Skip header and navigation

Refine By

25 records – page 1 of 3.

Amniotic fluid phthalate levels and male fetal gonad function.

https://arctichealth.org/en/permalink/ahliterature264835
Source
Epidemiology. 2015 Jan;26(1):91-9
Publication Type
Article
Date
Jan-2015
Author
Morten Søndergaard Jensen
Ravinder Anand-Ivell
Bent Nørgaard-Pedersen
Bo A G Jönsson
Jens Peter Bonde
David M Hougaard
Arieh Cohen
Christian H Lindh
Richard Ivell
Gunnar Toft
Source
Epidemiology. 2015 Jan;26(1):91-9
Date
Jan-2015
Language
English
Publication Type
Article
Keywords
Adult
Amniotic Fluid - chemistry
Case-Control Studies
Cryptorchidism - epidemiology
Denmark - epidemiology
Diethylhexyl Phthalate - analysis
Environmental Exposure - statistics & numerical data
Female
Gonadal Steroid Hormones - analysis
Humans
Hydrocortisone - analysis
Hypospadias - epidemiology
Immunoassay
Infant, Newborn
Insulin - analysis
Leydig Cells
Linear Models
Logistic Models
Male
Mass Spectrometry
Phthalic Acids - analysis
Pregnancy
Proteins - analysis
Abstract
Prenatal exposure to phthalates may pose a threat to human male reproduction. However, additional knowledge about the in vivo effect in humans is needed, and reported associations with genital abnormalities are inconclusive. We aimed to study prenatal di(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DiNP) exposure in relation to cryptorchidism, hypospadias, and human fetal Leydig cell function.
We studied 270 cryptorchidism cases, 75 hypospadias cases, and 300 controls. Second-trimester amniotic fluid samples were available from a Danish pregnancy-screening biobank (n = 25,105) covering 1980-1996. We assayed metabolites of DEHP and DiNP (n = 645) and steroid hormones (n = 545) by mass spectrometry. We assayed insulin-like factor 3 by immunoassay (n = 475) and analyzed data using linear or logistic regression.
Mono(2-ethyl-5-carboxypentyl) phthalate (5cx-MEPP, DEHP metabolite) was not consistently associated with cryptorchidism or hypospadias. However, we observed an 18% higher (95% confidence interval [CI] = 5%-33%) testosterone level, and a 41% lower (-56% to -21%) insulin-like factor 3 level in the highest 5cx-MEPP tertile compared with the lowest. Mono(4-methyl-7-carboxyheptyl) phthalate (7cx-MMeHP, DiNP metabolite) showed elevated odds ratio point estimates for having cryptorchidism (odds ratio = 1.28 [95% CI = 0.80 to 2.01]) and hypospadias (1.69 [0.78 to 3.67]), but was not consistently associated with the steroid hormones or insulin-like factor 3.
Data on the DEHP metabolite indicate possible interference with human male fetal gonadal function. Considering the DiNP metabolite, we cannot exclude (nor statistically confirm) an association with hypospadias and, less strongly, with cryptorchidism.
PubMed ID
25384265 View in PubMed
Less detail

Association between paternal smoking at the time of pregnancy and the semen quality in sons.

