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Association of blood lead levels with onset of puberty in Russian boys.

https://arctichealth.org/en/permalink/ahliterature156140
Source
Environ Health Perspect. 2008 Jul;116(7):976-80
Publication Type
Article
Date
Jul-2008
Author
Russ Hauser
Oleg Sergeyev
Susan Korrick
Mary M Lee
Boris Revich
Elena Gitin
Jane S Burns
Paige L Williams
Author Affiliation
Environmental and Occupational Medicine and Epidemiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA. rhauser@hohp.harvard.edu
Source
Environ Health Perspect. 2008 Jul;116(7):976-80
Date
Jul-2008
Language
English
Publication Type
Article
Keywords
Body Weights and Measures
Child
Cross-Sectional Studies
Humans
Lead - blood - toxicity
Logistic Models
Male
Puberty - drug effects
Russia - epidemiology
Socioeconomic Factors
Abstract
Epidemiologic studies suggest a temporal trend of earlier onset and longer duration of puberty, raising concerns regarding the potential impact of environmental factors on pubertal development. Lead exposure has been associated with delayed pubertal onset in girls; however, epidemiologic data in boys are limited.
We used multivariable logistic regression models to explore the cross-sectional association of blood lead levels with growth and pubertal onset based on physician-assessed testicular volume (TV) and pubertal staging in 489 boys 8-9 years of age from Chapaevsk, Russia. We used multivariable linear regression models to assess associations of blood lead levels with somatic growth at the study entry visit.
The median (25th-75th percentile) blood lead level was 3 microg/dL (2-5 microg/dL). Height, weight, body mass index, birth weight, and gestational age were predictive of the onset of puberty as assessed either by TV (> 3 mL), genitalia stage (G2), or both. Blood lead level was inversely associated with height (p or = 5 microg/dL had 43% reduced odds of having entered G2 compared with those with lower levels (odds ratio = 0.57; 95% confidence interval, 0.34-0.95, p = 0.03).
Relatively low environmental blood lead levels were associated with decreased growth and differences in pubertal onset in periadolescent Russian boys. Future analyses of this prospective cohort will address pubertal onset and progression in relation to lead and other environmental chemicals.
Notes
Cites: J Toxicol Environ Health A. 1998 May 22;54(2):77-999652546
Cites: Arch Environ Health. 1997 Sep-Oct;52(5):377-839546761
Cites: Vopr Pitan. 1998;(3):8-139752664
Cites: J Expo Anal Environ Epidemiol. 1993;3 Suppl 1:201-99857305
Cites: Environ Health. 2005;4(1):815918907
Cites: Endocrinol Metab Clin North Am. 2005 Sep;34(3):617-41, ix16085163
Cites: Mol Cell Endocrinol. 2006 Jul 25;254-255:22-516757105
Cites: Neurotoxicology. 2007 Mar;28(2):245-5116806481
Cites: J Pediatr. 1999 May;134(5):623-3010228299
Cites: Am J Epidemiol. 1999 Oct 1;150(7):747-5510512428
Cites: Eur J Clin Nutr. 2000 Mar;54(3):203-810713741
Cites: Arch Pediatr Adolesc Med. 2001 Sep;155(9):1022-811529804
Cites: Gig Sanit. 2001 Nov-Dec;(6):6-1111810913
Cites: J Adolesc Health. 2002 Mar;30(3):205-1211869928
Cites: Environ Health Perspect. 2002 Jun;110(6):559-6212055045
Cites: Horm Res. 2002;57 Suppl 2:19-3012065922
Cites: Environ Health Perspect. 2002 Sep;110(9):871-412204820
Cites: Pediatrics. 2002 Nov;110(5):911-912415029
Cites: Pediatrics. 2003 Apr;111(4 Pt 1):844-5012671122
Cites: N Engl J Med. 2003 Apr 17;348(16):1527-3612700372
Cites: J Pediatr Endocrinol Metab. 2003 Feb;16(2):169-7812713253
Cites: Environ Health Perspect. 2003 May;111(5):737-4112727603
Cites: Adv Data. 2003 Apr 17;(334):1-412743879
Cites: Arch Dis Child. 1970 Feb;45(239):13-235440182
Cites: Biol Reprod. 1985 Oct;33(3):722-83931714
Cites: Pediatrics. 1986 Mar;77(3):281-83951909
Cites: Environ Res. 1987 Apr;42(2):524-333106028
Cites: Biol Reprod. 1987 Dec;37(5):1135-83327539
Cites: Pediatrics. 1992 Aug;90(2 Pt 1):186-91641279
Cites: Toxicol Appl Pharmacol. 1995 Apr;131(2):297-3087716770
Cites: Toxicol Appl Pharmacol. 1996 Feb;136(2):361-718619245
Cites: Acta Paediatr. 1996 Jul;85(7):785-88819542
Cites: Pediatrics. 1997 Apr;99(4):505-129093289
Cites: Am J Clin Nutr. 1997 Apr;65(4 Suppl):1220S-1228S; discussion 1229S-1231S9094926
Cites: J Toxicol Environ Health A. 1998 May 22;54(2):101-209652547
PubMed ID
18629324 View in PubMed
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The association of peripubertal serum concentrations of organochlorine chemicals and blood lead with growth and pubertal development in a longitudinal cohort of boys: a review of published results from the Russian Children's Study.

