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• W2117455783 abstract "The 2007 Summit on Environmental Challenges to Reproductive Health and Fertility convened scientists, health care professionals, community groups, political representatives, and the media to hear presentations on the impact of environmental contaminants on reproductive health and fertility, and to discuss opportunities to improve health through research, education, communication, and policy. Environmental reproductive health focuses on exposures to environmental contaminants, particularly during critical periods of development, and their potential effects on future reproductive health, including conception, fertility, pregnancy, adolescent development, and adult health. Approximately 87,000 chemical substances are registered for commercial use in the United States, with ubiquitous human exposures to environmental contaminants in air, water, food, and consumer products. Exposures during critical windows of susceptibility may result in adverse effects with lifelong and even intergenerational health impacts. Effects can include impaired development and function of the reproductive tract and permanently altered gene expression, leading to metabolic and hormonal disorders, reduced fertility and fecundity, and illnesses such as testicular, prostate, uterine, and cervical cancers later in life. This executive summary reviews effects of pre- and postnatal exposures on male and female reproductive health, and provides a series of recommendations for advancing the field in the areas of research, policy, health care, and community action. The 2007 Summit on Environmental Challenges to Reproductive Health and Fertility convened scientists, health care professionals, community groups, political representatives, and the media to hear presentations on the impact of environmental contaminants on reproductive health and fertility, and to discuss opportunities to improve health through research, education, communication, and policy. Environmental reproductive health focuses on exposures to environmental contaminants, particularly during critical periods of development, and their potential effects on future reproductive health, including conception, fertility, pregnancy, adolescent development, and adult health. Approximately 87,000 chemical substances are registered for commercial use in the United States, with ubiquitous human exposures to environmental contaminants in air, water, food, and consumer products. Exposures during critical windows of susceptibility may result in adverse effects with lifelong and even intergenerational health impacts. Effects can include impaired development and function of the reproductive tract and permanently altered gene expression, leading to metabolic and hormonal disorders, reduced fertility and fecundity, and illnesses such as testicular, prostate, uterine, and cervical cancers later in life. This executive summary reviews effects of pre- and postnatal exposures on male and female reproductive health, and provides a series of recommendations for advancing the field in the areas of research, policy, health care, and community action. On January 28–30, 2007, the Summit on Environmental Challenges to Reproductive Health and Fertility was convened at the Mission Bay Campus of the University of California, San Francisco (UCSF). The Summit was the product of a collaboration between the UCSF Program on Reproductive Health and the Environment in the Department of Obstetrics, Gynecology and Reproductive Sciences, the UCSF National Center of Excellence in Women's Health, and the Collaborative on Health and the Environment. This unique gathering coalesced the field of environmental reproductive health by bringing together over 400 scientists, researchers, health care professionals, trainees, health-affected groups, community and political representatives, and the media to discuss what is currently known about the impacts of environmental contaminants on reproductive health and fertility. The compelling nature of the collective science, with observations in humans, animal models, and wildlife, raised concern for the future health of individuals and families. The Summit also set the stage to improve health through research, education, communication, and changes in public health policy. This executive summary presents the highlights from the accompanying Supplement on Environmental Challenges to Reproductive Health and the Environment (1Proceedings of the UCSF-CHE Summit on Environmental Challenges to Reproductive Health and Fertility.Fertil Steril. 