https://arctichealth.org/en/permalink/ahliterature299606
Source
PLoS One. 2018; 13(11):e0207221
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
2018
Author
Jonatan Axelsson
Sally Sabra
Lars Rylander
Anna Rignell-Hydbom
Christian H Lindh
Aleksander Giwercman
Author Affiliation
Molecular Reproductive Medicine, Department of Translational Medicine, Faculty of Medicine, Lund University, Malmö, Sweden.
Source
PLoS One. 2018; 13(11):e0207221
Date
2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adolescent
Cotinine - blood
Fathers
Female
Humans
Male
Maternal Exposure
Nuclear Family
Paternal Exposure
Pregnancy
Prenatal Exposure Delayed Effects
Semen Analysis
Smoking - adverse effects - blood
Sweden
Young Adult
Abstract
Maternal smoking during pregnancy has repeatedly been associated with decreased sperm counts in sons. Nevertheless, our team recently detected a lower total sperm count in the sons of smoking fathers as compared to sons of non-smoking fathers. Since paternal and maternal tobacco smoking often coincide, it is difficult to discriminate whether effects are mediated paternally or maternally when using questionnaire- or register-based studies. Therefore, getting an objective measure of the maternal nicotine exposure level during pregnancy might help disentangling the impact of paternally and maternally derived exposure.
Our aim was to study how paternal smoking at the time of the pregnancy was associated with semen quality in the sons after adjusting for the maternal levels of nicotine exposure during pregnancy.
We recruited 104 men (17-20 years old) from the general Swedish population. The participants answered a questionnaire about paternal smoking. Associations between smoking and semen volume, total sperm count, sperm concentration, morphology and motility were adjusted for levels of the nicotine metabolite cotinine in stored maternal serum samples obtained from rubella screening between the 6th and 35th week of pregnancy. We additionally adjusted for the estimated socioeconomic status.
After adjusting for the maternal cotinine, the men of smoking fathers had 41% lower sperm concentration and 51% lower total sperm count than the men of non-smoking fathers (p = 0.02 and 0.003, respectively). This was robust to the additional adjustment.
Our results suggest a negative association between paternal smoking and sperm counts in the sons, independent of the level maternal nicotine exposure during the pregnancy.
PubMed ID
30462692 View in PubMed
Less detail

Association between pregnancy loss and urinary phthalate levels around the time of conception.

https://arctichealth.org/en/permalink/ahliterature129391
Source
Environ Health Perspect. 2012 Mar;120(3):458-63
Publication Type
Article
Date
Mar-2012
Author
Gunnar Toft
Bo A G Jönsson
Christian H Lindh
Tina Kold Jensen
Niels H Hjollund
Anne Vested
Jens Peter Bonde
Author Affiliation
Danish Ramazzini Center, Department of Occupational Medicine, Aarhus University Hospital, Aarhus, Denmark. guntof@rm.dk
Source
Environ Health Perspect. 2012 Mar;120(3):458-63
Date
Mar-2012
Language
English
Publication Type
Article
Keywords
Abortion, Spontaneous - chemically induced - epidemiology
Adult
Cohort Studies
Denmark - epidemiology
Environmental Exposure
Environmental Pollutants - toxicity - urine
Female
Fertilization
Humans
Phthalic Acids - metabolism - toxicity - urine
Pregnancy
Prospective Studies
Young Adult
Abstract
Animal studies indicate that some phthalate metabolites may harm female reproductive function.
We assessed the associations between exposure to phthalate metabolites and pregnancy loss.
Using a previously established cohort of couples planning their first pregnancy, we analyzed four primary and two oxidized secondary phthalate metabolites in urine samples collected on day 10 after the first day of the last menstrual period before conception occurred (n = 128) and during the previous cycle (if any, n = 111). Subclinical embryonal loss was identified by repeated measurement of urinary human chorionic gonadotropin, and information on clinical spontaneous abortions was obtained by telephone interview with the mother.
Pregnancy loss (n = 48) was increased among women with urinary concentration of monoethylhexyl phthalate (MEHP) in the upper tertile in the conception sample compared with women in the lowest tertile [adjusted odds ratio (OR) = 2.9; 95% confidence interval (CI): 1.1, 7.6]. The corresponding OR for subclinical embryonal loss (n = 32) was 40.7 (95% CI: 4.5, 369.5).
The phthalate metabolite MEHP was associated with higher occurrence of pregnancy loss. Because this is the first human study to show this association and the sample size is small, the findings need to be corroborated in independent studies.
Notes
Cites: Int J Androl. 2008 Apr;31(2):118-3018194284
Cites: Int J Androl. 2008 Apr;31(2):131-818070048
Cites: Am J Epidemiol. 2009 Apr 15;169(8):1015-2419251754
Cites: J Expo Sci Environ Epidemiol. 2010 Mar;20(2):169-7519277068
Cites: Environ Res. 2011 Jul;111(5):656-6321429484
Cites: Epidemiology. 2000 Jan;11(1):18-2310615838
Cites: Scand J Work Environ Health. 2000 Jun;26(3):187-9210901109
Cites: Anal Chem. 2000 Sep 1;72(17):4127-3410994974
Cites: Environ Health Perspect. 2000 Sep;108(9):895-90011017896
Cites: Food Addit Contam. 2001 Dec;18(12):1068-7411761117
Cites: Environ Health Perspect. 2003 Feb;111(2):139-4512573895
Cites: Hum Reprod. 2003 Jul;18(7):1512-512832380
Cites: Environ Res. 2003 Oct;93(2):177-8512963402
Cites: Environ Health Perspect. 2003 Nov;111(14):1783-514594632
Cites: Gynecol Endocrinol. 2004 Jan;18(1):51-715106366
Cites: Am J Epidemiol. 2004 Oct 1;160(7):661-715383410
Cites: Toxicol Appl Pharmacol. 1987 Apr;88(2):255-693564043
Cites: J Occup Med. 1987 May;29(5):451-43598737
Cites: N Engl J Med. 1988 Jul 28;319(4):189-943393170
Cites: Am Ind Hyg Assoc J. 1993 Oct;54(10):615-278237794
Cites: Reprod Toxicol. 1998 Jan-Feb;12(1):19-279431569
Cites: Reprod Toxicol. 2005 Mar-Apr;19(4):505-1515749265
Cites: Am J Epidemiol. 2005 Oct 15;162(8):709-1616120699
Cites: Int J Androl. 2006 Feb;29(1):155-65; discussion 181-516466535
Cites: J Expo Sci Environ Epidemiol. 2006 Jan;16(1):39-4816007114
Cites: Risk Anal. 2006 Jun;26(3):803-2416834635
Cites: Toxicol Sci. 2006 Sep;93(1):189-9516763070
Cites: Int J Hyg Environ Health. 2007 Jan;210(1):21-3317182278
Cites: Int J Hyg Environ Health. 2007 May;210(3-4):319-3317400024
Cites: J Endocrinol. 2007 Sep;194(3):603-917761899
Cites: Environ Health Perspect. 2008 Aug;116(8):1092-718709157
PubMed ID
22113848 View in PubMed
Less detail