https://arctichealth.org/en/permalink/ahliterature283496
Source
Rev Environ Health. 2017 Mar 01;32(1-2):83-92
Publication Type
Article
Date
Mar-01-2017
Author
Oleg Sergeyev
Jane S Burns
Paige L Williams
Susan A Korrick
Mary M Lee
Boris Revich
Russ Hauser
Source
Rev Environ Health. 2017 Mar 01;32(1-2):83-92
Date
Mar-01-2017
Language
English
Publication Type
Article
Keywords
Adolescent
Child
Dioxins and Dioxin-like Compounds - blood
Endocrine Disruptors - blood
Environmental Exposure
Environmental pollutants - blood
Furans - blood
Humans
Hydrocarbons, Chlorinated - blood
Lead - blood
Longitudinal Studies
Male
Prospective Studies
Russia
Sexual Maturation - drug effects
Young Adult
Abstract
Organochlorine chemicals and lead are environmental exposures that have endocrine disrupting properties (EDCs) which interfere with many aspects of hormone action. Childhood and adolescence are windows of susceptibility for adverse health effects of EDCs. Our ongoing study, the Russian Children's Study (RCS), is one of the few longitudinal studies investigating the impact of EDCs on growth and puberty in boys. It is conducted in the historically contaminated city of Chapaevsk, in the Samara region. The study focuses on evaluating the associations of persistent organochlorine chemicals and lead with growth and pubertal timing. At enrollment in 2003-2005, we collected blood from 516 boys at ages 8-9 years to measure dioxins, furans, polychlorinated biphenyls (PCBs), chlorinated pesticides and lead. At enrollment and at annual visits through the ages of 18-19 years, a physician performed physical examinations that included pubertal staging and testicular volume measurements. We review the history of Chapaevsk as a research site and summarize published RCS data on the association of peripubertal serum concentrations of organochlorines and blood lead levels with growth, pubertal onset and sexual maturity. Overall, we found that persistent organochlorines and lead negatively affected growth during puberty. Our results also suggest that total toxic equivalents (TEQs), dioxin-like compounds, organochlorine pesticides and lead may delay, while nondioxin-like-PCBs may advance, the timing of male puberty. These findings promoted remediation programs in Chapaevsk, with improvement in health indicators, resulting in Chapaevsk being designated a member of the World Health Organization (WHO) network "Healthy Cities" in 2015.
PubMed ID
28231067 View in PubMed
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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
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Blood lead levels and delayed onset of puberty in a longitudinal study of Russian boys.

https://arctichealth.org/en/permalink/ahliterature144434
Source
Pediatrics. 2010 May;125(5):e1088-96
Publication Type
Article
Date
May-2010
Author
Paige L Williams
Oleg Sergeyev
Mary M Lee
Susan A Korrick
Jane S Burns
Olivier Humblet
Julie DelPrato
Boris Revich
Russ Hauser
Author Affiliation
Harvard School of Public Health, Department of Biostatistics, Boston, MA 02115, USA. paige@hsph.harvard.edu
Source
Pediatrics. 2010 May;125(5):e1088-96
Date
May-2010
Language
English
Publication Type
Article
Keywords
Adolescent
Body Size
Child
Cohort Studies
Food Habits
Health Surveys
Humans
Lead - blood
Lead Poisoning - blood - prevention & control
Longitudinal Studies
Male
Proportional Hazards Models
Puberty, Delayed - blood - chemically induced
Russia
Sexual Maturation - drug effects
Socioeconomic Factors
Abstract
We evaluated the association of blood lead levels (BLLs) with pubertal onset in a longitudinal cohort of Russian boys.
A total of 489 Russian boys were enrolled in 2003-2005, at 8 to 9 years of age, and were monitored annually through May 2008. Cox proportional-hazards models were used to evaluate the association of BLLs at enrollment with time to pubertal onset during follow-up monitoring.