2008; 89 (Available online at)http://www.fertstert.orgGoogle Scholar), which summarizes the state of the science presented at the Summit, and outlines the key “next steps” Summit participants recommended for research, policy, health care, community action, and safe work.Defining the fieldEnvironmental reproductive health focuses on exposures to environmental contaminants (synthetic chemicals and metals), particularly during critical periods of development (such as before conception and during pregnancy), and their potential effects on all aspects of future reproductive health throughout the life course, including conception, fertility, pregnancy, child and adolescent development, and adult health (Fig. 1).Environmental contaminantsSince World War II, there has been a dramatic increase in human exposures to both natural and synthetic chemicals. As of 2006, there are approximately 87,000 chemical substances registered for commerce in the United States (US) (2US EPAWhat is the TSCA Chemical Substance Inventory. Vol. 2007. US Environmental Protection Agency, Washington, DC2006Google Scholar). Common environmental pollutants include pesticides and herbicides such as atrazine and chlorpyrifos; volatile organic compounds such as benzene, toluene, and chloroform; heavy metals such as lead, mercury, and arsenic; air contaminants such as carbon monoxide, ozone, particulate matter, and environmental tobacco smoke (ETS); and persistent organic pollutants, such as the dioxins, polychlorinated biphenols (PCBs), the pesticide dichlorodiphenyltrichloroethane (DDT), and its breakdown product dichlorodiphenyldichloroethylene (DDE).Although many environmental contaminants can affect reproductive health (Table 1), there is an important class of chemicals called endocrine disrupting chemicals (EDCs) that interfere with the production, release, transport, metabolism, binding, action, or elimination of natural hormones in the body that are responsible for the maintenance of homeostasis and the regulation of developmental processes. Some of the common EDCs discussed at the Summit include bisphenol A (BPA), phthalates, and certain pesticides (e.g., vinclozolin, dicofol, atrazine). Many of these compounds alter estrogen, androgen, and thyroid signaling, which are essential for normal embryonic development and reproductive activity in all vertebrates studied to date (3McLachlan J.A. Environmental signaling: what embryos and evolution teach us about endocrine disrupting chemicals.Endocr Rev. 2001; 22: 319-341Crossref PubMed Scopus (328) Google Scholar, 4Zoeller R.T. Dowling A.L.S. Herzig C.T.A. Iannacone E.A. Gauger K.J. Bansal R. Thyroid hormone, brain development, and the environment.Environ Health Perspect. 2002; 110: 355-361Crossref PubMed Google Scholar, 5Gray LE Jr, Wilson VS, Stoker T, Lambright C, Furr J, Noriega N, et al. Adverse effects of environmental antiandrogens and androgens on reproductive development in mammals. Int J Androl 29:96–104.Google Scholar). They can also alter hormone synthesis, storage on plasma proteins, and hepatic biotransformation and clearance (6Guillette Jr., L.J. Gunderson M.P. Alterations in the development of the reproductive and endocrine systems of wildlife exposed to endocrine disrupting contaminants.Reproduction. 2001; 122: 857-864Crossref PubMed Google Scholar); disrupt neural and immune signaling pathways (7Fournier M. Brousseau P. Tryphonas H. Cyr D. Biomarkers of immunotoxicity: an evolutionary perspective.in: Guillette Jr., L.J. Crain D.A. Endocrine disrupting contaminants: an evolutionary perspective. Francis and Taylor Inc., Philadelphia, PA2000: 182-215Google Scholar, 8Guillette Jr., L.J. Endocrine disrupting contaminants—beyond the dogma.Environ Health Perspect. 2006; 114: 9-12PubMed Google Scholar, 9Osteen K.G. Sierra-Rivera E. Does disruption of immune and endocrine systems by environmental toxins contribute to development of endometriosis?.Semin Reprod Endocrinol. 