Parental occupational exposure to endocrine disrupting chemicals and male genital malformations: A study in the danish national birth cohort study
Background Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous hormonal signalling has received considerable scientific attention, but human evidence is scarce. Objectives We analyse occurrence of hypospadias...
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| Published in | Environmental health Vol. 10; no. 1; p. 3 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
BioMed Central
14.01.2011
BioMed Central Ltd BMC |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1476-069X 1476-069X |
| DOI | 10.1186/1476-069X-10-3 |
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| Abstract | Background
Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous hormonal signalling has received considerable scientific attention, but human evidence is scarce.
Objectives
We analyse occurrence of hypospadias and cryptorchidism according to maternal and paternal occupational exposure to possible endocrine disrupting chemicals.
Methods
We conducted a follow-up study of 45,341 male singleton deliveries in the Danish National Birth Cohort during 1997-2009. Information on work during pregnancy was obtained by telephone interviews around gestational week 16. Parents' job titles were classified according to DISCO-88. A job exposure matrix for endocrine disrupting chemicals (EDCs) was implemented to assess occupational exposures. The Medical Birth and National Hospital Register provided data on congenital anomalies diagnosed at birth or during follow-up, which ended in 2009. Crude and adjusted hazard ratios (HR) were obtained from Cox regression models.
Results
Among all pregnancies, 6.3% were classified as possibly or probably exposed to EDCs. The most prevalent occupations conferring possible exposure were cleaners, laboratory technicians, hairdressers and agricultural workers (58% of all potentially exposed). The final cumulative incidence of cryptorchidism in boys was 2.2% (1002 cases), and of hypospadias 0.6% (262 cases). The occurrence of hypospadias increased when mothers were probably [HRa = 1.8 (95% CI 1.0-2.6)] or possibly exposed to one or more EDCs [HRa = 2.6 (95% CI 1.8-3.4). Possible paternal exposure to heavy metals increased the risk of hypospadias [HRa 2.2 (95% CI: 1.0-3.4)] and cryptorchidism [HRa 1.9 (95% CI: 1.1-2.7)]. None of the exposure groups reached statistical significance.
Conclusion
The study provides some but limited evidence that occupational exposure to possible endocrine disrupting chemicals during pregnancy increases the risk of hypospadias. |
|---|---|
| AbstractList | Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous hormonal signalling has received considerable scientific attention, but human evidence is scarce.BACKGROUNDSex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous hormonal signalling has received considerable scientific attention, but human evidence is scarce.We analyse occurrence of hypospadias and cryptorchidism according to maternal and paternal occupational exposure to possible endocrine disrupting chemicals.OBJECTIVESWe analyse occurrence of hypospadias and cryptorchidism according to maternal and paternal occupational exposure to possible endocrine disrupting chemicals.We conducted a follow-up study of 45,341 male singleton deliveries in the Danish National Birth Cohort during 1997-2009. Information on work during pregnancy was obtained by telephone interviews around gestational week 16. Parents' job titles were classified according to DISCO-88. A job exposure matrix for endocrine disrupting chemicals (EDCs) was implemented to assess occupational exposures. The Medical Birth and National Hospital Register provided data on congenital anomalies diagnosed at birth or during follow-up, which ended in 2009. Crude and adjusted hazard ratios (HR) were obtained from Cox regression