Skip header and navigation

Refine By

31 records – page 1 of 4.

Androgen receptor gene CAG repeat length as a modifier of the association between persistent organohalogen pollutant exposure markers and semen characteristics.

https://arctichealth.org/en/permalink/ahliterature77700
Source
Pharmacogenet Genomics. 2007 Jun;17(6):391-401
Publication Type
Article
Date
Jun-2007
Author
Giwercman Aleksander
Rylander Lars
Rignell-Hydbom Anna
Jönsson Bo A G
Pedersen Henning S
Ludwicki Jan K
Lesovoy Vladimir
Zvyezday Valentyna
Spano Marcello
Manicardi Gian-Carlo
Bizzaro Davide
Bonefeld-Jørgensen Eva C
Toft Gunnar
Bonde Jens Peter
Giwercman Charlotte
Tiido Tarmo
Giwercman Yvonne Lundberg
Author Affiliation
Molecular Reproductive Medicine Research Unit, Department of Clinical Sciences, Reproductive Medicine Centre, Malmö University Hospital, Lund University, Malmö, Sweden. aleksander.giwercman@med.lu.se
Source
Pharmacogenet Genomics. 2007 Jun;17(6):391-401
Date
Jun-2007
Language
English
Publication Type
Article
Keywords
Adult
DNA Fragmentation - drug effects
Dichlorodiphenyl Dichloroethylene - blood - toxicity
Endocrine Disruptors - blood - toxicity
Environmental Exposure
Environmental Pollutants - blood - toxicity
Humans
Hydrocarbons, Halogenated - toxicity
Male
Minisatellite Repeats
Pharmacogenetics
Polychlorinated Biphenyls - blood - toxicity
Polymorphism, Genetic
Receptors, Androgen - genetics
Semen - drug effects - metabolism
Sperm Count
Trinucleotide Repeats
Abstract
OBJECTIVES: Exposure to persistent organohalogen pollutants was suggested to impair male reproductive function. A gene-environment interaction has been proposed. No genes modifying the effect of persistent organohalogen pollutants on reproductive organs have yet been identified. We aimed to investigate whether the CAG and GGN polymorphisms in the androgen receptor gene modify the effect of persistent organohalogen pollutant exposure on human sperm characteristics. METHODS: Semen and blood from 680 men [mean (SD) age 34 (10) years] from Greenland, Sweden, Warsaw (Poland) and Kharkiv (Ukraine) were collected. Persistent organohalogen pollutant exposure was assessed by measuring serum levels of 2,2',4,4',5,5'-hexachlorobiphenyl (CB-153) and dichlorodiphenyl dichloroethene (p,p'-DDE). Semen characteristics (volume, sperm concentration, total count, proportion of progressively motile and morphology) and DNA fragmentation index (DFI) were determined. CAG and GGN repeat lengths were determined by direct sequencing of leukocyte DNA. RESULTS: A statistically significant interaction was found between the CB-153 group and CAG repeat category in relation to sperm concentration and total sperm count (P=0.03 and 0.01, respectively). For p,p'-DDE, in the European cohorts a significant interaction was found in relation to DFI (P=0.01). For CAG
PubMed ID
17502831 View in PubMed
Less detail

Association between exposure to persistent organohalogen pollutants and epididymal and accessory sex gland function: multicentre study in Inuit and European populations.

https://arctichealth.org/en/permalink/ahliterature80475
Source
Reprod Toxicol. 2006 Nov;22(4):765-73
Publication Type
Article
Date
Nov-2006
Author
Elzanaty Saad
Rignell-Hydbom Anna
Jönsson Bo A G
Pedersen Henning S
Ludwicki Jan K
Shevets Maryna
Zvyezday Valentyna
Toft Gunnar
Bonde Jens Peter
Rylander Lars
Hagmar Lars
Bonefeld-Jorgensen Ewa
Spano Marcello
Bizzaro Davide
Manicardi Gian-Carlo
Giwercman Aleksander
Author Affiliation
Scanian Andrology Centre, Fertility Centre, Malmö University Hospital, Lund University, Malmö, Sweden. saad.elzanaty@kmed.lu.se
Source
Reprod Toxicol. 2006 Nov;22(4):765-73
Date
Nov-2006
Language
English
Publication Type
Article
Keywords
Adult
Biological Markers - analysis
Dichlorodiphenyl Dichloroethylene - blood - poisoning
Environmental Exposure - adverse effects
Environmental Pollutants - blood - poisoning
European Continental Ancestry Group
Female
Fisheries
Genitalia, Male - drug effects - physiology
Greenland
Humans
Inuits
Linear Models
Male
Middle Aged
Poland
Polychlorinated Biphenyls - blood - toxicity
Pregnancy
Prostate-Specific Antigen - analysis
Semen - chemistry - drug effects
Sperm Motility - drug effects
Ukraine
Abstract
Exposure to persistent organochlorine pollutants (POPs) may have negative impact on male reproductive function. We, therefore, investigated the association between serum levels of POPs and epididymal and accessory sex gland function. Serum levels of CB-153, p,p'-DDE and seminal markers of epididymal [neutral-alpha glucosidase (NAG)], prostatic [prostate specific-antigen (PSA)] and zinc, and seminal vesicle function (fructose) were measured from 135 Swedish fishermen and fertile men from Greenland (n=163), Warsaw, Poland (n=167) and Kharkiv, Ukraine (n=158). Multiple linear regression analyses, adjusting for potential confounders, were employed using both continuous and categorized exposure variables. Both exposure and outcome variables were log transformed. Considering the consistency between models with either continuous or categorized CB-153 levels, negative associations with the activity of NAG were found among Greenlandic men (mean difference 7.0 mU/ejaculate, 95% CI 3.0, 34), and in the aggregated cohort (mean difference 4.0 mU/ejaculate, 95% CI -0.2, 8.0). A positive association was observed between CB-153 and PSA as well as zinc among Kharkiv men. In the Swedish cohort, a negative association was found between CB-153 and fructose. In conclusion, the negative effects of POP on sperm motility, observed in the same study population might partly be caused by post-testicular mechanisms, involving a decreased epididymal function.
PubMed ID
17008049 View in PubMed
Less detail

