Of the 571 study participants 12–15 years of age with complete data, parents of 48 (8.4%) reported that their child had ADHD. Of those, 21 (3.6% of the study population) also reported using prescription medications approved for the treatment of ADHD within the last month. We included one child reported to be taking prescription medication for ADHD but not reported to have been diagnosed with ADHD in analyses as a noncase. Details regarding the total sample size are displayed in the Supplemental Material, Figure 1 (doi:10.1289/ehp.1001898).
Sex and maternal smoking during pregnancy were significantly associated with parental-report of ADHD in bivariate analyses (). Compared with non-Hispanic whites, Mexican Americans were less likely to report ADHD diagnosis [OR = 0.28; 95% confidence interval (CI), 0.11–0.72]. Associations between ETS and ADHD were similar whether ETS was indicated by categorical serum cotinine levels (data not shown) or report of living with someone who smokes cigarettes, cigars, or pipes inside the home. We controlled for ETS in models using report of living in a home with a smoker because data were missing less frequently. ETS was not associated with our stricter case definition of ADHD, having a reported diagnosis and taking prescription medication for the treatment of ADHD, which was similar to what Braun et al. (2006)
observed. We also observed a positive association between lead and ADHD similar to that reported previously in a larger NHANES sample (Braun et al. 2006
Selected population characteristics and bivariate analyses of parental-reported ADHD and covariates.
displays the median serum level of each PFC in the study population. Nearly all study participants had detectable serum concentrations of all four PFCs included in our analyses (> 96% for all PFCs). Other PFCs were detected infrequently in this population. displays the median serum PFC levels according to categorical covariates. Median serum concentrations were consistently higher in males than females and in children who attended preschool. Similarly, those who lived in a home with a smoker consistently had higher PFC levels. displays correlations between continuous covariates and each PFC. With the exception of PFOA, which was weakly correlated with lead, we did not observe evidence of an association between PFCs and lead. Additionally, we observed a small but significant correlation between each PFC and the PIR.
Distribution of PFC levels in the study population (μg/L).
Median serum PFC concentrations (μg/L) by categorical covariates.
Spearman correlations between continuous covariates and PFCs (p-value).
The results of the smoothed analyses suggested that the association between PFC levels and ADHD may be approximately linear over most of the data range; accordingly, we included PFCs in logistic regression models as continuous predictors [see details in Supplemental Material, Figure 2 (doi:10.1289/ehp.1001898)]. We observed a significant (p-value < 0.05) dose–response relationship between PFOS exposure and parent-reported ADHD; the OR for each 1-μg/L increase in serum PFOS was 1.03 (95% CI, 1.01–1.05) () after adjusting for confounding by NHANES sample cycle, age, race/ethnicity, sex, ETS, and maternal smoking during pregnancy. Crude estimates of the association between PFCs and ADHD were similar to adjusted estimates. The inclusion of other covariates, including the PIR, did not materially alter the association between PFCs and parent-reported ADHD (data not shown). PFOA and PFHxS levels were also positively associated with ADHD (PFOA: OR = 1.12; 95% CI, 1.01–1.23; PFHxS: OR = 1.06; 95% CI, 1.02–1.11). The odds of parent-reported ADHD also increased with PFNA concentrations, although not significantly (OR = 1.32; 95% CI, 0.86–2.02). Results were similar when we used the stricter case definition of ADHD that required both parental report and medication use (). The same covariates were evaluated for each case definition.
ORs (95% CIs) for 1-μg/L increase in serum level (n = 571).
Because the range of serum values varied considerably for the PFCs we assessed, we also calculated ORs standardized to an increase in units equal to the IQR for each PFC. An increase in serum PFOS levels equal to the IQR was associated with 1.60 times the odds of ADHD (95% CI, 1.10–2.31; IQR = 15.9 μg/L). For PFOA, the odds of ADHD increased 1.35 times for an increase equal to the IQR (95% CI, 1.04–1.77; IQR = 2.7 μg/L). A 2.9-μg/L increase in serum PFHxS increased the odds of ADHD 1.19 times (95% CI, 1.05–1.34). The IQR effect for PFNA increased ADHD odds 1.15 times (95% CI, 0.93–1.42; IQR = 0.5 μg/L).
Several children had very high serum PFC levels, particularly PFHxS, PFOA, and PFNA. Estimated ORs were slightly higher than those reported in when observations with PFC concentrations more than three times the value of the 75th percentile were excluded (data not shown).
Principal component analyses indicated that PFOS, PFOA, and PFHxS all loaded onto a single component that accounted for 58% of the total variability in all four PFC measures. A second component, which primarily represented PFNA exposure, accounted for an additional 22% of the total variability. We repeated multiple logistic regression analyses including both PFNA and the principal component that represented the weighted combination of PFOS, PFOA, and PFHxS. A positive association with ADHD remained for the combined PFC variable and for PFNA (data not shown; PFOS, PFOA, and PFHxS component p-value = 0.02; PFNA p-value = 0.72).