In utero dioxin exposure and cardiometabolic risk in the Seveso Second Generation Study

Background/objectives In utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) may alter risk of obesity and related metabolic disease later in life. We examined the relationship of prenatal exposure to TCDD with obesity and metabolic syndrome (MetS) i...

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Published inInternational Journal of Obesity Vol. 43; no. 11; pp. 2233 - 2243
Main Authors Warner, Marcella, Rauch, Stephen, Ames, Jennifer, Mocarelli, Paolo, Brambilla, Paolo, Signorini, Stefano, Eskenazi, Brenda
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.11.2019
Nature Publishing Group
Subjects
692/163/2743
692/499
Adipose tissue
Adolescent
Adult
Blood levels
Blood pressure
Blood Pressure - physiology
Body fat
Body mass index
Body size
Body Size - physiology
Child
Child, Preschool
Children
Cohort Studies
Dioxins
Disruption
Endocrine disruptors
Epidemiology
Explosions
Exposure
Female
Health Promotion and Disease Prevention
Health risk assessment
Health risks
Humans
Internal Medicine
Intrauterine exposure
Italy
Lipids
Male
Maternal Exposure - statistics & numerical data
Medicine
Medicine & Public Health
Metabolic Diseases
Metabolic disorders
Metabolic syndrome
Metabolic Syndrome - epidemiology
Metabolism
Obesity
Offspring
Polychlorinated Dibenzodioxins - analysis
Polychlorinated Dibenzodioxins - toxicity
Pregnancy
Prenatal experience
Prenatal exposure
Public Health
Risk
TCDD
Young Adult
Italy
Online AccessGet full text

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Abstract Background/objectives In utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) may alter risk of obesity and related metabolic disease later in life. We examined the relationship of prenatal exposure to TCDD with obesity and metabolic syndrome (MetS) in children born to a unique cohort of TCDD-exposed women resulting from a 1976 explosion in Seveso, Italy. Subjects/methods In 2014, nearly 40 years after the explosion, we enrolled 611 post-explosion offspring, 2 to 39 years of age, in the Seveso Second Generation Study. In utero TCDD exposure was defined primarily as TCDD concentration measured in maternal serum collected soon after the explosion and alternately as TCDD estimated at pregnancy. We measured height, weight, waist circumference, body fat, blood pressure, and fasting blood levels of lipids and glucose, which were combined to assess body mass index (BMI) and MetS. Results Children (314 female, 297 male) averaged 23.6 (±6.0) years of age. Among the 431 children ≥18 years, a 10-fold increase in initial maternal TCDD concentration was inversely associated with BMI in daughters (adj-β = −0.99 kg/m 2 ; 95% CI -1.86, -0.12), but not sons (adj-β = 0.41 kg/m 2 ; 95% CI −0.35, 1.18) ( p -int = 0.02). A similar relationship was found in the younger children (2–17 years); a 10-fold increase in initial maternal TCDD was inversely associated with BMI z -score (adj-β = −0.59 kg/m 2 ; 95% CI −1.12, −0.06) among daughters, but not sons (adj-β = 0.04 kg/m 2 ; 95% CI −0.34, 0.41) ( p -int = 0.03). In contrast, in sons only, initial maternal TCDD was associated with increased risk for MetS (adj-RR = 2.09, 95% CI 1.09, 4.02). Results for TCDD estimated at pregnancy were comparable. Conclusions These results suggest prenatal TCDD exposure alters cardiometabolic endpoints in a sex-specific manner. In daughters, in utero TCDD is inversely associated with adiposity measures. In sons, in utero TCDD is associated with increased risk for MetS.
AbstractList Background/objectivesIn utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may alter risk of obesity and related metabolic disease later in life. We examined the relationship of prenatal exposure to TCDD with obesity and metabolic syndrome (MetS) in children born to a unique cohort of TCDD-exposed women resulting from a 1976 explosion in Seveso, Italy.Subjects/methodsIn 2014, nearly 40 years after the explosion, we enrolled 611 post-explosion offspring, 2 to 39 years of age, in the Seveso Second Generation Study. In utero TCDD exposure was defined primarily as TCDD concentration measured in maternal serum collected soon after the explosion and alternately as TCDD estimated at pregnancy. We measured height, weight, waist circumference, body fat, blood pressure, and fasting blood levels of lipids and glucose, which were combined to assess body mass index (BMI) and MetS.ResultsChildren (314 female, 297 male) averaged 23.6 (±6.0) years of age. Among the 431 children ≥18 years, a 10-fold increase in initial maternal TCDD concentration was inversely associated with BMI in daughters (adj-β = −0.99 kg/m2; 95% CI -1.86, -0.12), but not sons (adj-β = 0.41 kg/m2; 95% CI −0.35, 1.18) (p-int = 0.02). A similar relationship was found in the younger children (2–17 years); a 10-fold increase in initial maternal TCDD was inversely associated with BMI z-score (adj-β = −0.59 kg/m2; 95% CI −1.12, −0.06) among daughters, but not sons (adj-β = 0.04 kg/m2; 95% CI −0.34, 0.41) (p-int = 0.03). In contrast, in sons only, initial maternal TCDD was associated with increased risk for MetS (adj-RR = 2.09, 95% CI 1.09, 4.02). Results for TCDD estimated at pregnancy were comparable.ConclusionsThese results suggest prenatal TCDD exposure alters cardiometabolic endpoints in a sex-specific manner. In daughters, in utero TCDD is inversely associated with adiposity measures. In sons, in utero TCDD is associated with increased risk for MetS.
Background/objectives In utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) may alter risk of obesity and related metabolic disease later in life. We examined the relationship of prenatal exposure to TCDD with obesity and metabolic syndrome (MetS) in children born to a unique cohort of TCDD-exposed women resulting from a 1976 explosion in Seveso, Italy. Subjects/methods In 2014, nearly 40 years after the explosion, we enrolled 611 post-explosion offspring, 2 to 39 years of age, in the Seveso Second Generation Study. In utero TCDD exposure was defined primarily as TCDD concentration measured in maternal serum collected soon after the explosion and alternately as TCDD estimated at pregnancy. We measured height, weight, waist circumference, body fat, blood pressure, and fasting blood levels of lipids and glucose, which were combined to assess body mass index (BMI) and MetS. Results Children (314 female, 297 male) averaged 23.6 (±6.0) years of age. Among the 431 children ≥18 years, a 10-fold increase in initial maternal TCDD concentration was inversely associated with BMI in daughters (adj-β = −0.99 kg/m 2 ; 95% CI -1.86, -0.12), but not sons (adj-β = 0.41 kg/m 2 ; 95% CI −0.35, 1.18) ( p -int = 0.02). A similar relationship was found in the younger children (2–17 years); a 10-fold increase in initial maternal TCDD was inversely associated with BMI z -score (adj-β = −0.59 kg/m 2 ; 95% CI −1.12, −0.06) among daughters, but not sons (adj-β = 0.04 kg/m 2 ; 95% CI −0.34, 0.41) ( p -int = 0.03). In contrast, in sons only, initial maternal TCDD was associated with increased risk for MetS (adj-RR = 2.09, 95% CI 1.09, 4.02). Results for TCDD estimated at pregnancy were comparable. Conclusions These results suggest prenatal TCDD exposure alters cardiometabolic endpoints in a sex-specific manner. In daughters, in utero TCDD is inversely associated with adiposity measures. In sons, in utero TCDD is associated with increased risk for MetS.
