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» Bisphenol A

Down the Drain: » Bisphenol A

July 12, 2007

In use since the 1950s, bisphenol A (BPA) is an industrial chemical and a building block for polycarbonate plastic and epoxy resins. BPA is found in many everyday products such as 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. By 1990, the annual U.S. production of this compound had exceeded 1 billion pounds (EPA 2006).

Bisphenol A been shown to leach into food and water from containers – particularly after heating or as the plastic ages. In studies conducted over the past 20 years, scientists have detected BPA in breast milk, serum, saliva, urine, amniotic fluid, and umbilical cord blood from people in Europe, North America, and Asia (CERHR 2006). Researchers at the Centers for Disease Control and Prevention (CDC) recently detected BPA in 95 percent of nearly 400 U.S. adults (Calafat 2005). A study of girls age 6 to 8 reported measurable amounts of BPA in 85 of 90 participants (Wolff 2007). EWG-led biomonitoring studies have detected BPA in 7 of 41 people tested for this chemical, located in 4 states and the District of Columbia (EWG 2007a). Bisphenol A is so common in products and industrial waste that it pollutes not only people but also rivers, streams, estuaries, house dust, and even air nearly everywhere it is tested (e.g. Kolpin 2002; Rudel 2003).

A large body of evidence indicates that BPA can disrupt the hormone system at very low concentrations. At some very low doses the chemical causes permanent alterations of breast and prostate cells that precede cancer, insulin resistance (a hallmark trait of Type 2 diabetes), and chromosomal damage linked to recurrent miscarriage and a wide range of birth defects including Down syndrome (vom Saal 2005). As of December 2004, 94 of 115 peer-reviewed studies had confirmed BPA's toxicity at low levels of exposure. Few chemicals have been found to consistently display such a diverse range of harm at such low doses. ("Low doses" are typically defined as those that produce tissue concentrations at or below those in the typical range of human exposures.)

One striking study found that very low doses of BPA (20 parts per billion) given to mice for just 1 week caused an error in cell division called aneuploidy (Hunt 2003). This type of cell division error results in the new cells having the wrong number of chromosomes, and is linked to miscarriages and certain birth defects in people, including Down syndrome.

Based on the results of this study, Japanese researchers recently looked at a small number of women to see if higher levels of bisphenol A in their bodies were associated with recurrent miscarriage. They not only found such an association, but also found evidence of aneuploidy in the miscarried fetuses, further suggesting that the higher rates of miscarriage could be BPA-related (Sugiura-Ogasawara 2005).

Japanese scientists found that women with polycystic ovarian syndrome had higher serum levels of BPA relative to women with normal ovarian function, and that there were positive correlations between BPA concentrations and androgen levels (Takeuchi 2006). Polycystic ovarian syndrome is the most common form of female infertility in the U.S., affecting as many as 5 percent of American women (Knochenhauer 1998).

Men with occupational exposure to epoxy resins were found to have decreased secretion of follicle stimulating hormone when compared with men without occupational exposure to epoxy resins (Hanaoka 2002). Follicle stimulating hormone is critical to sperm formation; diminished secretion of this hormone in men can result in reduced sperm concentration and infertility.

A recent animal study also found a link between exposure to low doses of bisphenol A and insulin resistance. In this study, adult mice were exposed to low doses of BPA – 10 parts per billion per day for 4 days (Alonso-Magdalena 2006). The exposed animals were found to have sustained increases in serum insulin levels after just 2 days of exposure, and impaired glucose tolerance after 4 days. Increased insulin levels are associated with Type 2 diabetes; interestingly, women with polycystic ovarian syndrome, epidemiologically associated with BPA exposures, often develop insulin resistance as well (AHA 2007). Over 60 million Americans exhibit insulin resistance, and one in four of these people develop Type 2 diabetes (AHA 2007).

The study of bisphenol A has opened a new chapter in our understanding of the effects of chemicals on our bodies. Where traditional toxicology asserts that higher doses confer greater harm, bisphenol A tests show that low doses can be the most toxic of all, below the radar screen of the body's compensatory detoxifying mechanisms, or below overtly toxic doses that destroy the tissues under study. In one investigation, a low dose of BPA produced a 70 percent higher growth rate of prostate cancer cells in lab animals than did higher doses (Wetherill 2002). In another study, lower doses of BPA resulted in higher rates of breast cell growth that can precede cancer (Markey 2001).

The unusually broad toxicity of BPA is explained by a prominent scientist as stemming from the fact that BPA can alter the behavior of over 200 genes – more than 1 percent of all human genes (Myers 2006). These genes control the growth and repair of nearly every organ and tissue in the body. Taken in its totality, the range of toxic effects linked to BPA is startlingly similar to the litany of human health problems on the rise or common across the population, including breast and prostate cancer, diabetes, obesity, infertility, and polycystic ovarian syndrome (Myers 2006).

Significantly, many of the studies showing adverse effects examine levels many times lower than what the Environmental Protection Agency (EPA) considers safe, 50 ug/kg/day, or 50 parts per billion per day. The EPA established this standard for BPA (the reference dose, or RfD) in 1987, a decade before the low-dose BPA literature developed (EPA 1987). The vast majority of studies finding BPA toxic at low doses have been published since 1997, the year that a pivotal study showed BPA's ability to harm the prostate at levels far below what was thought safe (Nagel 1997). EPA's safety standard is 25 times the dose now known to cause birth defects in lab studies, and has not been updated for 20 years. BPA is allowed in unlimited amounts in consumer products, drinking water, and food, the top exposure source for most people, despite studies that show that BPA is toxic to lab animals at doses overlapping with or very near to human exposures.

Researchers from around the world have detected BPA in surface waters, sometimes at levels approaching the EPA's safe reference dose. Bisphenol A was found in Dutch surface water at levels up to 330 parts per trillion; scientists documented one water sample that contained 21 parts per billion of BPA (Belfroid 2002). Fromme and others (2002) reported BPA levels in surface waters ranging from 0.5 to 410 parts per trillion, and levels in treated wastewater ranging from 18 to 702 parts per trillion. Scientists with the United States Geological Survey detected BPA in 41 percent of the 109 streams sampled in a recent investigation, with the highest concentration at 12 parts per billion (Kolpin 2002).

A number of studies have shown impacts to fish and other wildlife when exposed to bisphenol A. A study of brown trout exposed to BPA at concentrations found in the environment reported impacts to sperm quality in males and either inhibited or reduced ovulation in females (Lahnsteiner 2005). Iwamuro and others (2006) reported that in the parts per billion range, BPA affected tadpole tail development in Xenopus, a frog species often used in bioassays. Another study showed bisphenol A bioaccumulated in spotted halibut (Lee 2004).

Finally, BPA is known to react with the chlorine chemicals used to disinfect tapwater and treated wastewater, creating an array of chlorinated substances that themselves exhibit hormone-disrupting properties (Hu 2002).