Serum Perfluorinated Compound Concentration and Attention Deficit/Hyperactivity Disorder in Children 5–18 Years of Age

Department of Preventive Medicine, Mount Sinai School of Medicine, New York, New York, USA.
Environmental Health Perspectives (Impact Factor: 7.98). 06/2011; 119(10):1466-71. DOI: 10.1289/ehp.1003538
Source: PubMed


Perfluorinated compounds (PFCs) are persistent environmental pollutants. Toxicology studies demonstrate the potential for perfluorooctanoic acid (PFOA) and other PFCs to affect human growth and development. Attention deficit/hyperactivity disorder (ADHD) is a developmental disorder with suspected environmental and genetic etiology.
We examined the cross-sectional association between serum PFC concentration and parent or self-report of doctor-diagnosed ADHD with and without current ADHD medication.
We used data from the C8 Health Project, a 2005-2006 survey in a Mid-Ohio Valley community highly exposed to PFOA through contaminated drinking water, to study non-Hispanic white children 5-18 years of age. Logistic regression models were adjusted for age and sex.
Of the 10,546 eligible children, 12.4% reported ADHD and 5.1% reported ADHD plus ADHD medication use. We observed an inverted J-shaped association between PFOA and ADHD, with a small increase in prevalence for the second quartile of exposure compared with the lowest, and a decrease for the highest versus lowest quartile. The prevalence of ADHD plus medication increased with perfluorohexane sulfonate (PFHxS) levels, with an adjusted odds ratio of 1.59 (95% confidence interval, 1.21-2.08) comparing the highest quartile of exposure to the lowest. We observed a modest association between perfluorooctane sulfonate and ADHD with medication.
The most notable finding for PFOA and ADHD, a reduction in prevalence at the highest exposure level, is unlikely to be causal, perhaps reflecting a spurious finding related to the geographic determination of PFOA exposure in this population or to unmeasured behavioral or physiologic correlates of exposure and outcome. Possible positive associations between other PFCs and ADHD, particularly PFHxS, warrant continued investigation.