Background/objectives In utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may alter risk of obesity and related metabolic disease later in life. We examined the relationship of prenatal exposure to TCDD with obesity and metabolic syndrome (MetS) in children born to a unique cohort of TCDD-exposed women resulting from a 1976 explosion in Seveso, Italy. Subjects/methods In 2014, nearly 40 years after the explosion, we enrolled 611 post-explosion offspring, 2 to 39 years of age, in the Seveso Second Generation Study. In utero TCDD exposure was defined primarily as TCDD concentration measured in maternal serum collected soon after the explosion and alternately as TCDD estimated at pregnancy. We measured height, weight, waist circumference, body fat, blood pressure, and fasting blood levels of lipids and glucose, which were combined to assess body mass index (BMI) and MetS. Results Children (314 female, 297 male) averaged 23.6 ([plus or minus]6.0) years of age. Among the 431 children [greater than or equal to]18 years, a 10-fold increase in initial maternal TCDD concentration was inversely associated with BMI in daughters (adj-[beta] = -0.99 kg/m.sup.2; 95% CI -1.86, -0.12), but not sons (adj-[beta] = 0.41 kg/m.sup.2; 95% CI -0.35, 1.18) (p-int = 0.02). A similar relationship was found in the younger children (2-17 years); a 10-fold increase in initial maternal TCDD was inversely associated with BMI z-score (adj-[beta] = -0.59 kg/m.sup.2; 95% CI -1.12, -0.06) among daughters, but not sons (adj-[beta] = 0.04 kg/m.sup.2; 95% CI -0.34, 0.41) (p-int = 0.03). In contrast, in sons only, initial maternal TCDD was associated with increased risk for MetS (adj-RR = 2.09, 95% CI 1.09, 4.02). Results for TCDD estimated at pregnancy were comparable. Conclusions These results suggest prenatal TCDD exposure alters cardiometabolic endpoints in a sex-specific manner. In daughters, in utero TCDD is inversely associated with adiposity measures. In sons, in utero TCDD is associated with increased risk for MetS.
In utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may alter risk of obesity and related metabolic disease later in life. We examined the relationship of prenatal exposure to TCDD with obesity and metabolic syndrome (MetS) in children born to a unique cohort of TCDD-exposed women resulting from a 1976 explosion in Seveso, Italy. Children (314 female, 297 male) averaged 23.6 ([plus or minus]6.0) years of age. Among the 431 children [greater than or equal to]18 years, a 10-fold increase in initial maternal TCDD concentration was inversely associated with BMI in daughters (adj-[beta] = -0.99 kg/m.sup.2; 95% CI -1.86, -0.12), but not sons (adj-[beta] = 0.41 kg/m.sup.2; 95% CI -0.35, 1.18) (p-int = 0.02). A similar relationship was found in the younger children (2-17 years); a 10-fold increase in initial maternal TCDD was inversely associated with BMI z-score (adj-[beta] = -0.59 kg/m.sup.2; 95% CI -1.12, -0.06) among daughters, but not sons (adj-[beta] = 0.04 kg/m.sup.2; 95% CI -0.34, 0.41) (p-int = 0.03). In contrast, in sons only, initial maternal TCDD was associated with increased risk for MetS (adj-RR = 2.09, 95% CI 1.09, 4.02). Results for TCDD estimated at pregnancy were comparable. These results suggest prenatal TCDD exposure alters cardiometabolic endpoints in a sex-specific manner. In daughters, in utero TCDD is inversely associated with adiposity measures. In sons, in utero TCDD is associated with increased risk for MetS.
In utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may alter risk of obesity and related metabolic disease later in life. We examined the relationship of prenatal exposure to TCDD with obesity and metabolic syndrome (MetS) in children born to a unique cohort of TCDD-exposed women resulting from a 1976 explosion in Seveso, Italy.BACKGROUND/OBJECTIVESIn utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may alter risk of obesity and related metabolic disease later in life. We examined the relationship of prenatal exposure to TCDD with obesity and metabolic syndrome (MetS) in children born to a unique cohort of TCDD-exposed women resulting from a 1976 explosion in Seveso, Italy.In 2014, nearly 40 years after the explosion, we enrolled 611 post-explosion offspring, 2 to 39 years of age, in the Seveso Second Generation Study. In utero TCDD exposure was defined primarily as TCDD concentration measured in maternal serum collected soon after the explosion and alternately as TCDD estimated at pregnancy. We measured height, weight, waist circumference, body fat, blood pressure, and fasting blood levels of lipids and glucose, which were combined to assess body mass index (BMI) and MetS.SUBJECTS/METHODSIn 2014, nearly 40 years after the explosion, we enrolled 611 post-explosion offspring, 2 to 39 years of age, in the Seveso Second Generation Study. In utero TCDD exposure was defined primarily as TCDD concentration measured in maternal serum collected soon after the explosion and alternately as TCDD estimated at pregnancy. We measured height, weight, waist circumference, body fat, blood pressure, and fasting blood levels of lipids and glucose, which were combined to assess body mass index (BMI) and MetS.Children (314 female, 297 male) averaged 23.6 (±6.0) years of age. Among the 431 children ≥18 years, a 10-fold increase in initial maternal TCDD concentration was inversely associated with BMI in daughters (adj-β = -0.99 kg/m2; 95% CI -1.86, -0.12), but not sons (adj-β = 0.41 kg/m2; 95% CI -0.35, 1.18) (p-int = 0.02). A similar relationship was found in the younger children (2-17 years); a 10-fold increase in initial maternal TCDD was inversely associated with BMI z-score (adj-β = -0.59 kg/m2; 95% CI -1.12, -0.06) among daughters, but not sons (adj-β = 0.04 kg/m2; 95% CI -0.34, 0.41) (p-int = 0.03). In contrast, in sons only, initial maternal TCDD was associated with increased risk for MetS (adj-RR = 2.09, 95% CI 1.09, 4.02). Results for TCDD estimated at pregnancy were comparable.RESULTSChildren (314 female, 297 male) averaged 23.6 (±6.0) years of age. Among the 431 children ≥18 years, a 10-fold increase in initial maternal TCDD concentration was inversely associated with BMI in daughters (adj-β = -0.99 kg/m2; 95% CI -1.86, -0.12), but not sons (adj-β = 0.41 kg/m2; 95% CI -0.35, 1.18) (p-int = 0.02). A similar relationship was found in the younger children (2-17 years); a 10-fold increase in initial maternal TCDD was inversely associated with BMI z-score (adj-β = -0.59 kg/m2; 95% CI -1.12, -0.06) among daughters, but not sons (adj-β = 0.04 kg/m2; 95% CI -0.34, 0.41) (p-int = 0.03). In contrast, in sons only, initial maternal TCDD was associated with increased risk for MetS (adj-RR = 2.09, 95% CI 1.09, 4.02). Results for TCDD estimated at pregnancy were comparable.These results suggest prenatal TCDD exposure alters cardiometabolic endpoints in a sex-specific manner. In daughters, in utero TCDD is inversely associated with adiposity measures. In sons, in utero TCDD is associated with increased risk for MetS.CONCLUSIONSThese results suggest prenatal TCDD exposure alters cardiometabolic endpoints in a sex-specific manner. In daughters, in utero TCDD is inversely associated with adiposity measures. In sons, in utero TCDD is associated with increased risk for MetS.
In utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may alter risk of obesity and related metabolic disease later in life. We examined the relationship of prenatal exposure to TCDD with obesity and metabolic syndrome (MetS) in children born to a unique cohort of TCDD-exposed women resulting from a 1976 explosion in Seveso, Italy. In 2014, nearly 40 years after the explosion, we enrolled 611 post-explosion offspring, 2 to 39 years of age, in the Seveso Second Generation Study. In utero TCDD exposure was defined primarily as TCDD concentration measured in maternal serum collected soon after the explosion and alternately as TCDD estimated at pregnancy. We measured height, weight, waist circumference, body fat, blood pressure, and fasting blood levels of lipids and glucose, which were combined to assess body mass index (BMI) and MetS. Children (314 female, 297 male) averaged 23.6 (±6.0) years of age. Among the 431 children ≥18 years, a 10-fold increase in initial maternal TCDD concentration was inversely associated with BMI in daughters (adj-β = -0.99 kg/m ; 95% CI -1.86, -0.12), but not sons (adj-β = 0.41 kg/m ; 95% CI -0.35, 1.18) (p-int = 0.02). A similar relationship was found in the younger children (2-17 years); a 10-fold increase in initial maternal TCDD was inversely associated with BMI z-score (adj-β = -0.59 kg/m ; 95% CI -1.12, -0.06) among daughters, but not sons (adj-β = 0.04 kg/m ; 95% CI -0.34, 0.41) (p-int = 0.03). In contrast, in sons only, initial maternal TCDD was associated with increased risk for MetS (adj-RR = 2.09, 95% CI 1.09, 4.02). Results for TCDD estimated at pregnancy were comparable. These results suggest prenatal TCDD exposure alters cardiometabolic endpoints in a sex-specific manner. In daughters, in utero TCDD is inversely associated with adiposity measures. In sons, in utero TCDD is associated with increased risk for MetS.
Audience Academic
Author Eskenazi, Brenda
Ames, Jennifer
Warner, Marcella
Signorini, Stefano
Mocarelli, Paolo
Rauch, Stephen
Brambilla, Paolo
AuthorAffiliation 1 Center for Environmental Research and Children’s Health (CERCH), School of Public Health, University of California at Berkeley, Berkeley, California, USA
2 Department of Laboratory Medicine, University of Milano-Bicocca, School of Medicine, Hospital of Desio, Desio-Milano, Italy
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  surname: Warner
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  givenname: Stephen
  surname: Rauch
  fullname: Rauch, Stephen
  organization: Center for Environmental Research and Children’s Health (CERCH), School of Public Health, University of California at Berkeley
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  givenname: Jennifer
  surname: Ames
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  organization: Center for Environmental Research and Children’s Health (CERCH), School of Public Health, University of California at Berkeley
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  givenname: Paolo
  surname: Mocarelli
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  organization: Department of Laboratory Medicine, School of Medicine, Hospital of Desio, University of Milano-Bicocca
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  fullname: Signorini, Stefano
  organization: Department of Laboratory Medicine, School of Medicine, Hospital of Desio, University of Milano-Bicocca
– sequence: 7
  givenname: Brenda
  surname: Eskenazi
  fullname: Eskenazi, Brenda
  organization: Center for Environmental Research and Children’s Health (CERCH), School of Public Health, University of California at Berkeley
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30659254$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1007/978-1-4899-1462-0_3
10.1289/ehp.1104282
10.1016/j.envint.2013.11.005
10.1007/s11892-014-0494-0
10.1080/026520300283351
10.1016/0045-6535(90)90124-C
10.1016/j.yfrne.2010.07.002
10.1016/S0045-6535(99)00376-8
10.1016/S0021-9258(19)88622-2
10.1289/ehp.6573
10.1161/01.CIR.88.5.2460
10.1016/S0304-4165(02)00485-3
10.1530/REP-13-0422
10.1038/ijo.2015.13
10.1038/sj.jea.7500233
10.1146/annurev-physiol-012110-142200
10.1016/j.envres.2014.03.019
10.1161/CIRCULATIONAHA.109.192644
10.1016/0009-8981(89)90054-5
10.1007/s12012-008-9027-x
10.1016/j.envint.2018.08.051
10.1289/ehp.1206113
10.1007/BF03344156
10.1016/j.envint.2016.04.040
10.1021/ac00142a023
10.1007/s12012-008-9023-1
10.1515/dmdi-2011-0035
10.1016/j.taap.2007.12.029
10.1016/j.taap.2003.12.005
10.1016/S0140-6736(12)61766-8
10.1002/jat.2881
10.1152/ajpendo.90368.2008
10.1111/j.1399-5448.2007.00271.x
10.4137/EHI.S38343
10.1016/S0140-6736(16)30175-1
10.1016/j.taap.2007.08.018
10.1016/j.reprotox.2016.10.001
10.1016/0041-008X(84)90357-0
10.1016/j.taap.2015.09.017
10.1371/journal.pone.0184006
10.1203/PDR.0b013e3181c8f04b
10.1080/15287398909531288
10.1002/jbt.2570080206
10.1038/jes.2013.70
10.1111/j.2047-6310.2012.00064.x
10.1016/0147-6513(80)90032-9
10.1080/1047322X.1990.10389587
10.1002/jat.1459
10.1016/j.jpeds.2016.04.064
10.1093/ije/26.suppl_1.S152
10.1055/s-0036-1586427
10.1289/ehp.6080
10.1016/S0140-6736(14)60460-8
ContentType Journal Article
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References EnanEMatsumuraF2,3,7,8-Tetrachlorodibenzo-P-dioxin induced alterations in protein phosphorylation in guinea pig adipose tissueJ Biochem Toxicol19938899910.1002/jbt.25700802061:CAS:528:DyaK3sXlvFOlsr0%3D8394938
Casals-CasasCDesvergneBEndocrine disruptors: from endocrine to metabolic disruptionAnnu Rev Physiol2011731356210.1146/annurev-physiol-012110-1422001:CAS:528:DC%2BC3MXktVKjtb8%3D21054169
WarnerMMocarelliPBrambillaPWesselinkAPattersonDGTurnerWESerum TCDD and TEQ concentrations among Seveso women, 20 years after the explosionJ Expo Sci Environ Epidemiol2014245889410.1038/jes.2013.701:CAS:528:DC%2BC3sXhs1yitbjL24149975
Stata Corp.Stata Statistical Software: Release 13.12013College StationStata Press
Patterson DG, Turner WE. Method 28: Measurement of PCDDs, PCDFs, and Coplanar PCBs in Serum by HRGC/ID-HRMS. Atanta: National Center for Enviromental Health, CDC; 2005.
SugaiEYoshiokaWKakeyamaMOhsakoSTohyamaCIn utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin modulates dysregulation of the lipid metabolism in mouse offspring fed a high-calorie dietJ Appl Toxicol20143429630610.1002/jat.28811:CAS:528:DC%2BC3sXptVahsL0%3D23749557
MimuraJFujii-KuriyamaYFunctional role of AhR in the expression of toxic effects by TCDDBiochim Biophys Acta20031619263810.1016/S0304-4165(02)00485-31:CAS:528:DC%2BD3sXovFGrtg%3D%3D12573486
JaegerCTischkauSARole of aryl hydrocarbon receptor in circadian clock disruption and metabolic dysfunctionEnviron Health Insights2016101334110.4137/EHI.S38343275592984990151
Lim SS, Vos T, Flaxman AD, Danaei G, Shibuya K, Adair-Rohani H, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012;380:2224–60.
