From Environmental Health Perspectives
Jenny L. Carwile; Henry T. Luu; Laura S. Bassett; Daniel A. Driscoll; Caterina Yuan; Jennifer Y. Chang; Xiaoyun Ye; Antonia M. Calafat; Karin B. Michels
Abstract
Background: Bisphenol A (BPA) is a high-production-volume chemical commonly used in the manufacture of polycarbonate plastic. Low-level concentrations of BPA in animals and possibly in humans may cause endocrine disruption. Whether ingestion of food or beverages from polycarbonate containers increases BPA concentrations in humans has not been studied.
Objectives: We examined the association between use of polycarbonate beverage containers and urinary BPA concentrations in humans.
Methods: We conducted a nonrandomized intervention of 77 Harvard College students to compare urinary BPA concentrations collected after a washout phase of 1 week to those taken after an intervention week during which most cold beverages were consumed from polycarbonate drinking bottles. Pairedt-tests were used to assess the difference in urinary BPA concentrations before and after polycarbonate bottle use.
Results: The geometric mean urinary BPA concentration at the end of the washout phase was 1.2 μg/g creatinine, increasing to 2.0 μg/g creatinine after 1 week of polycarbonate bottle use. Urinary BPA concentrations increased by 69% after use of polycarbonate bottles (p < 0.0001). The association was stronger among participants who reported ≥ 90% compliance (77% increase; p < 0.0001) than among those reporting < 90% compliance (55% increase; p = 0.03), but this difference was not statistically significant (p = 0.54).
Conclusions: One week of polycarbonate bottle use increased urinary BPA concentrations by two-thirds. Regular consumption of cold beverages from polycarbonate bottles is associated with a substantial increase in urinary BPA concentrations irrespective of exposure to BPA from other sources.
Introduction
The endocrine-disrupting chemical bisphenol A (BPA) has recently garnered heightened attention because of widespread human exposure and disruption of normal reproductive development in laboratory animals [Center for the Evaluation of Risks to Human Reproduction (CERHR) 2008; Chapin et al. 2008; Goodman et al. 2006; European Union 2003; vom Saal and Hughes 2005]. BPA is thought to disrupt normal cell function by acting as an estrogen agonist (Wozniak et al. 2005) as well as an androgen antagonist (Lee et al. 2003). In animal studies, prenatal and neonatal exposure to BPA has been linked to early onset of sexual maturation (Howdeshell et al. 1999), altered development and tissue organization of the mammary gland (Markey et al. 2001), induction of preneoplastic mammary gland (Durando et al. 2007) and reproductive tract lesions (Newbold et al. 2007), increased prostate size (Timms et al. 2005), and decreased sperm production (vom Saal et al. 1998) in offspring. Most recently, exposure to BPA has also been associated with chronic disease in humans, including cardiovascular disease, diabetes, and serum markers of liver disease (Lang et al. 2008).
Orally administered BPA is rapidly metabolized by glucuronidation during first-pass metabolism, with a biological half-life of approximately 6 hr and nearly complete elimination within 24 hr (Volkel et al. 2002). However, because of continuous and widespread exposure, > 92% of the 2,517 participants ≥ 6 years of age in the U.S. 2003–2004 National Health and Nutrition Examination Survey (NHANES) had detectable concentrations of BPA in their urine (Calafat et al. 2008). The geometric mean (GM) urinary BPA concentration in that study was 2.6 μg/L (2.6 μg/g creatinine), and the 95th percentile was 15.9 μg/L (11.2 μg/g creatinine).
An important source of human exposure is thought to be the ingestion of food and drink that has been in contact with epoxy resins or polycarbonate plastics (Kang et al. 2006). Polycarbonate is a durable, lightweight, and heat-resistant plastic, making it popular for use in plastic food and beverage containers. Indeed, nearly three-fourths of the 1.9 billion pounds of BPA used in the United States in 2003 was used for the manufacture of polycarbonate resin (CERHR 2008). Other common uses of BPA include the manufacture of epoxy resins used as composites and sealants in dentistry and in the lacquer lining of aluminum food and beverage cans (CERHR 2008; European Union 2003).
Laboratory studies have demonstrated that biologically active BPA is released from polycarbonate bottles after simulated normal use (Brede et al. 2003; Le et al. 2008). High temperatures as well as acidic and alkali solutions cause polymer degradation via hydrolysis, resulting in increased BPA migration. After incubation for 8, 72, and 240 hr in food-simulating solvents (10% ethanol at 70°C and corn oil at 100°C), mean BPA migration increased with incubation time (Onn Wong et al. 2005). After a sequence of washing and rinsing, Le et al. (2008) found that new polycarbonate bottles leached 1.0 ± 0.3 μg/mL BPA (mean ± SD) into the bottle content after incubation at room temperature for 7 days. Although exposure to boiling water increased the rate of BPA migration up to 55-fold, used bottles did not leach significantly more BPA than new ones. However, other studies have found that higher concentrations of BPA leach from used polycarbonate plastic than from new. BPA has been observed to leach from polycarbonate animal cages after 1 week of incubation at room temperature, with higher levels of migration from used versus new cages (Howdeshell et al. 2003). Similarly, after incubation in 100°C water for 1 hr, the amount of BPA leached from baby bottles subjected to simulated use (including dishwashing, boiling, and brushing into the bottle) exceeded the amount that leached from new baby bottles (Brede et al. 2003).
Recently, some polycarbonate bottle manufacturers voluntarily eliminated BPA from their products (Nalgene Outdoor 2008), and several retailers withdrew polycarbonate bottles from their stores altogether (Mui 2008). Canada has imposed a ban on the use of BPA in polycarbonate baby bottles in order to reduce exposure of infants to BPA (Health Canada 2008), and similar legislation is being considered by several U.S. states (Austen 2008). However, such actions have been largely preemptive, as no epidemiologic study has evaluated the physiologic consequences of polycarbonate bottle use. Therefore, we studied the impact of cold beverage consumption from polycarbonate bottles on measurable urinary BPA concentrations among a Harvard College population. We also measured exposure to the phenols triclosan (TCS), methyl paraben (MePB), propyl paraben (PrPB), and benzophenone-3 (BP-3), which occurs mainly through the use of personal care products. Therefore, because exposure of these chemicals is considered unrelated to polycarbonate bottle use, we assessed their association with polycarbonate bottle use as a negative control
Furthermore, we assessed the impact of polycarbonate bottle use in a normal use setting. The present study could be considered a conservative estimate of true use, as students did not have access to dishwashers and were instructed to use their containers for cold beverages only, whereas the storage of hot liquids is common, especially in outdoor recreation settings. Because heating is thought to increase the amount of BPA leached from the polycarbonate (Le et al. 2008), we would anticipate higher urinary BPA concentrations after ingestion of hot beverages stored in the same bottles.
http://www.medscape.com/viewarticle/710617?src=mp&spon=9&uac=71630FV
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