Perfluorinated Sulfonamides in Indoor and Outdoor Air and Indoor Dust: Occurrence, Partitioning, and Human Exposure

Abstract
Perfluorinated alkyl sulfonamides (PFASs) which are used in a variety of consumer products for surface protection were investigated through a comprehensive survey of indoor air, house dust, and outdoor air in the city of Ottawa, Canada. This study revealed new information regarding the occurrence and indoor air source strength of several PFASs including N-methylperfluorooctane sulfonamidoethanol (MeFOSE), N-ethylperfluorooctane sulfonamidoethanol (EtFOSE), N-ethylperfluorooctane sulfonamide (EtFOSA), and N-methylperfluorooctane sulfonamidethylacrylate (MeFOSEA). Passive air samplers consisting of polyurethane foam disks were calibrated and used to conduct the indoor and outdoor survey. Indoor air concentrations for MeFOSE and EtFOSE (1490 and 740 pg m-3, respectively) were about 10−20 times greater than outdoor concentrations, establishing indoor air as an important source to the outside environment. EtFOSA and MeFOSEA concentrations were lower in indoor air (40 and 29 pg m-3 respectively) and below detection in outdoor air samples. For indoor dust, highest concentrations were recorded for MeFOSE and EtFOSE with geometric mean concentrations of 110 and 120 ng g-1, while concentrations for EtFOSA and MeFOSEA were below detection and 7.9 ng g-1 respectively. MeFOSE and EtFOSE concentrations in house dust followed levels in indoor air. However, resolution of the coupled air and dust data (for the same homes) was not successful using existing KOA-based models for surface-air exchange. The partitioning to house dust was greatly underpredicted. The difficulties with existing models may be due to the high activity coefficient of PFASs in octanol and/or a situation where the dust is greatly oversaturated with respect to the air due to components of the dust being contaminated with PFASs. A human exposure assessment based on median air and dust concentrations revealed that human exposure through inhalation (100% absorption assumed) and dust ingestion were ∼40 and ∼20 ng d-1, respectively. However, for children the dust ingestion pathway was dominant and accounted for ∼44 ng d-1.

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