You are currently viewing a new version of our website. To view the old version click .
MDPIMDPI
Search all articles
Environments
Download PDF
  • Editor’s Choice
  • Review
  • Open Access

1 September 2024

Impacts of PFAS Exposure on Neurodevelopment: A Comprehensive Literature Review

,
and
1
Interdisciplinary Toxicology Program, University of Georgia, Athens, GA 30602, USA
2
Department of Environmental Health Science, College of Public Health, University of Georgia, Athens, GA 30602, USA
*
Author to whom correspondence should be addressed.
Environments2024, 11(9), 188;https://doi.org/10.3390/environments11090188
Version Notes
Order Reprints

Abstract

Neurodevelopmental disorders (NDDs) encompass a range of conditions that begin during the developmental stage and cause deficits that lead to disruptions in normal functioning. One class of chemicals that is of increasing concern for neurodevelopmental disorders is made up of per- and polyfluoroalkyl substances (PFAS). In this comprehensive literature review, we investigated data from epidemiological studies to understand the connection between PFAS exposure and neurodevelopmental endpoints such as cognitive function, intelligence (IQ), and memory, along with behavioral changes like Attention-Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorders (ASD). When we reviewed the findings from individual studies that analyzed PFAS levels in biological samples and their association with NDD, we concluded that there was a correlation between PFAS and neurodevelopmental disorders. The findings suggest that children exposed to higher PFAS levels could potentially have an increased risk of ASD and ADHD along with an inhibitory effect on IQ. While the results vary from one study to another, there is increasing association between PFAS exposure and neurodevelopmental disorders. Importantly, the findings provide valuable insights into the adverse effects associated with PFAS exposure and neurodevelopment.

1. Introduction

According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), neurodevelopmental disorders (NDD) are defined as a group of conditions with onset in the developmental period, inducing deficits that produce impairments of functioning [1]. Impairments of cellular growth and metabolism during critical periods of prenatal brain development may result from the effects of environmental toxins, nutritional deficits, maternal illnesses, and genetic disorders, alone or in combination [2]. It has been established that the environment plays a crucial role in influencing juvenile health, with an increased risk of negatively affecting neurodevelopment [3]. Additionally, the significant increase in the occurrence of neurodevelopmental disorders suggests that environmental factors could be a major contributing cause [4]. There are approximately 200 chemicals that have been found to be neurotoxic in humans, and there is at least some evidence of neurotoxicity deriving from animal studies for many more [5,6]. However, of over 80,000 chemicals on the market, only a handful (approximately 200) have undergone developmental neurotoxicity testing according to the established guidelines [6,7]. One class of chemicals that is of increasing concern for neurodevelopmental disorders is made up of per- and polyfluoroalkyl substances.
Per- and polyfluoroalkyl substances (PFAS) are a varied collection of synthetic compounds defined by their chemical structure, which includes one or more carbon atoms bonded to fluorine atoms, forming fully fluorinated groups like −CF3 (perfluorinated methyl) or −CF2− (perfluorinated methylene). These substances differ in their carbon chain lengths, the degree of fluorination, and the types of additional chemical groups that they may contain [8]. The development of PFAS began in the 1930s, and their unique property of interacting with both hydrophobic and hydrophilic substances has driven their widespread adoption in a range of industrial and commercial uses [9]. PFAS are often used for their “non-stick” and surface-tension-lowering properties, which makes them useful for repelling oil and water (preventing stains) and modifying surface chemistry [10]. Humans are exposed to PFAS primarily through consuming contaminated food and water, inhaling or ingesting dust and fumes from PFAS-containing items found in residential and office environments, and through occupational contact in industries that manufacture or utilize PFAS [11,12]. The most significant source of human exposure to PFAS is dietary intake (food and water) [13]. In certain situations, the intake of PFAS through drinking water can be just as significant as dietary sources of these chemicals [14]. Several studies have detected PFAS in surface- and groundwater worldwide, both of which are important sources for drinking water production and as a result, public concern has arisen over human exposure risks to PFAS [15].
Despite the extensive and widespread use of PFAS over recent decades, it was only in recent years that significant attention was paid to human exposure to these chemicals and their potential negative health impacts [16]. PFAS pose numerous environmental and health risks. While some PFAS are regarded as having minimal health impact, others are linked to harmful effects in both humans and wildlife at present environmental exposure levels [17]. PFAS has been associated with adverse effects in many organs and systems, including reproductive [18,19], immune [20,21], endocrine [22,23,24,25], hepatic [26], cardiovascular [27,28], and neurodevelopmental effects [29,30,31,32]. Neurodevelopment begins shortly after conception, around three weeks into pregnancy, and progresses through the stages of infancy and into puberty [33]. Various pieces of evidence indicate that the nervous system in development may be more vulnerable, or differently affected, by toxic exposures compared to the adult nervous system [34].
Extensive research shows that various PFAS are frequently found in pregnant women [35,36,37], and that the placenta is a reasonable target for PFAS [38,39]. PFAS accumulate in the placenta and pass the placental barrier, affecting the developing embryo [40]. Studies have shown that PFAS can cross the placental barrier and are associated with fetal growth restriction, immunosuppression, neurotoxicity, and some other health effects [41,42]. The ability of PFAS to pass through the placenta varies depending on factors such as the length of the carbon-fluorine chain, the presence of functional groups, and the overall chemical structure. This process is largely influenced by the interaction of PFAS with serum carrier proteins and placental transport mechanisms [43]. Furthermore, It has been observed that young children tend to reach their highest PFAS concentrations before the age of two [44], possibly due to cumulative exposure via breastfeeding [45,46]. The combination of exposure routes from gestation through adolescence makes PFAS an agent of neurodevelopmental toxicity. Increasing evidence from epidemiological research suggests that exposure to PFAS during pregnancy might influence neurodevelopment in children. This could affect various cognitive functions, including learning, IQ, and memory, and may also be related to behavioral disorders such as ADHD and Autism Spectrum Disorders (ASD) [11,47]. While IQ, ASD, and ADHD constitute prominent endpoints in the study of neurodevelopmental disorders, the broader category of neurodevelopmental disorders encompass a range of complex conditions marked by impairments in cognitive function, communication abilities, behavioral patterns, and motor skills, all stemming from atypical brain development [48].
The US Centers for Disease Control and Prevention (CDC) has reported, based on findings from the National Health and Nutrition Examination Survey (NHANES), that PFAS have been found in the bloodstream of 97% of people in the United States [49]. With the omnipresence of PFAS in humans, there is an increasing concern of PFAS exposure throughout prenatal and postnatal development. Given the increasing concerns, through this review, we explore epidemiological studies examining the association between early-life PFAS exposure and childhood neurodevelopmental disorders, specifically focusing on IQ, ADHD, and ASD.