A total of 481 boys had BLLs, with a median of 3 microg/dL and 28% with values of > or =5 microg/dL. The proportion of pubertal boys increased with age, from 12% at age 8 to 83% at age 12 for testicular volume of >3 mL, from 22% to 90% for genitalia stage 2 or higher, and from 4% to 40% for pubic hair stage 2 or higher. After adjustment for potential confounders including BMI and height, boys with high BLLs (> or =5 microg/dL) had 24% to 31% reduced risk of pubertal onset, on the basis of testicular volume of >3 mL (hazard ratio [HR]: 0.73 [95% confidence interval [CI]: 0.55-0.97]; P = .03), genitalia staging (HR: 0.76 [95% CI: 0.59-0.98]; P = .04), and pubic hair staging (HR: 0.69 [95% CI: 0.44-1.07]; P = .10), compared with those with lower BLLs. Pubertal onset occurred 6 to 8 months later, on average, for boys with high BLLs, compared with those with BLLs of
Notes
Cites: Fertil Steril. 2008 Feb;89(2):281-30018275883
Cites: Pediatrics. 2008 Feb;121 Suppl 3:S172-9118245511
Cites: Environ Res. 2008 Jul;107(3):393-40018479682
Cites: Environ Health Perspect. 2008 Jul;116(7):976-8018629324
Cites: Curr Opin Endocrinol Diabetes Obes. 2009 Feb;16(1):25-3019115521
Cites: Pediatrics. 2009 Mar;123(3):e376-8519254973
Cites: Dev Psychol. 2004 Nov;40(6):1188-9815535766
Cites: J Pediatr. 1999 May;134(5):623-3010228299
Cites: Med Sci Monit. 2009 Jun;15(6):RA137-4519478717
Cites: Pediatrics. 2005 Feb;115(2):e127-3415653789
Cites: Sci Total Environ. 2000 Jul 10;256(2-3):95-10110902837
Cites: Am J Epidemiol. 2000 Sep 1;152(5):446-5210981459
Cites: Arch Pediatr Adolesc Med. 2001 Sep;155(9):1022-811529804
Cites: J Adolesc Health. 2002 Mar;30(3):205-1211869928
Cites: Environ Health Perspect. 2002 Jun;110(6):559-6212055045
Cites: Environ Health Perspect. 2002 Sep;110(9):871-412204820
Cites: Pediatrics. 2003 Apr;111(4 Pt 1):844-5012671122
Cites: N Engl J Med. 2003 Apr 17;348(16):1527-3612700372
Cites: J Pediatr Endocrinol Metab. 2003 Feb;16(2):169-7812713253
Cites: Environ Health Perspect. 2003 May;111(5):737-4112727603
Cites: J Pediatr. 2003 Jun;142(6):643-612838192
Cites: Arch Dis Child. 1970 Feb;45(239):13-235440182
Cites: N Engl J Med. 1982 Apr 29;306(17):1033-57062994
Cites: Pediatrics. 1986 Mar;77(3):281-83951909
Cites: Pediatrics. 1991 Nov;88(5):886-921945627
Cites: Toxicol Appl Pharmacol. 1995 Apr;131(2):297-3087716770
Cites: Environ Health Perspect. 1995 Oct;103(10):952-78529592
Cites: Toxicol Appl Pharmacol. 1996 Feb;136(2):361-718619245
Cites: Pediatrics. 1997 Apr;99(4):505-129093289
Cites: Prev Med. 1997 Nov-Dec;26(6):808-169388792
Cites: J Toxicol Environ Health A. 1998 May 22;54(2):77-999652546
Cites: J Toxicol Environ Health A. 1998 May 22;54(2):101-209652547
Cites: Vopr Pitan. 1998;(3):8-139752664
Cites: J Adolesc. 1999 Feb;22(1):157-7110066339
Cites: Environ Health. 2005;4(1):815918907
Cites: Mol Cell Endocrinol. 2006 Jul 25;254-255:172-816806671
Cites: Neurotoxicology. 2007 Mar;28(2):245-5116806481
Cites: Bull World Health Organ. 2007 Sep;85(9):660-718026621
Cites: Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):168-7518226071
Cites: Environ Health Perspect. 2008 Feb;116(2):243-818288325
PubMed ID
20368318 View in PubMed
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Blood lead levels and serum insulin-like growth factor 1 concentrations in peripubertal boys.

https://arctichealth.org/en/permalink/ahliterature114274
Source
Environ Health Perspect. 2013 Jul;121(7):854-8
Publication Type
Article
Date
Jul-2013
Author
Abby F Fleisch
Jane S Burns
Paige L Williams
Mary M Lee
Oleg Sergeyev
Susan A Korrick
Russ Hauser
Author Affiliation
Department of Endocrinology, Children's Hospital Boston, Boston, Massachusetts, USA.
Source
Environ Health Perspect. 2013 Jul;121(7):854-8
Date
Jul-2013
Language
English
Publication Type
Article
Keywords
Child
Cohort Studies
Dose-Response Relationship, Drug
Environmental Exposure
Environmental pollutants - blood
Humans
Insulin-Like Growth Factor I - metabolism
Lead - blood
Linear Models
Luminescence
Luminescent Measurements
Male
Russia
Spectrophotometry, Atomic
Abstract
Childhood lead exposure has been associated with growth delay. However, the association between blood lead levels (BLLs) and insulin-like growth factor 1 (IGF-1) has not been characterized in a large cohort with low-level lead exposure.