Biological monitoring of exposure to toluene diisocyanate.

https://arctichealth.org/en/permalink/ahliterature177488
Source
Scand J Work Environ Health. 2004 Oct;30(5):371-8
Publication Type
Article
Date
Oct-2004
Author
Carl Johan Sennbro
Christian H Lindh
Håkan Tinnerberg
Hans Welinder
Margareta Littorin
Bo A G Jönsson
Author Affiliation
Department of Occupational and Environmental Medicine, University Hospital, Lund, Sweden. carl-johan.sennbro@ymed.lu.se
Source
Scand J Work Environ Health. 2004 Oct;30(5):371-8
Date
Oct-2004
Language
English
Publication Type
Article
Keywords
Adult
Biological Markers
Chromatography, High Pressure Liquid
Female
Humans
Linear Models
Male
Middle Aged
Occupational Exposure
Sweden
Toluene 2,4-Diisocyanate - blood - metabolism - urine
Abstract
Toluene diisocyanate (TDI) is used in the manufacture of polyurethane and is a potent inducer of diseases of the airways. In this study, 2,4- and 2,6-toluenediamine in hydrolyzed urine and plasma were evaluated as biomarkers of exposure to 2,4- and 2,6-TDI, respectively.
For 81 exposed workers from nine different plants, the personal 8-hour time-weighted-average exposure to TDI was monitored by a filter method with 1-(2-methoxyphenyl)piperazine. In parallel, urinary samples (U1) were collected during the last 4 hours of the workshift. On a different occasion, blood samples and additional urinary samples (U2) were collected from the exposed workers, and also from a reference group consisting of 121 unexposed workers. The biomarker levels were determined in urine and plasma by the use of alkaline hydrolysis.
There were strong associations between the personal air and biomarker levels, with correlation coefficients in the range of 0.75-0.88 for the U1 samples and in the range of 0.50-0.78 for the plasma samples. By weighted linear regression, the relations were calculated between the air and biomarker levels. The slopes of the obtained regression curves ranged from 1.8 to 2.7 m3/1 for air-urine and from 2.2 to 2.9 m3/1 for air-plasma, and the intercepts were all close to the origin of the coordinates. Through the extrapolation of these regression curves, biological exposure limits were calculated.
The biological monitoring methods and strategies presented in this report are useful for assessing exposure to TDI in practice.
Notes
Erratum In: Scand J Work Environ Health. 2005 Feb;31(1):84
PubMed ID
15534959 View in PubMed
Less detail

