Despite the limitation of a small sample size (30 offices), this is the first systematic examination of air concentrations of PFCs in offices. Significantly different PFC concentrations were observed between buildings, with the highest FTOH air levels measured in the most recently constructed and furnished building, the next highest found in a partially renovated building, and the lowest air levels found in un-renovated buildings. We hypothesize that the differences in PFC air concentrations by building are due to off-gassing of FTOHs from new carpeting, upholstered furniture and/or paint in the renovated buildings. Dinglasan-Panlilio and Mabury22
identified residual unbound FTOHs in a commercially available carpet protector similar to industrial-scale products. 8:2-FTOH was in greatest abundance followed by 10:2-FTOH and then 6:2-FTOH, consistent with the trends we saw in office air. They concluded that the potential exists for a significant proportion of these unbound FTOHs to be released from products. The high air concentrations of FTOHs, particularly 8:2-FTOH, found in Building A in our study may thus be due to the presence of new carpeting and furniture. The low air concentrations of FOSAs/FOSEs observed in this new building may be a consequence of the absence of older carpeting and the withdrawal of sulfonamide products from the market in the early 2000s. The higher air concentrations of MeFOSE in Building B may be explained by the presence of older carpeting in 90% of offices and the fact that MeFOSE was widely used in the past as a stain repellent for carpets.28
Only a few studies have examined concentrations of neutral PFCs in indoor air. Levels of FOSAs/FOSEs measured in office air in this study were much lower than those previously measured in homes in Ottawa29
in 2002–2003 (n=59) and Norway3
in 2005 (n=4), but very similar to those measured more recently in 59 Vancouver homes.30
This difference may be attributable to the withdrawal of sulfonamides from the North American market in the early 2000s. 6:2-FTOH and 10:2-FTOH air levels were somewhat lower in the offices in our study compared to the Norwegian homes and somewhat higher than the Vancouver homes. However, the GM air concentration of 8:2-FTOH measured in our study was 3–5 times higher than those measured in these earlier studies suggesting that offices may represent a unique and important exposure environment.
Serum PFC concentrations among the 31 office workers in this study are consistent with those reported by Calafat and colleagues,4
including the decline in PFOS concentrations observed since the withdrawal from the market of its precursor compounds in the early 2000s. Geometric mean PFOS concentrations in serum of the US general population were 30.4 ng/mL in 1999–2000, 20.7 ng/mL in 2003–2004, and 17.1 ng/mL in 2005–2006.4,27
PFOS concentrations in the serum of workers in our study (collected in 2009) had a GM of 11 ng/mL. Calafat and colleagues4
observed a 100% increase in the GM concentration of PFNA from 0.5 to 1.0 ng/mL between 1999–2000 and 2003–2004. The geometric mean PFNA serum concentration found in our study, 1.6 ng/mL, could support a hypothesis of an increasing temporal trend in US body burdens of PFNA.
To our knowledge, this analysis represents the first PFC exposure assessment to measure both biologic and environmental air samples concurrently. In addition to differences in air concentrations by building, we also observed differences in serum PFCs by building, suggesting a link between the office environment and serum concentrations. We found a strong positive association between FTOH concentrations in office air and PFOA concentrations in serum. We also observed a marginally significant (p=0.10) positive association between FTOHs in office air and PFNA in serum. These results are the first empirical evidence suggesting that exposure to fluorotelomer alcohols in air contribute substantially to the body burden of PFOA and PFNA. The amount of time spent in the office was also an independent predictor of PFOA serum concentrations, providing further evidence that exposures in the office environment contribute to PFC body burden. As would be expected, serum PFOS was not associated with PFCA-precursors in office air. Concentrations of PFOS in serum were also not associated with PFSA-precursors in office air. However, serum PFOS was positively associated with both time spent in office and building, with the highest serum concentrations found in those who worked in the newly constructed Building A. For PFOS, building is likely a surrogate for some other unmeasured exposure—perhaps PFCs in dust.
