National Center for Environmental Assessment, Office of Research and Development, United States Environmental Protection Agency, Washington, DC, USA.
Environ Int. 2012 Dec 1;50:7-14. doi: 10.1016/j.envint.2012.09.002. Epub 2012 Sep 29.
Human biomonitoring studies measuring bisphenol A (BPA) in urine have shown widespread exposure in the general population. Diet is thought to be a major route of exposure. We studied urinary BPA patterns in five individuals over a 48-h period of fasting (bottled water only). Personal activity patterns were recorded with a diary to investigate non-dietary routes of exposure. All urine void events during the fast were collected, as well as events before and after the fast. The pattern of BPA concentrations was similar for all participants: they rose near the beginning of the fast (after the pre-fast meal), declined over the next 24h, fluctuated at lower levels during the second day, and then rose after the post-fast meal. Concentrations (2 μg/g creatine) and calculated BPA intakes (0.03 μg/kg-day) in these individuals during the first 24h were consistent with general population exposures. For the second 24h, concentrations and intakes declined by about two-thirds. One of the individuals had an extraordinary pre-fast exposure event with concentrations rising as high as 98 μg/g creatine but declining to <5 μg/g creatine by day 2. Given patterns found in day 1 and the subsequent decline to lower levels in day 2, we hypothesize that BPA exposures in these individuals were diet-driven. No events in the diary (use of personal care products, e.g.) appear associated with exposures. On day 2, non-dietary sources may still be present, such as from dust. Another hypothesis is that small reservoirs of BPA from past exposures are released from storage (lipid reservoirs, e.g.) and excreted.
人体生物监测研究表明，尿液中的双酚 A（BPA）在普通人群中广泛存在，饮食被认为是主要的暴露途径。我们研究了 5 名个体在禁食（仅瓶装水）48 小时期间的尿液 BPA 模式。通过日记记录个人活动模式，以调查非饮食暴露途径。所有在禁食期间的尿液排泌事件，以及禁食前后的尿液排泌事件都被收集。所有参与者的 BPA 浓度模式相似：它们在禁食开始时（在预禁食餐后）上升，在接下来的 24 小时内下降，在第二天以较低水平波动，然后在禁食后餐后再次上升。这些个体在最初 24 小时内的浓度（2μg/g 肌酸）和计算的 BPA 摄入量（0.03μg/kg-day）与一般人群的暴露量一致。在接下来的 24 小时内，浓度和摄入量下降了约三分之二。其中一名个体在预禁食时出现了异常的暴露事件，浓度高达 98μg/g 肌酸，但到第 2 天降至<5μg/g 肌酸。考虑到第 1 天发现的模式以及随后在第 2 天下降到较低水平，我们假设这些个体的 BPA 暴露是由饮食驱动的。日记中没有记录任何事件（例如，使用个人护理产品）与暴露有关。在第 2 天，非饮食来源（如灰尘）可能仍存在。另一种假设是，过去暴露产生的 BPA 小储存库从储存库（例如脂质储存库）中释放并排泄。