1997; 15: 301-308Crossref PubMed Google Scholar); and alter the regulation of gene expression (e.g., DNA methylation, RNA stability, protein degradation) [reviewed by (10Edwards T.M. Myers J.P. Environmental exposures and gene regulation in disease etiology.Environ Health Perspect. 2007; 115: 1264-1270Crossref PubMed Scopus (96) Google Scholar)]. In some cases, altered DNA methylation patterns have been shown to be heritable (11Anway M.D. Cupp A.S. Uzumcu M. Skinner M.K. Epigenetic transgenerational actions of endocrine disruptors and mate fertility.Science. 2005; 308: 1466-1469Crossref PubMed Scopus (763) Google Scholar, 12Crews D. Gore A.C. Hsu T.S. Dangleben N.L. Spinetta M. Schallert T. et al.Transgenerational epigenetic imprints on mate preference.Proc Nat Acad Sci USA. 2007; 104: 5942-5946Crossref PubMed Scopus (138) Google Scholar).Table 1Environmental contaminants: sources and selected health effects from developmental and adult exposures (animal and human data). (Adapted from Challenged Conceptions, Collaborative on Health and the Environment, 2005 254CHE. CHE Toxicant and Disease Database. Collaborative on Health and the Environment. Available at: http://database.healthhandenvironment.org. Accessed 16 October 2007.Google Scholar).ContaminantSourcesExamples of health effects associated with exposure during adulthoodExamples of health effects associated with exposure during developmentAir PollutionCommon air pollutants include carbon monoxide, lead, ground-level ozone, particulate matter, nitrogen dioxide, and sulfur dioxide. Air pollution arises from a variety of sources, including motor vehicles, industrial production, energy (coal) production, wood burning, and small local sources such as dry cleaners.fetal lossdMalformations of the reproductive tract: in males, could include shortened ano-genital distance in animals or hypospadias (humans), undescended testicles (cryptor-chidism), small testicles (hypoplasia), and structural abnormalities of the epididymis. In females, could include small ovaries, reduced number of follicles (eggs), and structural abnormalities of the oviducts, uterus, cervix, and/or vagina. 254CHE. CHE Toxicant and Disease Database. Collaborative on Health and the Environment. Available at: http://database.healthhandenvironment.org. Accessed 16 October 2007.Google Scholarlow birth weight 254CHE. CHE Toxicant and Disease Database. Collaborative on Health and the Environment. Available at: http://database.healthhandenvironment.org. Accessed 16 October 2007.Google Scholarpreterm delivery 254CHE. CHE Toxicant and Disease Database. Collaborative on Health and the Environment. Available at: http://database.healthhandenvironment.org. Accessed 16 October 2007.Google ScholarBisphenol A (BPA)Industrial chemical and building block for polycarbonate plastic and epoxy resins. Found in the lining of metal food and drink cans, plastic baby bottles, pacifiers and baby toys, dental sealants, computers, cell phones, hard plastic water bottles, paints, adhesives, enamels, varnishes, CDs and DVDs, and certain microwavable or reusable food and drink containers.oocyte chromosome abnomalities 162Hunt P.A. Koehler K.E. Susiarjo M. Hodges C.A. Ilagan A. Voigt R.C. et al.Bisphenol a exposure causes meiotic aneuploidy in the female mouse.Curr Biol. 2003; 13: 546-553Abstract Full Text Full Text PDF PubMed Scopus (237) Google Scholarrecurrent miscarriage 160Sugiura-Ogasawara M. Ozaki Y. Sonta S. Makino T. Suzumori K. Exposure to bisphenol A is associated with recurrent miscarriage.Hum Reprod. 2005; 20: 2325-2329Crossref PubMed Scopus (125) Google Scholardecreased semen quality 180Al-Hiyasat A.S. Darmani H. Elbetieha A.M. Effects of bisphenol A on adult male mouse fertility.Eur J Oral Sci. 2002; 110: 163-167Crossref PubMed Google Scholar, 181Sakaue M. Ohsako S. Ishimura R. Kurosawa S. Kurohmaru M. Hayashi Y. et al.Bisphenol-A affects spermatogenesis in the adult rat even at a low dose.J Occup Health. 2001; 43: 185-190Crossref Google Scholaraltered puberty onset 182Howdeshell K.L. Hotchkiss A.K. Thayer K.A. Vandenbergh J.G. vom Saal F.S. Exposure to bisphenol A advances puberty.Nature. 