|1. What are endocrine disruptors?|
|2. How can my family be exposed to EDs?|
|3. What are the health effects of endocrine disruptors?|
|4. Are there medical tests to see if my family has been exposed to endocrine
What are endocrine disruptors?
Endocrine disruptors (EDs) are environmental chemicals that affect the function of the endocrine system, the system involving the glands and hormones of the body. The endocrine system coordinates the functions of various organs and systems in the body. EDs may disrupt the endocrine system in several ways:
- they may act as "imposters" of naturally occurring hormones
- they may block the action of hormones
- they may alter the chemical message sent by hormones
- they may disrupt the production of hormones or hormone receptors (proteins used to receive information from hormones)
EDs are a diverse class of chemicals. They include:
- certain pesticides (DDT)
- industrial chemicals (PCBs, dioxins)
- phenols (bisphenol A, alkylphenol)
- plant hormones (phytoestrogens)
How can my family be exposed to EDs?
Exposure to each major class of EDs - pesticides, industrial chemicals, phthalates, phenol compounds, and plant hormones - will be discussed separately.
Pesticides are widely used for many purposes, including home, garden, commercial, and agricultural pest control. Thus, the potential for human exposure to these chemicals is great. Among the pesticides that may act as EDs, DDT is perhaps the most widely studied. Due to its negative reproductive effects on wildlife and tendency persist in the environment, DDT was banned in the U.S. in 1987. However, DDT is still used extensively in certain developing countries and may enter the U.S. from imported produce. One of the few remaining pesticides in this class still in use is lindane (Kwell), which is used mainly for treatment of head lice.
In general, pesticides can enter the body through the lungs, the mouth, and the skin. Each class of pesticide will differ somewhat in the specific way it is absorbed.
Young children may be at particularly increased risk of pesticide exposure for several reasons:
- their tendency to explore their environment with their mouths
- their closeness to the ground
- their increased time playing outdoors
Two industrial chemicals suspected as EDs are PCBs and dioxins. Each will be discussed separately.
PCBs, or polychlorinated biphenyls, are members of a chemical family that were widely used in the past in industry as lubricants, coatings, and insulation materials for dielectric equipment like transformers and capacitors.
PCBs were also used in common consumer items such as hydraulic fluid, fluorescent lights, televisions, and other appliances. Because PCBs tend to persist for long periods in the environment and have negative effects on wildlife, they were banned from use in the U.S. in 1977.
PCBs have been released into the environment from several sources:
- Poorly maintained hazardous waste dumps and city landfills
- Illegal or improper dumping of hydraulic fluids/coolants
- Leaks from electrical transformers and other equipment
- Burning of medical, industrial, or city waste
- From older consumer goods like televisions
Polychlorinated dibenzodioxins, commonly called dioxins, are a family of chemical compounds unintentionally produced by a variety of industrial processes, including:
- PVC plastic manufacturing
- Manufacturing of certain industrial chemicals and pesticides
- burning of medical /city wastes
- the chlorine bleaching process of pulp and paper mills
To learn more about exposure to dioxins, click here.
Phthalates are chemicals used as plasticizers, or plastic softeners. They make normally rigid plastics easier to bend. Phthalates are used in a variety of consumer products, including:
- plastics in food and beverage containers
- PVC pipes
- vinyl toys or products for children
- lining of metal cans
- medical supplies
- automotive parts
- Food -
People may be exposed to pthalates by eating food stored or cooked in plastic containers or drinking beverages from plastic containers.
- Direct Injection -
Certain medical procedures can put phthalates directly into the blood- stream. This may occur from certain medical products wrapped in plastic such as intra- venous (IV) tubing, IV bags, and indwelling catheters.
- Water -
Drinking water may contain low levels of pthalates. However, the levels found in water tend to be extremely low. Also, well water near certain hazardous waste sites may be contaminated with phthalates.
- Air -
People may be exposed to low concentrations of pthalates in indoor and workplace air. People can also be exposed to phthalates when they receive treatments involving inhalation of gases, such as during anesthesia prior to surgery.
The two members of this class of chemicals thought to be EDs are bisphenol A and alkylphenol. Each will be discussed separately.
