D'Eon Jessica C, Mabury Scott A
Department of Chemistry, University of Toronto, 80 St. George Street, Toronto, Ontario, Canada M5S 3H6.
Environ Sci Technol. 2007 Jul 1;41(13):4799-805. doi: 10.1021/es070126x.
Perfluorinated acids are detected in human blood world-wide, with increased levels observed in industrialized areas. The origin of this contamination is not well understood. A possible route of exposure, which has received little attention experimentally, is indirect exposure to perfluorinated acids through ingestion of chemicals applied to food contact paper packaging. The current investigation quantified the load of perfluorinated acids to Sprague-Dawley rats upon exposure to polyfluoroalkyl phosphate surfactants (PAPS), nonpolymeric fluorinated surfactants approved for application to food contact paper products. The animals were administered a single dose at 200 mg/kg by oral gavage of 8:2 fluorotelomer alcohol (8:2 FTOH) mono-phosphate (8:2 monoPAPS), or the corresponding di-phosphate (8:2 diPAPS), with blood taken over 15 days post-dosing to monitor uptake, biotransformation, and elimination. Upon completion of the time-course study the animals were redosed using an identical dosing procedure, with sacrifice and necropsy 24 h after the second dosing. Increased levels of perfluorooctanoic acid (PFOA), along with both 8:2 PAPS congeners, were observed in the blood of the dosed animals. In the 8:2 monoPAPS-dosed animals, 8:2 monoPAPS and PFOA blood concentrations peaked at 7900 +/- 1200 ng/g and 34 +/- 4 ng/g respectively. In the 8:2 diPAPS-dosed animals, 8:2 diPAPS peaked in concentration at 32 +/- 6 ng/g, and 8:2 monoPAPS and PFOA peaked at 900 +/- 200 ng/g and 3.8 +/- 0.3 ng/g, respectively. Several established polyfluorinated metabolites previously identified in 8:2 FTOH metabolism studies were also observed in the dosed animals. Consistent with other fluorinated contaminants, the tissue distributions showed increased levels of both PFOA and the 8:2 PAPS congeners in the liver relative to the other tissues measured. Previous investigations have found that PAPS can migrate into food from paper packaging. Here we link ingestion of PAPS with in vivo production of perfluorinated acids.
全氟辛酸在全球范围内的人体血液中均有检出,在工业化地区其含量更高。这种污染的来源尚不清楚。一种可能的接触途径在实验中很少受到关注,即通过摄入应用于食品接触纸包装的化学品而间接接触全氟辛酸。当前的研究对暴露于聚氟烷基磷酸酯表面活性剂(PAPS)的斯普拉格-道利大鼠体内全氟辛酸的负荷进行了量化,PAPS是被批准用于食品接触纸制品的非聚合氟化表面活性剂。通过口服灌胃以200mg/kg的单一剂量给动物施用8:2氟调聚物醇(8:2 FTOH)单磷酸盐(8:2 monoPAPS)或相应的二磷酸盐(8:2 diPAPS),给药后15天内采集血液以监测吸收、生物转化和消除情况。在时间进程研究完成后,使用相同的给药程序对动物进行再次给药,第二次给药后24小时进行处死和尸检。在给药动物的血液中观察到全氟辛酸(PFOA)以及两种8:2 PAPS同系物的水平升高。在8:2 monoPAPS给药的动物中,8:2 monoPAPS和PFOA的血液浓度分别在7900±1200 ng/g和34±4 ng/g时达到峰值。在8:2 diPAPS给药的动物中,8:2 diPAPS的浓度峰值为32±6 ng/g,8:2 monoPAPS和PFOA的峰值分别为900±200 ng/g和3.8±0.3 ng/g。在给药动物中还观察到了先前在8:2 FTOH代谢研究中鉴定出的几种已确定的多氟代谢物。与其他氟化污染物一致,组织分布显示相对于所测量的其他组织,肝脏中PFOA和8:2 PAPS同系物的水平均有所升高。先前的研究发现PAPS可从纸包装迁移到食品中。在此我们将PAPS的摄入与全氟辛酸的体内生成联系起来。