Perfluorinated chemicals (PFCs) such as perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) have been produced and used in a wide range of industrial and consumer products for many decades. Their resistance to degradation has led to their widespread distribution in the environment, but little is known about how humans become exposed. Recent studies have demonstrated that the application of PFC contaminated biosolids can have important effects on local environments, ultimately leading to demonstrable human exposures. This manuscript describes a situation in Decatur, Alabama where PFC contaminated biosolids from a local municipal wastewater treatment facility that had received waste from local fluorochemical facilities were used as a soil amendment in local agricultural fields for as many as twelve years. Ten target PFCs were measured in surface and groundwater samples. Results show that surface and well water in the vicinity of these fields had elevated PFC concentrations, with 22% of the samples exceeding the U.S. Environmental Protection Agency's Provisional Health Advisory level for PFOA in drinking water of 400 ng/L. Water/soil concentration ratios as high as 0.34 for perfluorohexanoic acid, 0.17 for perfluoroheptanoic acid, and 0.04 for PFOA verify decreasing mobility from soils with increasing chain length while indicating that relatively high transport from soils to surface and well water is possible.

Despite ongoing efforts to develop robust analytical methods for the determination of perfluorinated compounds (PFCs) such as perfluorooctanesulfonate (PFOS) and perfluorooctanoic acid (PFOA) in surface water, comparatively little has been published on method performance, and the environmental distribution of these materials remains poorly described worldwide. In this study, an existing method was improved and applied in a large-scale evaluation of the Upper Mississippi River Basin, one of the largest watersheds in the world. Samples were collected in 2008 in an effort that involved multiple sample sites and collection teams, long-range transport, and storage of up to 4 weeks before analysis. Ninety-four percent of the resulting 177 samples had quantifiable PFC concentrations, with 80% of the individual target compounds below 10 ng/L. The most abundant PFCs were perfluorobutanoic acid (C4; 77% above the limit of quantitation, LOQ), perfluorooctanoic acid (C8; 73%), perfluorooctanesulfonate (PFOS; 71%), perfluorohexanoic acid (C6; 70%), and perfluoroheptanoic acid (C7; 69%), with the remaining target compounds occurring above the LOQ in less than 50% of the samples. The highest concentrations recorded include C4 at 458 ng/L, PFOS at 245 ng/L, and C8 at 125 ng/L, suggesting various point source inputs within the Basin.

Previous studies in mice with multiple gestational exposures to perfluorooctanoic acid (PFOA) demonstrate numerous dose dependent growth and developmental effects which appeared to worsen if offspring exposed in utero nursed from PFOA-exposed dams. To evaluate the disposition of PFOA in the pregnant and lactating dam and her offspring, time-pregnant CD-1 mice received a single 0, 0.1, 1, or 5 mg PFOA/kg BW dose (n = 25/dose group) by gavage on gestation day 17. Maternal and pup fluids and tissues were collected over time. Pups exhibited significantly higher serum PFOA concentrations than their respective dams, and their body burden increased after birth until at least postnatal day 8, regardless of dose. The distribution of milk:serum PFOA varied by dose and time, but was typically in excess of 0.20. These data suggest that milk is a substantial PFOA exposure route in mice and should be considered in risk assessment modeling designs for this compound.