- Bisphenol A
Bisphenol A is a chemical used in the production of epoxy resins and polycarbonate plastics. It may be found in the following consumer products:
- food and drink packages
- baby bottles
- lacquers coating certain metal products
- cans and bottle tops water pipes
- some polymers used in dental treatment
Exposure may occur from:
- leaching of the chemical from cans into food
- leaching from plastic bottles into food or drink
- leaching from dental products into the mouth
Alkylphenols are chemicals used in a variety of consumer goods. They may be found in:
- liquid clothes detergents
- The spermicidal lubricant nonoxynol-9 used in some condoms
- some pesticide formulations
Exposure may occur through:
- Skin -
Absorption across skin may happen from shampoos, cosmetics, and laundry detergents. The spermicide nonoxynol-9 may be absorbed across skin or mucous membranes from condom use.
- Food -
Eating food from fields spread with sewage sludge containing alkylphenols may result in exposure to alkylphenols.
- Water -
Drinking water from polluted rivers may result in alkylphenol exposure. Drinking well water near certain hazardous waste sites may result in exposure as well.
- Air -
Breathing fumes from pesticide sprays may cause exposure to alkylphenols. Alkylphenols may also be present as background outdoor air pollutants.
- Skin -
The family of plant hormones suspected to act as endocrine disruptors (EDs) are called phytoestrogens. They are very similar to natural human estrogens, but tend to be much weaker than human estrogens. Phytoestrogens are in:
- soy products
- citrus fruits
- certain grains (wheat, alfalfa)
What are the health effects of endocrine disruptors?
The health effects from endocrine disruptors (EDs) will depend on:
- the specific ED involved
- the level of exposure
- the timecourse of exposure (hours, days, years)
- the underlying health status of the exposed individual
General Health Trends - Male Reproductive problems
- Testicular cancer
Several studies suggest that testicular cancer is increasing around the world. Some scientists believe that endocrine disrupting chemicals could be a cause for this increase. 
- Sperm Counts
Several studies suggest that sperm counts are decreasing in developed countries. Some scientists suspect that EDs may be a possible cause for this decrease. 
- Male reproductive abnormalities
There is limited evidence that male reproductive problems such as cryptorchidism and hypospadias are increasing around the world.  Crytporchidism is a condition where one or both testicles does not descend properly into the scrotum. Hypospadias is a condition where the urethra (opening on the penis where urine or semen comes out) opens on the underside rather than on the end of the penis. Some scientists suspect that EDs may be a possible cause for the increase in these conditions. 
- Breast cancer
Several studies suggest that breast cancer is increasing around the world. Some scientists believe that EDs may be one cause of this increase. 
- Early puberty
Some research suggests that girls in the US are entering puberty earlier than in the past.  Some scientists believe that EDs may be one cause of this trend
There are two main types of pesticides, the organo- chlorines and the organophosphates, and each type has a different set of effects. The two types are each discussed separately below.
- Organochlorine pesticides -
Some human studies suggest that pregnant mothers exposed to organochlorine pesticides may have increased risk of spontaneous abortions (stillbirths) and early delivery of infants. 
One human study suggests that mothers exposed to certain organochlorine pesticides may have not be able to produce milk for as long as unexposed mothers. 
There has been some concern that exposure to organochlorines is associated with increased risk of breast cancer and endometrial cancer, but the weight of the available evidence argues against these associations. [16-19][87-88]
The endocrine disrupting effects of lower levels of pesticides is still very controversial. Many studies do not support these relation- ships. However, many animal studies have given us reason for concern.
Several animal studies suggest that animals exposed to organochlorines have problems with their menstrual cycle, problems with fertility, and decreased litter size. [20-23]
- Organophosphate pesticides -
One study suggests that animals exposed to organophosphate pesticides have problems with hormone regulation and egg development. 
Another animal study suggests that certain organophosphates can block male sex hormones. 
Several animal studies suggest that the fungicides can block male sex hormones and cause problems in sperm quality and delays in puberty. [62-64]
Several human studies suggest that women exposed to PCBs may have problems with their menstrual cycle, children with abnormal growth, and increased risk of spontaneous abortion. 
