Outgas Designer Toxic Synthetic Hormones


By Peter Marino



Abstract Research on breast cancer, testicular cancer and male fertility shows that these diseases and ailments are caused in part by xenoestrogens found in pesticides, plastic products and synthetic hormones. Xenoestrogens are chemical substances that imitate the function of estrogen but have adverse effects on the human body. Unlike natural estrogen, xenoestrogens do not fit properly into the receptor sites of cells. Since the body cannot metabolize the foreign chemicals properly these are retained in the body and may interfere with proper hormonal signaling. Xenoestrogen effects were observed in aquatic animals and humans exposed to the different forms of these chemicals. Exposure to these chemicals can be reduced or removed through effective efforts from policy makers to identify all the products having xenoestrogen components and impose standards limiting or eliminating human and animal exposure to their adverse effects.

Table of Contents

Page Title Page 1

Abstract 2 Table of Contents 3 Introduction 4 Discussion 5 Sources of Xenoestrogens 5 Pesticides 5 Plastic Products 7

Hormones 8

Effects of Xenoestrogen 9 Effects on Aquatic Animals 9 Effects on Humans 10 Policies on Xenoestrogen 11 Recommendations 12 Conclusion 13 References 14

Estrogen is a hormone produced by ovaries and testes responsible for the development of sexual characteristics, preservation of normal brain functions, and the formation of nerve cells.

If estrogen is beneficial to the health, there are synthetic substances that mimic the function of estrogen but have adverse effects. Xenoestrogens are a group of many different synthetic and naturally occurring chemicals that mimic the behavior of natural hormones and attach to estrogen receptor sites of humans and animals (Chen, 2001). These chemicals enter the body mainly through absorption and ingestion. Unlike natural estrogen, xenoestrogens cause negative effects on the body, because the chemicals do not fit properly into the receptors sites of cells, thus the body cannot metabolize the foreign chemicals properly and may interfere with proper hormonal signaling (Soto, et. al. 1995). There are three classes of xenoestrogens, which are organochlorine pesticides, detergents used in the manufacture of plastics, and coumestrol present in alfalfa sprouts, soybeans, sunflower seeds/oil. (Eubanks, 2004)

Since it is estimated that 40% of all cancers in women are hormonally mediated (Feigelson et. al., 1996) a link between xenoestrogens and the incidence of breast cancer should be investigated. Breast cancer is currently the second leading cause of cancer deaths among American women. (USCS, 2004). Feigelson et al. (1994) showed that women who reach menopause at age 55 or greater are at twice the risk as those who reach menopause before the age of 45. (Feigelson et al., 1996). Therefore, women exposed to estrogen for a longer period are more likely to develop breast cancer.

In males, xenoestrogens also play a role in causing hormone disruption. An analysis of 101 studies performed by Swann et al. (2000) showed that the sperm density of males has decreased in the last 62 years. Swann concluded that common environmental exposures, such as xenoestrogens, could be attributed to the decreased sperm density of males throughout the world. The study also explained that regional differences in male sperm density coincide with the use, manufacturing and exposure of xenoestrogens.

This paper investigates some of the common sources of xenoestrogens synthetically placed in the environment. It will also discuss the association between the increase in environmental xenoestrogens and the incidence of breast cancer in women; the increased incidence of testicular cancer in men between the age of 12 and 50 from an expected 7,200 new cases in 2001 to 8,980 new cases in 2004; and the decline of fertility and sperm density in male semen.

Discussion Sources of Xenoestrogens

Xenoestrogens are found in plastics having bisphenol-A, polycarbonates, and phthalates (Chen 2001; Feldman and Krishna 1995; Stancel 1995; Murk et al 2001; Shioda et al

2000; Ackerman et al 2002; Leger et al 2001; Soto et al 1995; Kolpin et al 2002),

pesticides (Dich et al 1999; Hopenhayn-Rich et al 2001; Legler et al 2001; Kolpin et al.