models.METHODSWe conducted a follow-up study of 45,341 male singleton deliveries in the Danish National Birth Cohort during 1997-2009. Information on work during pregnancy was obtained by telephone interviews around gestational week 16. Parents' job titles were classified according to DISCO-88. A job exposure matrix for endocrine disrupting chemicals (EDCs) was implemented to assess occupational exposures. The Medical Birth and National Hospital Register provided data on congenital anomalies diagnosed at birth or during follow-up, which ended in 2009. Crude and adjusted hazard ratios (HR) were obtained from Cox regression models.Among all pregnancies, 6.3% were classified as possibly or probably exposed to EDCs. The most prevalent occupations conferring possible exposure were cleaners, laboratory technicians, hairdressers and agricultural workers (58% of all potentially exposed). The final cumulative incidence of cryptorchidism in boys was 2.2% (1002 cases), and of hypospadias 0.6% (262 cases). The occurrence of hypospadias increased when mothers were probably [HRa = 1.8 (95% CI 1.0-2.6)] or possibly exposed to one or more EDCs [HRa = 2.6 (95% CI 1.8-3.4). Possible paternal exposure to heavy metals increased the risk of hypospadias [HRa 2.2 (95% CI: 1.0-3.4)] and cryptorchidism [HRa 1.9 (95% CI: 1.1-2.7)]. None of the exposure groups reached statistical significance.RESULTSAmong all pregnancies, 6.3% were classified as possibly or probably exposed to EDCs. The most prevalent occupations conferring possible exposure were cleaners, laboratory technicians, hairdressers and agricultural workers (58% of all potentially exposed). The final cumulative incidence of cryptorchidism in boys was 2.2% (1002 cases), and of hypospadias 0.6% (262 cases). The occurrence of hypospadias increased when mothers were probably [HRa = 1.8 (95% CI 1.0-2.6)] or possibly exposed to one or more EDCs [HRa = 2.6 (95% CI 1.8-3.4). Possible paternal exposure to heavy metals increased the risk of hypospadias [HRa 2.2 (95% CI: 1.0-3.4)] and cryptorchidism [HRa 1.9 (95% CI: 1.1-2.7)]. None of the exposure groups reached statistical significance.The study provides some but limited evidence that occupational exposure to possible endocrine disrupting chemicals during pregnancy increases the risk of hypospadias.CONCLUSIONThe study provides some but limited evidence that occupational exposure to possible endocrine disrupting chemicals during pregnancy increases the risk of hypospadias. Background Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous hormonal signalling has received considerable scientific attention, but human evidence is scarce. Objectives We analyse occurrence of hypospadias and cryptorchidism according to maternal and paternal occupational exposure to possible endocrine disrupting chemicals. Methods We conducted a follow-up study of 45,341 male singleton deliveries in the Danish National Birth Cohort during 1997-2009. Information on work during pregnancy was obtained by telephone interviews around gestational week 16. Parents' job titles were classified according to DISCO-88. A job exposure matrix for endocrine disrupting chemicals (EDCs) was implemented to assess occupational exposures. The Medical Birth and National Hospital Register provided data on congenital anomalies diagnosed at birth or during follow-up, which ended in 2009. Crude and adjusted hazard ratios (HR) were obtained from Cox regression models. Results Among all pregnancies, 6.3% were classified as possibly or probably exposed to EDCs. The most prevalent occupations conferring possible exposure were cleaners, laboratory technicians, hairdressers and agricultural workers (58% of all potentially exposed). The final cumulative incidence of cryptorchidism in boys was 2.2% (1002 cases), and of hypospadias 0.6% (262 cases). The occurrence of hypospadias increased when mothers were probably [HRa = 1.8 (95% CI 1.0-2.6)] or possibly exposed to one or more EDCs [HRa = 2.6 (95% CI 1.8-3.4). Possible paternal exposure to heavy metals increased the risk of hypospadias [HRa 2.2 (95% CI: 1.0-3.4)] and cryptorchidism [HRa 1.9 (95% CI: 1.1-2.7)]. None of the exposure groups reached statistical significance. Conclusion The study provides some but limited evidence that occupational exposure to possible endocrine disrupting chemicals during pregnancy increases the risk of hypospadias. Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous hormonal signalling has received considerable scientific attention, but human evidence is scarce. We analyse occurrence of hypospadias and cryptorchidism according to maternal and paternal occupational exposure to possible endocrine disrupting chemicals. We conducted a follow-up study of 45,341 male singleton deliveries in the Danish National Birth Cohort during 1997-2009. Information on work during pregnancy was obtained by telephone interviews around gestational week 16. Parents' job titles were classified according to DISCO-88. A job exposure matrix for endocrine disrupting chemicals (EDCs) was implemented to assess occupational exposures. The Medical Birth and National Hospital Register provided data on congenital anomalies diagnosed at birth or during follow-up, which ended in 2009. Crude and adjusted hazard ratios (HR) were obtained from Cox regression models. Among all pregnancies, 6.3% were classified as possibly or probably exposed to EDCs. The most prevalent occupations conferring possible exposure were cleaners, laboratory technicians, hairdressers and agricultural workers (58% of all potentially exposed). The final cumulative incidence of cryptorchidism in boys was 2.2% (1002 cases), and of hypospadias 0.6% (262 cases). The occurrence of hypospadias increased when mothers were probably [HRa = 1.8 (95% CI 1.0-2.6)] or possibly exposed to one or more EDCs [HRa = 2.6 (95% CI 1.8-3.4). Possible paternal exposure to heavy metals increased the risk of hypospadias [HRa 2.2 (95% CI: 1.0-3.4)] and cryptorchidism [HRa 1.9 (95% CI: 1.1-2.7)]. None of the exposure groups reached statistical significance. The study provides some but limited evidence that occupational exposure to possible endocrine disrupting chemicals during pregnancy increases the risk of hypospadias. Abstract Background: Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous hormonal signalling has received considerable scientific attention, but human evidence is scarce. Objectives: We analyse occurrence of hypospadias and cryptorchidism according to maternal and paternal occupational exposure to possible endocrine disrupting chemicals. Methods: We conducted a follow-up study of 45,341 male singleton deliveries in the Danish National Birth Cohort during 1997-2009. Information on work during pregnancy was obtained by telephone interviews around gestational week 16. Parents' job titles were classified according to DISCO-88. A job exposure matrix for endocrine disrupting chemicals (EDCs) was implemented to assess occupational exposures. The Medical Birth and National Hospital Register provided data on congenital anomalies diagnosed at birth or during follow-up, which ended in 2009. Crude and adjusted hazard ratios (HR) were obtained from Cox regression models. Results: Among all pregnancies, 6.3% were classified as possibly or probably exposed to EDCs. The most prevalent occupations conferring possible exposure were cleaners, laboratory technicians, hairdressers and agricultural workers (58% of all potentially exposed). The final cumulative incidence of cryptorchidism in boys was 2.2% (1002 cases), and of hypospadias 0.6% (262 cases). The occurrence of hypospadias increased when mothers were probably [HRa = 1.8 (95% CI 1.0-2.6)] or possibly exposed to one or more EDCs [HRa = 2.6 (95% CI 1.8-3.4). Possible paternal exposure to heavy metals increased the risk of hypospadias [HRa 2.2 (95% CI: 1.0-3.4)] and