1999; 401: 763-764Crossref PubMed Scopus (430) Google Scholarobesity 182Howdeshell K.L. Hotchkiss A.K. Thayer K.A. Vandenbergh J.G. vom Saal F.S. Exposure to bisphenol A advances puberty.Nature. 1999; 401: 763-764Crossref PubMed Scopus (430) Google Scholaraltered prostate development 183Timms B.G. Howdeshell K.L. Barton L. Bradley S. Richter C.A. vom Saal F.S. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra.Proc Natl Acad Sci USA. 2005; 102: 7014-7019Crossref PubMed Scopus (154) Google Scholar, 184Gupta C. Reproductive malformation of the male offspring following maternal exposure to estrogenic chemicals.Proc Soc Exp Biol Med. 2000; 224: 61-68Crossref PubMed Scopus (184) Google Scholardecreased semen quality 181Sakaue M. Ohsako S. Ishimura R. Kurosawa S. Kurohmaru M. Hayashi Y. et al.Bisphenol-A affects spermatogenesis in the adult rat even at a low dose.J Occup Health. 2001; 43: 185-190Crossref Google Scholar, 185Herath C.B. Jin W. Watanabe G. Arai K. Suzuki A.K. Taya K. Adverse effects of environmental toxicants, octylphenol and bisphenol A, on male reproductive functions in pubertal rats.Endocrine. 2004; 25: 163-172Crossref PubMed Scopus (37) Google Scholarhormonal changes 185Herath C.B. Jin W. Watanabe G. Arai K. Suzuki A.K. Taya K. Adverse effects of environmental toxicants, octylphenol and bisphenol A, on male reproductive functions in pubertal rats.Endocrine. 2004; 25: 163-172Crossref PubMed Scopus (37) Google ScholarDisinfection by-productsOver 600 compounds formed by the reaction of chemical disinfectants (most often chlorine) with natural organic matter, primarily in surface waters. Most prevalent compounds are trihalomethanes.menstrual irregularitiescMenstrual irregularities could include short or long menstrual cycles, missed periods, abnormal bleeding, anovulaion. 131Windham G.C. Waller K. Anderson M. Fenster L. Mendola P. Swan S. Chlorination by-products in drinking water and menstrual cycle function.Environ Health Perspect. 2003; 111 (discussion A409): 935-941Crossref PubMed Google Scholar, 186del Rio Gomez I. Marshall T. Tsai P. Shao Y.S. Guo Y.L. Number of boys born to men exposed to polychlorinated byphenyls.Lancet. 2002; 360: 143-144Abstract Full Text Full Text PDF PubMed Scopus (60) Google Scholarfetal growth, IUGR 177Bove F. Shim Y. Zeitz P. Drinking water contaminants and adverse pregnancy outcomes: a review.Environ Health Perspect. 2002; 110: 61-74PubMed Google Scholar, 178Nieuwenhuijsen M.J. Toledano M.B. Eaton N.E. Fawell J. Elliott P. Chlorination disinfection byproducts in water and their association with adverse reproductive outcomes: a review.Occup Environ Med. 2000; 57: 73-85Crossref PubMed Scopus (224) Google Scholar, 179Tardiff R.G. Carson M.L. Ginevan M.E. Updated weight of evidence for an association between adverse reproductive and developmental effects and exposure to disinfection by-products.Regul Toxicol Pharmacol. 2006; 45: 185-205Crossref PubMed Scopus (47) Google ScholarEthylene oxideChemical sterilant used in dental and medical practices.fetal lossdMalformations of the reproductive tract: in males, could include shortened ano-genital distance in animals or hypospadias (humans), undescended testicles (cryptor-chidism), small testicles (hypoplasia), and structural abnormalities of the epididymis. In females, could include small ovaries, reduced number of follicles (eggs), and structural abnormalities of the oviducts, uterus, cervix, and/or vagina. 187Sharara F.I. Seifer D.B. Flaws J.A. Environmental toxicants and female reproduction.Fertil Steril. 1998; 70: 613-622Abstract Full Text Full Text PDF PubMed Scopus (135) Google Scholar, 188Hruska K.S. Furth P.A. Seifer D.B. Sharara F.I. Flaws J.A. Environmental factors in infertility.Clin Obstet Gynecol. 2000; 43: 821-829Crossref PubMed Scopus (37) Google Scholardecreased semen qualityaDecreased semen quality could include low semen, abnormal sperm shapes or motility, decreased sperm counts. 188Hruska K.S. Furth P.A. Seifer D.B. Sharara F.I. Flaws J.A. Environmental factors in infertility.Clin Obstet Gynecol. 2000; 43: 821-829Crossref PubMed Scopus (37) Google Scholarmiscarriage in female partner 188Hruska K.S. Furth P.A. Seifer D.B. Sharara F.I. Flaws J.A. Environmental factors in infertility.Clin Obstet Gynecol. 