Association between prenatal polychlorinated biphenyl exposure and obesity development at ages 5 and 7 y: a prospective cohort study of 656 children from the Faroe Islands.

https://arctichealth.org/en/permalink/ahliterature106521
Source
Am J Clin Nutr. 2014 Jan;99(1):5-13
Publication Type
Article
Date
Jan-2014
Author
Jeanett L Tang-Péronard
Berit L Heitmann
Helle R Andersen
Ulrike Steuerwald
Philippe Grandjean
Pál Weihe
Tina K Jensen
Author Affiliation
Department of Environmental Medicine, Institute of Public Health, University of Southern Denmark, Odense, Denmark (JLT-P, HRA, PG, and TKJ); the Research Unit for Dietary Studies, Institute of Preventive Medicine, Copenhagen University Hospitals, Frederiksberg, Denmark (JLT-P and BLH); the National Institute of Public Health, University of Southern Denmark, Copenhagen, Denmark (BLH); the Boden Institute of Obesity, Nutrition, Exercise & Eating Disorders, Sydney Medical School, Sydney, Australia (BLH); the Department of Occupational Medicine and Public Health, Tórshavn, Faroe Islands (US); and the Department of Environmental Medicine, Faroese Hospital System, Tórshavn, Faroe Islands (PW).
Source
Am J Clin Nutr. 2014 Jan;99(1):5-13
Date
Jan-2014
Language
English
Publication Type
Article
Keywords
Body mass index
Body Weight - drug effects
Child
Child, Preschool
Denmark
Dichlorodiphenyl Dichloroethylene - blood - toxicity
Female
Humans
Linear Models
Male
Maternal Exposure
Milk, human - chemistry
Obesity - chemically induced
Overweight - blood - metabolism
Polychlorinated Biphenyls - blood - toxicity
Pregnancy
Prenatal Exposure Delayed Effects - chemically induced
Prospective Studies
Waist Circumference - drug effects
Abstract
Chemicals with endocrine-disrupting abilities may act as obesogens and interfere with the body's natural weight-control mechanisms, especially if exposure occurs during prenatal life.
We examined the association between prenatal exposure to polychlorinated biphenyls (PCBs) and p,p'-dichlorodiphenyldichloroethylene (DDE) and subsequent obesity at 5 and 7 y of age.
From 1997 to 2000, 656 pregnant Faroese women were recruited. PCB and DDE were measured in maternal serum and breast milk, and children's weight, height, and waist circumference (WC) were measured at clinical examinations at 5 and 7 y of age. The change in body mass index (BMI) from 5 to 7 y of age was calculated. Analyses were performed by using multiple linear regression models for girls and boys separately, taking into account maternal prepregnancy BMI.
For 7-y-old girls who had overweight mothers, PCB was associated with increased BMI (ß = 2.07, P = 0.007), and PCB and DDE were associated with an increased change in BMI from 5 to 7 y of age (PCB: ß = 1.23, P = 0.003; DDE: ß = 1.11, P = 0.008). No association was observed with BMI in girls with normal-weight mothers. PCB was associated with increased WC in girls with overweight mothers (ß = 2.48, P = 0.001) and normal-weight mothers (ß = 1.25, P = 0.04); DDE was associated with increased WC only in girls with overweight mothers (ß = 2.21, P = 0.002). No associations were observed between PCB or DDE and BMI in 5-y-old girls. For boys, no associations were observed.
Results suggest that prenatal exposure to PCB and DDE may play a role for subsequent obesity development. Girls whose mothers have a high prepregnancy BMI seem most affected.
PubMed ID
24153349 View in PubMed
Less detail

Associations of Peripubertal Serum Dioxin and Polychlorinated Biphenyl Concentrations with Pubertal Timing among Russian Boys.