We recruited 394 boys 8-9 years of age from an industrial Russian town in 2003-2005 and followed them annually thereafter. We used linear regression models to estimate the association of baseline BLLs with serum IGF-1 concentration at two follow-up visits (ages 10-11 and 12-13 years), adjusting for demographic and socioeconomic covariates.
At study entry, median BLL was 3 µg/dL (range,
Notes
Cites: Life Sci. 1984 Oct 22;35(17):1747-546090848
Cites: Pediatrics. 1986 Mar;77(3):281-83951909
Cites: Clin Endocrinol (Oxf). 1986 Jul;25(1):67-743791658
Cites: Toxicol Appl Pharmacol. 1989 Jul;99(3):474-862749734
Cites: Toxicol Appl Pharmacol. 1990 Oct;106(1):80-72123580
Cites: Toxicology. 1991;68(2):169-791654001
Cites: Pediatrics. 1991 Nov;88(5):886-921945627
Cites: Neuroendocrinology. 1991 Oct;54(4):420-31758585
Cites: Pediatrics. 1992 Aug;90(2 Pt 1):186-91641279
Cites: Pediatrics. 1992 Dec;90(6):855-611437425
Cites: Toxicology. 1993 Oct 25;83(1-3):101-148248939
Cites: Arch Environ Health. 2001 Sep-Oct;56(5):449-5511777027
Cites: Environ Health Perspect. 2012 Jul;120(7):a26822759595
Cites: N Engl J Med. 2003 Apr 17;348(16):1527-3612700372
Cites: Am J Pathol. 1967 May;50(5):815-476023504
Cites: J Biol Chem. 1983 Jul 25;258(14):8618-226408091
Cites: Biol Reprod. 1994 Apr;50(4):802-118199261
Cites: Endocrinology. 1996 Sep;137(9):3717-288756538
Cites: Toxicol Appl Pharmacol. 1996 Sep;140(1):164-728806882
Cites: Mol Endocrinol. 1997 Jul;11(8):1145-559212061
Cites: Prev Med. 1997 Nov-Dec;26(6):808-169388792
Cites: Arch Environ Health. 1997 Sep-Oct;52(5):377-839546761
Cites: Circulation. 2006 Sep 26;114(13):1388-9416982939
Cites: Ann Hum Biol. 2009 May-Jun;36(3):331-4119381987
Cites: Pediatrics. 2010 May;125(5):e1088-9620368318
Cites: J Clin Invest. 2010 Aug;120(8):2900-920628204
Cites: Sci Total Environ. 2010 Oct 1;408(21):4949-5420692685
Cites: Environ Health Perspect. 2012 Feb;120(2):303-821984531
Cites: J Pediatr. 2012 Jun;160(6):1044-922284921
Cites: Endocr Rev. 2012 Jun;33(3):378-45522419778
Cites: Infertility. 1978;1(1):33-5112265605
Cites: Reprod Toxicol. 1998 May-Jun;12(3):347-559628557
Cites: J Toxicol Environ Health A. 1998 May 22;54(2):77-999652546
Cites: J Toxicol Environ Health A. 1998 May 22;54(2):101-209652547
Cites: Vopr Pitan. 1998;(3):8-139752664
Cites: J Pediatr. 1999 May;134(5):623-3010228299
Cites: Environ Health. 2005;4(1):515831097
Cites: Environ Health Perspect. 2005 Jul;113(7):894-916002379
Cites: Neurotoxicol Teratol. 2005 Jul-Aug;27(4):655-6515919179
Cites: Reprod Toxicol. 2006 Jan;21(1):104-916153799
PubMed ID
23632160 View in PubMed
Less detail

Dioxin and polychlorinated biphenyl concentrations in mother's serum and the timing of pubertal onset in sons.

https://arctichealth.org/en/permalink/ahliterature130773
Source
Epidemiology. 2011 Nov;22(6):827-35
Publication Type
Article
Date
Nov-2011
Author
Olivier Humblet
Paige L Williams
Susan A Korrick
Oleg Sergeyev
Claude Emond
Linda S Birnbaum
Jane S Burns
Larisa Altshul
Donald G Patterson
Wayman E Turner
Mary M Lee
Boris Revich
Russ Hauser
Author Affiliation
Environmental and Occupational Medicine and Epidemiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA.
Source
Epidemiology. 2011 Nov;22(6):827-35
Date
Nov-2011
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Child
Dioxins - adverse effects - blood
Female
Gestational Age
Humans
Lead - adverse effects - blood
Male
Multivariate Analysis
Polychlorinated biphenyls - adverse effects - blood
Pregnancy
Prenatal Exposure Delayed Effects - blood
Proportional Hazards Models
Prospective Studies
Puberty - drug effects
Russia - epidemiology
Young Adult
Abstract
Animal studies have demonstrated that timing of pubertal onset can be altered by prenatal exposure to dioxins or polychlorinated biphenyls (PCBs), but studies of human populations have been quite limited.