2002; Soto et al 1995, Hayes, 2003), and hormones (Kolpin et al. 2002; Baronti et al



Pesticides are a major source of xenoestrogens in the environment (Gagne 2001; Bolz 2001; Rogers-Gray et al. 2000; Kolpin et al 2002; Murk et al 2002). The xenoestrogens in pesticides are carried through land runoff and accumulate in wastewater processing plants. Most xenoestrogen waste that cannot be broken down by wastewater treatment is discharged into local streams.

The rate of pesticide and herbicide use in agricultural areas is alarming in relation to the xenoestrogen components in a number of pesticide and insecticides. The world pesticide production has annually doubled every year since 1995 (Dich et al 1997). In a study by Soto et al (1995) the insecticides dieldrin, endosulfan, and toxaphene were found to have estrogenic properties that would lead to a xenoestrogen effect on animals and humans through exposure. A study by Kolpin et al (1995) tested 95 chemicals in which seven were insecticides. The results showed that all seven (carbaryl, cis-chlordane, chlorpyrifos, diazinon, dieldrin, lindane, and methyl parathion) were xenoestrogens (1995).

There is a need to study the effects of all commonly used pesticides. In an earlier study, the organochlorine herbicides, atrazine and simazine did not show a xenoestrogen response when tested (Legler 2001). A study by Hopenhayn-Rich et al (2001) showed similar results agreeing with Legler (2001) that atrazine does not have xenoestrogen effects. However, in 2003 Hayes et al conducted a study, which demonstrated that atrazine exposure (0.1 ppb) resulted in retarded gonadal development (gonadal dysgenesis) and testicular oogenesis (hermaphroditism) in leopard frogs (Rana pipiens).

Wastewater facilities are collecting places for all of the xenoestrogen from pesticides as well as plastic wastes. Many studies have been conducted to determine the amount of xenoestrogen in the wastewater effluent. Experiments by Bolz et al (2001), Kolpin et al (2002), Murk et al (2001), Gagne et al (2000); and Roger-Gray et al (2000) determined that 25 samples, which included both rivers and streams, had levels up to 458 ng/l for 4-nonylphenol (4NP), 189 ng/l for 4-t-octylphenol (4tOP), 272 ng/l for bisphenol A (BPA) and 47 ng/l for 2-hydroxybiphenyl (2OHBiP), chemicals having xenoestrogenic affects Plastic Products

Many plastics have xenoestrogen properties. Based on experiments by Feldman and Krishnan (1995) the xenoestrogens in plastics have hormone mimicking and chromosomal damaging effect on animals and humans. The chemical bisphenol-A or BPA in plastics demonstrated moderate to slightly toxic effects on fish and chromosal defects in Chinese hamsters. This is significant because of the effects that BPA may possibly have on humans especially that BPA has a world production rate of more than

1.4 billion pounds in 1995 (Chen 2001). Studies by Stancel 1995, Murk et al. 2001, and Shioda et al. 2000, and Ackerman et al. 2002 agreed with results from Feldman and

Krishnan 1995 and Chen et al 2000. However, Feldman and Krishnan (1995) found that heating plastic and exposing plastic to acidic substances increased the estrogenic effect of BPA. (Feldman and Krishnan 1995).

Another chemical found in plastic are polycarbonates commonly used as lining of canned food, large water jugs, soda and beer bottles, baby bottles, and baby food (Feldman and Krishnan 1995; Chen et al 2001). The frequency of heating these plastic products results to heightened exposure to xenoestrogens. Water left near heated areas or soft drinks, with their phosphoric acid, can mimic these environmental situations in everyday life.

Phthalate ester is another component of plastics. Soto et al. (1995) determined that the phthalate ester butylbenzylphthalate also had xenoestrogen properties. An experiment by Legler et al (2001) agreed that butybenzylphthalate was a xenoestrogen although the potency of the chemical was less than that of natural hormones.