https://arctichealth.org/en/permalink/ahliterature282988
Source
Environ Health Perspect. 2016 Nov;124(11):1801-1807
Publication Type
Article
Date
Nov-2016
Author
Jane S Burns
Mary M Lee
Paige L Williams
Susan A Korrick
Oleg Sergeyev
Thuy Lam
Boris Revich
Russ Hauser
Source
Environ Health Perspect. 2016 Nov;124(11):1801-1807
Date
Nov-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Child
Dioxins - blood - toxicity
Environmental Exposure - analysis
Humans
Longitudinal Studies
Male
Polychlorinated Biphenyls - blood - toxicity
Russia
Sexual Maturation - drug effects
Time Factors
Abstract
Dioxins, furans, and polychlorinated biphenyls (PCBs), dioxin-like and non-dioxin-like, have been linked to alterations in puberty.
We examined the association of peripubertal serum levels of these compounds [and their toxic equivalents (TEQs)] with pubertal onset and maturity among Russian boys enrolled at ages 8-9 years and followed prospectively through ages 17-18 years.
At enrollment, 473 boys had serum dioxin-like compounds and PCBs measured. At the baseline visit and annually until age 17-18 years, a physician performed pubertal staging [genitalia (G), pubarche (P), and testicular volume (TV)]. Three hundred fifteen subjects completed the follow-up visit at 17-18 years of age. Pubertal onset was defined as TV > 3 mL, G2, or P2. Sexual maturity was defined as TV = 20 mL, G5, or P5. Multivariable interval-censored models were used to evaluate associations of lipid-standardized concentrations with pubertal timing.
Medians (interquartile ranges) of the sum of dioxin-like compounds, TEQs, and non-dioxin-like PCBs were 362 pg/g lipid (279-495), 21.1 pg TEQ/g lipid (14.4-33.2), and 250 ng/g lipid (164-395), respectively. In adjusted models, the highest compared to lowest TEQ quartile was associated with later pubertal onset [TV = 11.6 months (95% CI: 3.8, 19.4); G2 = 10.1 months (95% CI: 1.4, 18.8)] and sexual maturity [TV = 11.6 months (95% CI: 5.7, 17.6); G5 = 9.7 months (95% CI: 3.1, 16.2)]. However, the highest compared to the lowest quartile of non-dioxin-like PCBs, when co-adjusted by TEQs, was associated with earlier pubertal onset [TV = -8.3 months (95% CI:-16.2, -0.3)] and sexual maturity [TV = -6.3 months (95% CI:-12.2, -0.3); G5 = -7.2 months (95% CI:-13.8, -0.6)]; the non-dioxin-like PCB associations were only significant when adjusted for TEQs. TEQs and PCBs were not significantly associated with pubic hair development.
Our results suggest that TEQs may delay, while non-dioxin-like PCBs advance, the timing of male puberty. Citation: Burns JS, Lee MM, Williams PL, Korrick SA, Sergeyev O, Lam T, Revich B, Hauser R. 2016. Associations of peripubertal serum dioxin and polychlorinated biphenyl concentrations with pubertal timing among Russian boys. Environ Health Perspect 124:1801-1807; http://dx.doi.org/10.1289/EHP154.
Notes
Cites: Environ Int. 2014 Oct;71:20-824950161
Cites: Environ Health Perspect. 2011 Sep;119(9):1339-4421527364
Cites: Toxicol Sci. 2003 Jul;74(1):182-9112730615
Cites: J Pediatr. 2000 Apr;136(4):490-610753247
Cites: Horm Res Paediatr. 2012;77(3):137-4522508036
Cites: Vopr Pitan. 1998;(3):8-139752664
Cites: Reprod Toxicol. 2012 Dec;34(4):498-50322841741
Cites: Environ Health Perspect. 2002 Aug;110(8):771-612153757
Cites: Reprod Toxicol. 2014 Apr;44:73-8424211603
Cites: Chemosphere. 2008 Oct;73(6):999-100418707752
Cites: Pediatrics. 2008 Feb;121 Suppl 3:S172-9118245511
Cites: Acta Paediatr. 2015 Jun;104(6):e271-825664405
Cites: Horm Behav. 2013 Jul;64(2):262-923998670
Cites: Environ Health Perspect. 2009 Oct;117(10 ):1593-920019911
Cites: Environ Health Perspect. 2009 Mar;117(3):417-2519337517
Cites: Chemosphere. 2005 Aug;60(7):898-90615992596
Cites: Bull World Health Organ. 2007 Sep;85(9):660-718026621
Cites: J Expo Sci Environ Epidemiol. 2011 May-Jun;21(3):224-3320197795
Cites: Endocrinology. 2003 Mar;144(3):767-7612586752
Cites: J Toxicol Environ Health A. 2005 Sep;68(17-18):1447-5616076757
Cites: Am J Clin Nutr. 1996 Jul;64(1):18-248669409
Cites: Nat Rev Endocrinol. 2014 Feb;10(2):67-924275741
Cites: Endocrinology. 2012 Sep;153(9):4097-11022733974
Cites: Pediatrics. 2009 May;123(5):e932-919403485
Cites: Environ Health Perspect. 2015 Oct;123(10):1046-5225956003
Cites: Pediatrics. 2011 Jan;127(1):e59-6821187307
Cites: Asian J Androl. 2014 Jan-Feb;16(1):89-9624369137
Cites: Pediatrics. 2012 Nov;130(5):e1058-6823085608
Cites: Arch Dis Child. 1976 Mar;51(3):170-9952550
Cites: Prev Med. 1997 Nov-Dec;26(6):808-169388792
Cites: Front Neuroendocrinol. 2015 Jul;38:12-3625592640
Cites: J Endocrinol. 2013 Jul 11;218(2):R1-1223709001
Cites: J Pediatr Endocrinol Metab. 2003 Feb;16(2):169-7812713253
Cites: Int J Obes (Lond). 2013 Aug;37(8):1036-4323164700
Cites: Toxicol Sci. 2007 Sep;99(1):224-3317545211
Cites: Environ Health. 2005 May 26;4(1):815918907
Cites: Environ Health Perspect. 2008 Jul;116(7):976-8018629324
Cites: Toxicol Sci. 2006 Oct;93(2):223-4116829543
Cites: Stat Med. 1998 Jan 30;17(2):219-389483730
Cites: Semin Reprod Med. 2004 Nov;22(4):337-4715635501
Cites: Epidemiology. 2011 Nov;22(6):827-3521968773
Cites: J Biomed Biotechnol. 2010;2010:null20862379
Cites: Reproduction. 2005 Jun;129(6):675-8315923383
Cites: J Adolesc Health. 2010 Sep;47(3):282-920708568
Cites: J Clin Endocrinol Metab. 1996 Mar;81(3):1152-58772591
Cites: J Pediatr. 1995 Jul;127(1):100-27608791
Cites: Pediatrics. 1997 Apr;99(4):505-129093289
Cites: Environ Health Perspect. 2015 Sep;123(9):888-9425769180
PubMed ID
27187981 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

