dev. 2015 Dec;91(12):795-9 PMID 26549774
PubMed ID
29195489 View in PubMed
Less detail

Effects of breast feeding on neuropsychological development in a community with methylmercury exposure from seafood.

https://arctichealth.org/en/permalink/ahliterature29935
Source
J Expo Anal Environ Epidemiol. 2005 Sep;15(5):423-30
Publication Type
Article
Date
Sep-2005
Author
Tina Kold Jensen
Philippe Grandjean
Esben Budtz Jørgensen
Roberta F White
Frodi Debes
Pál Weihe
Author Affiliation
Department of Environmental Medicine, Institute of Public Health, University of Southern Denmark, Odense C, Denmark. tkjensen@health.sdu.dk
Source
J Expo Anal Environ Epidemiol. 2005 Sep;15(5):423-30
Date
Sep-2005
Language
English
Publication Type
Article
Keywords
Adult
Animals
Atlantic Ocean
Breast Feeding
Child
Child Development
Child, Preschool
Cognition Disorders - etiology - prevention & control
Environmental Exposure
Female
Fetal Blood - chemistry
Food Contamination
Geography
Hair - chemistry
Humans
Infant
Infant Welfare
Infant, Newborn
Intelligence Tests
Longitudinal Studies
Male
Methylmercury Compounds - pharmacokinetics
Neuropsychological Tests
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Seafood
Whales
Abstract
Breastfeeding has been associated with an advantage to infant neurobehavioral development, possibly in part due to essential nutrients in breast milk. However, breast milk may be contaminated by environmental neurotoxicants, such as methylmercury. In the Faroe Islands, where maternal consumption of pilot whale may cause transfer of marine toxicants into breast milk, a cohort of 1022 consecutive singleton births was generated during 1986-87. Methylmercury exposure was assessed from mercury concentrations in cord blood and in the hair of the child at age 12 months, and the duration of breastfeeding was recorded. At approximately 7 years of age, 917 (90%) of the children underwent detailed neurobehavioral examination. After adjustment for confounders, breastfeeding was associated with only marginally better neuropsychological performance on most tests. These associations were robust even after adjustment for cord-blood and hair mercury concentration at age 1 year. Thus, in this cohort of children with a relatively high prenatal toxicant exposure and potential exposure to neurotoxicants through breast milk, breastfeeding was associated with less benefits on neurobehavioral development than previously published studies though not associated with a deficit in neuropsychological performance at age 7. Although the advantage may be less, Faroese women can still safely breastfeed their children.
PubMed ID
15674318 View in PubMed
Less detail

Delayed brainstem auditory evoked potential latencies in 14-year-old children exposed to methylmercury.

https://arctichealth.org/en/permalink/ahliterature30532
Source
J Pediatr. 2004 Feb;144(2):177-83
Publication Type
Article
Date
Feb-2004
Author
Katsuyuki Murata
Pál Weihe
Esben Budtz-Jørgensen
Poul J Jørgensen
Philippe Grandjean
Author Affiliation
Division of Environmental Health Sciences, Akita University School of Medicine, Akita, Japan.
Source
J Pediatr. 2004 Feb;144(2):177-83
Date
Feb-2004
Language
English
Publication Type
Article
Keywords
Adolescent
Audiometry
Child
Cohort Studies
Denmark
Environmental Exposure - adverse effects
Evoked Potentials, Auditory, Brain Stem - drug effects - physiology
Female
Fetal Blood - chemistry
Food Contamination
Hair - chemistry
Humans
Male
Mercury Poisoning, Nervous System - physiopathology
Methylmercury Compounds - analysis - toxicity
Pregnancy
Prenatal Exposure Delayed Effects
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Seafood - adverse effects
Abstract
OBJECTIVE: To determine possible exposure-associated delays in auditory brainstem evoked potential latencies as an objective measure of neurobehavioral toxicity in 14-year-old children with developmental exposure to methylmercury (MeHg) from seafood. STUDY DESIGN: Prospective study of a birth cohort in the Faroe Islands, where 878 of eligible children (87%) were examined at age 14 years. Latencies of brainstem evoked potential peaks I, III, and V at 20 and 40 Hz constituted the outcome variables. Mercury concentrations were determined in cord blood and maternal hair, and in the child's hair at ages 7 and 14. RESULTS: Latencies of peaks III and V increased by about 0.012 ms when the cord blood mercury concentration doubled. As seen at age 7 years, this effect appeared mainly within the I-III interpeak interval. Despite lower postnatal exposures, the child's hair mercury level at age 14 years was associated with prolonged III-V interpeak latencies. All benchmark dose results were similar to those obtained for dose-response relationships at age 7 years. CONCLUSIONS: The persistence of prolonged I-III interpeak intervals indicates that some neurotoxic effects from intrauterine MeHg exposure are irreversible. A change in vulnerability to MeHg toxicity is suggested by the apparent sensitivity of the peak III-V component to recent MeHg exposure.
PubMed ID
14760257 View in PubMed
Less detail