Not all phthalate esters are xenoestrogens because the same experiment proved alkylalcohols including dibutylphthalate and diamylphthalate were not xenoestrogens. There is difficulty in testing and quantifying the xenoestrogenic effects of phthalate because of the non-selectivity of xenoestrogen properties in relation to compound categories. However, a common factor for all studies on phthalate is that a dose-response relationship occurs with xenoestrogens making the quantity and frequency of exposure important. The studies showed that exposure chances to xenoestrogen sources are increasingly higher at present because of the increase in the use and frequency of use and exposure to xenoestrogen. A measure of the chemicals discharged by the

population to wastewater was examined and found that plastics along with steroids anddetergent metabolites made up approximately 80% of total measured concentration (Kolpin et al 2002).


Hormones are another source of xenoestrogens (Kolpin et al 2002). Pharmaceutical companies manufacture chemicals that are meant to replicate the body’s natural hormones. The difference in structure does not allow the metabolism to break down and discard them in the same way as natural hormones. The synthetic hormone is then expelled to the environment through the wastewater plant. Currently wastewater plants are not designed and do not have the ability to break down the xenoestrogen compounds. According to an experiment by Kolpin et al (2000) hormones were found in the second highest frequency in wastewater. The experimental data by Baronti et al (2002) determined that synthetic hormones are hazardous to aquatic species even if levels were as low as 0.001ug/L. Effects of Xenoestrogen Effects on Marine Animals

The negative effects of animal exposure to xenoestrogen are the alteration of reproductive organs, stagnation of growth rate, and decrease in the number of eggs that will hatch (Huang et al. 2002; Schwaiger et al 2001; Ohtani et al 2001; Palace et al 2002; Gagne et al 2000; Murk et al 2001; Siligato et al 2001; Toft and Baatrup 2000, Vethaak et al, 2002).Roger-Gray et al (2000) examined the fishes in streams exposed to effluent discharge from sewage and found that there was sex reversal in young fishes. Similar data was collected in an experiment with the marine hermaphrodite Protandrous Black Porgy (Acanthopagrus schlegeli). The experimental data showed that the fish’s sex could be influenced early in the life cycle with the testicles being more susceptible to change. (Huang et al 2002) In an experiment on medaka, Oryzas latipes, a sex change occurred as early as 7 days after hatching and there was also reduction in growth rate (Papoulias, et al 1999). The same results were found using mature male common carp (Cyprinus carpio) (Gimeno et al 1998).

The experimental data showed that males developed ‘ovo-tests’ or the presence of both male and female reproductive parts (Gimeno et al, 1998). Another experiment using rainbow trout showed a reduction in the eggs that will hatch and the occurrence of intersex in both sexes (Schwaiger, 2001). An experiment testing the xenoestrogen effects on male rainbow trout and roach showed an increase in vitellogenin production and testicular growth (Murk et al 2001). An experiment using brown trout and stone loach observed a reduction of larval and juvenile stages from the xenoestrogen pollution (Siligato et al 2001).

An experiment by Gagne et al. (2000) proved that even freshwater bivalves are affected by xenoestrogens. The experiment showed health, survival, and reproduction problems occurred because of the increased in exposure to xenoestrogens (Gagne 2000). Frogs are also affected by xenoestrogens in the environment. Ohtani (2001) used the Japanese wrinkled frog (Rana rugosa) to determine xenoestrogen effects on the gonadal sex differentiation. The experiment determined that styrene monomer and trimers influenced the growth of ovaries in some of the sampled males. The data concluded that this was due to a weak xenoestrogen effect (2001)

Effects on Humans

The harmful effects of the excessive exposure to xenoestrogens on humans include illnesses and endocrinal abnormalities (Korner, 2001; Aldlecreutz, 1995). The effects of xenoestrogen on humans are more difficult to detect because of the impossibility of injecting xenoestrogens in humans similar to the experiments performed on animals. The effects of chemicals can be determined using samples of human tissue extracted from the body. The data from animal research also prove to be valuable when related to the possible xenoestrogen effects on humans such as abnormalities in reproductive organs and cycles. Research on the response of the body to xenoestrogens established a relationship between breast cancer and exposure to synthetic estrogen hormone. The synthetic estrogen given to supplement the natural estrogen of women has been proven to increase the chances of having breast cancer (Porch 2002; Lower et al 1999). Women that have never used any synthetic hormones were determined to have a 62% less chance of having breast tumors relating to synthetic estrogen (Lower, et al 1999).