CacciariEMilaniSBalsamoASpadaEBonaGCavalloLItalian cross-sectional growth charts for height, weight and BMI (2 to 20 yr)J Endocrinol Invest2006295819310.1007/BF033441561:STN:280:DC%2BD28rjt1Oiug%3D%3D16957405
van EsterikJCVerharenHWHodemaekersHMGremmerERNagarajahBKamstraJHCompound- and sex-specific effects on programming of energy and immune homeostasis in adult C57BL/6JxFVB mice after perinatal TCDD and PCB 153Toxicol Appl Pharmacol20152892627510.1016/j.taap.2015.09.0171:CAS:528:DC%2BC2MXhs1Cqu7vN26415833
di DomenicoASilanoVVivianoGZapponiGAccidental release of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at Seveso, Italy. II. TCDD distribution in the soil surface layerEcotoxicol Environ Saf1980429832010.1016/0147-6513(80)90032-97439100
ZimmetPAlbertiKGKaufmanFTajimaNSilinkMArslanianSThe metabolic syndrome in children and adolescents - an IDF consensus reportPediatr Diabetes2007829930610.1111/j.1399-5448.2007.00271.x17850473
Zook D, Rappe C. Environmental sources, distribution, and fate. In: Schecter A, editor. Dioxins and Health. New York: Plenum Press; 1994. p. 79–113.
SchecterAPapkeOBallMEvidence for transplacental transfer of dioxins from mother to fetus: chlorinated dioxin and dibenzofuran in te livers of stillborn infantsChemosphere19902110172210.1016/0045-6535(90)90124-C1:CAS:528:DyaK3MXhtFKmsLY%3D
BaroukiRAggerbeckMAggerbeckLCoumoulXThe aryl hydrocarbon receptor systemDrug Metabol Drug Interact2012273810.1515/dmdi-2011-00351:CAS:528:DC%2BC2cXmtV2mtbY%3D22718620
BirnbaumLSTuomistoJNon-carcinogenic effects of TCDD in animalsFood Addit Contam2000172758810.1080/0265203002833511:CAS:528:DC%2BD3cXktl2qtbc%3D10912242
IszattNStigumHGovartsEMurinovaLPSchoetersGTrnovecTPerinatal exposure to dioxins and dioxin-like compounds and infant growth and body mass index at seven years: a pooled analysis of three European birth cohortsEnviron Int20169439940710.1016/j.envint.2016.04.0401:CAS:528:DC%2BC28XhtVWgurbF27311652
SeefeldMDKeeseyREPetersonREBody weight regulation in rats treated with 2,3,7,8-tetrachlorodibenzo-p-dioxinToxicol Appl Pharmacol1984765263610.1016/0041-008X(84)90357-01:CAS:528:DyaL2MXlslCjsA%3D%3D6506077
LindenJLensuSTuomistoJPohjanvirtaRDioxins, the aryl hydrocarbon receptor and the central regulation of energy balanceFront Neuroendocrinol2010314527810.1016/j.yfrne.2010.07.0021:CAS:528:DC%2BC3cXhtleqt7jL20624415
DelvauxIVan CauwenbergheJDen HondESchoetersGGovartsENelenVPrenatal exposure to environmental contaminants and body composition at age 7-9 yearsEnviron Res2014132243210.1016/j.envres.2014.03.0191:CAS:528:DC%2BC2cXpvFWjtrg%3D24742724
EnanELiuPCMatsumuraF2,3,7,8-Tetrachlorodibenzo-p-dioxin causes reduction of glucose transporting activities in the plasma membranes of adipose tissue and pancreas from the guinea pigJ Biol Chem199226719785911:CAS:528:DyaK38XlsVGjsLs%3D1400292
AylwardLLHaysSMTemporal trends in human TCDD body burden: decreases over three decades and implications for exposure levelsJ Expo Anal Environ Epidemiol2002123192810.1038/sj.jea.75002331:CAS:528:DC%2BD38XnvVynsLc%3D12198580
EskenaziBMocarelliPWarnerMCheeWYGerthouxPMSamuelsSMaternal serum dioxin levels and birth outcomes in women of Seveso, ItalyEnviron Health Perspect20031119475310.1289/ehp.60801:CAS:528:DC%2BD3sXltlKitLs%3D127824971241530
LeijsMMKoppeJGVulsmaTOlieKvan AalderenWMCde VoogtPAlterations in the programming of energy metabolism in adolescents with background exposure to dioxins, dl-PCBs and PBDEsPLoS One201712e018400610.1371/journal.pone.01840061:CAS:528:DC%2BC1cXotVykt7c%3D288982415595283
World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO Consultation on Obesity. Geneva: World Health Organization; 1998.
Ng M, Fleming T, Robinson M, Thomson B, Graetz N, Margono C, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;384:766–81.
PattersonDGHamptonLLapezaCRBelserWTGreenVAlexanderLHigh-resolution gas chromatographic/high-resolution mass spectrometric analysis of human serum on a whole-weight and lipid basis for 2,3,7,8-tetrachlorodibenzo-p-dioxinAnal Chem1987592000510.1021/ac00142a0231:CAS:528:DyaL2sXktlCns7g%3D3631519
KirkleyAGSargisRMEnvironmental endocrine disruption of energy metabolism and cardiovascular riskCurr Diab Rep20141449410.1007/s11892-014-0494-01:CAS:528:DC%2BC2cXms1Cqtbw%3D247563434067479
RashidCSCarterLGHennigBPearsonKJPerinatal Polychlorinated Biphenyl 126 Exposure Alters Offspring Body CompositionJ Pediatr Biochem20133475310.1055/s-0036-1586427237412833670830
TaiPTNishijoMNghiTNNakagawaHVan LuongHAnhTHEffects of perinatal dioxin exposure on development of children during the first 3 years of lifeJ Pediatr201617515966.e210.1016/j.jpeds.2016.04.0641:CAS:528:DC%2BC28XnvFejsbY%3D27189679
AkinsJRWaldrepKBernertJTJr.The estimation of total serum lipids by a completely enzymatic ‘summation’ methodClin Chim Acta19891842192610.1016/0009-8981(89)90054-51:CAS:528:DyaL1MXmt1yhtr4%3D2611996
WarnerMMocarelliPBrambillaPWesselinkASamuelsSSignoriniSDiabetes, metabolic syndrome, and obesity in relation to serum dioxin concentrations: the Seveso women’s health studyEnviron Health Perspect20131219061110.1289/ehp.12061131:CAS:528:DC%2BC2cXovFWnsbY%3D236745063734493
ColeTJLobsteinTExtended international (IOTF) body mass index cut-offs for thinness, overweight and obesityPediatr Obes201272849410.1111/j.2047-6310.2012.00064.x1:STN:280:DC%2BC38jjt1ymsA%3D%3D22715120
DesaiMJellymanJKRossMGEpigenomics, gestational programming and risk of metabolic syndromeInt J Obes20153963310.1038/ijo.2015.131:CAS:528:DC%2BC2MXjt1Sns7o%3D
La MerrillMBastonDSDenisonMSBirnbaumLSPompDThreadgillDWMouse breast cancer model-dependent changes in metabolic syndrome-associated phenotypes caused by maternal dioxin exposure and dietary fatAm J Physiol Endocrinol Metab2009296E2031010.1152/ajpendo.90368.20081:CAS:528:DC%2BD1MXpsFCnug%3D%3D18840765
