My name is Martin Donohoe. I practice internal medicine and teach courses in the School of Community Health and Women’s Studies at PortlandStateUniversity. I am on the Board of Advisors of Oregon Physicians for Social Responsibility and am the Chief Science Advisor for Oregon PSR’s Campaign for Safe Foods. I have over 100 publications of various types and speak nationally and internationally about environmental health.
Oregon Physicians for Social Responsibility supports SJM 8, SB944, and SB 945. These bills will allow consumers to make better-informed choices to protect the health of their families, protect children from exposure to toxins, and enhance our knowledge about known and suspected hazardous chemicals.
Every day, babies drink out of plastic baby bottles and physicians administer medicine through plastic IV bags. Through common situations like these, people are exposed to bisphenol A (BPA) and the phthalate class of chemicals. While acute poisonings from these chemicals are rare, low dose exposure is associated with a variety of detrimental health effects. Bisphenol A and phthalates are endocrine disruptors; exposure during fetal and child development can disrupt hormone function critical to normal development.
Exposures to Bisphenol A and phthalates are widespread, through water, food and other residues that are inhaled or ingested by children. Oregon PSR believes that the evidence we have is strong enough that we should act now to prevent children’s exposure to these toxic chemicals.
Several studies suggest that the constant exposure to these chemicals may be related to widespread trends of lower sperm count, obesity and diabetes, and breast cancer.2,4,5,7,9,10
Potential health effects of Bisphenol A
One of the main uses of bisphenol A is in the manufacture of polycarbonate plastics and epoxy resins. A large number of consumer products are made with polycarbonate plastic (plastic #7): baby bottles, water, milk and juice bottles, microwavable plastic and plastic eating utensils. BPA is also used in metal can lining, nail polish, cds, water pipes, artificial teeth and as an inert ingredient in pesticides and flame retardants. In total, BPA production exceeds six billion pounds per year[1].
BPA is a persistent toxin found in waterways and in our bodies. BPA has been measured at levels shown to alter development in umbilical cords and placental tissue and transfers rapidly to the fetus after maternal uptake.[2] The ester bond connecting BPA monomers is unstable and when the polymers degrade, BPA is released into the food or liquid in the container. BPA leaches from plastic easily; plastics leach BPA at room temperature water. Acidic liquids, high temperatures and cut or scratched plastics increase the speed of leaching[3].
Recent studies find that exposure to BPA, especially perinatal exposure, has an alarming number of potential health effects. In animals, perinatal exposure is linked to precancerous lesions,[4] aneuploidy,[5] abnormal sexual differentiation, altered patterns of estrous cyclicity, altered plasma LH levels[6] and abnormal prostate development.[7] In adult human and animal studies, exposure corresponds with insulin resistance,[8] miscarriages,[9] prostate cancer,[10] hyperactivity, altered female and male reproductive organs, changes in brain structure,[11] oocyte genetic damage,[12] changes in maternal behavior,[13] acceleration of the conversion of 3T3-L1 fibroblasts to adipocytes,[14] abnormal androgen receptor activation and mitogenesis,[15] altered glandular cell function,[16] altered mammary gland development,[17] lower sperm production, lower testosterone levels, polycystic ovarian disease and accelerated growth and puberty.[18]
Bisphenol-A mimics estrogen and attaches to the estrogen receptor, which can lead to similar physiological effects as those caused by the body's own estrogen. In addition, BPA has the capacity to bind to a membrane receptor in cells and initiate a more rapid response than the traditional estrogen receptor does in the nucleus.[19] BPA also affects gene activity normally stimulated by thyroid hormone (T3) in a dose-dependentmanner.[20]
Potential Health Effects of Phthalates
Phthalates are used in a number of plastic products in order to soften the plastic. One billion pounds of phthalates are produced per year and are used in perfumes, children’s toys, hairspray, lubricants, wood finishers, car interiors, medical equipment, paints, adhesives and cosmetics. The Center for Disease Control conducted a study[21] released in 2000 that found high levels of several phthalates compounds in Americans; of most concern was the disproportionate number of women of child bearing age with high levels of a particular metabolite, DBP. The CDC study also found that African Americans have higher levels of several phthalates.
Phthalates have been measured in urine, serum, breast milk and amniotic fluid. Humans are exposed through ingestion, inhalation, dermal absorption, and percutaneous exposure. [22] Phthalates are not chemically bound in plastics and leach easily from the plastic.[23] They are also widespread in household dust.