Policies on Xenoestrogen

In recognition of the harmful effects of xenoestrogens, a federal advisory committee was formed in 1996 called the Endocrine Disruptor Screening and Testing Advisory Committee (EDSTAC, 2004). EDSTAC develops and oversees screening and testing programs. In the same year the Food Quality Protection Act (FPQA, 1996) was passed providing a mandatory screening and testing of endocrine disrupting effects of chemicals and pesticides.

The amendment to the Safe Drinking Water Act (SDWA, 1996) called for the screening and testing of endocrine disrupting effects of pesticides and chemicals found in water.

In 2001, the EPA created the National Advisory Council for Environmental Policy and Technology the Endocrine Disruptor Methods Validation Subcommittee (EDMVS) to give technical advice and counsel to EPA on scientific issues associated with the validation of Tier 1 and Tier 2 assays on topics including the development and choice of initial protocols; prevalidation study designs; and validation study designs (EPA: EDSP Chronology, 2005). In 2004, the Endocrine Disruptor Methods Validation Advisory Committee (EDMVAC) replaced EDMVS and will perform the same vital technical and advisory functions as the EDMVS in fulfilling the Endocrine Disruptor Screening Program.

In September of 2005, the EPA published their first notice for Chemical Selection Approach for Initial Round of Screening (Federal Register, 2005). EPA will start to select 50 to 100 endocrine disrupting chemicals based on their high potential for human exposure rather than using a mixture of exposure-and effects-related factors. The U.S. Congress explicitly instructed the EPA to test active and inert pesticide chemicals for possible endocrine effects.


Actions need to be taken to stop and avoid further negative effects from harmful xenoestrogens. The efforts of identifying the xenoestrogen content of many products should be heightened to speed up the process to eliminating the use of these harmful chemicals. This approach will stop the source of the problem instead of trying to regulate a harmful chemical. This will also cause policy makers to protect public health by imposing standards for manufacturers to exclude materials with xenoestrogen.

The level and frequency of exposure to xenoestrogen that will cause harm should also be determined because the effect of these chemical depend upon the circumstances of exposure. Where low levels could be proven safe, regulations could enforce limits. Allowing amounts of xenoestrogen to be used would only occur if the process could be changed to lower levels of xenoestrogens to reasonable amounts. Then regulatory guidelines can be set by the FDA to ensure good manufacturing methods and a safer product for consumers. Labeling a product if it contains a xenoestrogen and in what amounts would encourage the company to limit or eliminate the use of the harmful products. This requirement would allow consumers to have a choice to purchase the products that contain xenoestrogen chemicals or those that do not.

The structural make up of these chemicals should be studies to find ways of breaking down the chemicals in wastewater facilities before discharging the effluent out to the local stream. This solution would minimize the xenoestrogen exposure of the aquatic environment.


Current proposed interventions to reduce breast and testicular cancer mainly focus on changing individual behaviors, including self-imposed restrictions akin to lifelong administration of pharmaceutical agents or radical changes in diet, exercise regime, or reproductive behavior. However, some of the causes of both breast and testicular cancer and related diseases can only be controlled by social and political action aimed at reducing the production, use, transport, and disposal of agents that directly or indirectly affect cancer risks.

The identification of contributing and vulnerability risk factors will provide a missing key component for fostering the promotion of guidelines that require public policy interventions. The public and private sectors should devise policies to prevent, restrict, or reduce exposures to agents in the household, workplace, and general environment that extend the duration and onset of breast or testicular growth or lack thereof, or alter the hormonal environment of persons in hormonally sensitive phases of life. For these policies to succeed, experimental screening tests to identify and research the effects of xenohormones and other disruptive agents merit high priority. It is up to the media, with the influence of public health officials, to make the detrimental effects of xenohormones known to the public. Doing so will pressure manufacturers to change or eliminate the use of xenohormone chemicals in products. It will also make the public perceptive when choosing products.