2. Materials and Methods

2.1. Data Sourcing

To investigate the neurodevelopmental toxicity of per- and polyfluoroalkyl substances, a comprehensive literature search was conducted using PubMed. The search strategy included a combination of keywords related to PFAS and neurodevelopmental outcomes. The primary search terms used were: “PFAS”, “per- and polyfluoroalkyl substances”, “neurodevelopment”, “IQ”, “intelligence quotient”, “ASD”, “autism spectrum disorder”, “ADHD”, and “attention deficit hyperactivity disorder”. These terms were combined using the Boolean operators “AND” and “OR” to form the search string: (“PFAS” OR “per- and polyfluoroalkyl substances”) AND (“neurodevelopment” OR “IQ” OR “intelligence quotient” OR “ASD” OR “autism spectrum disorder” OR “ADHD” OR “attention deficit hyperactivity disorder”). Studies had to include clear exposure assessment for PFAS in humans. We included all primary epidemiological studies that presented quantitative measures of the association between at least one type of PFAS and at least one neurodevelopmental disorder. Specifically, this encompassed research that provided statistical estimates of how PFAS exposure correlates with neurodevelopmental outcomes. We excluded studies that were reviews or focused on non-epidemiological aspects, such as mechanistic studies, in vitro experiments, or animal research. Additionally, we did not consider human studies that failed to provide quantitative estimates of the relationship between PFAS and neurodevelopmental disorders. (Figure 1).
Figure 1. Study Flow Design.

2.2. Exposure Assessment

Exposure assessment in the included studies primarily involved measuring concentrations of PFAS compounds in biological samples, such as serum or plasma, from participants. These measurements were typically obtained through high-performance liquid chromatography coupled with tandem mass spectrometry (HPLC–MS/MS), a highly sensitive and specific analytical method [50,51]. However, a subset of studies employed liquid chromatography (LC), indicating a variability of results. The studies varied in the specific PFAS compounds assessed, with common ones including perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), and perfluorohexanesulfonic acid (PFHxS). Additionally, the timing of exposure assessment ranged from prenatal (e.g., maternal blood or cord blood) to postnatal periods, reflecting critical windows of neurodevelopmental susceptibility [52]. These observations highlight the diversity in methods and compounds analyzed, as well as the broad range of timing the exposure assessments, which collectively contribute to our understanding of PFAS exposure in relation to neurodevelopmental disorders.

2.3. Outcomes

The assessment of neurodevelopmental outcomes such as the Intelligence Quotient (IQ), Autism Spectrum Disorder (ASD), and Attention-Deficit Hyperactivity Disorder (ADHD) in the included studies utilized standard and accepted means of evaluating neurodevelopmental disorders. The Intelligence Quotient (IQ) was evaluated using widely recognized tests including Wechsler Intelligence Scale for Children-Fourth Edition (WISC-IV) and the Full-Scale Intelligence Quotient (FSIQ) [53,54]. For the diagnosis of ASD, studies often relied on established diagnostic criteria from the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), employing tools like Mullen Scales of Early Learning (MSEL) and the Behavioral Assessment System for Children-2 (BASC-2) [55,56]. Finally, ADHD was assessed and diagnosed using the criteria laid out in the DSM-5. These diagnostic tools included ADHD Rating Scale (ADHD-RS) and the Child Behavior Checklist (CBCL) [57,58]. These assessment tools ensure that the neurodevelopmental outcomes were accurately assessed to allow comparison between studies.