2000; 43: 821-829Crossref PubMed Scopus (37) Google ScholarGlycol ethersUsed in paints, varnishes, thinners, printing inks, electronics, semi-conductor industry, leather, photographic film, varnish, enamels, cosmetics, perfumes, brake fluids, wood stains.longer menstrual cycles 135Hsieh G.Y. Wang J.D. Cheng T.J. Chen P.C. Prolonged menstrual cycles in female workers exposed to ethylene glycol ethers in the semiconductor manufacturing industry.Occup Environ Med. 2005; 62: 510-516Crossref PubMed Scopus (18) Google Scholardecreased semen qualityaDecreased semen quality could include low semen, abnormal sperm shapes or motility, decreased sperm counts. 100Figa-Talamanca I. Traina M.E. Urbani E. Occupational exposures to metals, solvents and pesticides: recent evidence on male reproductive effects and biological markers.Occup Med (Lond). 2001; 51: 174-188Crossref PubMed Scopus (62) Google Scholar, 189LaDou J. Occupational and environmental medicine. 3rd ed. Lange Medical/McGraw Hill, Stamford, CT2004Google Scholarreduced fertilitybReduced fertility could include both infertility and increased time to pregnancy (reduced fecundity). 190Correa A. Gray R.H. Cohen R. Rothman N. Shah F. Seacat H. et al.Ethylene glycol ethers and risks of spontaneous abortion and subfertility.Am J Epidemiol. 1996; 143: 707-717Crossref PubMed Google Scholar, 191Eskenazi B. Gold E.B. Samuels S.J. Wight S. Lasley B.L. Hammond S.K. et al.Prospective assessment of fecundability of female semiconductor workers.Am J Ind Med. 1995; 28: 817-831Crossref PubMed Google Scholarfetal lossdMalformations of the reproductive tract: in males, could include shortened ano-genital distance in animals or hypospadias (humans), undescended testicles (cryptor-chidism), small testicles (hypoplasia), and structural abnormalities of the epididymis. In females, could include small ovaries, reduced number of follicles (eggs), and structural abnormalities of the oviducts, uterus, cervix, and/or vagina. 189LaDou J. Occupational and environmental medicine. 3rd ed. Lange Medical/McGraw Hill, Stamford, CT2004Google Scholar, 190Correa A. Gray R.H. Cohen R. Rothman N. Shah F. Seacat H. et al.Ethylene glycol ethers and risks of spontaneous abortion and subfertility.Am J Epidemiol. 1996; 143: 707-717Crossref PubMed Google ScholarPesticidesBroad category that includes many classes of insecticides, fungicides, herbicides, rodenticides, and fumigants. Pesticides are used on food, in residential and industrial settings. Exposures can occur through food, drinking water, or from home use.menstrual irregularitiescMenstrual irregularities could include short or long menstrual cycles, missed periods, abnormal bleeding, anovulaion. 133Farr S.L. Cooper G.S. Cai J. Savitz D.A. Sandler D.P. Pesticide use and menstrual cycle characteristics among premenopausal women in the Agricultural Health Study.Am J Epidemiol. 2004; 160: 1194-1204Crossref PubMed Scopus (39) Google Scholar, 166Farr S.L. Cai J. Savitz D.A. Sandler D.P. Hoppin J.A. Cooper G.S. Pesticide exposure and timing of menopause: the Agricultural Health Study.Am J Epidemiol. 2006; 163: 731-742Crossref PubMed Scopus (11) Google Scholarreduced fertilitybReduced fertility could include both infertility and increased time to pregnancy (reduced fecundity). 147Greenlee A.R. Arbuckle T.E. Chyou P.H. Risk factors for female infertility in an agricultural region.Epidemiology. 2003; 14: 429-436PubMed Google Scholar, 148Abell A. Juul S. Bonde J.P. Time to pregnancy among female greenhouse workers.Scand J Work Environ Health. 2000; 26: 131-136Crossref PubMed Google Scholar, 188Hruska K.S. Furth P.A. Seifer D.B. Sharara F.I. Flaws J.A. Environmental factors in infertility.Clin Obstet Gynecol. 2000; 43: 821-829Crossref PubMed Scopus (37) Google Scholar, 192Fuortes L. Clark M.K. Kirchner H.L. Smith E.M. Association between female infertility and agricultural work history.Am J Ind Med. 1997; 31: 445-451Crossref PubMed Scopus (48) Google Scholardecreased semen qualityaDecreased semen quality could include low semen, abnormal sperm shapes or motility, decreased sperm counts. 189LaDou J. Occupational and environmental medicine. 