HornungRWReedLDEstimation of average concentration in the presence of non-detectable valuesAppl Occup Environ Hyg19905485110.1080/1047322X.1990.10389587
EskenaziBWarnerMBrambillaPSignoriniSAmesJMocarelliPThe Seveso accident: a look at 40years of health research and beyondEnviron Int2018121Pt 1718410.1016/j.envint.2018.08.0511:CAS:528:DC%2BC1cXhs1Gqs7fI301797666221983
SatoSShirakawaHTomitaSOhsakiYHaketaKTooiOLow-dose dioxins alter gene expression related to cholesterol biosynthesis, lipogenesis, and glucose metabolism through the aryl hydrocarbon receptor-mediated pathway in mouse liverToxicol Appl Pharmacol200822910910.1016/j.taap.2007.12.0291:CAS:528:DC%2BD1cXlslWrtrc%3D18295293
KaurJA comprehensive review on metabolic syndromeCardiol Res Pract20142014943162247119543966331
ZhuBTGalloMABurgerCWJr.MeekerRJCaiMXXuSEffect of 2,3,7,8-tetrachlorodibenzo-p-dioxin administration and high-fat diet on the body weight and hepatic estrogen metabolism in female C3H/HeN miceToxicol Appl Pharmacol20082261071810.1016/j.taap.2007.08.0181:CAS:528:DC%2BD2sXhsVOls7bL17945325
EskenaziBMocarelliPWarnerMNeedhamLPattersonDGSamuelsSRelationship of serum TCDD concentrations and age at exposure of female residents of Seveso, ItalyEnviron Health Perspect200411222710.1289/ehp.65731:CAS:528:DC%2BD2cXhtVSju7o%3D146989261241792
KopfPGHuweJKWalkerMKHypertension, cardiac hypertrophy, and impaired vascular relaxation induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin are associated with increased superoxideCardiovasc Toxicol200881819310.1007/s12012-008-9027-x1:CAS:528:DC%2BD1cXhsVyms7jL188500752648846
PerloffDGrimCFlackJFrohlichEDHillMMcDonaldMHuman blood pressure determination by sphygmomanometryCirculation1993885 Pt 124607010.1161/01.CIR.88.5.24601:STN:280:DyaK2c%2Fjslerug%3D%3D8222141
CimafrancaMAHanlonPRJefcoateCRTCDD administration after the pro-adipogenic differentiation stimulus inhibits PPARgamma through a MEK-dependent process but less effectively suppresses adipogenesisToxicol Appl Pharmacol20041961566810.1016/j.taap.2003.12.0051:CAS:528:DC%2BD2cXisFyrtrY%3D15050417
GBMC.Body-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continentsLanc
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References_xml – reference: SchecterAPapkeOBallMEvidence for transplacental transfer of dioxins from mother to fetus: chlorinated dioxin and dibenzofuran in te livers of stillborn infantsChemosphere19902110172210.1016/0045-6535(90)90124-C1:CAS:528:DyaK3MXhtFKmsLY%3D
– reference: CacciariEMilaniSBalsamoASpadaEBonaGCavalloLItalian cross-sectional growth charts for height, weight and BMI (2 to 20 yr)J Endocrinol Invest2006295819310.1007/BF033441561:STN:280:DC%2BD28rjt1Oiug%3D%3D16957405
– reference: van EsterikJCVerharenHWHodemaekersHMGremmerERNagarajahBKamstraJHCompound- and sex-specific effects on programming of energy and immune homeostasis in adult C57BL/6JxFVB mice after perinatal TCDD and PCB 153Toxicol Appl Pharmacol20152892627510.1016/j.taap.2015.09.0171:CAS:528:DC%2BC2MXhs1Cqu7vN26415833
– reference: Casals-CasasCDesvergneBEndocrine disruptors: from endocrine to metabolic disruptionAnnu Rev Physiol2011731356210.1146/annurev-physiol-012110-1422001:CAS:528:DC%2BC3MXktVKjtb8%3D21054169
– reference: Needham L, Patterson DG, VN H. Levels of TCDD in selected human populations and their relevance to human risk assessment. In: Gallo MA, editor. Cold Spring Harbor: Cold Spring Harbor Laboratory Press; 1991. 229–57 p.
– reference: ZhuBTGalloMABurgerCWJr.MeekerRJCaiMXXuSEffect of 2,3,7,8-tetrachlorodibenzo-p-dioxin administration and high-fat diet on the body weight and hepatic estrogen metabolism in female C3H/HeN miceToxicol Appl Pharmacol20082261071810.1016/j.taap.2007.08.0181:CAS:528:DC%2BD2sXhsVOls7bL17945325
– reference: di DomenicoASilanoVVivianoGZapponiGAccidental release of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at Seveso, Italy. II. TCDD distribution in the soil surface layerEcotoxicol Environ Saf1980429832010.1016/0147-6513(80)90032-97439100
– reference: SeefeldMDKeeseyREPetersonREBody weight regulation in rats treated with 2,3,7,8-tetrachlorodibenzo-p-dioxinToxicol Appl Pharmacol1984765263610.1016/0041-008X(84)90357-01:CAS:528:DyaL2MXlslCjsA%3D%3D6506077
– reference: RashidCSCarterLGHennigBPearsonKJPerinatal Polychlorinated Biphenyl 126 Exposure Alters Offspring Body CompositionJ Pediatr Biochem20133475310.1055/s-0036-1586427237412833670830
– reference: MimuraJFujii-KuriyamaYFunctional role of AhR in the expression of toxic effects by TCDDBiochim Biophys Acta20031619263810.1016/S0304-4165(02)00485-31:CAS:528:DC%2BD3sXovFGrtg%3D%3D12573486
– reference: LeijsMMKoppeJGVulsmaTOlieKvan AalderenWMCde VoogtPAlterations in the programming of energy metabolism in adolescents with background exposure to dioxins, dl-PCBs and PBDEsPLoS One201712e018400610.1371/journal.pone.01840061:CAS:528:DC%2BC1cXotVykt7c%3D288982415595283
– reference: WarnerMMocarelliPBrambillaPWesselinkASamuelsSSignoriniSDiabetes, metabolic syndrome, and obesity in relation to serum dioxin concentrations: the Seveso women’s health studyEnviron Health Perspect20131219061110.1289/ehp.12061131:CAS:528:DC%2BC2cXovFWnsbY%3D236745063734493
– reference: KirkleyAGSargisRMEnvironmental endocrine disruption of energy metabolism and cardiovascular riskCurr Diab Rep20141449410.1007/s11892-014-0494-01:CAS:528:DC%2BC2cXms1Cqtbw%3D247563434067479
– reference: AylwardLLHaysSMTemporal trends in human TCDD body burden: decreases over three decades and implications for exposure levelsJ Expo Anal Environ Epidemiol2002123192810.1038/sj.jea.75002331:CAS:528:DC%2BD38XnvVynsLc%3D12198580
– reference: PerloffDGrimCFlackJFrohlichEDHillMMcDonaldMHuman blood pressure determination by sphygmomanometryCirculation1993885 Pt 124607010.1161/01.CIR.88.5.24601:STN:280:DyaK2c%2Fjslerug%3D%3D8222141
– reference: Lim SS, Vos T, Flaxman AD, Danaei G, Shibuya K, Adair-Rohani H, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012;380:2224–60.