2.4. Covariates

Throughout the various studies between PFAS and neurodevelopment, several covariates were considered to control for potential confounding variables within each study. Commonly adjusted covariates included sociodemographic variables such as child’s age, sex, parental education, household income, and maternal age at childbirth. Additionally, studies accounted for smoking, country of birth, and quality of the child’s home environment. By controlling for certain covariates, the studies reduced bias and confounding variables to more accurately assess the relationship between PFAS and neurodevelopmental endpoints, such as IQ, ASD, and ADHD.

2.5. Data Extraction

Data extraction was conducted systematically using a standardized form to ensure consistency and comprehensiveness across all included studies. Key information collected included the following: authors’ names, publication year, study design, sample size, and population characteristics such as age, sex, and geographic location. PFAS exposure assessment was recorded, including the types of PFAS compounds measured, biological sample type, and concentration levels. For neurodevelopmental outcomes, data on assessment methods for IQ, ASD, and ADHD were extracted, specifying the tools/criteria used for evaluation, such as standardized intelligence tests, diagnostic interviews, and rating scales. Further, sample sizes, confidence intervals, and significance were also noted. Finally, any covariates that were adjusted for throughout the studies were recorded. Using a systematic data extraction process, all necessary information was collected in detail for accurate comparison between studies.

3. Results

3.1. The Intelligence Quotient (IQ)

Within a literature search (Table 1), ten studies focusing on the association between PFAS exposure throughout childhood and the Intelligence Quotient were included [11,59,60,61,62,63,64,65,66,67]. In total, 14 individual PFAS were included, but only PFOS, PFHxS, and PFOA were seen in every study. Cognitive assessments were performed using various standardized tests, primarily the Wechsler Preschool and Primary Scale of Intelligence (WPPSI) and the Full-Scale Intelligence Quotient (FSIQ). Most studies used either one of these main tests or a combination of them. However, Harris et al., 2018 chose to use the Kaufman Brief Intelligence Test (KBIT-2), while Skogheim et al., 2020 employed the Stanford–Binet Intelligence Test. While each study has different testing parameters, an extensive body of research has demonstrated that IQs obtained from different intelligence tests substantially correlate at the group level [68]. The results of the included studies showed conflicting results, but some studies indicated that there was some significant evidence that PFAS could have an inhibitory effect on the Intelligence Quotient. Some of the inconsistent results could be associated with the several covariates such as PFAS exposure levels, child’s age, and child’s sex.
Table 1. Summary of articles, results, and evidence on PFAS exposure to the Intelligence Quotient (IQ).

3.2. Attention-Deficit Hyperactivity Disorder (ADHD)

As a results of the literature search (Table 2), nine primary research studies were identified that focused on PFAS exposure on Attention-Deficit Hyperactivity Disorder (ADHD) [61,66,70,71,72,73,74,75,76]. While eleven PFAS were examined throughout the different studies, PFOS and PFOA were the only PFAS that were included in every study. While there is not a current standardized ADHD test, various tests with the main ADHD criteria being outlined in the Diagnostic and Statistical Manual of Mental Disorders were utilized in the different studies. These include commonly used diagnostic exams such as Attention Syndrome Scale of the Child Behavior Checklist (CBCL-ADHD) and Behavioral Assessment System for Children-2 (BASC-2). Most studies did not show any association between PFAS exposure and ADHD. However, a few studies showed conflicting results. Skogheim et al., 2021 [74] and Itoh et al., 2022 [75] indicated that there could be an inverse, protective effect of PFAS. Furthermore, Kim et al., 2023 [72] and Vuong et al., 2021 [61] indicated that there could be an positive association between PFAS exposure and ADHD. These conflicting results could be associated with the inability to conduct consistent ADHD diagnosis.
Table 2. Summary of articles, results, and evidence on PFAS exposure to Attention-Deficit Hyperactivity Disorder (ADHD).

3.3. Autism Spectrum Disorder (ASD)

Through a systematic literature review (Table 3), six primary clinical studies were identified that focus on associating PFAS exposure with Autism Spectrum Disorder (ASD) [31,74,77,78,79,80]. While ten different PFAS were analyzed, PFOA PFOS, PFHxS, and PFNA appeared in every study. The diagnosis of Autism Spectrum Disorder was conducted through several different standardized exams. The Mullen Scales of Early Leaning (MSEL) or the International Classification of Diseases (ICD)-8 were used in diagnosis in every study, except for Lyall et al., 2018 [80], which used the DSM-5 criteria for diagnosis. Additionally, the Vineland Adaptive Behavioral Scale (VABS) and the Autism Diagnostic Observation Schedule (ADOS) were utilized in corroborating the results of the MSEL and the ICD-8. A majority of the studies showed significant association between PFAS exposure and increased odds of ASD. However, two studies that showed a low protective effect were Lyall et al., 2018 [80] and Skogheim et al., 2021 [74]. This conflicting result could be due to the difference in diagnostic method utilized in the study. The results of these studies indicate that PFAS could have an inhibitory effect on neurodevelopment leading to ASD.
Table 3. Summary of articles, results, and evidence on PFAS exposure to Autism Spectrum Disorder (ASD).