One human study suggests that boys exposed to PCBs while in the womb had shorter penis lengths than unexposed boys. 
One human study suggests that girls exposed to polybrominated biphenyls during breastfeeding (closely related to PCBs) experienced an earlier start of menstrual bleeding than less exposed girls. 
There has been some concern that PCBs are linked with increased risk of breast cancer, but the weight of the available evidence argues against this. 
Some studies suggest that PCBs can alter thyroid function. There is also evidence against such an association, but there appears to be more evidence in favor of this association. 
One study suggests that men exposed to dioxin have an altered ratio of males to female children. 
Several studies of Vietnam veterans do not support a link between a father’s dioxin exposure and spontaneous abortion (stillbirth), birth defects, and developmental problems in his children. 
Another study of Vietnam veterans shows no association between dioxin exposures and changes in levels of male reproductive hormones. 
One human study suggests that together, dioxins and PCBs may cause thyroid abnormalities. 
One human study suggests that phthalates may cause premature puberty in young girls. 
One occupational study linked exposure to phthalates in PVC plastic with increased testicular cancer. 
Overall, the human evidence supporting the endocrine disrupting effects of phthalates is limited. However, several animal studies have given us reason for concern. Some animal studies suggest that phthalates can cause spontaneous abortions, birth defects, altered menstrual cycle, and other reproductive problems. 
However, these findings are very controversial. Not all studies support the notion that phthalates are EDs. 
Phenols (Bisphenol A, Alkylphenol)
- Bisphenol A
There is little human evidence that Bisphenol A acts as an endocrine disruptor (ED). However, several animal studies and cell culture studies have given us reason for concern:
- One study found that Bisphenol A acts as an ED with human breast cancer cells. 
- One animal study suggests that Bisphenol A may cause changes in hormone levels, menstrual cycle irregularities, delays in reproductive development, and other reproductive problems 
- Several animal studies suggests that Bisphenol A may cause various reproductive abnormalities in males 
- These finding are controversial. Not all studies agree with these effects of Bisphenol A. 
There is little human evidence that alkylphenols act as EDs. However, several animal studies and cell culture studies have given us reason for concern:
- One study found that certain alkylphenols act as EDs with human breast cancer cells. 
- Several animal studies suggest that alkylphenols may negatively effect the female reproductive system. [43-45]
- Another animal study suggests that alkylphenols may decrease sperm production in males. 
- One animal study also suggests that alkyphenols may alter energy balance. 
The health effects of phytoestrogens are controversial. Some studies suggest that phytoestrogens are harmful to the female reproductive system, whereas others suggest that they are actually beneficial to women.
- Potentially harmful effects -
One human study suggests that phytoestrogens may cause small changes in the lining of the vagina. The significance of this finding is not clear. 
One human study suggests that some phytoestrogens may increase the risk of prostate cancer. 
One human study suggests that phytoestrogens may increase risk of thyroid disease. 
Another human study suggests that phytoestrogens may alter an infant’s ability to make cholesterol.  The significance of this finding is not clear.
One animal study suggests that phytoestrogens may cause problems with the menstrual cycle. 
One animal study suggests that phytoestrogens may worsen certain cancers. 
Potentially beneficial effects -
One human study suggests that phytoestrogens may lead to favorable changes in reproductive hormones in postmenopausal women. 
Several laboratory studies suggests that phytoestrogens may decrease the risk of breast cancer. 
One laboratory study suggests that phytoestrogens may decrease risk of prostate cancer. 
These findings are controversial. Not all studies support these relationships. 
Are there medical tests to see if my family has been exposed to endocrine disruptors?
The answer to this question depends on the endocrine disruptor of interest. Each is discussed separately below (pesticides, industrial chemicals, phenols, phthalates, and plant hormones).
- To learn more about medical tests for pesticides, click here.
- Industrial chemicals
- To learn more about medical tests for PCBs, click here.
- To learn more about medical tests for dioxins, click here.
- Bisphenol A
- There are no medical test available to measure levels of bisphenol A in the – body.
- There are no medical tests available to measure levels of alkylphenols in the body.
