High frequencies of detection were obtained for most of the PFCs ( and ), and PFOS was detected in all samples analyzed. By contrast, PFDoA was detected infrequently—in less than 25% of the samples—and will not be discussed further. Correlations between paired results from the 7 and 14-year-old subjects (N = 79) were relatively poor, with Pearson’s r values of 0.144 for PFOS and 0.168 for PFOA. Likewise, concentrations in the pregnant mothers (N = 12) were poorly associated with those seen in their children five years later.
Serum concentrations (in ng/mL) in 12 Faroese mothers (collected in 2000) and their 5 year old children (collected in 2005)
Serum concentrations (in ng/mL) in the Faroese 7-year-old children (n = 103, collected in 1993–1994) and in the 14-year-old children (n=79, collected in 2000–2001)
The highest average concentrations were for PFOS (with one child at age 7 years exceeding 100 ng/mL), followed by PFOA and the rest of the PFCs ( and ). The PFOS mean increased from 29 ng/mL to 33 ng/mL (p = 0.09) between 7 and 14 years of age, and a 3-fold increase was seen in the PFHxS (p < 0.001, paired t-test) concentrations. However, decreases were observed for PFOA (p = 0.001) and PFOSA (p < 0.001), and Et-PFOSA-AcOH between 7 and 14 years (p < 0.001) (). During the same period, the children did not change their frequency of fish dinners, but whale meat dinners decreased from an average of 1.9 per month at age 7 years to 0.8 at age 14.
We found statistically significant correlations between the concentrations of PFOS and PFOA (r = 0.632, p < 0.0001 for the 7-year-old children and r = 0.494, p < 0.0001 for the 14-year-olds), and between the concentrations of PFOA and PFNA (r = 0.401 for the 7-year-old children, p < 0.0001). The correlation between the concentrations of PFOA and PFNA for the 14-year-olds was not as strong (r = 0.269). Furthermore, the PFOS concentrations correlated well with the combined concentrations of fluorooctanyl sulfonamide derivatives (i.e., PFOSA, Me-PFOSA-AcOH, and Et-PFOSA-AcOH, which are considered precursors of PFOS (15
)), with r = 0.546 (p < 0.0001) for the 7-year-old children and r = 0.635 (p<0.0001) for the 14-year-olds.
In the Faroese paired mother-children samples, mothers had higher PFOS concentrations than their children (p = 0.002; paired t test), but the children had higher concentrations of PFOA (p < 0.001) and PFNA (p = 0.007) than their mothers had five years previously.
Four of the 12 pregnant mothers did not eat pilot whale at all, and their concentrations of Me-PFOSA-AcOH and PFDeA were all <LOD, and the same was true for Et-PFOSA-AcOH for three mothers. Results <LOD were obtained for PFDeA and Et-PFOSA-AcOH only for mothers not eating whale. In children aged 7 years, a tendency of higher PFC concentrations was seen in those who included whale in their diet (data not shown). At age 14 years, PFOS, PFDeA, and PFNA were significantly associated with the frequency of pilot whale dinners (). Fish and whale intakes were poorly correlated (r = 0.07), and the PFCs were not associated with the frequency of fish dinners, except for PFHxS at age 14 (r = 0.24; p < 0.05); adjustment for whale intake decreased the r to 0.19. There was no association with sex.
Mean serum concentrations (in ng/mL) in 79 Faroese adolescents at age 14 years (in 2000–2001) in relation to the monthly number of pilot whale dinners (numbers in parenthesis).
On a relative scale, a high intake of two pilot whale dinners per month is associated with increases in the 14-year serum concentrations of PFOS, PFNA, and PFDeA by almost 25%, 50%, and 100%, when compared to concentrations in subjects eating little or no whale at all (). Fish dinners had a much weaker effect, although each weekly fish dinner augmented the PFHxS concentration by about 10%.