cryptorchidism [HRa 1.9 (95% CI: 1.1-2.7)]. None of the exposure groups reached statistical significance. Conclusion: The study provides some but limited evidence that occupational exposure to possible endocrine disrupting chemicals during pregnancy increases the risk of hypospadias. Background Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous hormonal signalling has received considerable scientific attention, but human evidence is scarce. Objectives We analyse occurrence of hypospadias and cryptorchidism according to maternal and paternal occupational exposure to possible endocrine disrupting chemicals. Methods We conducted a follow-up study of 45,341 male singleton deliveries in the Danish National Birth Cohort during 1997-2009. Information on work during pregnancy was obtained by telephone interviews around gestational week 16. Parents' job titles were classified according to DISCO-88. A job exposure matrix for endocrine disrupting chemicals (EDCs) was implemented to assess occupational exposures. The Medical Birth and National Hospital Register provided data on congenital anomalies diagnosed at birth or during follow-up, which ended in 2009. Crude and adjusted hazard ratios (HR) were obtained from Cox regression models. Results Among all pregnancies, 6.3% were classified as possibly or probably exposed to EDCs. The most prevalent occupations conferring possible exposure were cleaners, laboratory technicians, hairdressers and agricultural workers (58% of all potentially exposed). The final cumulative incidence of cryptorchidism in boys was 2.2% (1002 cases), and of hypospadias 0.6% (262 cases). The occurrence of hypospadias increased when mothers were probably [HRa = 1.8 (95% CI 1.0-2.6)] or possibly exposed to one or more EDCs [HRa = 2.6 (95% CI 1.8-3.4). Possible paternal exposure to heavy metals increased the risk of hypospadias [HRa 2.2 (95% CI: 1.0-3.4)] and cryptorchidism [HRa 1.9 (95% CI: 1.1-2.7)]. None of the exposure groups reached statistical significance. Conclusion The study provides some but limited evidence that occupational exposure to possible endocrine disrupting chemicals during pregnancy increases the risk of hypospadias. Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous hormonal signalling has received considerable scientific attention, but human evidence is scarce. We analyse occurrence of hypospadias and cryptorchidism according to maternal and paternal occupational exposure to possible endocrine disrupting chemicals. We conducted a follow-up study of 45,341 male singleton deliveries in the Danish National Birth Cohort during 1997-2009. Information on work during pregnancy was obtained by telephone interviews around gestational week 16. Parents' job titles were classified according to DISCO-88. A job exposure matrix for endocrine disrupting chemicals (EDCs) was implemented to assess occupational exposures. The Medical Birth and National Hospital Register provided data on congenital anomalies diagnosed at birth or during follow-up, which ended in 2009. Crude and adjusted hazard ratios (HR) were obtained from Cox regression models. Among all pregnancies, 6.3% were classified as possibly or probably exposed to EDCs. The most prevalent occupations conferring possible exposure were cleaners, laboratory technicians, hairdressers and agricultural workers (58% of all potentially exposed). The final cumulative incidence of cryptorchidism in boys was 2.2% (1002 cases), and of hypospadias 0.6% (262 cases). The occurrence of hypospadias increased when mothers were probably [HRa = 1.8 (95% CI 1.0-2.6)] or possibly exposed to one or more EDCs [HRa = 2.6 (95% CI 1.8-3.4). Possible paternal exposure to heavy metals increased the risk of hypospadias [HRa 2.2 (95% CI: 1.0-3.4)] and cryptorchidism [HRa 1.9 (95% CI: 1.1-2.7)]. None of the exposure groups reached statistical significance. The study provides some but limited evidence that occupational exposure to possible endocrine disrupting chemicals during pregnancy increases the risk of hypospadias. |