There are medical that can measure the levels of a certain phthalate called di(2-ethylhexyl)phthalate, or DEHP. The test measures a breakdown product of DEHP called (2-ethylhexyl)phthalate, or MEHP, in the urine or blood. This test is good only for recent exposures because DEHP remains in the body for a short time. These tests are generally performed in research settings and are not routinely available in a doctor's office.
No routine blood or urine test is available for other phthalate species such as diethyl phthalate. There are medical tests to measure levels of diethylphthalate in semen, fat, and kidney tissue. However, these tests are only useful in specialized research settings. They are not available at most doctors' offices.
There are medical tests available that can measure the levels of certain phytoestrogens in the blood and saliva. These have been useful mainly in research settings and are not widely available in a doctor’s office. However, some manufacturers have advertised tests for phytoestrogens in saliva on the inter
 Etzel R, Balk S. Handbook of Pediatric Environmental Health. Endocrine Disruptors. American Academy of Pediatrics Committee on Environmental Health Affairs 1999:83-87.
 Schettler T, Stein J, et al. In Harm’s Way: Toxic Threats to Child Development. Greater Boston Physicians for Social Responsibility 2000.
 Guillette L, Gross T, et al. Developmental abnormalities of the gonad and abnormal sex hormone concentrations in juvenile alligators from contaminated and control lakes in Florida. Environmental Health Perspectives 1994;102(8):680-8.
 Fry DM. Reproductive effects in birds exposed to pesticides and industrial chemicals. Environmental Health Perspectives 1995;103 Suppl 7:165-71.
 Skakkebaek NE, Rajpert-De Meyts E, et al. Germ cell cancer and disorders of spermatogenesis: an environmental connection? APMIS 1998;106(1):3-11.
 Giwercman A, Bonde J. Declining male fertility and environmental factors. Endocrinology & Metabolism Clinics of North America 1998;27(4):807-30.
 Swann, S, Elkin, E, Fenster L. Have sperm densities declined? A reanalysis of global trend data. Environmental Health Perspectives 1997;105: 1228-1232.
 Jensen, T.K., Toppari, J., Keiding, N., Skakkebaek, N.E. 1995. Do environmental estrogens contribute to the decline in male reproductive health? Clinical Chemistry 41: 1896-1901.
 Wolff M, Weston A. Breast cancer risk and environmental exposures. Environmental Health Perspectives 1997;105:891-6.
 Ohlson CG, Hardell L. Testicular cancer and occupational exposures with a focus on xenoestrogens in polyvinyl chloride plastics. Chemosphere 2000; 40(9-11):1277-82.
 Herman-Giddens M, Slora E, et al. Secondary sexual characteristics and menses in young girls seen in office practice: a study from the Pediatric Research in Office Settings network. Pediatrics 1997;99(4):505-12.
 Saxena M, Siddiqui M, et al. Organochlorine pesticides in specimens from women undergoing spontaneous abortion, premature or full-term delivery. Journal of Analytic Toxicology 1981;5:6-9.
 Mobed K, Gold E, Schenker M. Occupational health problems among migrant and seasonal farmworkers. Western Journal of Medicine 1992;157:367-73.
 Gladen B, Rogan W. DDE and shortened duration of lactation in a Northern Mexican Town. American Journal of Public Health 1995;85:504-8.
 Wolff M, Zeleniuch-Jacquotte A, et al. Risk of breast cancer and organochlorine exposure. Cancer Epidemiology, Biomarkers & Prevention 2000;9(3):271-7.
 Hoyer A, Jorgensen T, et al. Organochlorine exposure and breast cancer survival. Journal of Clinical Epidemiology 2000;53(3):323-30.
 Romieu I, Hernandez-Avila M, et al. Breast cancer, lactation history, and serum organochlorines. American Journal of Epidemiology 2000;152(4):363-70.
 Sturgeon S, Brock J, et al. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Cancer Causes & Control 1998;9(4):417-24.
 Eroschenko V. Estrogenic activity of the insecticide chlordecone in the reproductive tract of birds and mammals. Journal of Toxicology and Environmental Health 1981;8:731-42.
 Gray L, Ostby J, et al. Methoxychlor induces estrogen-like alterations of behavior and the reproductive tract in the female rat and hamster: Effects on sex behavior, running wheel activity, and uterine morphology. Toxicology and Applied Pharmacology 1988;96:525-40.