Cardiac autonomic activity in methylmercury neurotoxicity: 14-year follow-up of a Faroese birth cohort.

https://arctichealth.org/en/permalink/ahliterature30533
Source
J Pediatr. 2004 Feb;144(2):169-76
Publication Type
Article
Date
Feb-2004
Author
Philippe Grandjean
Katsuyuki Murata
Esben Budtz-Jørgensen
Pál Weihe
Author Affiliation
Institute of Public Health, University of Southern Denmark, Odense, Denmark. pgrand@hsph.harvard.edu
Source
J Pediatr. 2004 Feb;144(2):169-76
Date
Feb-2004
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Blood Pressure - physiology
Child
Cohort Studies
Denmark
Environmental Exposure - adverse effects
Evoked Potentials, Auditory, Brain Stem - drug effects - physiology
Female
Follow-Up Studies
Food Contamination
Heart - drug effects - physiology
Heart Rate - physiology
Humans
Male
Methylmercury Compounds - toxicity
Parasympathetic Nervous System - drug effects - physiopathology
Pregnancy
Prenatal Exposure Delayed Effects
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Seafood - adverse effects
Sex Factors
Sympathetic Nervous System - drug effects - physiopathology
Abstract
OBJECTIVE: To determine whether heart function in childhood is affected by exposure to methylmercury (MeHg) from seafood. STUDY DESIGN: Prospective study of a Faroese birth cohort (N=1022). Examinations at ages 7 and 14 years included blood pressure, heart rate variability (HRV) and its frequency components of autonomic origin, and brainstem auditory evoked potentials (BAEPs). Mercury concentrations were determined in cord blood and in the child's hair. RESULTS: Both low-frequency (LF) and high-frequency (HF) activities decreased by about 25% from 7 to 14 years; they correlated well with the blood pressures. A doubling of prenatal MeHg exposure was associated with a decrease in LF and HF powers of about 6.7% (P=.04) and in the coefficient of variation of the electrocardiographic R-R interval of 2.7% (P=.04) at age 14 years. No discernible effect on blood pressure was apparent. Decreased LF variability was associated with increased latency of BAEP peak III, but adjustment for MeHg exposure substantially attenuated this correlation. CONCLUSIONS: Methylmercury exposure was associated with decreased sympathetic (LF) and parasympathetic (HF) modulation of the HRV. Parallel MeHg-related delays of BAEP latencies may be caused by underlying MeHg neurotoxicity to brainstem nuclei.
PubMed ID
14760255 View in PubMed
Less detail

Umbilical cord mercury concentration as biomarker of prenatal exposure to methylmercury.

https://arctichealth.org/en/permalink/ahliterature29620
Source
Environ Health Perspect. 2005 Jul;113(7):905-8
Publication Type
Article
Date
Jul-2005
Author
Philippe Grandjean
Esben Budtz-Jørgensen
Poul J Jørgensen
Pál Weihe
Author Affiliation
Institute of Public Health, University of Southern Denmark, Odense, Denmark. pgrand@health.sdu.uk
Source
Environ Health Perspect. 2005 Jul;113(7):905-8
Date
Jul-2005
Language
English
Publication Type
Article
Keywords
Atlantic Islands
Biological Markers - analysis - blood
Child
Comparative Study
Environmental monitoring
Female
Fetal Blood - chemistry
Food Contamination
Hair - chemistry
Humans
Infant, Newborn
Maternal Exposure
Maternal-Fetal Exchange
Methylmercury Compounds - analysis - blood - toxicity
Neuropsychological Tests
Neurotoxicity Syndromes - blood - epidemiology
Pregnancy
Prospective Studies
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Seafood
Umbilical Cord - chemistry
Abstract
Biomarkers are often applied to assess prenatal exposure to methylmercury in research and surveillance. In a prospective study in the Faroe Islands, the main exposure biomarkers were the mercury concentrations in cord blood and maternal hair obtained at parturition. We have now supplemented these exposure biomarkers with mercury analyses of umbilical cord tissue from 447 births. In particular, when expressed in relation to the dry weight of the tissue, the cord mercury concentration correlated very well with that in cord blood. Structural equation model analysis showed that these two biomarkers have average total imprecision of about 30%, which is much higher than the laboratory error. The imprecision of the dry-weight-based concentration was lower than that of the wet-weight-based parameter, and it was intermediate between those of the cord blood and the hair biomarkers. In agreement with this finding, regression analyses showed that the dry-weight cord mercury concentration was almost as good a predictor of methylmercury-associated neuropsychologic deficits at 7 years of age as was the cord-blood mercury concentration. Cord mercury analysis can therefore be used as a valid measure of prenatal methylmercury exposure, but appropriate adjustment for the imprecision should be considered.
PubMed ID
16002381 View in PubMed
Less detail

21 records – page 1 of 2.