– reference: AlbertiKGEckelRHGrundySMZimmetPZCleemanJIDonatoKAHarmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of ObesityCirculation20091201640510.1161/CIRCULATIONAHA.109.1926441:CAS:528:DC%2BD1MXht1OrtrrK19805654
– reference: SatoSShirakawaHTomitaSOhsakiYHaketaKTooiOLow-dose dioxins alter gene expression related to cholesterol biosynthesis, lipogenesis, and glucose metabolism through the aryl hydrocarbon receptor-mediated pathway in mouse liverToxicol Appl Pharmacol200822910910.1016/j.taap.2007.12.0291:CAS:528:DC%2BD1cXlslWrtrc%3D18295293
– reference: EnanELiuPCMatsumuraF2,3,7,8-Tetrachlorodibenzo-p-dioxin causes reduction of glucose transporting activities in the plasma membranes of adipose tissue and pancreas from the guinea pigJ Biol Chem199226719785911:CAS:528:DyaK38XlsVGjsLs%3D1400292
– reference: KuritaHYoshiokaWNishimuraNKubotaNKadowakiTTohyamaCAryl hydrocarbon receptor-mediated effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on glucose-stimulated insulin secretion in miceJ Appl Toxicol2009296899410.1002/jat.14591:CAS:528:DC%2BD1MXhsVKgsrbO19623578
– reference: KopfPGHuweJKWalkerMKHypertension, cardiac hypertrophy, and impaired vascular relaxation induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin are associated with increased superoxideCardiovasc Toxicol200881819310.1007/s12012-008-9027-x1:CAS:528:DC%2BD1cXhsVyms7jL188500752648846
– reference: IszattNStigumHGovartsEMurinovaLPSchoetersGTrnovecTPerinatal exposure to dioxins and dioxin-like compounds and infant growth and body mass index at seven years: a pooled analysis of three European birth cohortsEnviron Int20169439940710.1016/j.envint.2016.04.0401:CAS:528:DC%2BC28XhtVWgurbF27311652
– reference: Wohlfahrt-VejeCAudouzeKBrunakSAntignacJPle BizecBJuulAPolychlorinated dibenzo-p-dioxins, furans, and biphenyls (PCDDs/PCDFs and PCBs) in breast milk and early childhood growth and IGF1Reproduction2014147391910.1530/REP-13-04221:CAS:528:DC%2BC2cXms1equr8%3D24586095
– reference: HeindelJJBlumbergBCaveMMachtingerRMantovaniAMendezMAMetabolism disrupting chemicals and metabolic disordersReprod Toxicol20176833310.1016/j.reprotox.2016.10.0011:CAS:528:DC%2BC28XhvVWmtLvI27760374
– reference: EnanEMatsumuraF2,3,7,8-Tetrachlorodibenzo-P-dioxin induced alterations in protein phosphorylation in guinea pig adipose tissueJ Biochem Toxicol19938899910.1002/jbt.25700802061:CAS:528:DyaK3sXlvFOlsr0%3D8394938
– reference: ColeTJLobsteinTExtended international (IOTF) body mass index cut-offs for thinness, overweight and obesityPediatr Obes201272849410.1111/j.2047-6310.2012.00064.x1:STN:280:DC%2BC38jjt1ymsA%3D%3D22715120
– reference: TaiPTNishijoMNghiTNNakagawaHVan LuongHAnhTHEffects of perinatal dioxin exposure on development of children during the first 3 years of lifeJ Pediatr201617515966.e210.1016/j.jpeds.2016.04.0641:CAS:528:DC%2BC28XnvFejsbY%3D27189679
– reference: EskenaziBMocarelliPWarnerMCheeWYGerthouxPMSamuelsSMaternal serum dioxin levels and birth outcomes in women of Seveso, ItalyEnviron Health Perspect20031119475310.1289/ehp.60801:CAS:528:DC%2BD3sXltlKitLs%3D127824971241530
– reference: EskenaziBMocarelliPWarnerMNeedhamLPattersonDGSamuelsSRelationship of serum TCDD concentrations and age at exposure of female residents of Seveso, ItalyEnviron Health Perspect200411222710.1289/ehp.65731:CAS:528:DC%2BD2cXhtVSju7o%3D146989261241792
– reference: Ng M, Fleming T, Robinson M, Thomson B, Graetz N, Margono C, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;384:766–81.
– reference: MocarelliPPocchiariFNelsonNPreliminary report: 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure to humans--Seveso, ItalyMMWR Morb Mortal Wkly Rep1988377336
– reference: Stata Corp.Stata Statistical Software: Release 13.12013College StationStata Press
– reference: GBMC.Body-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continentsLancet20163887768610.1016/S0140-6736(16)30175-1
– reference: PattersonDGHamptonLLapezaCRBelserWTGreenVAlexanderLHigh-resolution gas chromatographic/high-resolution mass spectrometric analysis of human serum on a whole-weight and lipid basis for 2,3,7,8-tetrachlorodibenzo-p-dioxinAnal Chem1987592000510.1021/ac00142a0231:CAS:528:DyaL2sXktlCns7g%3D3631519
– reference: EskenaziBWarnerMBrambillaPSignoriniSAmesJMocarelliPThe Seveso accident: a look at 40years of health research and beyondEnviron Int2018121Pt 1718410.1016/j.envint.2018.08.0511:CAS:528:DC%2BC1cXhs1Gqs7fI301797666221983
– reference: DelvauxIVan CauwenbergheJDen HondESchoetersGGovartsENelenVPrenatal exposure to environmental contaminants and body composition at age 7-9 yearsEnviron Res2014132243210.1016/j.envres.2014.03.0191:CAS:528:DC%2BC2cXpvFWjtrg%3D24742724
– reference: WarnerMMocarelliPBrambillaPWesselinkAPattersonDGTurnerWESerum TCDD and TEQ concentrations among Seveso women, 20 years after the explosionJ Expo Sci Environ Epidemiol2014245889410.1038/jes.2013.701:CAS:528:DC%2BC3sXhs1yitbjL24149975
– reference: SuPHChenJYChenJWWangSLGrowth and thyroid function in children with in utero exposure to dioxin: a 5-year follow-up studyPediatr Res2010672051010.1203/PDR.0b013e3181c8f04b1:CAS:528:DC%2BC3cXktVKkug%3D%3D20091939
– reference: Zook D, Rappe C. Environmental sources, distribution, and fate. In: Schecter A, editor. Dioxins and Health. New York: Plenum Press; 1994. p. 79–113.
– reference: CookSAuingerPHuangTTGrowth curves for cardio-metabolic risk factors in children and adolescentsJ Pediatr2009155S6 e1526
– reference: PisaniPFaggianoFKroghVPalliDVineisPBerrinoFRelative validity and reproducibility of a food frequency dietary questionnaire for use in the Italian EPIC centresInt J Epidemiol199726Suppl 1S1526010.1093/ije/26.suppl_1.S1529126543
– reference: KimMJPellouxVGuyotETordjmanJBuiLCChevallierAInflammatory pathway genes belong to major targets of persistent organic pollutants in adipose cellsEnviron Health Perspect20121205081410.1289/ehp.11042821:CAS:528:DC%2BC38XmslCmt7s%3D222627113339464
– reference: LindenJLensuSTuomistoJPohjanvirtaRDioxins, the aryl hydrocarbon receptor and the central regulation of energy balanceFront Neuroendocrinol2010314527810.1016/j.yfrne.2010.07.0021:CAS:528:DC%2BC3cXhtleqt7jL20624415
– reference: HornungRWReedLDEstimation of average concentration in the presence of non-detectable valuesAppl Occup Environ Hyg19905485110.1080/1047322X.1990.10389587
– reference: World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO Consultation on Obesity. Geneva: World Health Organization; 1998.