4. Discussion

In this review, we systematically gathered the current available evidence on the effects of early development PFAS exposure with respect to the outcome of neurobehavioral defects in children. Our results indicated that there is a potential effect of PFAS exposure throughout development on the Intelligence Quotient, but the results are inconclusive. Furthermore, recent evidence (since 2022) highlights that PFAS exposure throughout gestation and early childhood has significant adverse effects on both ASD and ADHD. Although some studies have produced conflicting results, the latest research underscores the serious impact of PFAS on these neurodevelopmental disorders, emphasizing the importance of continued investigation to better understand these associations.
Within the past decade, researchers have considered PFAS exposure during gestation and childhood and its association with a variety of neurodevelopmental disorders. There are data supporting the plausibility of PFAS exposure as a risk factor on neurodevelopment through various routes of exposure. Initial exposure of PFAS begins with exposure of the developing fetus [81]. This is due to the ability for PFAS to cross the placenta barrier from a pregnant woman to her fetus [82,83,84]. PFAS has also been shown to expose developing children through breast milk [85,86,87,88]. These early exposure pathways have been positively associated with cardiovascular [89], immunologic [90,91], sexual maturation [92,93], thyroid function [94,95,96], kidney function [97,98], and neurodevelopment outcomes [99,100,101]. Neurodevelopmental Disorders are a class of disorders affecting brain development and function and are characterized by wide genetic and clinical variability [102]. According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), NDDs comprise of Autism Spectrum Disorder, attention-deficit/hyperactivity disorder, and intellectual disabilities [103].
Environmental chemicals and toxins have been correlated with a higher risk of neurodevelopmental impairments [104]. Epidemiological research supports these conclusions by documenting higher rates of birth defects, developmental disabilities, and reduced IQ levels in areas where mothers and children are exposed to various environmental pollutants [105]. The Intelligence Quotient (IQ) is a measure of the progress an individual had made in mental or cognitive development compared to same-aged peers [106]. For groups with neurodevelopmental disorders, mean IQ scores are generally below the population normative mean [107]. The Intelligence Quotient was utilized to assess generalized intellectual disabilities to PFAS exposure. Studies using the Wechsler Preschool and Primary scales of Intelligence (WPPSI) and the Full-Scale Intelligence Quotient (FSIQ) showed conflicting results on early PFAS exposure to intelligence disabilities. Some studies indicated that there was no association between PFAS and inhibition of IQ [11,62,63,66,69]. However, other studies found associations with multiple PFAS and their adverse effects on intelligence [59,60,64,65,67]. There were a few confounding variables that adjusted the association. Goodman et al., 2023 noted that there was a significant association difference between the sex of the child with intellectual deficiencies and that this could be due to sex-specific effect by one or more mechanisms. This suggests that sex could act as an effect modifier rather than just a confounder. While some studies controlled for sex, they may have missed important variations by not examining how sex modifies the association between PFAS exposure and neurodevelopmental outcomes. Future studies should consider stratified analyses or interaction terms to better understand how sex influences these associations.
Attention-Deficit Hyperactivity Disorder (ADHD) is among the most prevalent neurodevelopmental disorders in children, marked by difficulties with attention, excessive activity, and impulsive behavior [108]. Various epidemiological studies have explored the link between early exposure to PFAS and the onset of ADHD during childhood [61,66,70,71,72,73,74,75,76]. Early studies did not find any associations between PFAS and ADHD, however more recent studies have discovered that there is a significant association. In 2022, there were significant changes within the DSM-5 for the diagnosis of ADHD to make the diagnosis more accurate [109]. It was previously presumed that any symptoms of inattention and/or hyperactivity–impulsivity was secondary to ASD and not due to an additional ADHD diagnosis [110]. This could lead to misdiagnosis in ADHD diagnosis, potentially distorting the results of earlier studies on the link between PFAS and ADHD. However, newer research has found a relationship between PFAS exposure at age 2 and the risk of developing ADHD by age 8 [72].
Over the past two decades, the prevalence of Autism Spectrum Disorders has progressively increased [111]. Autism Spectrum Disorder (ASD), characterized by deficits in social communication and restricted, repetitive behaviors or interests, affects approximately 2.3% of 8-year-old children in the US [112]. Studies using the Mullen Scales of Early Learning (MSEL) determined that PFOA had the strongest association with risk of ASD with an odds ratio [OR] per ng/mL increase: 1.99 (95% confidence interval [CI]: 1.20–3.29) [31]. PFOS and PFHxS exhibited borderline associations with elevated risks of Autism Spectrum Disorder (ASD). Specifically, PFOS had an odds ratio of 1.46 (95% CI: 0.98–2.18), suggesting a potential increase in risk, while PFHxS had an odds ratio of 1.03 (95% CI: 0.99–1.08), indicating a similar, though less pronounced, association [79]. However, the remaining PFAS investigated did not show any significant relationship with ASD. The inability to determine association between some PFAS and ASD could be due to the inability to measure PFAS in biological samples over the limit of detection (LOD). Furthermore, evaluating co-occurring conditions in Autism Spectrum Disorder (ASD) is difficult due to the overlap of symptoms with other disorders, the risk of diagnostic overshadowing, and the often unclear presentation of symptoms. These factors make it challenging to accurately assess and differentiate additional conditions in individuals with ASD [113].
Previous studies have considered neurodevelopment as one of the most sensitive endpoints for PFAS exposure. The findings of this extensive review have found significant associations between early-life PFAS exposure and the prevalence neurodevelopmental disorders. Given there is a ubiquitous exposure to PFAS, investigating the association between early-life exposure and neurodevelopmental disorders provides valuable information in understanding PFAS toxicity. Furthermore, the increasing prevalence and improved diagnostic techniques for neurodevelopmental disorders makes it essential to understand the detrimental impacts of environmental pollutants on human health.