We assessed the association between maternal serum concentrations of dioxins and PCBs and the sons' age of pubertal onset in a prospective cohort of 489 mother-son pairs from Chapaevsk, Russia, a town contaminated with these chemicals during past industrial activity. The boys were recruited at ages 8 to 9 years, and 4 years of annual follow-up data were included in the analysis. Serum samples were collected at enrollment from both mothers and sons for measurement of dioxin and PCB concentrations using high-resolution mass spectrometry. The sons' pubertal onset--defined as pubertal stage 2 or higher for genitalia (G) or pubic hair (P), or testicular volume >3 mL--was assessed annually by the same physician.
In multivariate Cox models, elevated maternal serum PCBs were associated with earlier pubertal onset defined by stage G2 or higher (4th quartile hazard ratio = 1.7 [95% confidence interval = 1.1- 2.5]), but not for stage P2 or higher or for testicular volume >3 mL. Maternal serum concentrations of dioxin toxic equivalents were not consistently associated with the sons' pubertal onset, although a dose-related delay in pubertal onset (only for G2 or higher) was seen among boys who breast-fed for 6 months or more.
Maternal PCB serum concentrations measured 8 or 9 years after sons' births--which may reflect sons' prenatal and early-life exposures--were associated with acceleration in some, but not all, measures of pubertal onset.
Notes
Cites: Horm Res. 2002;57 Suppl 2:19-3012065922
Cites: J Expo Sci Environ Epidemiol. 2011 May-Jun;21(3):224-3320197795
Cites: Pediatrics. 2011 Jan;127(1):e59-6821187307
Cites: Epidemiology. 2004 Sep;15(5):615-2515308962
Cites: Environ Health Perspect. 2011 Sep;119(9):1339-4421527364
Cites: Environ Health Perspect. 2011 May;119(5):713-821262597
Cites: J Pediatr. 2000 Apr;136(4):490-610753247
Cites: J Vet Med Sci. 2001 Jan;63(1):5-911217063
Cites: Chemosphere. 2001 May-Jun;43(4-7):951-6611372889
Cites: Eur J Endocrinol. 2002 Mar;146(3):357-6311888842
Cites: J Pediatr Endocrinol Metab. 2003 Feb;16(2):169-7812713253
Cites: Toxicol Sci. 2003 Jul;74(1):182-9112730615
Cites: Arch Dis Child. 1970 Feb;45(239):13-235440182
Cites: Arch Dis Child. 1976 Mar;51(3):170-9952550
Cites: Biol Reprod. 1977 Sep;17(2):298-303889997
Cites: Anal Chem. 1987 Aug 1;59(15):2000-53631519
Cites: Arch Environ Contam Toxicol. 1989 Jul-Aug;18(4):495-5002505694
Cites: Arch Environ Contam Toxicol. 1993 May;24(4):504-128507107
Cites: Toxicol Appl Pharmacol. 1995 Mar;131(1):108-187878665
Cites: Toxicol Appl Pharmacol. 1996 Jan;136(1):112-78560463
Cites: Environ Health Perspect. 1997 Jan;105(1):13-49074863
Cites: Prev Med. 1997 Nov-Dec;26(6):808-169388792
Cites: Vopr Pitan. 1998;(3):8-139752664
Cites: Toxicol Ind Health. 1999 Jan-Mar;15(1-2):65-7910188192
Cites: New Dir Child Adolesc Dev. 2004 Winter;(106):23-3415707160
Cites: Environ Health. 2005;4(1):815918907
Cites: Mol Cell Endocrinol. 2006 Jul 25;254-255:154-6216765510
Cites: Toxicol Sci. 2006 Oct;93(2):223-4116829543
Cites: Toxicol Sci. 2007 Sep;99(1):224-3317545211
Cites: Rev Endocr Metab Disord. 2007 Jun;8(2):143-5917674209
Cites: Bull World Health Organ. 2007 Sep;85(9):660-718026621
Cites: Environ Health Perspect. 2008 Jan;116(1):70-718197302
Cites: Environ Sci Technol. 2009 Feb 15;43(4):1211-819320182
Cites: Environ Health Perspect. 2009 Mar;117(3):417-2519337517
Cites: Environ Health Perspect. 2009 Oct;117(10):1593-920019911
Cites: Pediatrics. 2010 May;125(5):e1088-9620368318
Cites: Clin Endocrinol (Oxf). 2010 Jun;72(6):731-719912242
Cites: Environ Sci Technol. 2010 Jul 15;44(14):5633-4020578718
PubMed ID
21968773 View in PubMed
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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
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A Longitudinal Study of Peripubertal Serum Organochlorine Concentrations and Semen Parameters in Young Men: The Russian Children's Study.