Biomarkers of exposure in Monday morning urine samples as a long-term measure of exposure to aromatic diisocyanates.

https://arctichealth.org/en/permalink/ahliterature259224
Source
Int Arch Occup Environ Health. 2014 May;87(4):365-72
Publication Type
Article
Date
May-2014
Author
Håkan Tinnerberg
Karin Broberg
Christian H Lindh
Bo A G Jönsson
Source
Int Arch Occup Environ Health. 2014 May;87(4):365-72
Date
May-2014
Language
English
Publication Type
Article
Keywords
Air Pollutants, Occupational - blood - urine
Biological Markers - blood - urine
Environmental Monitoring - methods
Female
Genotype
Glutathione Transferase - genetics
Humans
Isocyanates - blood - urine
Male
Occupational Exposure - analysis
Polymorphism, Genetic
Sweden
Toluene 2,4-Diisocyanate - blood - urine
Abstract
Exposure to diisocyanates is a known occupational hazard. One method for monitoring occupational exposure is by analyzing biomarkers in hydrolyzed urine and plasma. The half-life of the biomarkers in plasma is about 3 weeks, and the urinary elimination is divided into one fast (hours) and one slow phases (weeks). Polymorphism in glutathione S-transferase enzymes (GST) is earlier shown to modify the metabolism. The aim of the study was to assess whether biomarkers of exposure in urine collected after two non-exposed days correlate with levels in plasma and whether they can be used as a measure for long-term exposure to aromatic diisocyanates and further whether polymorphisms in GST influenced the correlations.
Biomarkers of exposure was analyzed in urine and blood samples collected from 24 workers, exposed to at least one of toluene-, methylenediphenyl- or naphthalene diisocyanate, on a Monday morning after at least two unexposed days. Moreover, genotype was determined for 19 of the workers.
The corresponding specific gravity-adjusted biomarkers in urine and plasma levels for the different diisocyanates correlated well (r between 0.689 and 0.988). When taking all samples together, the correlation coefficient was 0.926. Polymorphism in the GSTM1 genotype seemed to modify the association.
Urine collected after two unexposed days can possibly be used as long-term biomarker of exposure for aromatic diisocyanates.
PubMed ID
23558852 View in PubMed
Less detail

Cotinine Validation of Self-Reported Smoking During Pregnancy in the Swedish Medical Birth Register.

https://arctichealth.org/en/permalink/ahliterature274714
Source
Nicotine Tob Res. 2016 Jan;18(1):79-83
Publication Type
Article
Date
Jan-2016
Author
Kristina Mattsson
Karin Källén
Anna Rignell-Hydbom
Christian H Lindh
Bo A G Jönsson
Peik Gustafsson
Per Olofsson
Sten A Ivarsson
Lars Rylander
Source
Nicotine Tob Res. 2016 Jan;18(1):79-83
Date
Jan-2016
Language
English
Publication Type
Article
Keywords
Adult
Cotinine - blood
Female
Fetal Blood - chemistry
Humans
Maternal-Fetal Exchange
Pregnancy - blood - psychology
Prenatal Exposure Delayed Effects
Prevalence
Registries
Self Report
Smoking - blood - epidemiology
Sweden - epidemiology
Young Adult
Abstract
Self-reported data on smoking during pregnancy from the Medical Birth Register of Sweden (MBR) are widely used. However, underreporting of such behavior may occur, leading to biases. It is of importance to validate the smoking data in the MBR. The main objective was to investigate the agreement between self-reported smoking data from the MBR and cotinine levels in maternal serum among women from the general population in the region of Skåne, Sweden. We also estimated the transfer of cotinine from mother to fetus.
From a cohort used previously to investigate the relationship between intrauterine environmental exposures and offspring neuropsychiatric outcomes, there were 204 control children retrieved from the MBR with data on maternal smoking in early pregnancy registered. Data on maternal and umbilical cord cotinine at delivery were available for these children from a regional biobank.
There was a high agreement between cotinine levels and MBR smoking data (? = 0.82) and a high correlation between cotinine levels in maternal and umbilical cord serum (r s = 0.90, P
PubMed ID
25895950 View in PubMed
Less detail