5. Conclusions

In this review, PFAS exposure through neurodevelopment was strongly associated with neurodevelopmental disorders, such as ADHD and ASD, and potentially an inhibitory effect on IQ. Importantly, these findings indicate that the ubiquitous exposure of PFAS throughout gestation and into early childhood development could lead to neurodevelopmental disorders. However, there are notable data gaps that need addressing. For instance, high limits of detection (LODs) may have hindered the identification of associations between PFAS and NDD. Developing more sensitive analytical methods for detecting PFAS in biological matrices could enable the identification of lower levels of PFAS and provide crucial data. Further investigation using larger prospective cohort studies with standardized diagnostic methods is essential to confirm these results and elucidate the relationships between PFAS structures and associated risks. Expanding research to fill these data gaps will offer valuable insights into the potential biological mechanisms underlying these adverse effects and guide future studies in this field.

Author Contributions

S.D.C., investigation, formal analysis, writing—original draft, and writing—reviewing and editing. J.-S.W., writing—reviewing and validation and writing. L.T., resources, supervision, funding acquisition, and writing—reviewing and editing. All authors have read and agreed to the published version of the manuscript.

Funding

This research was supported by funding from the U.S Environmental Protection Agency (# 84045301, to L.T.).

Conflicts of Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

References

  1. Morris-Rosendahl, D.J.; Crocq, M.A. Neurodevelopmental disorders—The history and future of a diagnostic concept. Dialogues Clin. Neurosci. 2020, 22, 65–72. [Google Scholar] [CrossRef]
  2. Graf, W.D.; Kekatpure, M.V.; Kosofsky, B.E. Prenatal-onset neurodevelopmental disorders secondary to toxins, nutritional deficiencies, and maternal illness. Handb. Clin. Neurol. 2013, 111, 143–159. [Google Scholar]
  3. Ijomone, O.M.; Olung, N.F.; Akingbade, G.T.; Okoh, C.O.A.; Aschner, M. Environmental influence on neurodevelopmental disorders: Potential association of heavy metal exposure and autism. J. Trace Elem. Med. Biol. 2020, 62, 126638. [Google Scholar] [CrossRef] [PubMed]
  4. Landrigan, P.J.; Lambertini, L.; Birnbaum, L.S. A research strategy to discover the environmental causes of autism and neurodevelopmental disabilities. Environ. Health Perspect. 2012, 120, a258–a260. [Google Scholar] [CrossRef] [PubMed]
  5. Grandjean, P.; Landrigan, P.J. Developmental neurotoxicity of industrial chemicals. Lancet 2006, 368, 2167–2178. [Google Scholar] [CrossRef] [PubMed]
  6. Giordano, G.; Costa, L.G. Developmental neurotoxicity: Some old and new issues. ISRN Toxicol. 2012, 2012, 814795. [Google Scholar] [CrossRef] [PubMed]
  7. Makris, S.L.; Raffaele, K.; Allen, S.; Bowers, W.J.; Hass, U.; Alleva, E.; Calamandrei, G.; Sheets, L.; Amcoff, P.; Delrue, N.; et al. A retrospective performance assessment of the developmental neurotoxicity study in support of OECD test guideline 426. Environ. Health Perspect. 2009, 117, 17–25. [Google Scholar] [CrossRef]
  8. Panieri, E.; Baralic, K.; Djukic-Cosic, D.; Buha Djordjevic, A.; Saso, L. PFAS Molecules: A Major Concern for the Human Health and the Environment. Toxics 2022, 10, 44. [Google Scholar] [CrossRef]
  9. Di Nisio, A.; Pannella, M.; Vogiatzis, S.; Sut, S.; Dall’Acqua, S.; Santa Rocca, M.; Antonini, A.; Porzionato, A.; De Caro, R.; Bortolozzi, M.; et al. Toni and C. Foresta. Impairment of human dopaminergic neurons at different developmental stages by perfluoro-octanoic acid (PFOA) and differential human brain areas accumulation of perfluoroalkyl chemicals. Environ. Int. 2022, 158, 106982. [Google Scholar] [CrossRef]