Contribution of methylmercury, polychlorinated biphenyls and organochlorine pesticides to the toxicity of a contaminant mixture based on Canadian Arctic population blood profiles.

https://arctichealth.org/en/permalink/ahliterature90943
Source
Toxicol Lett. 2009 Feb 10;184(3):176-85
Publication Type
Article
Date
Feb-10-2009
Author
Pelletier Guillaume
Masson Sheila
Wade Mike J
Nakai Jamie
Alwis Ramona
Mohottalage Susantha
Kumarathasan Premkumari
Black Paleah
Bowers Wayne J
Chu Ih
Vincent Renaud
Author Affiliation
Hazard Identification Division, Environmental Health, Science and Research Bureau, Chemicals Management Directorate, Health Canada, Canada. guillaume_pelletier@hc-sc.gc.ca
Source
Toxicol Lett. 2009 Feb 10;184(3):176-85
Date
Feb-10-2009
Language
English
Publication Type
Article
Keywords
Age Factors
Animals
Arctic Regions
Body Weight - drug effects
Brain - drug effects - metabolism
Canada
Cerebellum - drug effects - metabolism
Complex Mixtures - toxicity
Disease Models, Animal
Electrophoresis, Gel, Two-Dimensional
Female
Gestational Age
Hippocampus - drug effects - metabolism
Hydrocarbons, Chlorinated - blood - toxicity
Hypothyroidism - blood - chemically induced
Male
Methylmercury Compounds - blood - toxicity
Mitochondrial Proteins - metabolism
Nerve Tissue Proteins - metabolism
Pesticides - blood - toxicity
Polychlorinated Biphenyls - blood - toxicity
Propylthiouracil
Rats
Rats, Sprague-Dawley
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Taurine - metabolism
Thyroid Gland - drug effects - metabolism
Thyroid Hormones - blood
Water Pollutants, Chemical - blood - toxicity
Abstract
Human populations are simultaneously exposed to a variety of anthropogenic contaminants. However, despite extensive literature on animal exposure to single compounds, data on the toxicity of complex mixtures are scarce. The Northern Contaminant Mixture (NCM) was formulated to contain the 27 most abundant contaminants in the same relative proportions found in the blood of Canadian Arctic populations. Sprague-Dawley rat dams were dosed from the first day of gestation until weaning with methylmercury (MeHg), polychlorinated biphenyls (PCBs) or organochlorines pesticides (OCs) administered either separately or together in the NCM. An additional control group for hypothyroxinemia was included by dosing dams with the goitrogen 6-propyl-2-thiouracil (PTU). Offspring growth, survival, serum thyroxine and Thyroid Stimulating Hormone (TSH) levels, thyroid gland morphology, brain taurine content and cerebellum and hippocampus protein expression patterns resulting from such exposures were monitored. Pups' increased mortality rate and impaired growth observed in the NCM treatment group were attributed to MeHg, while decreased circulating thyroxine levels and perturbations of thyroid gland morphology were mostly attributable to PCBs. Interestingly, despite comparable reduction in serum thyroxine levels, PCBs and PTU exposures produced markedly different effects on pup's growth, serum TSH level and brain taurine content. Analysis of cerebellum and hippocampus protein expression patterns corroborated previous cerebellum gene expression data, as contaminant co-exposure in the NCM significantly masked the effects of individual components on protein two-dimensional electrophoresis patterns. Identification by MALDI-TOF/TOF MS of differentially expressed proteins involved notably in neuronal and mitochondrial functions provided clues on the cellular and molecular processes affected by these contaminant mixtures.
PubMed ID
19059321 View in PubMed
Less detail

A cross-sectional study of the association between persistent organochlorine pollutants and diabetes.