Dioxin-like activities in serum across European and Inuit populations.

https://arctichealth.org/en/permalink/ahliterature169143
Source
Environ Health. 2006;5:14
Publication Type
Article
Date
2006
Author
Manhai Long
Birgitte S Andersen
Christian H Lindh
Lars Hagmar
Aleksander Giwercman
Gian-Carlo Manicardi
Davide Bizzaro
Marcello Spanò
Gunnar Toft
Henning S Pedersen
Valentyna Zvyezday
Jens Peter Bonde
Eva C Bonefeld-Jorgensen
Author Affiliation
Unit of Cellular & Molecular Toxicology, Department of Environmental and Occupational Medicine, Institute of Public Health, University of Aarhus, Vennelyst Boulevard 6, DK-8000 Aarhus C, Denmark. ml@mil.au.dk
Source
Environ Health. 2006;5:14
Date
2006
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Biological Markers - blood
Cohort Studies
Dichlorodiphenyl Dichloroethylene - blood
Dioxins - blood - toxicity
Environmental Exposure
Environmental Pollutants - toxicity
Europe
Humans
Insecticides - blood
Inuits
Male
Middle Aged
Polychlorinated biphenyls - blood
Receptors, Aryl Hydrocarbon - blood - metabolism
Tetrachlorodibenzodioxin - toxicity
Abstract
Persistent organic pollutants (POPs) such as polychlorinated dibenzo-p-dioxins/furans, polychlorinated biphenyls (PCBs) and organochlorine pesticides can cause a series of adverse effects on e.g. reproduction in animals and humans, many of which involve the aryl hydrocarbon receptor (AhR). The aim of the present study was to compare the integrated serum level of AhR mediated activity among European and Inuit populations, and evaluate whether the activity was associated to the selected POP markers, 2,2',4,4',5,5'-hexachlorobiphenyl (CB-153) and 1,1-dichloro-2,2-bis(p-chlorophenyl)-ethylene (p,p'-DDE).
The study included 338 males from Greenland (Inuit's), Sweden, Warsaw (Poland) and Kharkiv (Ukraine). The AhR transactivity of serum extracts alone (AhRag) and competitive AhR activity (AhRcomp) upon co-exposure with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were determined in the lipophilic serum fraction containing the POPs using the AhR mediated luciferase reporter Hepa1.12cR cell assay.
The European groups showed higher median level of AhR-TEQ (TCDD toxic equivalents) compared to the Inuit's, whereas higher incidence of Inuits sample further induced AhRcomp activity. Neither AhRag nor AhR-TEQ were correlated to CB-153 or p,p'-DDE for any of the study groups. Multiple regressions showed a significant heterogeneity of association between the CB-153 and the AhRcomp across the study groups, and accordingly a negative association between AhRcomp and CB-153 was found for the Kharkiv group.
No consistent correlation between AhR activities and two POP markers was found. Although the difference of AhRag between European and Inuit men could not be explained by CB-153 or p,p'-DDE levels alone, we believe that the variation of AhR serum activity reflects different pattern of POP exposure, genetics and/or life style factors.
Notes