  10. Sunderland, E.M.; Hu, X.C.; Dassuncao, C.; Tokranov, A.K.; Wagner, C.C.; Allen, J.G. A review of the pathways of human exposure to poly- and perfluoroalkyl substances (PFASs) and present understanding of health effects. J. Expo. Sci. Environ. Epidemiol. 2019, 29, 131–147. [Google Scholar] [CrossRef]
  11. Spratlen, M.J.; Perera, F.P.; Lederman, S.A.; Rauh, V.A.; Robinson, M.; Kannan, K.; Trasande, L.; Herbstman, J. The association between prenatal exposure to perfluoroalkyl substances and childhood neurodevelopment. Environ. Pollut. 2020, 263 Pt B, 114444. [Google Scholar] [CrossRef]
  12. Trudel, D.; Horowitz, L.; Wormuth, M.; Scheringer, M.; Cousins, I.T.; Hungerbühler, K. Estimating consumer exposure to PFOS and PFOA. Risk Anal. 2008, 28, 251–269. [Google Scholar] [CrossRef]
  13. Death, C.; Bell, C.; Champness, D.; Milne, C.; Reichman, S.; Hagen, T. Per-and polyfluoroalkyl substances (PFAS) in livestock and game species: A review. Sci. Total Environ. 2021, 774, 144795. [Google Scholar] [CrossRef]
  14. Ericson, I.M.; Nadal, B.; van Bavel, G.; Lindstrom, J.L. Domingo. Levels of perfluorochemicals in water samples from Catalonia, Spain: Is drinking water a significant contribution to human exposure? Environ. Sci. Pollut. Res. Int. 2008, 15, 614–619. [Google Scholar] [CrossRef]
  15. Banzhaf, S.; Filipovic, M.; Lewis, J.; Sparrenbom, C.J.; Barthel, R. A review of contamination of surface-, ground-, and drinking water in Sweden by perfluoroalkyl and polyfluoroalkyl substances (PFASs). Ambio 2017, 46, 335–346. [Google Scholar] [CrossRef] [PubMed]
  16. Domingo, J.L.; Nadal, M. Human exposure to per- and polyfluoroalkyl substances (PFAS) through drinking water: A review of the recent scientific literature. Environ. Res. 2019, 177, 108648. [Google Scholar] [CrossRef] [PubMed]
  17. Cousins, I.T.; DeWitt, J.C.; Glüge, J.; Goldenman, G.; Herzke, D.; Lohmann, R.; Ng, C.A.; Scheringer, M.; Wang, Z. The high persistence of PFAS is sufficient for their management as a chemical class. Environ. Sci. Process. Impacts 2020, 22, 2307–2312. [Google Scholar] [CrossRef]
  18. Cui, Q.; Pan, Y.; Wang, J.; Liu, H.; Yao, B.; Dai, J. Exposure to per- and polyfluoroalkyl substances (PFASs) in serum versus semen and their association with male reproductive hormones. Environ. Pollut. 2020, 266 Pt 2, 115330. [Google Scholar] [CrossRef] [PubMed]
  19. Gardener, H.; Sun, Q.; Grandjean, P. PFAS concentration during pregnancy in relation to cardiometabolic health and birth outcomes. Environ. Res. 2021, 192, 110287. [Google Scholar] [CrossRef]
  20. Stein, C.R.; McGovern, K.J.; Pajak, A.M.; Maglione, P.J.; Wolff, M.S. Perfluoroalkyl and polyfluoroalkyl substances and indicators of immune function in children aged 12–19 y: National Health and Nutrition Examination Survey. Pediatr. Res. 2016, 79, 348–357. [Google Scholar] [CrossRef]
  21. Papadopoulou, E.; Stratakis, N.; Basagaña, X.; Brantsæter, A.L.; Casas, M.; Fossati, S.; Gražulevičienė, R.; Haug, L.S.; Heude, B.; Maitre, L.; et al. Prenatal and postnatal exposure to PFAS and cardiometabolic factors and inflammation status in children from six European cohorts. Environ. Int. 2021, 157, 106853. [Google Scholar] [CrossRef] [PubMed]
  22. Alderete, T.L.; Jin, R.; Walker, D.I.; Valvi, D.; Chen, Z.; Jones, D.P.; Peng, C.; Gilliland, F.D.; Berhane, K.; Conti, D.V.; et al. Perfluoroalkyl substances, metabolomic profiling, and alterations in glucose homeostasis among overweight and obese Hispanic children: A proof-of-concept analysis. Environ. Int. 2019, 126, 445–453. [Google Scholar] [CrossRef] [PubMed]