It is widely recognized that PFOA and PFOS are commonly correlated in human serum, as they were in this study (r = 0.53, p = 0.002), suggesting at least some common exposure pathway. However, because concentrations in serum represent exposure from many sources and over a long period of time, it is difficult to determine the true reason for the correlation in serum of these two compounds. Interestingly, we observed a negative correlation between 8:2-FTOH and EtFOSA in office air (r = −0.36, p = 0.048), precursors of PFOA and PFOS, respectively. This was likely due, in large part, to the withdrawal of sulfonamide compounds from the market in the early 2000s and the continued use of FTOHs since that time. Supporting this theory is the fact that a building-by-building correlation analysis of 8:2-FTOH and EtFOSA revealed that the negative association is driven by data from Building A, the newly constructed office building (r = −0.74, p = 0.09). For Building B and the Other office buildings, the association between the two compounds is positive, weaker, and non-significant (Building B: r = 0.31, p = 0.24; Other: r = 0.53, p = 0.17). We observed an association between 8:2-FTOH in office air and PFOA in serum, suggesting a possible exposure pathway for PFOA body burden. The fact that a similar pathway was not observed for exposure to PFOS could mean that there are other important exposure pathways that PFOA and PFOS share (such as diet or dust) and/or that the correlation of PFOA and PFOS in serum is being strongly influenced by past exposures (when 8:2-FTOH and EtFOSA may possibly have been more correlated in office air).
While our sample size of 31 office workers is fairly small, the study was sufficiently powered to observe statistically significant differences in PFC concentrations by building as well as significant air-serum associations. Dietary factors were evaluated and not found to be significant predictors of PFCs in serum. However, dietary contributions of PFCs are unlikely to confound the observed relationship between FTOHs in office air and PFOA in serum since diet would not be expected to vary by building or be associated with PFCs measured in office air. A more important limitation is the possibility of confounding by exposure to PFOA in air (unmeasured) and to a lower extent, PFCs in office dust. Dust samples were collected from offices in this study and PFC dust results will be presented in a later manuscript. However, preliminary analyses indicate that PFOA in office dust was not correlated with FTOH concentrations in air. Office air concentrations of PFOA would likely be orders of magnitude lower than the much more volatile FTOHs.3,30
Nevertheless, while our results suggest an important contribution of FTOHs in air to PFOA in serum, we cannot rule out contributions by FTOHs in dust or PFOA in dust and air.
While we found a strong association between serum PFOA and PFCA-precursor factor, it is biologically implausible that 6:2-FTOH contributes to serum PFOA. Instead the association is probably being driven by 8:2-FTOH and 10:2-FTOH. 8:2-FTOH metabolizes to PFOA and PFNA in vivo
and in vitro
using rats and rat hepatocytes; 10:2-FTOH can also be metabolized to PFOA.19
Most participants from Buildings A and B had worked in those offices for little more than a year at the time of sampling. If the four days of air sampling is somewhat representative of the entire one-year exposure period, then air exposure during that period is more likely to be predictive of serum levels of PFOA with a serum half-life of 2.3 years7
than PFHxS with a serum
half-life of 7.3 years.8
Some research suggests that exposure to residual FTOHs from consumer products is not likely to be a significant source of PFOA in humans. Vestergren and colleagues18
provide multiple exposure estimates based on a wide range of human behaviors. Notably, in the high-exposure scenario, precursors account for 48–55% of total daily intake for adults and teens, though much of this is attributed to migration of FTOHs from food packaging materials. However, these conclusions were based on exposure models that relied on minimal air data for PFOA-precursors (data from 4 Norwegian homes reported by Barber and colleagues3
). The authors noted that particular sub-groups in the population may receive considerably higher doses from precursor compounds. We posit that residents and workers of newly renovated buildings may be one such sub-group. Importantly, Vestergren and colleagues18
stress that their conclusions are limited by lack of knowledge on the occurrence of PFOA precursors in exposure media such as indoor air and food. Our study specifically addresses this data gap and provides evidence that exposure to PFCs via indoor air in the office environment contributes to PFC body burdens.
Though previous studies have focused on PFCs in the home environment and suggest diet to be the dominant exposure pathway for PFOA,15,16
our results suggest that inhalation of indoor air may represent an important exposure pathway, particularly for office workers. Future studies of PFC exposure should aim to concurrently investigate diet and indoor exposure, but we stress the need to consider the impact of indoor air and varied microenvironments, in particular.