Cites: Food Chem Toxicol. 2002 Jun;40(6):781-811983272
Cites: Int J Epidemiol. 1999 Apr;28(2):179-8810342677
Cites: Chemosphere. 2002 Sep;48(8):763-7012222769
Cites: Chemosphere. 2002 Sep;48(8):811-2512222775
Cites: Chemosphere. 2002 Sep;48(8):827-3212222776
Cites: Sci Total Environ. 2003 Jan 20;302(1-3):27-5212526896
Cites: Toxicol Appl Pharmacol. 2003 Feb 15;187(1):11-2112628580
Cites: Environ Sci Pollut Res Int. 2003;10(1):49-5612635959
Cites: Toxicology. 2003 Dec 15;194(1-2):77-9314636698
Cites: Toxicol Sci. 2000 Mar;54(1):183-9310746945
Cites: Environ Health Perspect. 2000 Jun;108(6):553-710856030
Cites: Arch Environ Health. 2000 May-Jun;55(3):195-20010908103
Cites: Food Addit Contam. 2000 Apr;17(4):347-5810912248
Cites: Environ Health Perspect. 2000 Nov;108(11):1035-4111102293
Cites: Toxicology. 2001 Feb 14;158(3):141-5311275356
Cites: Environ Toxicol Chem. 2001 Dec;20(12):2736-4311764156
Cites: Environ Health Perspect. 2001 Dec;109(12):1291-911748038
Cites: Environ Health Perspect. 2002 Feb;110(2):125-811836138
Cites: Biofactors. 2004;20(1):11-2215096657
Cites: Sci Total Environ. 2004 Sep 1;330(1-3):55-7015325158
Cites: Environ Health Perspect. 2004 Sep;112(13):1265-815345337
Cites: Environ Toxicol. 2004 Oct;19(5):480-915352264
Cites: Arch Biochem Biophys. 1989 Apr;270(1):344-552539049
Cites: Crit Rev Toxicol. 1990;21(1):51-882124811
Cites: Environ Health Perspect. 1994 Jan;102 Suppl 1:205-98187710
Cites: Crit Rev Toxicol. 1994;24(2):87-1498037844
Cites: Arch Toxicol Suppl. 1995;17:99-1157786196
Cites: Environ Health Perspect. 1995 Mar;103 Suppl 2:135-427614935
Cites: Scand J Work Environ Health. 1995 Apr;21(2):96-1057618064
Cites: Eur J Pharmacol. 1995 May 26;293(1):1-407545581
Cites: Fundam Appl Toxicol. 1996 Apr;30(2):194-2038812265
Cites: Eur J Pharmacol. 1995 Dec 7;293(4):463-748748700
Cites: Scand J Work Environ Health. 1995 Dec;21(6):419-268824747
Cites: Crit Rev Toxicol. 1997 Mar;27(2):109-349099515
Cites: Bull Environ Contam Toxicol. 1997 May;58(5):769-759115141
Cites: Carcinogenesis. 1997 Aug;18(8):1651-49276643
Cites: Chemosphere. 1998 Oct-Nov;37(9-12):2279-919828342
Cites: Environ Health Perspect. 1998 Dec;106(12):775-929831538
Cites: Environ Health Perspect. 1999 Jun;107(6):459-6210339445
Cites: Environ Health Perspect. 2005 Feb;113(2):175-915687046
Cites: Reproduction. 2005 Apr;129(4):379-8915798013
Cites: J Expo Anal Environ Epidemiol. 2005 Jul;15(4):310-815383834
Cites: Environ Health Perspect. 2005 Oct;113(10):1277-8416203234
Cites: Environ Health Perspect. 2005 Oct;113(10):1318-2416203240
Cites: Environ Sci Technol. 2005 Oct 1;39(19):7357-6416245802
Cites: Mol Cell Endocrinol. 2005 Dec 1;244(1-2):20-3016219411
Cites: Environ Health. 2005;4:2716283941
Cites: Environ Health. 2005;4:2616280075
Cites: Environ Health Perspect. 2006 Sep;114(9):1348-5316966087
Cites: Thromb Haemost. 1999 Apr;81(4):547-5210235437
Cites: Environ Health Perspect. 2002 Jul;110(7):617-2412117636
PubMed ID
16725033 View in PubMed
Less detail