  23. Chen, Z.; Yang, T.; Walker, D.I.; Thomas, D.C.; Qiu, C.; Chatzi, L.; Alderete, T.L.; Kim, J.S.; Conti, D.V.; Breton, C.V.; et al. Dysregulated lipid and fatty acid metabolism link perfluoroalkyl substances exposure and impaired glucose metabolism in young adults. Environ. Int. 2020, 145, 106091. [Google Scholar] [CrossRef]
  24. Fan, Y.; Li, X.; Xu, Q.; Zhang, Y.; Yang, X.; Han, X.; Du, G.; Xia, Y.; Wang, X.; Lu, C. Serum albumin mediates the effect of multiple per- and polyfluoroalkyl substances on serum lipid levels. Environ. Pollut. 2020, 266 Pt 2, 115138. [Google Scholar] [CrossRef]
  25. Blomberg, A.J.; Shih, Y.-H.; Messerlian, C.; Jørgensen, L.H.; Weihe, P.; Grandjean, P. Early-life associations between per- and polyfluoroalkyl substances and serum lipids in a longitudinal birth cohort. Environ. Res. 2021, 200, 111400. [Google Scholar] [CrossRef]
  26. Ojo, A.F.; Xia, Q.; Peng, C.; Ng, J.C. Evaluation of the individual and combined toxicity of perfluoroalkyl substances to human liver cells using biomarkers of oxidative stress. Chemosphere 2021, 281, 130808. [Google Scholar] [CrossRef] [PubMed]
  27. Lind, P.M.; Salihovic, S.; van Bavel, B.; Lind, L. Circulating levels of perfluoroalkyl substances (PFASs) and carotid artery atherosclerosis. Environ. Res. 2017, 152, 157–164. [Google Scholar] [CrossRef]
  28. Bjorke-Monsen, A.-L.; Varsi, K.; Averina, M.; Brox, J.; Huber, S. Perfluoroalkyl substances (PFASs) and mercury in never-pregnant women of fertile age: Association with fish consumption and unfavorable lipid profile. BMJ Nutr. Prev. Health 2020, 3, 277–284. [Google Scholar] [CrossRef]
  29. Carstens, K.E.; Freudenrich, T.; Wallace, K.; Choo, S.; Carpenter, A.; Smeltz, M.; Clifton, M.S.; Henderson, W.M.; Richard, A.M.; Patlewicz, G.; et al. Evaluation of Per- and Polyfluoroalkyl Substances (PFAS) In Vitro Toxicity Testing for Developmental Neurotoxicity. Chem. Res. Toxicol. 2023, 36, 402–419. [Google Scholar] [CrossRef]
  30. Chen, N.; Li, J.; Li, D.; Yang, Y.; He, D. Chronic exposure to perfluorooctane sulfonate induces behavior defects and neurotoxicity through oxidative damages, in vivo and in vitro. PLoS ONE 2014, 9, 113453. [Google Scholar] [CrossRef]
  31. Oh, J.; Shin, H.-M.; Kannan, K.; Busgang, S.A.; Schmidt, R.J.; Schweitzer, J.B.; Hertz-Picciotto, I.; Bennett, D.H. Childhood exposure to per- and polyfluoroalkyl substances and neurodevelopment in the CHARGE case-control study. Environ. Res. 2022, 215 Pt 2, 114322. [Google Scholar] [CrossRef]
  32. Yao, H.; Fu, Y.; Weng, X.; Zeng, Z.; Tan, Y.; Wu, X.; Zeng, H.; Yang, Z.; Li, Y.; Liang, H.; et al. The Association between Prenatal Per- and Polyfluoroalkyl Substances Exposure and Neurobehavioral Problems in Offspring: A Meta-Analysis. Int. J. Environ. Res. Public Health 2023, 20, 1668. [Google Scholar] [CrossRef]
  33. Rock, K.D.; Patisaul, H.B. Environmental Mechanisms of Neurodevelopmental Toxicity. Curr. Environ. Health Rep. 2018, 5, 145–157. [Google Scholar] [CrossRef] [PubMed]
  34. Costa, L.G.; Cole, T.B.; Dao, K.; Chang, Y.-C.; Garrick, J.M. Developmental impact of air pollution on brain function. Neurochem. Int. 2019, 131, 104580. [Google Scholar] [CrossRef] [PubMed]
  35. Hamm, M.P.; Cherry, N.M.; Chan, E.; Martin, J.W.; Burstyn, I. Maternal exposure to perfluorinated acids and fetal growth. J. Expo. Sci. Environ. Epidemiol. 2010, 20, 589–597. [Google Scholar] [CrossRef]
  36. Szilagyi, J.T.; Avula, V.; Fry, R.C. Perfluoroalkyl Substances (PFAS) and Their Effects on the Placenta, Pregnancy, and Child Development: A Potential Mechanistic Role for Placental Peroxisome Proliferator-Activated Receptors (PPARs). Curr. Environ. Health Rep. 2020, 7, 222–230. [Google Scholar] [CrossRef] [PubMed]