| ArticleNumber | 3 |
| Audience | Academic |
| Author | Kaerlev, Linda Thulstrup, Ane-Marie Bonde, Jens P Olsen, Jørn Morales-Suárez-Varela, María M Jensen, Morten S Ramlau-Hansen, Cecilia Toft, Gunnar V Llopis-González, Agustín |
| AuthorAffiliation | 6 Center for National Clinical Databases South, Department of Research and HTA, Odense University Hospital, Denmark 5 Perinatal Epidemiology Research Unit, Departments of Obstetrics and Paediatrics, Aarhus University Hospital, Skejby, Denmark 1 Unit of Public Health and Environmental Care, Department of Preventive Medicine, University of Valencia. Valencia, Spain 2 CIBER Epidemiology and Public Health (CIBERESP), Spain 3 Center for Public Health Research (CSISP), Valencia, Spain 7 Department of Epidemiology, School of Public Health, UCLA, Los Angeles, USA 9 Institute of Public Health, University of Copenhagen, Denmark 8 Department of Occupational and Environmental Medicine, Bispebjerg Hospital, Denmark 4 Department of Occupational Medicine, Aarhus University Hospital, Denmark |
| AuthorAffiliation_xml | – name: 1 Unit of Public Health and Environmental Care, Department of Preventive Medicine, University of Valencia. Valencia, Spain – name: 8 Department of Occupational and Environmental Medicine, Bispebjerg Hospital, Denmark – name: 5 Perinatal Epidemiology Research Unit, Departments of Obstetrics and Paediatrics, Aarhus University Hospital, Skejby, Denmark – name: 6 Center for National Clinical Databases South, Department of Research and HTA, Odense University Hospital, Denmark – name: 3 Center for Public Health Research (CSISP), Valencia, Spain – name: 7 Department of Epidemiology, School of Public Health, UCLA, Los Angeles, USA – name: 2 CIBER Epidemiology and Public Health (CIBERESP), Spain – name: 4 Department of Occupational Medicine, Aarhus University Hospital, Denmark – name: 9 Institute of Public Health, University of Copenhagen, Denmark |
| Author_xml | – sequence: 1 givenname: María M surname: Morales-Suárez-Varela fullname: Morales-Suárez-Varela, María M email: maria.m.morales@uv.es organization: Unit of Public Health and Environmental Care, Department of Preventive Medicine, University of Valencia, CIBER Epidemiology and Public Health (CIBERESP), Center for Public Health Research (CSISP) – sequence: 2 givenname: Gunnar V surname: Toft fullname: Toft, Gunnar V organization: Department of Occupational Medicine, Aarhus University Hospital – sequence: 3 givenname: Morten S surname: Jensen fullname: Jensen, Morten S organization: Department of Occupational Medicine, Aarhus University Hospital, Perinatal Epidemiology Research Unit, Departments of Obstetrics and Paediatrics, Aarhus University Hospital – sequence: 4 givenname: Cecilia surname: Ramlau-Hansen fullname: Ramlau-Hansen, Cecilia organization: Department of Occupational Medicine, Aarhus University Hospital – sequence: 5 givenname: Linda surname: Kaerlev fullname: Kaerlev, Linda organization: Center for National Clinical Databases South, Department of Research and HTA, Odense University Hospital – sequence: 6 givenname: Ane-Marie surname: Thulstrup fullname: Thulstrup, Ane-Marie organization: Department of Occupational Medicine, Aarhus University Hospital – sequence: 7 givenname: Agustín surname: Llopis-González fullname: Llopis-González, Agustín organization: Unit of Public Health and Environmental Care, Department of Preventive Medicine, University of Valencia, CIBER Epidemiology and Public Health (CIBERESP), Center for Public Health Research (CSISP) – sequence: 8 givenname: Jørn surname: Olsen fullname: Olsen, Jørn organization: Department of Epidemiology, School of Public Health, UCLA – sequence: 9 givenname: Jens P surname: Bonde fullname: Bonde, Jens P organization: Department of Occupational and Environmental Medicine, Bispebjerg Hospital, Institute of Public Health, University of Copenhagen |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21235764$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | Morales-Suárez-Varela et al; licensee BioMed Central Ltd. 2011 COPYRIGHT 2011 BioMed Central Ltd. 2011 Morales-Suárez-Varela et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright ©2011 Morales-Suárez-Varela et al; licensee BioMed Central Ltd. 2011 Morales-Suárez-Varela et al; licensee BioMed Central Ltd. |
