Dietary intake has been estimated to be the major ongoing pathway of human exposure to perfluoroalkyl carboxylic acids (PFCAs) and perfluoroalkane sulfonic acids (PFSAs). However, difficulties associated with the analysis of food samples have hampered the reliable quantification of dietary exposure. Here the dietary exposure of the average Swedish population to PFCAs and PFSAs is estimated through analysis of a range of homologues in representative food basket samples from 1999, 2005 and 2010. Exposure to perfluorooctane sulfonate (796−1424 pg kg

-1day-1), perfluoroundecanoic acid (88−212 pg kg-1day-1), perfluorodecanoic acid (52−102 pg kg-1day-1) and perfluorononanoic acid (62−83 pg kg-1day-1) was dominated by the consumption of fish and meat. In contrast, exposure to perfluorooctanoic acid (322−513 pg kg-1day-1) originated from low levels (8−62 pg g-1) found in several ―high consumption‖ food categories including cereals, dairy products, vegetables and fruit. The average body weight normalized dietary intakes (pg kg-1day-1) were fairly constant between 1999 and 2010 for all PFCAs and PFSAs demonstrating that dietary intake has been a continuous exposure pathway for these compounds during this period when many manufacturing changes occurred. Although statistically significant temporal trends in the average dietary intake estimates could not be determined, there is preliminary evidence of a downward time trend in the concentrations of PFOS in eggs and meat products and an upward trend of PFDA, PFUnDA, perfluorododecanoic acid and perfluorotridecanoic acid in fish products, which both warrant further investigation. In line with recent studies, dietary intake was found to be the major ongoing human exposure pathway for both PFOA and PFOS (~70% of the total exposure) for the Swedish population compared to exposure via ingestion of household dust and drinking water. The calculated higher total dietary exposure to PFOA compared to PFNA is consistent with the pattern observed in human serum, although there are several other exposure pathways which could explain this homologue pattern in serum.