https://arctichealth.org/en/permalink/ahliterature46956
Source
Environ Health. 2005;4:28
Publication Type
Article
Date
2005
Author
Lars Rylander
Anna Rignell-Hydbom
Lars Hagmar
Author Affiliation
Division of Occupational and Environmental Medicine and Psychiatric Epidemiology, Department of Laboratory Medicine, University Hospital, SE-221 85 Lund, Sweden. lars.rylander@med.lu.se
Source
Environ Health. 2005;4:28
Date
2005
Language
English
Publication Type
Article
Keywords
Adult
Aged
Cross-Sectional Studies
Diabetes Mellitus, Type 2 - chemically induced - epidemiology
Dichlorodiphenyl Dichloroethylene - blood - toxicity
Environmental Pollutants - blood - toxicity
Female
Fisheries
Food chain
Humans
Hydrocarbons, Chlorinated - blood - toxicity
Logistic Models
Male
Mass Fragmentography
Middle Aged
Polychlorinated Biphenyls - blood - toxicity
Prevalence
Seafood
Sweden - epidemiology
Abstract
BACKGROUND: Experimental evidence supports the hypothesis that persistent organochlorine pollutants (POPs) may cause type 2 diabetes mellitus, whereas there is no fully convincing epidemiological evidence for such an association. In Sweden the most important source of POP exposure is fatty fish. We have assessed the association between serum levels of POPs and prevalence of diabetes in Swedish fishermen and their wives, with high consumption of fatty fish from the Baltic Sea. METHODS: In 196 men (median age 60 years) and 184 women (median age 64 years), we analyzed 2,2',4,4',5,5'-hexachlorobiphenyl (CB-153) and 1,1-dichloro-2,2-bis(p-chlorophenyl)-ethylene (p,p'-DDE) in serum using gas chromatography-mass spectrometry. The participants were asked if they had diabetes and, if so, since which year and about medication and diet. The Odds Ratios (OR) for diabetes with respect to continuous exposure variables were analyzed with logistic regression, adjusting for potential confounders. Moreover trends of diabetes prevalence with respect to trichotomized exposure variables were tested with Jonckheere-Terpstra's test. RESULTS: Six percent of the men and 5% of the women had diabetes. After confounder adjustment CB-153 was significantly associated with diabetes prevalence using both categorized and continuous exposure data (an increase of 100 ng/g lipid corresponded to an OR of 1.16, 95% confidence interval [CI] 1.03, 1.32, p = 0.03). Similar associations were observed for p,p'-DDE (an increase of 100 ng/g lipid corresponded to an OR of 1.05, 95% CI 1.01, 1.09, p = 0.006). Gender stratified analyses showed among men consistent positive associations with CB-153, but a more ambiguous pattern with respect to DDE. In contrast, among the women the associations with p,p'-DDE were stronger than with CB-153. CONCLUSION: The study provides support that POP exposure might contribute to type 2 diabetes mellitus.
PubMed ID
16316471 View in PubMed
Less detail

Dioxin exposure and age of pubertal onset among Russian boys.