NOTE: If you are unsure of which products contain Xenoestrogens please see the Amazon.com page I made with xenoestrogen free products that can be used in place of your current cosmetic/personal care products. Click here to go to the store. If you’d like more information and want to learn about what you can do to stop companies from putting these dangerous chemicals in products click here.


Ackermann, Gabriele E., Eva Brombacher, and Kari Fent. (2002). Development of a Fish Reporter Gene System for the Assessment of Estrogenic Compounds and Sewage Treatment Plant Effluents, Environmental Toxicology and Chemistry, 21, 9: 1864-1875.

Adlercreutz H, (1995) Phytoestrogens: epidemiology and a possible role in cancer protection. Environmental Health Perspectives 103; 103–112

Arai Y, Mori T, Suzuki Y, Bern HA. (1983) Long-term effects of perinatal exposure to sex steroids and diethylstilbestrol on the reproductive system of male mammals. Int Rev Cytol 84:235-268.

Aravindakshan J., (2004)Consequences of xenoestrogen exposure on male reproductive function in spottail shiners (Notropis hudsonius), Toxicol Sci. Mar; Vol. 78 (1), pp. 156­


Aravindakshan J, (2004) Consumption of xenoestrogen-contaminated fish during lactation alters adult male reproductive function. Toxicol Sci. Sep; Vol. 81 (1), pp. 179­


Bolz, U., H. Hagenmaier, W. Korner. (2001). Phenolic xenoestrogens in surface water, sediments, and sewage sludge from Baden-Wurttemberg, south-west Germany, Environmental Pollution, 115: 291-301.

Baronti, C., R. Curini, G. D’Ascenzo, A. Di Corcia, A. Gentili and R. Samperi (2000). Monitoring Natural and Synthetic Estrogens at Activated Sludge Sewage TreatmentPlants and in a Receiving River Water. Environmental Science & Technology 34 (24): 5059-5065.

Bushee, E.L., D.R. Edwards, P.A. Moore Jr. (1998). Quality of Runoff from Plots Treated with Municipal Sludge and Horse Bedding, Transactions of the ASEA, 41, 4: 1035-1041.

Carlsen E, Giwercman A, Keiding N, Skakkebæk NE. (1992). Evidence for decreasing quality of semen during past 50 years. Br Med J 305:609-613.

Chen, Min-Yu, Michihiko Ike, and Masanori Fujita. (2001). Acute Toxicity, Mutagenicity, and Estroenicity of Bisphenol-A and Other Bisphenols Environmental Toxicology, 17, 1: 80-86.

Devesa SS, Grauman DJ, Blot WJ, Pennello GA, Hoover RN, Fraumeni JF Jr (1999) Atlas of cancer mortality in the United States, 1950–1994. Washington DC: US Govt Print Off; (NIH) 99-4564].

Dich, J., SH Zahm, A. Hanberg, HO Adami. (1997). Pesticides and Cancer, Cancer Causes Control, 8: 420-433.

Endocrine Disruptor Screening and Testing Advisory (EDSTAC) Chronology, EPA (February 6, 2004). Retrieved on October 12, 2005:


Chen, M, Michihiko I, Masanori F., (2001). Acute Toxicity,

Mutagenicity, and Estroenicity of Bisphenol-A and Other Bisphenols Environmental

Toxicology 17, 1: 80-86.

Endocrine Disruptor Screening Program; Chemical Selection Approach for Initial

Round of Screening, (September 27, 2005) Federal Register Vol. 70, No. 186.

Retrieved on October 27, 2005:

Click to access t19260.pdf

Eubanks, M (2004). The Safety of Xenoestrogens: Challenging the Genomic Model of Effects. Environmental Health Perspectives, 112(15), 897+.

Feigelson HS, Henderson BE. Estrogens and breast cancer. Carcinogenesis (1996); 17: 2279–84.