https://arctichealth.org/en/permalink/ahliterature286153
Source
Environ Health Perspect. 2017 Mar;125(3):460-466
Publication Type
Article
Date
Mar-2017
Author
Lidia Mínguez-Alarcón
Oleg Sergeyev
Jane S Burns
Paige L Williams
Mary M Lee
Susan A Korrick
Luidmila Smigulina
Boris Revich
Russ Hauser
Source
Environ Health Perspect. 2017 Mar;125(3):460-466
Date
Mar-2017
Language
English
Publication Type
Article
Keywords
Adolescent
Environmental Exposure - statistics & numerical data
Environmental pollutants - blood
Humans
Hydrocarbons, Chlorinated - blood
Longitudinal Studies
Male
Russia - epidemiology
Semen - physiology
Young Adult
Abstract
Exposures to endocrine-disrupting chemicals during critical phases of testicular development may be related to poorer semen parameters. However, few studies have assessed the association between childhood organochlorine (OC) exposure and adult semen parameters.
We examined whether peripubertal serum OC concentrations are associated with semen parameters among young Russian men.
From 2003 through 2005, 516 boys were enrolled at age 8-9 years and followed for up to 10 years. Serum OCs were measured in the enrollment samples using high-resolution mass spectrometry. At 18-19 years, 133 young men provided 1 or 2 semen samples (256 samples) collected approximately 1 week apart, which were analyzed for volume, sperm concentration, and motility. Unadjusted and adjusted linear mixed models were used to examine the associations of quartiles of lipid-standardized concentrations of dioxins [2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), polychlorinated dibenzo-p-dioxins (PCDDs)], furans, polychlorinated biphenyls (PCBs), and corresponding toxic equivalents (TEQs) with semen parameters.
The median (range) for TCDD was 2.9 (0.4-12.1) pg/g lipid and PCDD TEQ was 8.7 (1.0-36.0) pg TEQ/g lipid. Higher quartiles of TCDD and PCDD TEQs were associated with lower sperm concentration, total sperm count, and total motile sperm count (p-trends = 0.05). The highest quartile of peripubertal serum TCDD concentrations was associated with a decrease (95% CI) of 40% (18, 66%), 29% (3, 64%), and 30% (2, 70%) in sperm concentration, total sperm count, and total motile sperm count, respectively, compared with the lowest quartile. Similar associations were observed for serum PCDD TEQs with semen parameters. Serum PCBs, furans, and total TEQs were not associated with semen parameters.
Higher peripubertal serum TCDD concentrations and PCDD TEQs were associated with poorer semen parameters. Citation: M?nguez-Alarc?n L, Sergeyev O, Burns JS, Williams PL, Lee MM, Korrick SA, Smigulina L, Revich B, Hauser R. 2017. A longitudinal study of peripubertal serum organochlorine concentrations and semen parameters in young men: the Russian Children's Study. Environ Health Perspect 125:460-466; http://dx.doi.org/10.1289/EHP25.
Notes
Cites: Toxicol Appl Pharmacol. 1998 Jun;150(2):383-929653070
Cites: Arch Environ Contam Toxicol. 1989 Jul-Aug;18(4):495-5002505694
Cites: Environ Health Perspect. 2011 Sep;119(9):1339-4421527364
Cites: Epidemiology. 2009 Jul;20(4):488-9519525685
Cites: Environ Health Perspect. 2008 Jan;116(1):70-718197302
Cites: Best Pract Res Clin Endocrinol Metab. 2006 Mar;20(1):91-11016522522
Cites: Chemosphere. 2008 Oct;73(6):999-100418707752
Cites: Environ Health Perspect. 2003 Apr;111(4):414-2012676592
Cites: Environ Health Perspect. 2009 Oct;117(10 ):1593-920019911
Cites: Anal Chem. 1987 Aug 1;59(15):2000-53631519
Cites: Chemosphere. 2005 Aug;60(7):898-90615992596
Cites: Syst Biol Reprod Med. 2010 Apr;56(2):122-3120377311
Cites: Endocrinology. 2003 Mar;144(3):767-7612586752
Cites: BMJ. 1992 Sep 12;305(6854):609-131393072
Cites: J Endocrinol Invest. 2015 Jul;38(7):745-5225770454
Cites: Environ Health Perspect. 2000 Oct;108(10):961-611049816
Cites: Pediatrics. 2011 Jan;127(1):e59-6821187307
Cites: Chemosphere. 2005 Mar;58(9):1185-20115667840
Cites: Environ Health Perspect. 2011 May;119(5):713-821262597
Cites: Epidemiology. 2006 Jul;17(4):450-816755259
Cites: Pediatrics. 2010 May;125(5):e1088-9620368318
Cites: Hum Reprod. 2001 May;16(5):1012-911331653
Cites: Anal Chem. 2004 Apr 1;76(7):1921-715053652
Cites: Andrologia. 2013 Aug;45(4):225-3122762285