https://arctichealth.org/en/permalink/ahliterature134923
Source
Environ Health Perspect. 2011 Sep;119(9):1339-44
Publication Type
Article
Date
Sep-2011
Author
Susan A Korrick
Mary M Lee
Paige L Williams
Oleg Sergeyev
Jane S Burns
Donald G Patterson
Wayman E Turner
Larry L Needham
Larisa Altshul
Boris Revich
Russ Hauser
Author Affiliation
Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA. susan.korrick@channing.harvard.edu
Source
Environ Health Perspect. 2011 Sep;119(9):1339-44
Date
Sep-2011
Language
English
Publication Type
Article
Keywords
Child
Cohort Studies
Confidence Intervals
Dioxins - blood - toxicity
Environmental Pollutants - blood - toxicity
Furans - blood - toxicity
Humans
Logistic Models
Male
Polychlorinated Biphenyls - blood - toxicity
Proportional Hazards Models
Prospective Studies
Puberty - drug effects
Questionnaires
Russia - epidemiology
Sensitivity and specificity
Statistics, nonparametric
Abstract
Animal data demonstrate associations of dioxin, furan, and polychlorinated biphenyl (PCB) exposures with altered male gonadal maturation. It is unclear whether these associations apply to human populations.
We investigated the association of dioxins, furans, PCBs, and corresponding toxic equivalent (TEQ) concentrations with pubertal onset among boys in a dioxin-contaminated region.
Between 2003 and 2005, 499 boys 8-9 years of age were enrolled in a longitudinal study in Chapaevsk, Russia. Pubertal onset [stage 2 or higher for genitalia (G2+) or testicular volume (TV) > 3 mL] was assessed annually between ages 8 and 12 years. Serum levels at enrollment were analyzed by the Centers for Disease Control and Prevention, Atlanta, Georgia, USA. We used Cox proportional hazards models to assess age at pubertal onset as a function of exposure adjusted for potential confounders. We conducted sensitivity analyses excluding boys with pubertal onset at enrollment.
The median (range) total serum TEQ concentration was 21 (4-175) pg/g lipid, approximately three times higher than values in European children. At enrollment, boys were generally healthy and normal weight (mean body mass index, 15.9 kg/m2), with 30% having entered puberty by G2+ and 14% by TV criteria. Higher dioxin TEQs were associated with later pubertal onset by TV (hazard ratio = 0.68, 95% confidence interval, 0.49-0.95 for the highest compared with the lowest quartile). Similar associations were observed for 2,3,7,8-tetrachlorodibenzo-p-dioxin and dioxin concentrations for TV but not G2+. Results were robust to sensitivity analyses.
Findings support an association of higher peripubertal serum dioxin TEQs and concentrations with later male pubertal onset reflected in delayed testicular maturation.
Notes
Cites: Environ Health Perspect. 2003 May;111(5):737-4112727603
Cites: J Clin Endocrinol Metab. 2010 Jan;95(1):263-7019926714
Cites: J Pediatr. 2003 Jun;142(6):643-612838192
Cites: J Chromatogr B Analyt Technol Biomed Life Sci. 2003 Aug 25;794(1):137-4812888206
Cites: Anal Chem. 2004 Apr 1;76(7):1921-715053652
Cites: J Am Acad Child Adolesc Psychiatry. 2004 Jun;43(6):718-2615167088
Cites: Mol Cell Endocrinol. 2004 Jun 30;221(1-2):87-9615223135
Cites: Arch Dis Child. 1976 Mar;51(3):170-9952550
Cites: Anal Chem. 1987 Aug 1;59(15):2000-53631519
Cites: Arch Environ Contam Toxicol. 1989 Jul-Aug;18(4):495-5002505694
Cites: J Pediatr. 1995 Jul;127(1):100-27608791
Cites: Arch Pediatr Adolesc Med. 2010 Feb;164(2):166-7320124146
Cites: Pediatrics. 2010 May;125(5):e1088-9620368318
Cites: Int J Androl. 2010 Apr;33(2):279-8720002220
Cites: Pediatrics. 2010 Sep;126(3):e583-9020696727
Cites: J Expo Sci Environ Epidemiol. 2011 May-Jun;21(3):224-3320197795
Cites: Am J Clin Nutr. 1996 Jul;64(1):18-248669409
Cites: J Clin Endocrinol Metab. 1996 Oct;81(10):3812-38855844
Cites: Pediatrics. 1997 Apr;99(4):505-129093289
Cites: Vopr Pitan. 1998;(3):8-139752664
Cites: J Steroid Biochem Mol Biol. 1998 Nov;67(4):347-549883992
Cites: J Pediatr. 2000 Apr;136(4):490-610753247
Cites: Int J Androl. 2000 Aug;23(4):248-5310886429
Cites: J Toxicol Environ Health A. 2001 May 11;63(1):1-1811346131
Cites: Arch Pediatr Adolesc Med. 2001 Sep;155(9):1022-811529804
Cites: Environ Health Perspect. 2002 Aug;110(8):771-612153757
Cites: N Engl J Med. 2003 Apr 17;348(16):1527-3612700372
Cites: Comp Biochem Physiol C Toxicol Pharmacol. 2004 Jul;138(3):375-8115533795
Cites: Chemosphere. 2005 Mar;58(9):1185-20115667840
Cites: J Toxicol Environ Health A. 2005 Sep;68(17-18):1447-5616076757
Cites: J Adolesc Health. 2005 Nov;37(5):345-5516227118
Cites: Mol Cell Endocrinol. 2006 Jul 25;254-255:172-816806671
Cites: Toxicol Sci. 2006 Oct;93(2):223-4116829543
Cites: Eur J Endocrinol. 2007 Jan;156(1):105-1117218732
Cites: J Epidemiol Community Health. 2007 Jul;61(7):564-517568044
Cites: Toxicol Sci. 2007 Sep;99(1):224-3317545211
Cites: Bull World Health Organ. 2007 Sep;85(9):660-718026621
Cites: Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):168-7518226071
Cites: Pediatrics. 2008 Feb;121 Suppl 3:S172-9118245511
Cites: J Endocrinol. 2008 May;197(2):351-818434365
Cites: Environ Health Perspect. 2008 Jul;116(7):976-8018629324
Cites: Chemosphere. 2008 Oct;73(6):999-100418707752
Cites: Curr Opin Endocrinol Diabetes Obes. 2009 Feb;16(1):25-3019115521
Cites: Reprod Toxicol. 2009 Jul;28(1):38-4519490993
Cites: Environ Health Perspect. 2009 Oct;117(10):1593-920019911
Cites: Toxicol Sci. 2003 Jul;74(1):182-9112730615
PubMed ID
21527364 View in PubMed
Less detail

Dioxin-like compounds and bone quality in Cree women of Eastern James Bay (Canada): a cross-sectional study.