 Guzelian P. Comparative toxicology of chlordecone (kepone) in humans and experimental animals. Annual Review of Pharmacology and Toxicology 1982;22:89-113.
 Cooper R, Stoker T, et al. Effect of atrazine on ovarian function in the rat. Reproductive Toxicology 1996;10:257-64.
 Rattner BA, Michael S. Organophosphorous insecticide induced decrease in plasma luteinizing hormone concentration in white-footed mice. Toxicology Letters 1985;24:65-9.
 Gladen B, Ragan N, Rogan W. Pubertal growth and development and prenatal and lactational exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene. Journal of Pediatrics 2000;136(4):490-6.
 Zheng T, Holford T, et al. Breast cancer risk associated with congeners of polychlorinated biphenyls. American Journal of Epidemiology 2000;152(1):50-8.
 Graham S. Ambrosone C. Polychlorinated biphenyls, cytochrome P4501A1 polymorphism, and postmenopausal breast cancer risk. Cancer Epidemiology, Biomarkers & Prevention 1999;8(1):41-4.
 Longnecker M, Gladen B, et al. Polychlorinated biphenyl (PCB) exposure in relation to thyroid hormone levels in neonates. Epidemiology 2000;11(3):249-54.
 Langer P, Tajtakova M, et al. Increased thyroid volume and prevalence of thyroid disorders in an area heavily polluted by polychlorinated biphenyls. European Journal of Endocrinology 1998;139(4):402-9.
 Mocarelli P, Gerthoux P, et al. Paternal concentrations of dioxin and sex ratio of offspring. Lancet 2000;355(9218):1858-63.
 Wolfe W, Michalek J, et al. Paternal serum dioxin and reproductive outcomes among veterans of Operation Ranch Hand. Epidemiology 1995;6(1):17-22.
 Henriksen G, Michalek J, et al. Serum dioxin, testosterone, and gonadotropins in veterans of Operation Ranch Hand. Epidemiology 1996;7(4):352-7.
 Koopman-Esseboom C, Morse D, et al. Effects of dioxins and polychlorinated biphenyls on thyroid status of pregnant women and their infants. Pediatric Research 1994;36(4):468-73.
 Erickson J, Mulinare , et al. Vietnam veterans’ risk for fathering babies with birth defects. JAMA 1984;252:903-12.
 Davis BJ, Maronpot RR, Heindel JJ. Di-(2-ethylhexyl) phthalate suppresses estradiol and ovulation in cycling rats. Toxicology and Applied Pharmacology 1994;128:216-23.
 Heindel JJ, Gulati DK, et al. Reproductive toxicity of three phthalic acid esters in a continuous breeding protocol. Fundamentals of Applied Toxicology 1989;12:508-18.
 Colon I. Caro D, et al. Identification of phthalate esters in the serum of young Puerto Rican girls with premature breast development. Environmental Health Perspectives 2000;108(9):895-900.
 Fredricsson B, Moller L, et al. Human sperm motility is affected by plasticizers and diesel particle extracts. Pharmacology & Toxicology 1993;72(2):128-33.
 Gray LE, Ostby J, et al. Perinatal exposure to the phthalates DEHP, BBP, and DINP, but not DEP, DMP, or DOTP, alters sexual differentiation of the male rat. Toxicological Sciences 2000;58(2):350-65.
 Krishnan, AV, Starhis, P, et al. Bisphenol-A: an estrogenic substance is released from polycarbonate flasks during autoclaving. Endocrinology 1993;132: 2279-2286.
 Howdeshell K, Hotchkiss, A, et al. Exposure to bisphenol A advances puberty. Nature 1999;401:763-764.
 Soto A, Justicia H, et al. .P-Nonylphenol, an estrogenic xenobiotic released from 'modified' polystyrene. Environmental Health Perspectives 1991;92: 167-173.
 Jobling S, Sumpter J. Detergent components in sewage effluent are weakly estrogenic to fish - An in-vitro study using rainbow-trout (Oncorhynchus mykiss) hepatocytes. Aquatic Toxicology 1993;27: 361-372.