3rd ed. Lange Medical/McGraw Hill, Stamford, CT2004Google Scholar, 193Schettler T. Solomon G. Valenti M. Huddle A. Generations at risk. Reproductive health and the environment. MIT Press, Cambridge, MA1999Google Scholar, 194Oliva A. Spira A. Multigner L. Contribution of environmental factors to the risk of male infertility.Hum Reprod. 2001; 16: 1768-1776Crossref PubMed Google Scholar, 195Swan S.H. Kruse R.L. Liu F. Barr D.B. Drobnis E.Z. Redmon J.B. et al.Semen quality in relation to biomarkers of pesticide exposure.Environ Health Perspect. 2003; 111: 1478-1484Crossref PubMed Google Scholarmiscarriage in female partner 151Crisostomo L. Molina V.V. Pregnancy outcomes among farming households of Nueva Ecija with conventional pesticide use versus integrated pest management.Int J Occup Environ Health. 2002; 8: 232-242PubMed Google Scholar, 153Arbuckle T.E. Savitz D.A. Mery L.S. Curtis K.M. Exposure to phenoxy herbicides and the risk of spontaneous abortion.Epidemiology. 1999; 10: 752-760Crossref PubMed Google Scholar, 196Goldsmith J.R. Dibromochloropropane: epidemiological findings and current questions.Ann N Y Acad Sci. 1997; 837: 300-306Crossref PubMed Google Scholar, 197Savitz D.A. Arbuckle T. Kaczor D. Curtis K.M. Male pesticide exposure and pregnancy outcome.Am J Epidemiol. 1997; 146: 1025-1036Crossref PubMed Google Scholarsperm chromosomeabnormalities 198Recio R. Robbins W.A. Borja-Aburto V. Moran-Martinez J. Froines J.R. Hernandez R.M. et al.Organophosphorous pesticide exposure increases the frequency of sperm sex null aneuploidy.Environ Health Perspect. 2001; 109: 1237-1240Crossref PubMed Google Scholar, 199Sanchez-Pena L.C. Reyes B.E. Lopez-Carrillo L. Recio R. Moran-Martinez J. Cebrian M.E. et al.Organophosphorous pesticide exposure alters sperm chromatin structure in Mexican agricultural workers.Toxicol Appl Pharmacol. 2004; 196: 108-113Crossref PubMed Scopus (76) Google Scholarhormonal changes 100Figa-Talamanca I. Traina M.E. Urbani E. Occupational exposures to metals, solvents and pesticides: recent evidence on male reproductive effects and biological markers.Occup Med (Lond). 2001; 51: 174-188Crossref PubMed Scopus (62) Google Scholar, 193Schettler T. Solomon G. Valenti M. Huddle A. Generations at risk. Reproductive health and the environment. MIT Press, Cambridge, MA1999Google Scholar, 200Garry V.F. Holland S.E. Erickson L.L. Burroughs B.L. Male reproductive hormones and thyroid function in pesticide applicators in the Red River Valley of Minnesota.J Toxicol Environ Health A. 2003; 66: 965-986Crossref PubMed Scopus (24) Google Scholaraltered sex ratio (H,A) 100Figa-Talamanca I. Traina M.E. Urbani E. Occupational exposures to metals, solvents and pesticides: recent evidence on male reproductive effects and biological markers.Occup Med (Lond). 2001; 51: 174-188Crossref PubMed Scopus (62) Google Scholar, 201Garry V.F. Schreinemachers D. Harkins M.E. Griffith J. Pesticide appliers, biocides, and birth defects in rural Minnesota.Environ Health Perspect. 1996; 104: 394-399Crossref PubMed Google Scholaraltered puberty onset 202Laws S.C. Ferrell J.M. Stoker T.E. Schmid J. Cooper R.L. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function.Toxicol Sci. 2000; 58: 366-376Crossref PubMed Scopus (79) Google Scholar, 203Monosson E. Kelce W.R. Lambright C. Ostby J. Gray Jr., L.E. Peripubertal exposure to the antiandrogenic fungicide, vinclozolin, delays puberty, inhibits the development of androgen-dependent tissues, and alters androgen receptor function in the male rat.Toxicol Ind Health. 1999; 15: 65-79PubMed Google Scholar, 204Stoker T.E. Guidici D.L. Laws S.C. Cooper R.L. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat.Toxicol Sci. 2002; 67: 198-206Crossref PubMed Scopus (61) Google Scholarmalformations of reproductive tractdMalformations of the reproductive tract: in males, could include shortened ano-genital distance in animals or hypospadias (humans), undescended testicles (cryptor-chidism), small testicles (hypoplasia), and structural abnormalities of the epididymis. In females, could include small ovaries, reduced number of follicles (eggs), and structural abnormalities of the oviducts, uterus, cervix, and/or vagina. 205Kristensen P. Irgens L.M. Andersen A. Bye A.S. Sundheim L. Birth defects among offspring of Norwegian farmers, 1967–1991.Epidemiology. 