Food Quality Protection Act of 1996, EPA. Retrieved on October 12, 2005: http://www.epa.gov/scipoly/oscpendo/docs/fqpa.pdf

Forman D, Møller H. (1992). Testicular cancer. Cancer Survey, 19/20:323-341.

Gagne, F., D.J. Marcogliese, C. Blaise, A.D. Gendron. (2001). Occurrence of Compounds Estrogenic to Freshwater Mussels in Surface Waters in an Urban Area, Environmental Toxicology, 16, 3: 260-268.

Gimeno, Sylvia, Hans Komen, Susan Jobling, John Sumpter, and Tim Bowmer. (1998). Demasculinisation of sexually mature male common carp, Cyprinus carpio, exposed to 4-tertpentylphenol during spermatogenesis, Aquatic Toxicology 43: 93-109.

Haung, Yu-Shan, Wen-Shium Yueh, Jing-Duan Huang, Jin-Lien Du, Lian-Tien Sun, Yoshitaka Nagahama, and Ching-Fong Chang. (2002). Cloning and Expression of Estrogen Receptors in the Protandrous Black Porgy (Acanthopagrus schlegeli): Implications of Sex Change Mechanism, Marine Biotechnology, 4:236-246.

Hayes T, Haston K, Tsui M, Hoang A, Haeffele C, Vonk A. (2003). Atrazine-induced hermaphroditism at 0.1 ppb in American leopard frogs (Rana pipiens): laboratory and field evidence, Environ Health Perspect. 111(4):568-75. Retrieved on November 4, 2005:


Hopenhayn-Rich, C., M.L. Stump, S.R. Browning. (2002). Regional Assessment of Atrazine Exposure and Incidence of Breast and Ovarian Cancers in Kentucky, Archives of Environmental Contamination and Toxicology, 42: 127-136. Retrieved on October 21, 2005:

Click Here

Kolpin, Dana W., Edward T. Furlong, Michael T. Meyer, E. Michael Thurman, Steven D. Zaugg, Larry B. Barber, and Herbert T. Buxton. (2002). Pharmaceuticals, Hormones, and Other Organic Wastewater Contaminants in U.S. Streams, 1999-2000: A National Reconnaissance, Environmental Science & Technology 36, 6: 1202-1211.

Korner, Wolfgang, Ulrike Bolz, Rita Triebskorn, Julia Schwaiger, Rolf- Dieter Negele, Alexander Marx and Hanspaul Hagenmaier. (2001). Steroid Analysis and Xenosteroid Potentials in the Small Streams in Southwest Germany, Journal of Aquatic Ecosystem Stress and Recovery 8: 215-229.

Legler, Juliette, Martine Dennekamp, A. Dick Vethaak, Abraham Brouwer, Jan H. Koeman, Bart van der Burg and Albertinka J. Murk. (2002). Detection of estrogenic activity in sediment-associated compounds using in vitro-reporter gene assays The Science of the Total Environment, 293: 69-83.

Lower, Elyse E., Robbin Blau, Paula Gazder, and Donna L. Stahl. (1999). The effects of estrogen usage on the subsequent hormone receptor status of primary breast cancer, Breast Cancer Research and Treatment, 58, 3: 205-210.

Murk, Albertinka J., Juliette Legler, Marola M.H. Van Lipzig, John H.N. Meerman, Angelique C. Belfroid, Albertus Spenkelink, Bart Van Der Burg, Gerald B.J. Rus, and Dick Vethaak. (2002). Detection of Estrogenic Potency in Wastewater and Surface r with Three in Vitro Bioassays, Environmental Toxicology and Chemistry 21, 1: 16-23.

Ohtani, Hiromi, Youko Ichikawa, Etsurou Iwamoto, and Ikuo Miura. (2001). Effects of Styrene Monomer and Trimer on Gonadal Sex Differentiation of Genetic Males of the Frog Rana rugosa, Environmental Research A87: 175-180.

Orth JM. (1984). The role of follicle-stimulating hormone in controlling Sertoli cell proliferation in testes of fetal rats. Endocrinology 115:1248-1255.