Diverging temporal trends of human exposure to bisphenols and plastizisers, such as phthalates, caused by substitution of legacy EDCs?

https://arctichealth.org/en/permalink/ahliterature282775
Source
Environ Res. 2017 Feb;153:48-54
Publication Type
Article
Date
Feb-2017
Author
Irina Gyllenhammar
Anders Glynn
Bo A G Jönsson
Christian H Lindh
Per Ola Darnerud
Kettil Svensson
Sanna Lignell
Source
Environ Res. 2017 Feb;153:48-54
Date
Feb-2017
Language
English
Publication Type
Article
Keywords
Adult
Benzhydryl Compounds - urine
Chlorpyrifos - metabolism - urine
Environmental Exposure - analysis
Environmental Pollutants - urine
Female
Humans
Mothers
Phenols - urine
Phthalic Acids - metabolism - urine
Plasticizers - analysis
Sweden
Triclosan - urine
Abstract
Phthalates and phenolic substances were investigated in urine samples from first-time mothers in Uppsala, Sweden, collected between 2009 and 2014. These substances have a comparably fast metabolism and urinary metabolites are predominantly analysed. The main aim was to investigate if measures to decrease production and use of certain phthalates and bisphenol A (BPA) have resulted in decreased human exposure, and to determine if exposures to replacement chemicals have increased. Temporal trends were evaluated for metabolites (n=13) of seven phthalates, a phthalate replacer, four different bisphenols, triclosan, one organophosphate-based flame retardant, and for two pesticides. The results showed downward trends of several phthalates which are in the process of being regulated and phased out. Concomitantly, an increasing trend was seen for a metabolite of the phthalate replacer Di-iso-nonylcyclohexane 1,2-dicarboxylate (DiNCH). Bisphenol A (BPA) showed a downward trend, whereas bisphenol F, identified as one of the substitutes for BPA, showed an increasing trend. The decreasing trend of triclosan is likely due to declining use within the EU. Temporal trend studies of urine samples make it possible to investigate human exposure to rapidly metabolised substances and study how measures taken to regulate and replace problematic chemicals affect human exposure.
PubMed ID
27898309 View in PubMed
Less detail

Exposure-response relationships for hexahydrophthalic and methylhexahydrophthalic anhydrides with total plasma protein adducts as biomarkers.

https://arctichealth.org/en/permalink/ahliterature50681
Source
Scand J Work Environ Health. 2003 Aug;29(4):297-303
Publication Type
Article
Date
Aug-2003
Author
Seema Rosqvist
Jörn Nielsen
Hans Welinder
Lars Rylander
Christian H Lindh
Bo A G Jönsson
Author Affiliation
Department of Occupational and Environmental Medicine, Institute of Laboratory Medicine, University Hospital, Lund, Sweden.
Source
Scand J Work Environ Health. 2003 Aug;29(4):297-303
Date
Aug-2003
Language
English
Publication Type
Article
Keywords
Adult
Air Pollutants, Occupational - chemistry - toxicity
Biological Markers - blood
Blood Proteins - analysis
Comparative Study
Enzyme-Linked Immunosorbent Assay
Epoxy Resins - chemistry - toxicity
Female
Humans
Male
Middle Aged
Occupational Exposure - adverse effects
Phthalic Acids - chemistry - toxicity
Phthalic Anhydrides - chemistry - toxicity
Research Support, Non-U.S. Gov't
Sweden
Abstract
OBJECTIVES: This study investigated the exposure-response relationships of hexahydrophthalic anhydride (HHPA) and methylhexahydrophthalic anhydride (MHHPA) and evaluated the applicability of the total plasma protein adducts (TPPA) of these anhydrides as biomarkers of exposure and risk. METHODS: In a cross-sectional study of 139 workers in a plant manufacturing electrical capacitors, the long-term exposure to HHPA and MHHPA was assessed through the quantification of TPPA using gas chromatography-mass spectrometry. Smoking and medical histories were obtained through questionnaires. Work-related symptoms of the eyes and airways were recorded. Specific immunoglobulin (Ig) E (radioallergosorbent test) and IgG (enzyme-linked immunosorbent assay) were determined in serum. RESULTS: The mean level of the TPPA of HHPA was 840 fmol/ml and that of the TPPA of MHHPA was 1700 fmol/ml. There was no correlation between the TPPA of HHPA and the TPPA of MHHPA. Of all the workers, 19% were found to be positive for specific IgE and 17-19% for IgG. Positive associations were observed between HHPA exposure and specific IgE and IgG and between MHHPA exposure and specific IgG. Regarding work-related symptoms, 27% of the workers had symptoms of the nose, 21% had symptoms of the eyes, 11% had symptoms of the lower airways, and 8% had nose bleeding. There were significant exposure-response relationships for symptoms of the eyes and nose for HHPA exposure. CONCLUSIONS: The results show that there is an exposure-response relationship for HHPA both with specific antibodies and with work-related symptoms and down to adduct levels of 40 fmol/ml plasma. In addition, the results elucidate the potential power of TPPA as a relevant index of exposure and risk.
PubMed ID
12934723 View in PubMed
Less detail