https://arctichealth.org/en/permalink/ahliterature260305
Source
Environ Health. 2013;12(1):54
Publication Type
Article
Date
2013
Author
Alexandra-Cristina Paunescu
Eric Dewailly
Sylvie Dodin
Evert Nieboer
Pierre Ayotte
Source
Environ Health. 2013;12(1):54
Date
2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
American Native Continental Ancestry Group
Bone and Bones - drug effects - physiology
Cross-Sectional Studies
Dioxins - blood
Environmental monitoring
Environmental Pollutants - blood - toxicity
Female
Humans
Metals, Heavy - blood
Middle Aged
Polychlorinated Biphenyls - blood - toxicity
Quebec
Abstract
Aboriginal populations living in Canada's northern regions are exposed to a number of persistent organic pollutants through their traditional diet which includes substantial amounts of predator fish species. Exposure to dioxin-like compounds (DLCs) can cause a variety of toxic effects including adverse effects on bone tissue. This descriptive cross-sectional study was conducted to investigate the relationship between plasma concentrations of DLCs and bone quality parameters in Cree women of Eastern James Bay (Canada).
Two hundred and forty-nine Cree women from seven communities in Eastern James Bay (Canada), aged 35 to 74 years old, participated in the study. In order to determine the total DLC concentration in plasma samples of participants, we measured the aryl hydrocarbon receptor-mediated transcriptional activity elicited by plasma sample extracts using a luciferase reporter gene assay. Plasma concentrations of mono-ortho-substituted dioxin-like polychlorinated biphenyls (DL-PCBs) 105, 118 and 156 were measured by gas chromatography-mass spectrometry. Bone quality parameters (speed of sound, m/s; broadband ultrasound attenuation, dB/MHz; stiffness index, %) were assessed by quantitative ultrasound at the right calcaneus with the Achilles InSight system. Several factors known to be associated with osteoporosis were documented by questionnaire. Multiple linear regression models were constructed for the three ultrasound parameters.
DL-PCBs 105 and 118 concentrations, but not the global DLC concentration, were inversely associated with the stiffness index, even after adjusting for several confounding factors. The stiffness index (log) decreased by -0.22% (p=0.0414) and -0.04% (p=0.0483) with an increase of one µg/L in plasma concentrations of DL-PCB 105 and DL-PCB 118, respectively. Other factors, including age, height, smoking status, menopausal status and the percentage of omega-6 polyunsaturated fatty acids (PUFAs) in erythrocyte membranes were negatively associated with one of the ultrasound parameters, while the percentage of omega-3 PUFAs in these membranes and levels of physical activity and education were positively associated with them.
Our results show that an increase in plasma concentrations of DL-PCBs 105 and 118 was negatively associated with stiffness index, a measure of bone quality/strength, in women of this population. In addition to environmental contaminants, future studies should also consider PUFA intake as a factor influencing bone quality.
Notes
Cites: Can J Public Health. 2005 Jan-Feb;96 Suppl 1:S45-5015686153
Cites: Bone. 2008 May;42(5):990-518329354
Cites: Am J Clin Nutr. 2005 Apr;81(4):934-815817874
Cites: Environ Health Perspect. 2005 Jul;113(7):853-716002372
Cites: Curr Osteoporos Rep. 2005 Jun;3(2):64-916036104
Cites: Sci Total Environ. 2005 Dec 1;351-352:165-24616297438
Cites: QJM. 2006 Apr;99(4):231-616565521
Cites: Osteoporos Int. 2006;17(9):1358-6816770522
Cites: Osteoporos Int. 2006 Dec;17(12):1755-6216960648
Cites: Environ Health. 2006;5:3317184534
Cites: J Nutr. 2007 Feb;137(2):461-517237327
Cites: Osteoporos Int. 2008 Jan;19(1):79-8617641811
Cites: J Clin Densitom. 2008 Jan-Mar;11(1):163-8718442758
Cites: Bone. 2008 Mar;42(3):498-50418191628
Cites: Front Biosci. 2008;13:4015-2018508495
Cites: Environ Health Perspect. 2008 Sep;116(9):1162-618795157
Cites: Toxicol Sci. 2009 Apr;108(2):330-4319201780
Cites: Chemosphere. 2009 May;75(5):680-419152955
Cites: Chemosphere. 2009 Oct;77(5):640-5119733382
Cites: Arthritis Res Ther. 2009;11(5):25119849819
Cites: J Biomech. 2010 Apr 19;43(6):1097-10320132933
Cites: Chemosphere. 2010 Jun;80(2):75-8220435334
Cites: Toxicology. 2010 Jun 29;273(1-3):1-1120403408
Cites: Menopause. 2010 Jan-Feb;17(1):25-54; quiz 55-620061894
Cites: Osteoporos Int. 2000;11(12):1036-4211256895
Cites: Curr Rheumatol Rep. 2001 Jun;3(3):245-811352794
Cites: Lancet. 2002 May 18;359(9319):1761-712049882
Cites: Med Sci Sports Exerc. 2003 Aug;35(8):1381-9512900694
Cites: Osteoporos Int. 2003 Nov;14(11):895-90412920507
Cites: CMAJ. 2004 Oct 12;171(8):869-7315477625
Cites: Arch Environ Contam Toxicol. 1989 Jul-Aug;18(4):495-5002505694
Cites: Osteoporos Int. 1994 Nov;4(6):368-817696835
Cites: J Med Assoc Thai. 1997 Nov;80(11):738-419385772
Cites: Aging (Milano). 1998 Oct;10(5):385-949932142
Cites: Am J Epidemiol. 2005 Feb 15;161(4):307-2015692074
PubMed ID
23816203 View in PubMed
Less detail

Direct assessment of cumulative aryl hydrocarbon receptor agonist activity in sera from experimentally exposed mice and environmentally exposed humans.