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    • "Among these studies, two reported increased attention deficit and hyperactivity disorder (ADHD) prevalence and symptomatology associated with PFASs exposure (Gump et al., 2011; Hoffman et al., 2010). The third study reported increased prevalence of ADHD associated with PFOS exposure (and other PFASs), but a nonmonotonic dose response curve with a marked decreased risk in the highest exposure concentrations of PFOA (Stein and Savitz, 2011). Five longitudinal studies were based on the general population in Denmark, Taiwan and United States (Chen et al., 2013; Fei and Olsen, 2011; Fei et al., 2008; Stein et al., 2013; Strøm et al., 2014). "
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    ABSTRACT: Perfluoroalkyl substances (PFASs) are chemicals with potential neurotoxic effects although the current evidence is still limited. This study investigated the association between perinatal exposure to perfluorooctanesulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) and neuropsychological development assessed at 6, 12 and 24months. We measured PFOS and PFOA in breast milk samples collected one month after delivery by mothers of children participating in the HUMIS study (Norway). Cognitive and psychomotor development was measured at 6 and at 24months using the Ages and Stages Questionnaire (ASQ-II). Behavioral development was assessed using the infant-toddler symptom checklist (ITSC) at 12 and at 24months. Weighted logistic regression and weighted negative binomial regression models were applied to analyze the associations between PFASs and ASQ-II and ITSC, respectively. The median concentration of PFOS was 110ng/L, while the median for PFOA was 40ng/L. We did not detect an increased risk of having an abnormal score in ASQ-II at 6months or 24months. Moreover, no consistent increase in behavioral problems assessed at 12 and 24months by ITSC questionnaire was detected. We observed no association between perinatal PFOS and PFOA exposure and early neuropsychological development. Further longitudinal studies are needed to confirm the effects of these compounds on neuropsychological development in older children. Copyright © 2015. Published by Elsevier Ltd.
    Environment international 07/2015; 83:176-182. DOI:10.1016/j.envint.2015.06.013 · 5.56 Impact Factor
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    • "These include hepatotoxicity, tumor induction, developmental toxicity, immunotoxicity, endocrine disruption , and neurotoxicity. In humans, epidemiological findings based on cross-sectional designs are equivocal; whereas some studies have suggested associations between PFAA exposure and adverse effects on reproductive health, birth weight and pubertal and behavioral development [11] [12] [13] [14] [15] [16] [17] [18], lipid and hormone metabolism [19] [20] [21] [22] and immune responses [23] [24], others failed to detect such linkages [25] [26] [27] [28] [29] [30] [31]. The mechanisms of PFAA toxicity remain largely to be explored, although involvement of peroxisome proliferator-activated receptor-alpha (PPAR␣) pathway has been widely implicated [4] [10] [32]. "
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    ABSTRACT: Perfluorononanoic acid (PFNA) is a ubiquitous and persistent environmental contaminant. Although its levels in the environment and in humans are lower than those of perfluorooctane sulfonate (PFOS) or perfluorooctanoic acid (PFOA), a steady trend of increases in the general population in recent years has drawn considerable interest and concern. Previous studies with PFOS and PFOA have indicated developmental toxicity in laboratory rodent models. The current study extends the evaluation of these adverse outcomes to PFNA in mice. PFNA was given to timed-pregnant CD-1 mice by oral gavage daily on gestational day 1-17 at 1, 3, 5 or 10mg/kg; controls received water vehicle. Dams given 10mg/kg PFNA could not carry their pregnancy successfully and effects of this dose group were not followed. Similar to PFOS and PFOA, PFNA at 5mg/kg or lower doses produced hepatomegaly in the pregnant dams, but did not affect the number of implantations, fetal viability, or fetal weight. Mouse pups were born alive and postnatal survival in the 1 and 3mg/kg PFNA groups was not different from that in controls. In contrast, although most of the pups were also born alive in the 5mg/kg PFNA group, 80% of these neonates died in the first 10 days of life. The pattern of PFNA-induced neonatal death differed somewhat from those elicited by PFOS or PFOA. A majority of the PFNA-exposed pups survived a few days longer after birth than those exposed to PFOS or PFOA, which typically died within the first 2 days of postnatal life. Surviving neonates exposed to PFNA exhibited dose-dependent delays in eye opening and onset of puberty. In addition, increased liver weight seen in PFNA-exposed offspring persisted into adulthood and was likely related to the persistence of the chemical in the tissue. Evaluation of gene expression in fetal and neonatal livers revealed robust activation of peroxisome proliferator-activated receptor-alpha (PPARα) target genes by PFNA that resembled the responses of PFOA. Our results indicate that developmental toxicity of PFNA in mice is comparable to that of PFOS and PFOA, and that these adverse effects are likely common to perfluoroalkyl acids that persist in the body. Copyright © 2014. Published by Elsevier Inc.
    Reproductive Toxicology 12/2014; 51:133-144. DOI:10.1016/j.reprotox.2014.12.012 · 3.23 Impact Factor
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    • "Grandjean et al. (2012) found that elevated exposures to PFAAs were associated with lower serum vaccine antibody concentrations in children. Moreover, potential association between perfluorooctanoic acid (PFOA) exposure and attention deficit/hyperactivity disorder (ADHD) was also determined (Stein et al. 2011). So far, dietary (Fromme et al. 2007), drinking water (Hölzer et al. 2008), house dust (Strynar and Lindstrom 2008), inhalation (Nilsson et al. 2010), as well as biotransformation of potential precursors, such as FTOHs and polyfluoroalkyl phosphate esters (PAPs) (D'eon and Mabury 2011; Nilsson et al. 2010), have been estimated to be significant human exposure pathways to PFAA contaminations. "
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    ABSTRACT: Severe perfluoroalkyl acid (PFAA) contamination resulting from the fast-growing semiconductor, electrochemical, and optoelectronic industries has been determined in the river water in the vicinity of the Taipei area, Taiwan, during recent years. However, little is known about body burdens of the PFAA contaminations in local residents, especially children living in the Taipei area recently. In this study, ten target PFAA analytes consisted of three perfluorosulfonates (PFSAs) and seven perfluorocarboxylates (PFCAs) in the blood serum samples, collected from 225 healthy children with an average age of 13.6 years in the Taipei area from 2009 to 2010, were analyzed via high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). As the dominant PFAA contaminant in the blood serum samples from Taiwanese children, perfluorooctane sulfonate (PFOS) contributed 86 % of all the target PFAA analytes, while the other nine analytes contributed less than 5 % individually. PFOS showed the highest median up to 29 ng/mL, ranging from 0.03 to 148 ng/mL, which was higher than that observed in the serum samples collected from Taiwanese children between 2006 and 2008. Statistically, serum concentrations of perfluorobutane sulfonate (PFBS), perfluorohexane sulfonate (PFHxS), and perfluorooctanoic acid (PFOA) had significantly positive correlations with ages of children (p < 0.05). Furthermore, serum PFBS, PFHxS, and PFOA concentrations in the male children were considerably higher than those in the female children (p = 0.049, p = 0.000, p = 0.000).
    Environmental Science and Pollution Research 03/2014; 21(12). DOI:10.1007/s11356-014-2594-4 · 2.83 Impact Factor
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