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Vol. 14 Issue 2, Spring/Summer 2009
Research Commentary
By Suzanne Snedeker, Ph.D., Associate Director for Translational Research, BCERF
Bisphenol A, commonly known as BPA, is an environmental estrogen whose health effects, especially from early life exposures, have been hotly debated in the scientific community during the last two years. The National Toxicology Program (NTP) reviewed evidence of whether early life exposures affect various health endpoints, from breast development and possible breast cancer risk to effects on the brain and prostate, and has called for more research to clarify the uncertainties about BPA’s possible health effects from current levels of exposure (NTP, 2008).
One of the main assumptions about BPA has been that the primary route of exposure to this chemical is through the diet (NTP, 2008). About 40% of the BPA in use is for epoxy resins, including linings of canned foods and beverages. The high-heat canning process results in BPA leaching from the can lining into the food or beverage. The other approximately 60% of BPA is used in the manufacturing of polycarbonate plastic. Until recently, polycarbonate was used extensively in sports and baby bottles. (In the past year, many manufacturers have voluntarily switched to using BPA-free plastics for food and beverage containers.) Putting hot foods or beverages into containers made of polycarbonate plastic, or microwaving in them, can cause low levels of BPA to leach from the plastic into the beverage or food. While polycarbonate plastics have many uses, including CDs, car headlight covers, and sports gear (from goggles to bike helmets), less is known about human exposure to these sources of BPA. Again, the primary source of exposure has been thought to be through the BPA that leaches into food or beverages from can linings or heated polycarbonate containers.
However, research from the University of Rochester and the University of Missouri-Columbia (Stahlhut et al., 2009) is questioning the assumption that diet is the exclusive source of exposure to BPA. BPA is rapidly metabolized and is excreted from the body in the urine. The authors hypothesize that if food and beverages were the primary sources of exposure, then longer periods of fasting time (time between last food intake and urine collection) would result in lower levels of BPA excreted into the urine. In contrast, individuals with short fasting times should have higher levels of BPA in their urine. Using data from 1,469 participants in the 2003-04 National Health and Nutrition Examination Survey (NHANES), these researchers analyzed BPA excretion in urine as a function of fasting time. Surprisingly, they did not observe a rapid decline in urinary levels with increasing fasting time.
The authors suggest two alternative explanations for this finding. Perhaps there is substantial non-food exposure to BPA, or, some BPA may be stored in body fat and is slowly released. It should be stressed that this study offers these as hypothetical explanations. They do not present new data showing that BPA is stored in body fat or data on alternative sources of exposure. They do cite the few studies done to date that have shown some evidence of BPA being detected in body fat. They also cite a study that detected migration of BPA from water hoses made with polyvinylchloride plastic and the need to investigate this as a possible source of exposure. They call for more in-depth studies to closely examine possible alternative sources of exposure, including breathing BPA from household dust or exposure through hand-to-mouth behavior in handling items (like carbonless paper) known to contain BPA. One possible route of exposure seldom considered is BPA in household products (like CDs and DVDs) that may heat up in players or computers and possibly release BPA on the surface of the materials.
The authors note several limitations of their study, including possible bias due to the self-reporting of fasting times by the study subjects and the possibility of contamination of the urine samples. Given that the processing and analysis of the urine samples were done by the Centers for Disease Control and Prevention (CDC), possible sources of contamination were minimized. However, few details were given on the quality control procedures used by the CDC in this paper. The authors did note that field blanks (surrogate liquids that could not have BPA that are put in the same collection containers) were not collected by the CDC for the NHANES study. This and other quality control and assurance procedures should be reviewed to make sure the widely variable BPA levels in study subjects were not due to any procedures that may have resulted in the contamination of the urine samples.
There is another possible explanation to this study’s results. Studies looking at how humans absorb, metabolize, and excrete BPA have been based on a small number of human subjects (only about a dozen subjects from several studies; see Völkel et al., 2002, and 2005; Tsukioka et al., 2004). These studies have indicated that ingested BPA is rapidly excreted over a very short time. Ingested BPA in humans is thought to be metabolized in the liver into a form called BPA-glucuronide and this form is then rapidly excreted in the urine. This is in contrast to how other mammals, e.g. young rats, handle BPA (EFSA, 2007; NTP, 2008). In rats, some of the BPA-glucuronide made in the liver is excreted into the bile and then into the gastrointestinal tract, where some it is cleaved to release “free” BPA. This free BPA is reabsorbed, while the rest is excreted in the urine as the BPA-glucuronide (ESFA, 2005). It is possible that the human studies need to reexamine BPA absorption and excretion patterns, and follow a larger number of individuals with a greater age range to see if there is any evidence that some proportion of adult humans metabolize BPA more like their young rodent counterparts. A slower elimination of BPA because of cleavage and reabsorption of free BPA would also explain why the NHANES-based study did not see a rapid fall in urinary BPA levels with long periods of fasting.
The authors point out that both the European and NTP evaluations of possible health risks from BPA have largely been based on the assumption that exposure is almost exclusively from food. The results presented in this NHANES-based study question this dogma and more studies are needed to see if another paradigm may more accurately explain whether sources of BPA exposure other than food and beverages should be determined and quantified, and if BPA may have some capacity to be stored in the body. I would also recommend that perhaps more humans studies are needed to reevaluate how BPA is absorbed, metabolized to its glucuronide form, and whether this form is entirely excreted or if some is reabsorbed as free BPA and stored in fat tissue. As always, assumptions need to be questioned, and they also need to be tested.
Bibliography
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