– reference: KaurJA comprehensive review on metabolic syndromeCardiol Res Pract20142014943162247119543966331
– reference: CimafrancaMAHanlonPRJefcoateCRTCDD administration after the pro-adipogenic differentiation stimulus inhibits PPARgamma through a MEK-dependent process but less effectively suppresses adipogenesisToxicol Appl Pharmacol20041961566810.1016/j.taap.2003.12.0051:CAS:528:DC%2BD2cXisFyrtrY%3D15050417
– reference: BirnbaumLSTuomistoJNon-carcinogenic effects of TCDD in animalsFood Addit Contam2000172758810.1080/0265203002833511:CAS:528:DC%2BD3cXktl2qtbc%3D10912242
– reference: SugaiEYoshiokaWKakeyamaMOhsakoSTohyamaCIn utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin modulates dysregulation of the lipid metabolism in mouse offspring fed a high-calorie dietJ Appl Toxicol20143429630610.1002/jat.28811:CAS:528:DC%2BC3sXptVahsL0%3D23749557
– reference: JaegerCTischkauSARole of aryl hydrocarbon receptor in circadian clock disruption and metabolic dysfunctionEnviron Health Insights2016101334110.4137/EHI.S38343275592984990151
– reference: DesaiMJellymanJKRossMGEpigenomics, gestational programming and risk of metabolic syndromeInt J Obes20153963310.1038/ijo.2015.131:CAS:528:DC%2BC2MXjt1Sns7o%3D
– reference: La MerrillMBastonDSDenisonMSBirnbaumLSPompDThreadgillDWMouse breast cancer model-dependent changes in metabolic syndrome-associated phenotypes caused by maternal dioxin exposure and dietary fatAm J Physiol Endocrinol Metab2009296E2031010.1152/ajpendo.90368.20081:CAS:528:DC%2BD1MXpsFCnug%3D%3D18840765
– reference: BaroukiRAggerbeckMAggerbeckLCoumoulXThe aryl hydrocarbon receptor systemDrug Metabol Drug Interact2012273810.1515/dmdi-2011-00351:CAS:528:DC%2BC2cXmtV2mtbY%3D22718620
– reference: WesselinkAWarnerMSamuelsSParigiABrambillaPMocarelliPMaternal dioxin exposure and pregnancy outcomes over 30 years of follow-up in SevesoEnviron Int201463143810.1016/j.envint.2013.11.0051:CAS:528:DC%2BC3sXitVWmur3L24291766
– reference: EskenaziBMocarelliPWarnerMSamuelsSVercelliniPOliveDSeveso Women’s Health Study: a study of the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on reproductive healthChemosphere20004012475310.1016/S0045-6535(99)00376-81:CAS:528:DC%2BD3cXhslSmtbo%3D10739069
– reference: Patterson DG, Turner WE. Method 28: Measurement of PCDDs, PCDFs, and Coplanar PCBs in Serum by HRGC/ID-HRMS. Atanta: National Center for Enviromental Health, CDC; 2005.
– reference: AkinsJRWaldrepKBernertJTJr.The estimation of total serum lipids by a completely enzymatic ‘summation’ methodClin Chim Acta19891842192610.1016/0009-8981(89)90054-51:CAS:528:DyaL1MXmt1yhtr4%3D2611996
– reference: ZimmetPAlbertiKGKaufmanFTajimaNSilinkMArslanianSThe metabolic syndrome in children and adolescents - an IDF consensus reportPediatr Diabetes2007829930610.1111/j.1399-5448.2007.00271.x17850473
– reference: AragonACGoensMBCarbettEWalkerMKPerinatal 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure sensitizes offspring to angiotensin II-induced hypertensionCardiovasc Toxicol200881455410.1007/s12012-008-9023-11:CAS:528:DC%2BD1cXht1ems7fI186709073613254
– reference: PirkleJLWolfeWHPattersonDGNeedhamLLMichalekJEMinerJCEstimates of the half-life of 2,3,7,8-tetrachlorodibenzo-p-dioxin in Vietnam Veterans of Operation Ranch HandJ Toxicol Environ Health1989271657110.1080/152873989095312881:CAS:528:DyaL1MXkslaksL0%3D2733058
– ident: 306_CR9
  doi: 10.1007/978-1-4899-1462-0_3
– volume: 120
  start-page: 508
  year: 2012
  ident: 306_CR56
  publication-title: Environ Health Perspect
  doi: 10.1289/ehp.1104282
– volume: 63
  start-page: 143
  year: 2014
  ident: 306_CR60
  publication-title: Environ Int
  doi: 10.1016/j.envint.2013.11.005
– volume: 14
  start-page: 494
  year: 2014
  ident: 306_CR13
  publication-title: Curr Diab Rep
  doi: 10.1007/s11892-014-0494-0
– volume: 17
  start-page: 275
  year: 2000
  ident: 306_CR10
  publication-title: Food Addit Contam
  doi: 10.1080/026520300283351
– volume: 21
  start-page: 1017
  year: 1990
  ident: 306_CR12
  publication-title: Chemosphere
  doi: 10.1016/0045-6535(90)90124-C
– volume: 31
  start-page: 452
  year: 2010
  ident: 306_CR53
  publication-title: Front Neuroendocrinol
  doi: 10.1016/j.yfrne.2010.07.002
– volume: 40
  start-page: 1247
  year: 2000
  ident: 306_CR35
  publication-title: Chemosphere
  doi: 10.1016/S0045-6535(99)00376-8
– volume: 267
  start-page: 19785
  year: 1992
  ident: 306_CR14
  publication-title: J Biol Chem
  doi: 10.1016/S0021-9258(19)88622-2
– volume: 112
  start-page: 22
  year: 2004
  ident: 306_CR40
  publication-title: Environ Health Perspect
  doi: 10.1289/ehp.6573
– volume: 88
  start-page: 2460
  issue: 5 Pt 1
  year: 1993
  ident: 306_CR38
  publication-title: Circulation
  doi: 10.1161/01.CIR.88.5.2460
– volume: 155
  start-page: S6 e15
  year: 2009
  ident: 306_CR47
  publication-title: J Pediatr
– volume: 1619
  start-page: 263
  year: 2003
  ident: 306_CR51
  publication-title: Biochim Biophys Acta
  doi: 10.1016/S0304-4165(02)00485-3
– volume: 147
  start-page: 391
  year: 2014
  ident: 306_CR29
  publication-title: Reproduction
  doi: 10.1530/REP-13-0422
– volume: 39
  start-page: 633
  year: 2015
  ident: 306_CR8
  publication-title: Int J Obes
  doi: 10.1038/ijo.2015.13
– volume-title: Stata Statistical Software: Release 13.1
  year: 2013
  ident: 306_CR50
– volume: 12
  start-page: 319
  year: 2002
  ident: 306_CR58
  publication-title: J Expo Anal Environ Epidemiol
  doi: 10.1038/sj.jea.7500233
– volume: 73
  start-page: 135
  year: 2011
  ident: 306_CR7
  publication-title: Annu Rev Physiol
  doi: 10.1146/annurev-physiol-012110-142200
– volume: 132
  start-page: 24
  year: 2014
  ident: 306_CR28
  publication-title: Environ Res
  doi: 10.1016/j.envres.2014.03.019
– volume: 120
  start-page: 1640
  year: 2009
  ident: 306_CR4
  publication-title: Circulation
  doi: 10.1161/CIRCULATIONAHA.109.192644
– volume: 184
  start-page: 219
  year: 1989
  ident: 306_CR43
  publication-title: Clin Chim Acta
  doi: 10.1016/0009-8981(89)90054-5
– volume: 8
  start-page: 181
  year: 2008
  ident: 306_CR17
  publication-title: Cardiovasc Toxicol
  doi: 10.1007/s12012-008-9027-x
– volume: 121
  start-page: 71
  issue: Pt 1
  year: 2018
  ident: 306_CR36
  publication-title: Environ Int
  doi: 10.1016/j.envint.2018.08.051
– volume: 121
  start-page: 906
  year: 2013