Cites: Horm Res. 2002;57 Suppl 2:2-1412065920
Cites: J Pediatr. 1999 May;134(5):579-8310228293
Cites: Environ Health Perspect. 2008 Jul;116(7):976-8018629324
Cites: Toxicol Sci. 2006 Oct;93(2):223-4116829543
Cites: Drug Chem Toxicol. 2011 Oct;34(4):347-5621714773
Cites: J Biomed Biotechnol. 2010;2010:null20862379
Cites: Toxicol Appl Pharmacol. 1998 Jun;150(2):427-429653074
Cites: Chemosphere. 2008 Aug;73(1 Suppl):S261-7718511103
Cites: Andrologia. 2014 Sep;46(7):744-5223879235
Cites: J Chromatogr B Analyt Technol Biomed Life Sci. 2003 Aug 25;794(1):137-4812888206
Cites: Hum Reprod. 2002 Aug;17(8):2199-20812151459
Cites: Reproduction. 2003 Jun;125(6):769-8412773099
Cites: J Toxicol Environ Health A. 2001 May 11;63(1):1-1811346131
Cites: Environ Health Perspect. 2016 Nov;124(11):1801-180727187981
Cites: Reprod Toxicol. 2009 Dec;28(4):495-50219703549
PubMed ID
27713107 View in PubMed
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Low dietary nutrient intakes and respiratory health in adolescents.

https://arctichealth.org/en/permalink/ahliterature163804
Source
Chest. 2007 Jul;132(1):238-45
Publication Type
Article
Date
Jul-2007
Author
Jane S Burns
Douglas W Dockery
Lucas M Neas
Joel Schwartz
Brent A Coull
Mark Raizenne
Frank E Speizer
Author Affiliation
Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA. jburns@hsph.harvard.edu
Source
Chest. 2007 Jul;132(1):238-45
Date
Jul-2007
Language
English
Publication Type
Article
Keywords
Adolescent
Antioxidants - physiology
Canada - ethnology
Diet Surveys
Fatty Acids, Omega-3 - physiology
Female
Food
Health Surveys
Humans
Linear Models
Logistic Models
Lung Diseases - epidemiology - ethnology - physiopathology
Male
Nutritional Status - physiology
Respiratory Physiological Phenomena
United States - ethnology
Vitamins - physiology
Abstract
Epidemiologic studies have indicated that a diet rich in fruit, antioxidants, and n-3 fatty acids may contribute to optimal respiratory health. We investigated whether low dietary nutrient intakes were associated with lower pulmonary function and higher reporting of respiratory symptoms in adolescents.
We examined the association of dietary factors (fruit, vegetables, vitamins C and E, beta-carotene, retinol, n-3 fatty acids) with respiratory health in a cohort of 2,112 twelfth-grade students in 13 communities in the United States and Canada during the 1998 to 1999 school year. We assessed the associations between dietary factors and pulmonary function with linear mixed models, and respiratory symptoms with logistic regression using a generalized estimating equation adjusted for individual and group-level covariates.
Low dietary fruit intake was associated with lower FEV(1) (- 1.3% of predicted; 95% confidence interval [CI], - 2.4 to - 0.2% of predicted), and increased odds of chronic bronchitic symptoms (odds ratio [OR], 1.36; 95% CI, 1.03 to 1.73) compared with higher intake. Low dietary n-3 fatty acids intake was associated with increased odds of chronic bronchitic symptoms (OR, 1.37; 95% confidence interval [CI], 1.05 to 1.81), wheeze (OR, 1.34; 95% CI, 1.06 to 1.69), and asthma (OR, 1.68; 95% CI, 1.18 to 2.39) compared with higher intake. Smokers with lower dietary vitamin C intake had higher ORs of respiratory symptoms compared with smokers who had higher intake.
Adolescents with the lowest dietary intakes of antioxidant and antiinflammatory micronutrients had lower pulmonary function and increased respiratory symptoms, especially among smokers, suggesting that adequate dietary intake may promote respiratory health and lessen the effects of oxidative stress.
PubMed ID
17475634 View in PubMed
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Peripubertal blood lead levels and growth among Russian boys.

https://arctichealth.org/en/permalink/ahliterature289798
Source
Environ Int. 2017 09; 106:53-59
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Date
09-2017
Author
Jane S Burns
Paige L Williams
Mary M Lee
Boris Revich
Oleg Sergeyev
Russ Hauser
Susan A Korrick
Author Affiliation
Environmental and Occupational Medicine and Epidemiology Program, Department of Environmental Health, Harvard T.H. Chan School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA. Electronic address: jburns@hsph.harvard.edu.