While the mechanisms of toxicity for the range of phthalates varies, several forms including DEHP, BBP, DBP, and perhaps DINP are all anti-androgens. They interfere with steroid (testosterone) synthesis.[24]
At high levels, exposure to phthalates causes cancer and infertility. Low level exposure is of great concern because of the common use of phthalates in consumer and medical products. Low level exposure to phthalates and their metabolites is associated with developmental effects including premature birth, sperm and DNA damage[25] and something called “phthalate syndrome:” low testosterone in fetal males, hypospadias, inhibition of normal scrotal development, undescended testes, and testicular tumors.[26] AmericanAcademy of Pediatrics has recommended research on the effects of phthalates on fetuses and infants.[27] One human infant study found phthalate levels significantly correlated with scrotal size, penile volume, and degree of testicular descent.[28] Phthalate exposure is also correlated to allergies and asthma in children and low sperm count in adults.[29] Most human exposure is to a combination of phthalates in products and dust. Recent animal studies found that exposure to a combination of several types of phthalates increases detrimental health effects.[30]
The European Union has banned phthalates in cosmetics and children’s toys.31San Francisco has banned the sale of phthlatate and bispehno-containing toys to children under age three.32 Some state legislatures are considering similar bills. The Food and Drug Administration has recommended that health care providers use alternatives to DEHP-IV tubing for certain groups, such as neonates and pregnant and lactating hemodialysis patients.33
To summarize, the known and suspected health hazards of phthalates and related compounds are very serious. The 3 bills we are discussing today will enhance consumer awareness, protect children from toxic exposures, and lead to increased understanding of the role of hazardous chemicals.
Martin Donohoe, MD, FACP
Internal Medicine, Kaiser Sunnyside Medical Center
Adjunct Lecturer, Department of Community Health
Portland State University
Chief Science Advisor, Campaign for Safe Foods
and Member, Board of Advisors
Oregon Physicians for Social Responsibility
Public Health and Social Justice Website
References:
[1]Wade V. Welshons, Susan C. Nagel and Frederick S. vom Saal (2006)Large Effects from Small Exposures. III. Endocrine Mechanisms Mediating Effects of Bisphenol A at Levels of Human ExposureEndocrinology Vol. 147, No. 6 s56-s69
[2] Takahashi, O and S Oishi. (2000) Disposition of Orally Administered 2,2-Bis(4-hydroxyphenyl) propane (Bisphenol A) in Pregnant Rats and the Placental Transfer to Fetuses. Environmental Health Perspectives 108:931-935.
[3] Howdeshell, KA, PH Peterman, BM Judy, JA Taylor, CE Orazio, RL Ruhlen, FS vom Saal, and WV Welshons (2003) Bisphenol A is released from used polycarbonate animal cages into water at room temperature.Environmental Health Perspectives Vol 111, No. 9
[4] Ho, S-M, W-Y Tang, J Belmonte de Frausto, and GS Prins. (2006) Developmental Exposure to Estradiol and Bisphenol A Increases Susceptibility to Prostate Carcinogenesis and Epigenetically Regulates Phosphodiesterase Type 4 Variant 4. Cancer Research 66: 5624-5632.
[5] Hunt, PA, KE Koehler, M Susiarjo, CA Hodges, A Ilagan, RC Voigt, S Thomas, BF Thomas and TJ Hassold. (2003) Bisphenol A exposure causes meiotic aneuploidy in the female mouse. Current Biology 13: 546-553.
[6] Rubin, BS, MK Murray, DA Damassa, JC King and AM Soto. (2001) Perinatal Exposure to Low Doses of Bisphenol A Affects Body Weight, Patterns of Estrous Cyclicity, and Plasma LH Levels. Environmental Health Perspectives 109: 675-680.
[7] vom Saal, F, Plastic Promises: Better Living or Bodily Harm? Presentation at the Oregon Environmental Council’s Forum, February 16,2006.
[8] Alonso-Magdalena, P, S Morimoto, C Ripoll, E Fuentes and A Nadal. (2006) The Estrogenic Effect of Bisphenol-A Disrupts the Pancreatic ß-Cell Function in vivo and Induces Insulin Resistance.Environmental Health Perspectives 114:106-112.
[9] Sugiura-Ogasawara, M, Y Ozaki, S Sonta, T Makino and Kaoru Suzumori (2005) Exposure to bisphenol A is associated with recurrent miscarriage. Human Reproduction 20:2325-2329.
[10] Timms, BG, KL Howdeshell, L Barton, S Bradley, CA Richter and FS vom Saal. (2005) Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. May 2, 2005,Proceedings of the National Academy of Sciences102: 7014-7019.