https://arctichealth.org/en/permalink/ahliterature143850
Source
Environ Health Perspect. 2010 May;118(5):693-8
Publication Type
Article
Date
May-2010
Author
Jennifer J Schlezinger
Pamela L Bernard
Amelia Haas
Philippe Grandjean
Pal Weihe
David H Sherr
Author Affiliation
Department of Environmental Health, Boston University School of Public Health, Boston, Massachusetts 02118 , USA. jschlezi@bu.edu
Source
Environ Health Perspect. 2010 May;118(5):693-8
Date
May-2010
Language
English
Publication Type
Article
Keywords
Animals
Cell Line
Cohort Studies
Denmark
Environmental Exposure
Environmental Pollutants - blood - toxicity
Female
Humans
Ligands
Mice
Mice, Inbred C57BL
Polychlorinated Biphenyls - blood - toxicity
Pregnancy
Receptors, Aryl Hydrocarbon - agonists - blood
Risk assessment
Tetrachlorodibenzodioxin - blood - toxicity
Abstract
Aryl hydrocarbon receptor (AhR) ligands adversely affect many biological processes. However, assessment of the significance of human exposures is hampered by an incomplete understanding of how complex mixtures affect AhR activation/inactivation.
These studies used biological readouts to provide a broader context for estimating human risk than that obtained with serum extraction and gas chromatography/mass spectroscopy (GC/MS)-based assays alone.
AhR agonist activity was quantified in sera from dioxin-treated mice, commercial human sources, and polychlorinated biphenyl (PCB)-exposed Faroe Islanders using an AhR-driven reporter cell line. To validate relationships between serum AhR agonist levels and biological outcomes, AhR agonist activity in mouse sera correlated with toxic end points. AhR agonist activity in unmanipulated ("neat") human sera was compared with these biologically relevant doses and with GC/MS-assayed PCB levels.
Mouse serum AhR agonist activity correlated with injected dioxin dose, thymic atrophy, and heptomegaly, validating the use of neat serum to assess AhR agonist activity. AhR agonist activity in sera from Faroe Islanders varied widely, was associated with the frequency of recent pilot whale dinners, but did not correlate with levels of PCBs quantified by GC/MS. Surprisingly, significant "baseline" AhR activity was found in commercial human sera.
An AhR reporter assay revealed cumulative levels of AhR activation potential in neat serum, whereas extraction may preclude detection of important non-dioxin-like biological activity. Significant levels of AhR agonist activity in commercial sera and in Faroe Islander sera, compared with that from experimentally exposed mice, suggest human exposures that are biologically relevant in both populations.
Notes
Cites: Toxicol Appl Pharmacol. 1999 Nov 15;161(1):10-2210558919
Cites: Environ Health Perspect. 2009 Jul;117(7):1070-519654915
Cites: Environ Health Perspect. 2000 Jun;108(6):553-710856030
Cites: Toxicol Lett. 2001 Aug 6;123(1):59-6711514106
Cites: Endocrinology. 2002 Feb;143(2):615-2011796517
Cites: Toxicol Sci. 2002 Feb;65(2):200-1011812924
Cites: Environ Health Perspect. 2002 Jun;110(6):595-60012055051
Cites: Chem Biol Interact. 2002 Sep 20;141(1-2):3-2412213382
Cites: Chemosphere. 2002 Sep;48(8):827-3212222776
Cites: Annu Rev Pharmacol Toxicol. 2003;43:309-3412540743
Cites: Toxicol Appl Pharmacol. 2003 Feb 15;187(1):11-2112628580
Cites: Regul Toxicol Pharmacol. 2003 Apr;37(2):202-1712726754
Cites: Fundam Appl Toxicol. 1995 Aug;27(1):131-97589923
Cites: Environ Res. 1995 Oct;71(1):29-388757236
Cites: Toxicol Appl Pharmacol. 1996 Sep;140(1):173-98806883
Cites: J Anim Sci. 1998 Jan;76(1):134-419464894
Cites: Mol Pharmacol. 1998 Apr;53(4):623-99547351
Cites: J Immunol. 1998 Apr 15;160(8):3844-549558089
Cites: Environ Health Perspect. 1998 Dec;106(12):775-929831538
Cites: Arch Environ Contam Toxicol. 2005 Jan;48(1):1-915657799
Cites: J Expo Anal Environ Epidemiol. 2005 Jul;15(4):310-815383834
Cites: J Immunol. 2005 Oct 1;175(7):4184-816177056
Cites: Environ Sci Technol. 2005 Oct 1;39(19):7357-6416245802
Cites: Mol Pharmacol. 2006 Jun;69(6):1871-816540597
Cites: Toxicol Lett. 2006 Sep 10;165(3):230-4116750337
Cites: Toxicol Sci. 2006 Oct;93(2):223-4116829543
Cites: PLoS Med. 2006 Aug;3(8):e31116942395
Cites: Eur J Clin Pharmacol. 2006 Dec;62(12):1041-817089110
Cites: Environ Toxicol Chem. 2007 Jun;26(6):1122-917571676
Cites: Nature. 2008 May 1;453(7191):106-918362914
Cites: Nature. 2008 May 1;453(7191):65-7118362915
Cites: J Expo Sci Environ Epidemiol. 2008 Jul;18(4):369-8017912254
Cites: Neurotoxicology. 2008 Sep;29(5):846-5418761371
Cites: Chem Biol Interact. 2008 Oct 22;176(1):19-2918762178
Cites: Biochem Pharmacol. 2009 Feb 15;77(4):642-5319027719
Cites: Biochem Pharmacol. 2009 Feb 15;77(4):746-6019100241
Cites: Toxicol Sci. 2000 Mar;54(1):183-9310746945
PubMed ID
20435556 View in PubMed
Less detail

31 records – page 1 of 4.