Source
Environ Int. 2017 09; 106:53-59
Date
09-2017
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Keywords
Adolescent
Body Height
Body mass index
Body Weight
Child
Cohort Studies
Environmental pollutants - blood
Humans
Lead - blood
Male
Puberty
Russia
Abstract
Childhood blood lead levels (BLL) have been associated with growth impairment.
We assessed associations of peripubertal BLL with adolescent growth and near adult height in a longitudinal cohort of Russian boys.
481 boys were enrolled at ages 8-9years and followed annually to age 18. At enrollment, BLL was measured, and height, weight, and pubertal staging were obtained annually during 10years of follow-up. Mixed effects models were used to assess the associations of BLL with longitudinal age-adjusted World Health OrganizationZ-scores for height (HT-Z) and body mass index (BMI-Z), and annual height velocity (HV). Interactions between boys' age and BLL on growth outcomes were evaluated.
The median (range) BLL was 3.0 (0.5-31.0) µg/dL. At age 18years, 79% of boys had achieved near adult height (HV
Notes
Cites: Environ Health. 2015 Dec 30;14:95 PMID 26715556
Cites: J Pediatr. 1999 May;134(5):623-30 PMID 10228299
Cites: Environ Health Perspect. 2013 Jul;121(7):854-8 PMID 23632160
Cites: J Child Psychol Psychiatry. 2016 Jul;57(7):775-93 PMID 26987761
Cites: Vopr Pitan. 1998;(3):8-13 PMID 9752664
Cites: Environ Health Perspect. 2003 May;111(5):737-41 PMID 12727603
Cites: Arch Environ Health. 1997 Sep-Oct;52(5):377-83 PMID 9546761
Cites: Toxicology. 1993 Oct 25;83(1-3):101-14 PMID 8248939
Cites: Environ Sci Pollut Res Int. 2013 Jul;20(7):4441-7 PMID 23247522
Cites: MMWR Morb Mortal Wkly Rep. 2015 Oct 23;62(54):76-80 PMID 26505220
Cites: Environ Res. 2017 Jan;152:226-232 PMID 27810680
Cites: Environ Int. 2010 May;36(4):330-7 PMID 20181395
Cites: N Engl J Med. 2003 Apr 17;348(16):1527-36 PMID 12700372
Cites: Int J Hyg Environ Health. 2008 Mar;211(1-2):82-7 PMID 17588495
Cites: Bull World Health Organ. 2007 Sep;85(9):660-7 PMID 18026621
Cites: Int J Environ Res Public Health. 2011 Jul;8(7):2593-628 PMID 21845148
Cites: Toxicol Appl Pharmacol. 1996 Sep;140(1):164-72 PMID 8806882
Cites: Pediatrics. 2014 Dec;134(6):1151-9 PMID 25422017
Cites: Toxicol Appl Pharmacol. 2013 Dec 15;273(3):516-23 PMID 24099784
Cites: Ann Hum Biol. 2009 May-Jun;36(3):331-41 PMID 19381987
Cites: J Toxicol Environ Health A. 1998 May 22;54(2):101-20 PMID 9652547
Cites: Environ Health Perspect. 1991 Feb;91:17-32 PMID 2040247
Cites: PLoS Med. 2008 May 27;5(5):e101 PMID 18507497
Cites: Prev Med. 1997 Nov-Dec;26(6):808-16 PMID 9388792
Cites: Pediatrics. 2010 May;125(5):e1088-96 PMID 20368318
Cites: J Pediatr Endocrinol Metab. 2003 Feb;16(2):169-78 PMID 12713253
Cites: Environ Res. 2014 Oct;134:17-23 PMID 25042032
Cites: J Environ Public Health. 2016;2016:8791686 PMID 27042184
Cites: Environ Health Perspect. 2011 Oct;119(10):1436-41 PMID 21715242
Cites: Am J Public Health. 2016 Feb;106(2):283-90 PMID 26691115
Cites: Biol Trace Elem Res. 2016 May;171(1):41-7 PMID 26358768
Cites: Pediatrics. 1991 Nov;88(5):886-92 PMID 1945627
Cites: Environ Health. 2005 May 26;4(1):8 PMID 15918907
Cites: Environ Health Perspect. 2008 Jul;116(7):976-80 PMID 18629324
Cites: Environ Health Perspect. 2012 Feb;120(2):303-8 PMID 21984531
Cites: Ann Hum Biol. 2006 Jul-Aug;33(4):401-14 PMID 17060065
Cites: J Pediatr. 2012 Jun;160(6):1044-9 PMID 22284921
Cites: Pediatrics. 1986 Mar;77(3):281-8 PMID 3951909
Cites: Environ Res. 2015 Jan;136:141-7 PMID 25460630
Cites: Environ Health Perspect. 2016 Nov;124(11):1801-1807 PMID 27187981
Cites: Int J Environ Res Public Health. 2016 Mar 25;13(4):358 PMID 27023578
PubMed ID
28599171 View in PubMed
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