Papoulias, Diana M., Douglas B. Noltie and Donald E. Tillitt. (1999). An In Vivo Model Fish System to Test Chemical Effects on Sexual Differentiation and Development: Exposure to Ethinyl Estradiol, Aquatic Toxicology 48: 37-50.

Rodgers-Gray, Trevor P., Susan Jobling, Steven Morris, Carole Kelly, Sonia Kirby, Afsaneh Janbakhsh, Jule E. Harries, Michael J. Waldock, John P. Sumpter, and Charles

R. Tyler. (2000). Long-Term Temporal Changes in the Estrogenic Composition of Treated Sewage Effluent and Its Biological Effects on Fish, Environmental Science & Technology 34: 1521-1528. Retrieved on October 24, 2005:

Click Here

Safe Drinking Water Act [Amendments from 1996] (SDWA), EPA. Retrieved on October 12, 2005: http://www.epa.gov/safewater/sdwa/basicinformation.html

Schwaiger, J., U. Mallow, H. Ferling, S. Knoerr, Th. Braunbeck, W. Kalbfus, and R. D. Negele. (2002). How estrogenic is nonulphenol? A transgenerational study using rainbow trout (Oncorhynchus mykiss) as a test organism, Aquatic Toxicology 59: 177­


Sharman M, Read WA, Castle L, Gilbert J. (1994). Levels of di-(2-ethylhexyl)phthalate and total phthalate esters in milk, cream, butter and cheese. J. Food Add. & Contam. 11:375-385.

Siligato, S. and J. Bohmer. (2001). Using indicators of fish health at multiple levels of biological organization to assess effects of stream pollution in southwest Germany, Journal of Aquatic Ecosystem Stress Recovery 8: 371-386.

Soto, AM., Sonnenschein C, Chung KL, Fernandez MF, Olea N, Serrano FO, (1995). The E-SCREEN Assay as a Tool to Identify Estrogens: An Update on Estrogenic Environmental Pollutants, Environment Health Perspective 103: 7; 113-122

Starek A, (2003) Estrogens and organochlorine xenoestrogens and breast cancer risk. Int J Occup Med Environ Health. 16: 2;113-24.

Swan SH, Elkin EP, Fenster L. (2000). The question of declining sperm density revisited: an analysis of 101 studies published 1934-1996. Environ Health Perspectives Oct;108(10):961-6. Retrieved on November 6: 2005:

Click Here

Toft, Gunnar and Erik Baatrup. (2000). Sexual Characteristics are Altered by 4-tert-Octylphenol and 17 B-Estradiol in the Adult Male Guppy (Poecilia reticulata), Ecotoxicology and Environmental Safety, 48: 76-84.

U.S. Cancer Statistics Working Group. United States Cancer Statistics: 2001 Incidence and Mortality. Atlanta, Georgia: Department of Health and Human Services, the Centers for Disease Control and Prevention and the National Cancer Institute, 2004. Retrieved on November 6, 2005: http://www.cdc.gov/cancer/npcr/uscs/pdf/USCS.pdf (refer to Table D.1.2M and Table D.1.2F).

Vethaak AD, Rijs GBJ, Schrap SM, Ruiter H, Gerritsen A, Lahr J. (2002). Estrogens and Xeno-estrogens in the Aquatic Environment of the Netherlands. Occurrence, Potency and Biological Effects. Riza/RikZ Report no. 2002.001. Lelystad, Netherlands:Ministry of Transport, Public Works and Water Management. Retrieved on October 27, 2005:

Click Here

Wozniak AL, (2005) Xenoestrogens at picomolar to nanomolar concentrations trigger membrane estrogen receptor-alpha-mediated Ca2+ fluxes and prolactin release in GH3/B6 pituitary tumor cells. Environ Health Perspect. Apr; Vol. 113 (4), pp. 431-9.

Zimmerman PA, (1995) Hormone-containing cosmetics may cause signs of early sexual development, Mil Med. Dec; Vol. 160 (12), pp. 628-30.