 White R, Jobling, S, et al. Environmentally persistent alkylphenolic compounds are estrogenic. Endocrinology 1994;35: 175-182.
 Routledge E, Sumpter J. Estrogenic activity of surfactants and some of their degradation products assessed using a recombinant yeast screen. Environmental Toxicology & Chemistry 1996;15: 241-248.
 Steinmetz R, Mitchner N, et al. The xenoestrogen bisphenol a induces growth, differentiation, and c-fos gene expression in the female reproductive tract. Endocrinology 1998;139: 2741-2747.
 Yu ML. Guo YL, et al. Menstruation and reproduction in women with polychlorinated biphenyl (PCB) poisoning: long-term follow-up interviews of the women from the Taiwan Yucheng cohort. International Journal of Epidemiology 2000;29(4):672-7.
 Guo YL, Yu ML, et al. Neuro-endocrine developmental effects in children exposed in utero to PCBs: studies in Taiwan. Neurotoxicology 1995;16:752.
 Michels-Blanck H, Marcus M, et al. Age at menarche in girls exposed perinatally to polybrominated biphenyl. American Journal of Epidemiology 1999;149:S21.
 Nunez AA, Kannan K, et al. Effects of bisphenol A on energy balance and accumulation in brown adipose tissue in rats. Chemosphere 2001;42(8):917-22.
 Adlercreutz H. Phytoestrogens: epidemiology and a possible role in cancer protection. Environmental Health Perspectives 1995;103:103-12.
 Whitten PL, Lewis C, et al. Potential adverse effects of phytoestrogens. Journal of Nutrition 1995;125:771S-6S.
 Whitten PL, Lewis C, et al. Phytoestrogen influences on the development of behavior and gonadotropin function. Proceedings of the Society of Experimental Biological Medicine 1995;208:82-6.
 Whitten PL, Russel E, Naftolin F. Influence of phytoestrogen diets on estradiol action in the rat uterus. Steroids 1994;59:443-9.
 Adams NR. Detection of the effects of phytoestrogens on sheep and cattle. Journal of Animal Sciences 1995;73:1509-15.
 Toppari J, Skakkebaek NE. Sexual differentiation and environmental endocrine disrupters. Clinical Endocrinology & Metabolism 1998;12(1):143-56.
 McLachlan JA, Newbold RR, et al. Are estrogens carcinogenic during development of the testes? APMIS 1998;106(1):240-2.
 Carlsen E, Giwercman A, et al. Declining semen quality and increasing incidence of testicular cancer: is there a common cause? Environmental Health Perspectives 1995;103 Suppl 7:137-9.
 Harrison PT, Holmes P, Humfrey CD. Reproductive health in humans and wildlife: are adverse trends associated with environmental chemical exposure? Science of the Total Environment 1997;205(2-3):97-106.
 Wolff MS, Weston A. Breast cancer risk and environmental exposures. Environmental Health Perspectives 1997;105 Suppl 4:891-6.
 Tamura H, Maness SC, et al. Androgen receptor antagonism by the organophosphate insecticide fenitrothion. Toxicological Sciences 2001;60(1):56-62.
 Kelce WR, Lambright CR, et al. Vinclozolin and p,p'-DDE alter androgen-dependent gene expression: in vivo confirmation of an androgen receptor-mediated mechanism. Toxicology & Applied Pharmacology 1997;142(1):192-200.
 Ostby J, Kelce WR, et al. The fungicide procymidone alters sexual differentiation in the male rat by acting as an androgen-receptor antagonist in vivo and in vitro. Toxicology & Industrial Health 1999;15(1-2):80-93.
 Monosson E, Kelce WR., et al. 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. Toxicology & Industrial Health 1999; 15(1-2):65-79.
 Lim J, Miller MG. The role of the benomyl metabolite carbendazim in benomyl-induced testicular toxicity. Toxicology & Applied Pharmacology 1997;142(2):401-10.
 Harris CA, Henttu P, et al. The estrogenic activity of phthalate esters in vitro. Environmental Health Perspectives 1997;105(8):802-11.