  ident: 306_CR34
  publication-title: Environ Health Perspect
  doi: 10.1289/ehp.1206113
– volume: 29
  start-page: 581
  year: 2006
  ident: 306_CR46
  publication-title: J Endocrinol Invest
  doi: 10.1007/BF03344156
– volume: 94
  start-page: 399
  year: 2016
  ident: 306_CR26
  publication-title: Environ Int
  doi: 10.1016/j.envint.2016.04.040
– volume: 59
  start-page: 2000
  year: 1987
  ident: 306_CR39
  publication-title: Anal Chem
  doi: 10.1021/ac00142a023
– volume: 8
  start-page: 145
  year: 2008
  ident: 306_CR20
  publication-title: Cardiovasc Toxicol
  doi: 10.1007/s12012-008-9023-1
– volume: 2014
  start-page: 943162
  year: 2014
  ident: 306_CR5
  publication-title: Cardiol Res Pract
– volume: 27
  start-page: 3
  year: 2012
  ident: 306_CR52
  publication-title: Drug Metabol Drug Interact
  doi: 10.1515/dmdi-2011-0035
– ident: 306_CR33
– volume: 229
  start-page: 10
  year: 2008
  ident: 306_CR55
  publication-title: Toxicol Appl Pharmacol
  doi: 10.1016/j.taap.2007.12.029
– volume: 196
  start-page: 156
  year: 2004
  ident: 306_CR57
  publication-title: Toxicol Appl Pharmacol
  doi: 10.1016/j.taap.2003.12.005
– ident: 306_CR3
  doi: 10.1016/S0140-6736(12)61766-8
– volume: 34
  start-page: 296
  year: 2014
  ident: 306_CR21
  publication-title: J Appl Toxicol
  doi: 10.1002/jat.2881
– volume: 296
  start-page: E203
  year: 2009
  ident: 306_CR24
  publication-title: Am J Physiol Endocrinol Metab
  doi: 10.1152/ajpendo.90368.2008
– volume: 8
  start-page: 299
  year: 2007
  ident: 306_CR48
  publication-title: Pediatr Diabetes
  doi: 10.1111/j.1399-5448.2007.00271.x
– volume: 10
  start-page: 133
  year: 2016
  ident: 306_CR54
  publication-title: Environ Health Insights
  doi: 10.4137/EHI.S38343
– volume: 388
  start-page: 776
  year: 2016
  ident: 306_CR2
  publication-title: Lancet
  doi: 10.1016/S0140-6736(16)30175-1
– volume: 226
  start-page: 107
  year: 2008
  ident: 306_CR19
  publication-title: Toxicol Appl Pharmacol
  doi: 10.1016/j.taap.2007.08.018
– volume: 68
  start-page: 3
  year: 2017
  ident: 306_CR6
  publication-title: Reprod Toxicol
  doi: 10.1016/j.reprotox.2016.10.001
– volume: 76
  start-page: 526
  year: 1984
  ident: 306_CR18
  publication-title: Toxicol Appl Pharmacol
  doi: 10.1016/0041-008X(84)90357-0
– volume: 289
  start-page: 262
  year: 2015
  ident: 306_CR22
  publication-title: Toxicol Appl Pharmacol
  doi: 10.1016/j.taap.2015.09.017
– volume: 12
  start-page: e0184006
  year: 2017
  ident: 306_CR25
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0184006
– volume: 67
  start-page: 205
  year: 2010
  ident: 306_CR30
  publication-title: Pediatr Res
  doi: 10.1203/PDR.0b013e3181c8f04b
– volume: 27
  start-page: 165
  year: 1989
  ident: 306_CR11
  publication-title: J Toxicol Environ Health
  doi: 10.1080/15287398909531288
– volume: 8
  start-page: 89
  year: 1993
  ident: 306_CR15
  publication-title: J Biochem Toxicol
  doi: 10.1002/jbt.2570080206
– volume: 24
  start-page: 588
  year: 2014
  ident: 306_CR42
  publication-title: J Expo Sci Environ Epidemiol
  doi: 10.1038/jes.2013.70
– volume: 7
  start-page: 284
  year: 2012
  ident: 306_CR49
  publication-title: Pediatr Obes
  doi: 10.1111/j.2047-6310.2012.00064.x
– ident: 306_CR45
– volume: 4
  start-page: 298
  year: 1980
  ident: 306_CR31
  publication-title: Ecotoxicol Environ Saf
  doi: 10.1016/0147-6513(80)90032-9
– volume: 5
  start-page: 48
  year: 1990
  ident: 306_CR44
  publication-title: Appl Occup Environ Hyg
  doi: 10.1080/1047322X.1990.10389587
– volume: 37
  start-page: 733
  year: 1988
  ident: 306_CR32
  publication-title: MMWR Morb Mortal Wkly Rep
– volume: 29
  start-page: 689
  year: 2009
  ident: 306_CR16
  publication-title: J Appl Toxicol
  doi: 10.1002/jat.1459
– volume: 175
  start-page: 159
  year: 2016
  ident: 306_CR27
  publication-title: J Pediatr
  doi: 10.1016/j.jpeds.2016.04.064
– ident: 306_CR41
– volume: 26
  start-page: S152
  issue: Suppl 1
  year: 1997
  ident: 306_CR37
  publication-title: Int J Epidemiol
  doi: 10.1093/ije/26.suppl_1.S152
– volume: 3
  start-page: 47
  year: 2013
  ident: 306_CR23
  publication-title: J Pediatr Biochem
  doi: 10.1055/s-0036-1586427
– volume: 111
  start-page: 947
  year: 2003
  ident: 306_CR59
  publication-title: Environ Health Perspect
  doi: 10.1289/ehp.6080
– ident: 306_CR1
  doi: 10.1016/S0140-6736(14)60460-8
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Snippet Background/objectives In utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) may alter risk of obesity and...
In utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may alter risk of obesity and related metabolic disease...
Background/objectives In utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may alter risk of obesity and...
Background/objectivesIn utero exposure to endocrine-disrupting compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may alter risk of obesity and...
SourceID pubmedcentral
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pubmed
crossref
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SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 2233
SubjectTerms 692/163/2743
692/499
Adipose tissue
Adolescent
Adult
Blood levels
Blood pressure
Blood Pressure - physiology
Body fat
Body mass index
Body size
Body Size - physiology
Child
Child, Preschool
Children
Cohort Studies
Dioxins
Disruption
Endocrine disruptors
Epidemiology
Explosions
Exposure
Female
Health Promotion and Disease Prevention
Health risk assessment
Health risks
Humans
Internal Medicine
Intrauterine exposure
Italy
Lipids
Male
Maternal Exposure - statistics & numerical data
Medicine
Medicine & Public Health
Metabolic Diseases
Metabolic disorders
Metabolic syndrome
Metabolic Syndrome - epidemiology
Metabolism
Obesity
Offspring
Polychlorinated Dibenzodioxins - analysis
Polychlorinated Dibenzodioxins - toxicity
Pregnancy
Prenatal experience
Prenatal exposure
Public Health
Risk
TCDD
Young Adult
Title In utero dioxin exposure and cardiometabolic risk in the Seveso Second Generation Study
URI https://link.springer.com/article/10.1038/s41366-018-0306-8
https://www.ncbi.nlm.nih.gov/pubmed/30659254
https://www.proquest.com/docview/2312251812
https://www.proquest.com/docview/2179366842
https://pubmed.ncbi.nlm.nih.gov/PMC6639155
Volume 43
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