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| Keywords | Cryptorchidism Phthalate Occupational Exposure Hypospadias Phthalate Ester |
| Language | English |
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| References_xml | – volume: 67 start-page: 585 year: 2009 ident: 381_CR16 publication-title: Occup Environ Med doi: 10.1136/oem.2009.048272 – volume: 32 start-page: 423 year: 2009 ident: 381_CR1 publication-title: Int J Androl doi: 10.1111/j.1365-2605.2008.00946.x – volume: 60 start-page: 15 year: 2005 ident: 381_CR17 publication-title: Nippon Eiseigaku Zasshi doi: 10.1265/jjh.60.15 – volume: 46 start-page: 465 year: 2002 ident: 381_CR14 publication-title: Ann Occup Hyg doi: 10.1093/annhyg/46.5.465 – volume: 3 start-page: e3051 year: 2008 ident: 381_CR22 publication-title: PLoS One doi: 10.1371/journal.pone.0003051 – volume: 26 start-page: 2 year: 2003 ident: 381_CR13 publication-title: Int J Androl doi: 10.1046/j.1365-2605.2003.00367.x – volume: 21 start-page: 4 year: 2006 ident: 381_CR29 publication-title: Reprod Toxicol doi: 10.1016/j.reprotox.2005.05.006 – volume: 20 start-page: 305 year: 2002 ident: 381_CR11 publication-title: Semin Reprod Med doi: 10.1055/s-2002-35377 – volume: 90 start-page: 4041 year: 2005 ident: 381_CR30 publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2005-0302 – volume: 55 start-page: 143 year: 2000 ident: 381_CR36 publication-title: Toxicol Sci doi: 10.1093/toxsci/55.1.143 – volume: 117 start-page: 1472 year: 2009 ident: 381_CR19 publication-title: Environ Health Perspect doi: 10.1289/ehp.0800389 – volume: 29 start-page: 300 year: 2001 ident: 381_CR24 publication-title: Scand J Public Health doi: 10.1177/14034948010290040201 – volume: 114 start-page: 270 year: 2006 ident: 381_CR23 publication-title: Environ Health Perspect doi: 10.1289/ehp.8075 – volume: 363 start-page: 1264 year: 2004 ident: 381_CR2 publication-title: Lancet doi: 10.1016/S0140-6736(04)15998-9 – volume: 115 start-page: 1519 year: 2007 ident: 381_CR21 publication-title: Environ Health Perspect doi: 10.1289/ehp.9924 – ident: 381_CR3 doi: 10.1136/adc.67.7.892 – volume: 29 start-page: 172 year: 2006 ident: 381_CR39 publication-title: Int J Androl doi: 10.1111/j.1365-2605.2005.00642.x – volume: 112 start-page: 1570 year: 2004 ident: 381_CR32 publication-title: Environ Health Perspect doi: 10.1289/ehp.7243 – volume: 88 start-page: 241 year: 2010 ident: 381_CR15 publication-title: Birth Defects Res A Clin Mol Teratol doi: 10.1002/bdra.20657 – volume: 97 start-page: 127 year: 2005 ident: 381_CR18 publication-title: Environ Res doi: 10.1016/S0013-9351(03)00108-7 – volume: 94 start-page: 868 year: 2009 ident: 381_CR5 publication-title: Arch Dis Child doi: 10.1136/adc.2008.150219 – volume: 117 start-page: 1175 year: 2009 ident: 381_CR20 publication-title: Environ Health Perspect doi: 10.1289/ehp.0800058 – volume: 93 start-page: 124 year: 2010 ident: 381_CR27 publication-title: Fertil Steril doi: 10.1016/j.fertnstert.2008.09.041 – volume: 108 start-page: 463 year: 2000 ident: 381_CR8 publication-title: Environ Health Perspect doi: 10.1289/ehp.00108463 – volume: 17 start-page: 413 year: 2006 ident: 381_CR25 publication-title: Epidemiology doi: 10.1097/01.ede.0000220549.14177.60 – volume-title: Statistics Denmark's Standard Classification of Occupations year: 1996 ident: 381_CR26 – volume: 16 start-page: 972 year: 2001 ident: 381_CR12 publication-title: Hum Reprod doi: 10.1093/humrep/16.5.972 – volume: 155 start-page: 313 year: 2002 ident: 381_CR41 publication-title: Am J Epidemiol doi: 10.1093/aje/155.4.313 – volume: 107 start-page: 297 year: 1999 ident: 381_CR9 publication-title: Environ Health Perspect doi: 10.1289/ehp.99107297 – volume: 114 start-page: 1133 year: 2006 ident: 381_CR40 publication-title: Environ Health Perspect doi: 10.1289/ehp.8741 – volume: 92 start-page: 44 year: 1993 ident: 381_CR4 publication-title: Pediatrics doi: 10.1542/peds.92.1.44 – volume: 30 start-page: 3 year: 2007 ident: 381_CR33 publication-title: Int J Androl doi: 10.1111/j.1365-2605.2006.00703.x – volume: 7 start-page: 282 year: 2001 ident: 381_CR10 publication-title: Human Reprod Update doi: 10.1093/humupd/7.3.282 – volume: 113 start-page: 1056 year: 2005 ident: 381_CR37 publication-title: Environ Health Perspect doi: 10.1289/ehp.8100 – volume-title: An assessment and analysis of existing surveillance data on hypospadias in UK and Europe year: 2003 ident: 381_CR7 – volume: 60 start-page: 543 year: 2003 ident: 381_CR31 publication-title: Occup Environ Med doi: 10.1136/oem.60.8.543 – volume: 16 start-page: 19 year: 2002 ident: 381_CR38 publication-title: Reprod Toxicol doi: 10.1016/S0890-6238(01)00201-5 – volume: 14 start-page: 3075 year: 2000 ident: 381_CR28 publication-title: Genes Dev doi: 10.1101/gad.843800 – volume: 17 start-page: 1112 year: 2002 ident: 381_CR6 publication-title: Hum Reprod doi: 10.1093/humrep/17.4.1112 – volume: 117 start-page: 303 year: 2009 ident: 381_CR34 publication-title: Environ Health Perspect doi: 10.1289/ehp.11933 – volume: 115 start-page: 8 year: 2007 ident: 381_CR35 publication-title: Environ Health Perspect doi: 10.1289/ehp.9351 – reference: 18725961 - 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Environ Health Perspect. 2006 Feb;114(2):270-6 – reference: 10788569 - Toxicol Sci. 2000 May;55(1):143-51 – reference: 16079079 - Environ Health Perspect. 2005 Aug;113(8):1056-61 – reference: 12428210 - Semin Reprod Med. 2002 Aug;20(3):305-12 – reference: 1355643 - Arch Dis Child. 1992 Jul;67(7):892-9 – reference: 19270804 - Environ Health Perspect. 2009 Feb;117(2):303-7 – reference: 10090709 - Environ Health Perspect. 1999 Apr;107(4):297-302 – reference: 19654930 - Environ Health Perspect. 2009 Jul;117(7):1175-9 |
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Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous... Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous hormonal... Background Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt endogenous... Abstract Background: Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt... Abstract Background Sex hormones closely regulate development of the male genital organs during fetal life. The hypothesis that xenobiotics may disrupt... |
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| SubjectTerms | Chemicals Child, Preschool Codes Cohort Studies Congenital defects Congenital diseases Cryptorchidism - chemically induced Cryptorchism Denmark - epidemiology Diagnosis Earth and Environmental Science Endocrine disruptors Endocrine Disruptors - adverse effects Environment Environmental Health Epidemiology Farmworkers Female Follow-Up Studies Health aspects Heavy metals Hormones Hospitals Humans Hypospadias Hypospadias - chemically induced Infant Infant, Newborn Interviews Interviews as Topic Male Maternal Exposure Medical research Medicine Mothers Occupational exposure Occupational Exposure - adverse effects Occupational Medicine/Industrial Medicine Pesticides Pregnancy Prenatal Exposure Delayed Effects - chemically induced Preventive medicine Public Health Risk factors Technicians Womens health Xenobiotics |
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| Title | Parental occupational exposure to endocrine disrupting chemicals and male genital malformations: A study in the danish national birth cohort study |
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