1997; 8: 537-544Crossref PubMed Scopus (109) Google Scholar, 206Fisher J.S. Environmental anti-androgens and male reproductive health: focus on phthalates and testicular dysgenesis syndrome.Reproduction. 2004; 127: 305-315Crossref PubMed Google Scholar, 207Gray L.E. Ostby J. Furr J. Wolf C.J. Lambright C. Parks L. et al.Effects of environmental antiandrogens on reproductive development in experimental animals.Hum Reprod Update. 2001; 7: 248-264Crossref PubMed Scopus (247) Google Scholarreduced fertility 193Schettler T. Solomon G. Valenti M. Huddle A. Generations at risk. Reproductive health and the environment. MIT Press, Cambridge, MA1999Google Scholar, 208Anway M.D. Cupp A.S. Uzumcu M. Skinner M.K. Epigenetic transgenerational actions of endocrine disruptors and male fertility.Science. 2005; 308: 1466-1469Crossref PubMed Scopus (763) Google Scholarfetal growth, IUGR 209Whyatt R.M. Rauh V. Barr D.B. Camann D.E. Andrews H.F. Garfinkel R. et al.Prenatal insecticide exposures and birth weight and length among an urban minority cohort.Environ Health Perspect. 2004; 112: 1125-1132Crossref PubMed Google Scholar, 210Perera F.P. Rauh V. Tsai W.Y. Kinney P. Camann D. Barr D. et al.Effects of transplacental exposure to environmental pollutants on birth outcomes in a multiethnic population.Environ Health Perspect. 2003; 111: 201-205Crossref PubMed Google Scholar, 211Levario-Carrillo M. Amato D. Ostrosky-Wegman P. Gonzalez-Horta C. Corona Y. Sanin L.H. Relation between pesticide exposure and intrauterine growth retardation.Chemosphere. 2004; 55: 1421-1427Crossref PubMed Scopus (34) Google ScholarPhthalatesPlasticizers added to soften plastics like PVC; also found in cosmetics, perfumes, toys, pharmaceuticals, medical devices, lubricants and wood finishers.altered (earlier) menarche onset 127Colon I. Caro D. Bourdony C.J. Rosario O. Identification of phthalate esters in the serum of young Puerto Rican girls with premature breast development.Environ Health Perspect. 2000; 108: 895-900Crossref PubMed Google Scholarestrous cycle, ovulatory irregularities 187Sharara F.I. Seifer D.B. Flaws J.A. Environmental toxicants and female reproduction.Fertil Steril. 1998; 70: 613-622Abstract Full Text Full Text PDF PubMed Scopus (135) Google Scholardecreased semen qualityaDecreased semen quality could include low semen, abnormal sperm shapes or motility, decreased sperm counts. 212Duty S.M. Silva M.J. Barr D.B. Brock J.W. Ryan L. Chen Z. et al.Phthalate exposure and human semen parameters.Epidemiology. 2003; 14: 269-277PubMed Google Scholarreduced fertilitybReduced fertility could include both infertility and increased time to pregnancy (reduced fecundity). 213Lovekamp-Swan T. Davis B.J. Mechanisms of phthalate ester toxicity in the female reproductive system.Environ Health Perspect. 2003; 111: 139-145Crossref PubMed Google Scholarfetal lossdMalformations of the reproductive tract: in males, could include shortened ano-genital distance in animals or hypospadias (humans), undescended testicles (cryptor-chidism), small testicles (hypoplasia), and structural abnormalities of the epididymis. In females, could include small ovaries, reduced number of follicles (eggs), and structural abnormalities of the oviducts, uterus, cervix, and/or vagina. 187Sharara F.I. Seifer D.B. Flaws J.A. Environmental toxicants and female reproduction.Fertil Steril. 1998; 70: 613-622Abstract Full Text Full Text PDF PubMed Scopus (135) Google Scholarendometriosis 141Cobellis L. Latini G. De Felice C. Razzi S. Paris I. Ruggieri F. et al.High plasma concentrations of di-(2-ethylhexyl)-phthalate in women with endometriosis.Hum Reprod. 2003; 18: 1512-1515Crossref PubMed Scopus (76) Google Scholar, 142Reddy B.S. Rozati R. Reddy B.V. Raman N.V. Association of phthalate esters with endometriosis in Indian women.BJOG. 2006; 113: 515-520Crossref PubMed Scopus (41) Google Scholarshortened anogenital distance 214Couse J.F. Korach K.S. Estrogen receptor-alpha mediates the detrimental effects of neonatal diethylstilbestrol (DES) exposure in the murine reproductive tract.Toxicology. 2004; 205: 55-63Crossref PubMed Scopus (62) Google Scholarmalformations of reproductive tract 215Gray Jr., L.E. Ostby J. Furr J. Price M. Veeramachaneni D.N. Parks L. Perinatal exposure to the phthalates di(2-" @default.