[11] vom Saal, F and C Hughes. (2005) An Extensive New Literature Concerning Low-Dose Effects of Bisphenol A Shows the Need for a New Risk Assessment. Environmental Health PespectivesVolume 113, Number 8, August 2005
[12] Hunt, PA, KE Koehler, M Susiarjo, CA Hodges, A Ilagan, RC Voigt, S Thomas, BF Thomas and TJ Hassold. (2003) Bisphenol A exposure causes meiotic aneuploidy in the female mouse. Current Biology 13: 546-553.
[13] Palanza, P, KL Howdeshell, S Parmigiani and FS vom Saal. (2002) Exposure to a low dose of bisphenol A during fetal life or in adulthood alters maternal behavior in mice. Environmental Health Perspectives 110 (suppl 3): 415-422.
[14] H. Masuno, et al., (2002) Bisphenol A in combination with insulin can accelerate the conversion of 3T3- L1 fibroblasts to adipocytesJournal of Lipid Research: 3:676-684
[15] Wetherill, YB, CE Petre, KR Monk, A Puga, and KE Knudsen. (2002) The Xenoestrogen Bisphenol A Induces Inappropriate Androgen Receptor Activation and Mitogenesis in Prostatic Adenocarcinoma Cells. Molecular Cancer Therapeutics 1: 515–524.
[16] Ramos, JG, J Varayoud, C Sonnenschein, AM Soto, M Muñoz de Toro and EH Luque. (2001) Prenatal Exposure to Low Doses of Bisphenol A Alters the Periductal Stroma and Glandular Cell Function in the Rat Ventral Prostate.Biology of Reproduction :65: 1271–1277.
[17] C.M. Markey, et al., (2001) In Utero Exposure to Bisphenol A Alters the Development and Tissue Organization of the Mouse Mammary GlandBiology of Reproduction: 65:1215–1223.
[18] K. Howdeshell, et al., (1999) Plastic bisphenol A speeds growth and pubertyNature: 401:762-764
[19] Correspondence with Ted Schettler, MD, MPH, Science Director, Science and Environment Health Network, August 24, 2006
[20]Moriyama, Kenji, Tagami, Tetsuya, et al(2002) Thyroid Hormone Action Is Disrupted by Bisphenol A as an AntagonistThe Journal of Clinical Endocrinology & Metabolism Vol. 87, No. 11 5185-5190
[21] Blount, BC, MJ Silva, SP Caudill, LL Needham, JL Pirkle, EJ Sampson, GW Lucier, RJ Jackson, JW Brock. (2000) Levels of Seven Urinary Phthalate Metabolites in a Human Reference Population. Environmental Health Perspectives 108:979-982.
[22] Shea, Katherine M. MD, MPH (2003) Pediatric Exposure and Potential Toxicity ofPhthalate PlasticizersPediatrics :111: 1467-1474
[23] Latini, G. (2000) Potential Hazards of Exposure to Di-(2-Ethylhexyl)-Phthalate in BabiesBiology of the Neonate 78:269-276
[24] Correspondence with Ted Schettler, MD, MPH, Science Director, Science and Environment Health Network, August 24, 2006
[25] Duty, SM, NP Singh, MJ Silva, DB Barr, JW Brock, L Ryan, RF Herrick, DC Christiani and R Hauser 2003. The relationship between environmental exposures to phthalates and DNA damage in human sperm using the neutral comet assay. Environmental Health Perspectives: doi:10.1289/ehp.5756
[26] Swan, Shanna H, 2006. New Science on the Potential Health Impacts of Phthalates. Presentation at Oregon Environmental Council Health Environment Forum, March 22, 2006.
[27]Shea, Katherine et al.Pediatric Exposure and Potential Toxicity of Phthalate Plasticizers. PEDIATRICS Vol. 111 No. 6 June 2003, pp. 1467-1474.
[28] Swan, SH, et al. 2005. Decrease in Anogenital Distance Among Male Infants with Prenatal Phthalate Exposure. Environmental Health Perspectives113: 1056-1061.
[29] Duty, SM, MJ Silva, DB Barr, JW Brock, L Ryan, Z Chen, RF Herrick, DC Christiani and R Hauser 2003. Phthalate Exposure and Human Semen ParametersEpidemiology 14:269 –277.
[30] Gray Jr, L. Earl, Wilson, Vickie S. et al (2006)Adverse effects of environmental antiandrogens and androgens on reproductive development in mammals International Journal of Andrology:29:96
31 Natural Resources Defense Council. EPA to weaken health standard for common consumer product ingredient. Posted January 8, 2007.
32Roosevelt M. What’s toxic in toyland. TIME 2006 (Dec 11). Available at Accessed 4/18/07.
33US Food and Drug Administration. FDA Public Health Notification: PVC devices containing the plasticizer DEHP. Updated 7/1/02. Available at Accessed 4/18/07.