Half-lives of PFOS, PFHxS and PFOA after end of exposure to contaminated drinking water.

https://arctichealth.org/en/permalink/ahliterature287931
Source
Occup Environ Med. 2018 Jan;75(1):46-51
Publication Type
Article
Date
Jan-2018
Author
Ying Li
Tony Fletcher
Daniel Mucs
Kristin Scott
Christian H Lindh
Pia Tallving
Kristina Jakobsson
Source
Occup Environ Med. 2018 Jan;75(1):46-51
Date
Jan-2018
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Alkanesulfonic Acids - blood - pharmacokinetics
Caprylates - blood - pharmacokinetics
Child
Child, Preschool
Drinking Water - chemistry
Environmental Exposure - analysis
Female
Fluorocarbons - blood - pharmacokinetics
Humans
Male
Middle Aged
Sex Factors
Sulfonic Acids - blood - pharmacokinetics
Sweden
Water Pollutants, Chemical - blood - pharmacokinetics
Water Quality
Water supply
Young Adult
Abstract
Municipal drinking water contaminated with perfluorinated alkyl acids had been distributed to one-third of households in Ronneby, Sweden. The source was firefighting foam used in a nearby airfield since the mid-1980s. Clean water was provided from 16 December 2013.
To determine the rates of decline in serum perfluorohexane sulfonate (PFHxS), perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA), and their corresponding half-lives.
Up to seven blood samples were collected between June 2014 and September 2016 from 106 participants (age 4-84 years, 53% female).
Median initial serum concentrations were PFHxS, 277?ng/mL (range 12-1660); PFOS, 345?ng/mL (range 24-1500); and PFOA, 18?ng/mL (range 2.4-92). The covariate-adjusted average rates of decrease in serum were PFHxS, 13% per year (95%?CI 12% to 15%); PFOS, 20% per year (95%?CI 19% to 22%); and PFOA, 26% per year (95%?CI 24% to 28%). The observed data are consistent with a first-order elimination model. The mean estimated half-life was 5.3 years (95%?CI 4.6 to 6.0) for PFHxS, 3.4 years (95%?CI 3.1 to 3.7) for PFOS and 2.7 years (95%?CI 2.5 to 2.9) for PFOA. The interindividual variation of half-life was around threefold when comparing the 5th and 95th percentiles. There was a marked sex difference with more rapid elimination in women for PFHxS and PFOS, but only marginally for PFOA.
The estimated half-life for PFHxS was considerably longer than for PFOS and PFOA. For PFHxS and PFOS, the average half-life is shorter than the previously published estimates. For PFOA the half-life is in line with the range of published estimates.
PubMed ID
29133598 View in PubMed
Less detail

25 records – page 1 of 3.