 Lamb JC, Chapin RE, et al. Reproductive effects of four phthalic acid esters in the mouse. Toxicology & Applied Pharmacology 1987;88(2):255-69.
 Gupta C. Reproductive malformation of the male offspring following maternal exposure to estrogenic chemicals. Proceedings of the Society for Experimental Biology and Medicine 2000;224:61-68.
 vom Saal FS, Cooke PS, et al. A physiologically based approach to the study of bisphenol A and other estrogenic chemicals on the size of reproductive organs, daily sperm production, and behavior. Toxicology and Industrial Health 1998;14:239-260.
 Steinmetz R, Brown NG, et al. The environmental estrogen bisphenol A stimulates prolactin release in vitro and in vivo. Endocrinology 1997;138:1780-1786.
 Colerangle JB, Roy D. Profound effects of the weak environmental estrogen-like chemical bisphenol A on the growth of the mammary gland of noble rats. Journal of Steroid Biochemistry and Molecular Biology 1997;60:153-160.
 Ashby J, Tinwell H, Haseman J. Lack of effects for low dose levels of bisphenol A (BPA) and diethylstilbestrol (DES) on the prostate gland of CF1 mice exposed in utero. Regulatory Toxicology and Pharmacology 1999;30:156-166.
 Paulozzi LJ; Erickson JD, Jackson RJ. Hypospadias trends in two US surveillance systems. Pediatrics 1997;100(5):831-4.
 Bicknell RJ, Herbison AE, Sumpter JP. Oestrogenic activity of an environmentally persistent alkylphenol in the reproductive tract but not the brain of rodents. Journal of Steroid Biochemistry & Molecular Biology 1995;54(1-2):7-9.
 Baird DD, Umbach DM, et a. Dietary intervention study to assess estrogenicity of dietary soy among postmenopausal women. Journal of Clinical Endocrinology & Metabolism 1995;80(5):1685-90.
 Cruz ML, Wong WW, et al. Effects of infant nutrition on cholesterol synthesis rates. Pediatric Research 1994;35(2):135-40.
 den Tonkelaar I, Keinan-Boker L, et al. Urinary phytoestrogens and postmenopausal breast cancer risk. Cancer Epidemiology, Biomarkers & Prevention 2001;10(3):223-8.
 Charland SL, Hui JW, Torosian MH. The effects of a soybean extract on tumor growth and metastasis. International Journal of Molecular Medicine 1998;2(2):225-228.
 Berrino F, Bellati C, et al. Reducing bioavailable sex hormones through a comprehensive change in diet: the diet and androgens (DIANA) randomized trial. Cancer Epidemiology, Biomarkers & Prevention 2001;10(1):25-33.
 Cappelletti V, Fioravanti L, et al. Genistein blocks breast cancer cells in the G(2)M phase of the cell cycle. Journal of Cellular Biochemistry 2000;79(4):594-600.
 Tamir S, Eizenberg M, et al. Estrogenic and antiproliferative properties of glabridin from licorice in human breast cancer cells. Cancer Research 2000;60(20):5704-9.
 Choi YH, Lee WH., et al. p53-independent induction of p21 (WAF1/CIP1), reduction of cyclin B1 and G2/M arrest by the isoflavone genistein in human prostate carcinoma cells. Japanese Journal of Cancer Research 2000;91(2):164-73.
 Strom SS, Yamamura Y, et al. Phytoestrogen intake and prostate cancer: a case-control study using a new database. Nutrition & Cancer 1999;33(1):20-5.
 Fort P, Moses N, et al. Breast and soy-formula feedings in early infancy and the prevalence of autoimmune thyroid disease in children. Journal of the American College of Nutrition 1990;9(2):164-7.
 Blanck HM, Marcus M, et al. Age at menarche and tanner stage in girls exposed in utero and postnatally to polybrominated biphenyl. Epidemiology 2000;11(6):641-7.
 Dorgan J, Brock J, et al. Serum organochlorine pesticides and PCBs and breast cancer risk: results from a prospective analysis (US). Cancer Causes & Control 1999;10(1):1-11.
 Weiderpass E, Adami H, et al. Organochlorines and endometrial cancer risk. Cancer Epidemiology, Biomarkers & Prevention 2000;9(5):487-93.