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• W2117455783 title "Proceedings of the Summit on Environmental Challenges to Reproductive Health and Fertility: executive summary" @default.
• W2117455783 cites W1006217371 @default.
• W2117455783 cites W134664743 @default.
• W2117455783 cites W1517854322 @default.
• W2117455783 cites W1543950566 @default.
• W2117455783 cites W158834731 @default.
• W2117455783 cites W1964951926 @default.
• W2117455783 cites W1964963472 @default.
• W2117455783 cites W1966341238 @default.
• W2117455783 cites W1967647179 @default.
• W2117455783 cites W1967982144 @default.
• W2117455783 cites W1968426311 @default.
• W2117455783 cites W1969501884 @default.
• W2117455783 cites W1969738900 @default.
• W2117455783 cites W1969866333 @default.
• W2117455783 cites W1970723200 @default.
• W2117455783 cites W1971425761 @default.
• W2117455783 cites W1972208841 @default.
• W2117455783 cites W1974059553 @default.
• W2117455783 cites W1974172315 @default.
• W2117455783 cites W1974822734 @default.
• W2117455783 cites W1975682947 @default.
• W2117455783 cites W1976878552 @default.
• W2117455783 cites W1977341519 @default.
• W2117455783 cites W1977489946 @default.
• W2117455783 cites W1977738542 @default.
• W2117455783 cites W1979301875 @default.
• W2117455783 cites W1982358764 @default.
• W2117455783 cites W1984017352 @default.
• W2117455783 cites W1987393396 @default.
• W2117455783 cites W1987850248 @default.
• W2117455783 cites W1990355089 @default.
• W2117455783 cites W1992045585 @default.
• W2117455783 cites W1992127626 @default.
• W2117455783 cites W1992990880 @default.
• W2117455783 cites W1993198178 @default.
• W2117455783 cites W1994048261 @default.
• W2117455783 cites W1995148252 @default.
• W2117455783 cites W1995453561 @default.
• W2117455783 cites W1995895212 @default.
• W2117455783 cites W1995905836 @default.
• W2117455783 cites W1996202698 @default.
• W2117455783 cites W1997096869 @default.
• W2117455783 cites W1998367565 @default.
• W2117455783 cites W1999133723 @default.
• W2117455783 cites W1999536031 @default.
• W2117455783 cites W2001120190 @default.
• W2117455783 cites W2001210351 @default.
• W2117455783 cites W2002104241 @default.
• W2117455783 cites W2003669217 @default.
• W2117455783 cites W2006044949 @default.
• W2117455783 cites W2006532904 @default.
• W2117455783 cites W2008797749 @default.
• W2117455783 cites W2009180756 @default.
• W2117455783 cites W2009305534 @default.
• W2117455783 cites W2010164990 @default.
• W2117455783 cites W2013077789 @default.
• W2117455783 cites W2013965546 @default.
• W2117455783 cites W2014249169 @default.
• W2117455783 cites W2014287839 @default.
• W2117455783 cites W2016567184 @default.
• W2117455783 cites W2016762488 @default.
• W2117455783 cites W2017135654 @default.
• W2117455783 cites W2017340526 @default.
• W2117455783 cites W2019310882 @default.
• W2117455783 cites W2020310293 @default.
• W2117455783 cites W2022977525 @default.
• W2117455783 cites W2023704290 @default.
• W2117455783 cites W2024385326 @default.
• W2117455783 cites W2024554347 @default.
• W2117455783 cites W2026302267 @default.
• W2117455783 cites W2026372585 @default.
• W2117455783 cites W2027917454 @default.
• W2117455783 cites W2028002462 @default.
• W2117455783 cites W2028279068 @default.
• W2117455783 cites W2031302504 @default.
• W2117455783 cites W2032743237 @default.
• W2117455783 cites W2037760262 @default.
• W2117455783 cites W2037886734 @default.
• W2117455783 cites W2038397637 @default.
• W2117455783 cites W2040462127 @default.
• W2117455783 cites W2040609979 @default.
• W2117455783 cites W2041002646 @default.
• W2117455783 cites W2041554939 @default.
• W2117455783 cites W2042412736 @default.
• W2117455783 cites W2044258134 @default.
• W2117455783 cites W2044272924 @default.
• W2117455783 cites W2045153097 @default.
• W2117455783 cites W2048681453 @default.
• W2117455783 cites W2049692820 @default.

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