  37. Erinc, A.; Davis, M.B.; Padmanabhan, V.; Langen, E.; Goodrich, J.M. Considering environmental exposures to per- and polyfluoroalkyl substances (PFAS) as risk factors for hypertensive disorders of pregnancy. Environ. Res. 2021, 197, 111113. [Google Scholar] [CrossRef] [PubMed]
  38. Blake, B.E.; Fenton, S.E. Early life exposure to per- and polyfluoroalkyl substances (PFAS) and latent health outcomes: A review including the placenta as a target tissue and possible driver of peri- and postnatal effects. Toxicology 2020, 443, 152565. [Google Scholar] [CrossRef]
  39. Liu, D.; Yan, S.; Liu, Y.; Chen, Q.; Ren, S. Association of prenatal exposure to perfluorinated and polyfluoroalkyl substances with childhood neurodevelopment: A systematic review and meta-analysis. Ecotoxicol. Environ. Saf. 2024, 271, 115939. [Google Scholar] [CrossRef]
  40. McAdam, J.; Bell, E.M. Determinants of maternal and neonatal PFAS concentrations: A review. Environ. Health 2023, 22, 41. [Google Scholar] [CrossRef]
  41. Cai, D.; Li, Q.-Q.; Chu, C.; Wang, S.-Z.; Tang, Y.-T.; Appleton, A.A.; Qiu, R.-L.; Yang, B.-Y.; Hu, L.-W.; Dong, G.-H.; et al. High trans-placental transfer of perfluoroalkyl substances alternatives in the matched maternal-cord blood serum: Evidence from a birth cohort study. Sci. Total Environ. 2020, 705, 135885. [Google Scholar] [CrossRef]
  42. Gützkow, K.B.; Haug, L.S.; Thomsen, C.; Sabaredzovic, A.; Becher, G.; Brunborg, G. Placental transfer of perfluorinated compounds is selective—A Norwegian Mother and Child sub-cohort study. Int. J. Hyg. Environ. Health 2012, 215, 216–219. [Google Scholar] [CrossRef] [PubMed]
  43. Bloom, M.S.; Varde, M.; Newman, R.B. Environmental toxicants and placental function. Best Pract. Res. Clin. Obstet. Gynaecol. 2022, 85 Pt B, 105–120. [Google Scholar] [CrossRef]
  44. Liu, Y.; Li, A.; Buchanan, S.; Liu, W. Exposure characteristics for congeners, isomers, and enantiomers of perfluoroalkyl substances in mothers and infants. Environ. Int. 2020, 144, 106012. [Google Scholar] [CrossRef]
  45. Brantsæter, A.; Whitworth, K.; Ydersbond, T.; Haug, L.; Haugen, M.; Knutsen, H.; Thomsen, C.; Meltzer, H.; Becher, G.; Sabaredzovic, A.; et al. Determinants of plasma concentrations of perfluoroalkyl substances in pregnant Norwegian women. Environ. Int. 2013, 54, 74–84. [Google Scholar] [CrossRef] [PubMed]
  46. Liew, Z.; Goudarzi, H.; Oulhote, Y. Developmental Exposures to Perfluoroalkyl Substances (PFASs): An Update of Associated Health Outcomes. Curr. Environ. Health Rep. 2018, 5, 1–19. [Google Scholar] [CrossRef] [PubMed]
  47. Gao, X.-X.; Zuo, Q.-L.; Fu, X.-H.; Song, L.-L.; Cen, M.-Q.; Wu, J. Association between prenatal exposure to per- and polyfluoroalkyl substances and neurodevelopment in children: Evidence based on birth cohort. Environ. Res. 2023, 236 Pt 2, 116812. [Google Scholar] [CrossRef] [PubMed]
  48. Mullin, A.P.; Gokhale, A.; Moreno-De-Luca, A.; Sanyal, S.; Waddington, J.L.; Faundez, V. Neurodevelopmental disorders: Mechanisms and boundary definitions from genomes, interactomes and proteomes. Transl. Psychiatry 2013, 3, 329. [Google Scholar] [CrossRef]
  49. Lewis, R.C.; Johns, L.E.; Meeker, J.D. Serum Biomarkers of Exposure to Perfluoroalkyl Substances in Relation to Serum Testosterone and Measures of Thyroid Function among Adults and Adolescents from NHANES 2011–2012. Int. J. Environ. Res. Public Health 2015, 12, 6098–6114. [Google Scholar] [CrossRef]
  50. Da Silva, B.F.; Ahmadireskety, A.; Aristizabal-Henao, J.J.; Bowden, J.A. A rapid and simple method to quantify per- and polyfluoroalkyl substances (PFAS) in plasma and serum using 96-well plates. MethodsX 2020, 7, 101111. [Google Scholar] [CrossRef]
  51. Marra, V.; Abballe, A.; Dellatte, E.; Iacovella, N.; Ingelido, A.M.; De Felip, E. A Simple and Rapid Method for Quantitative HPLC MS/MS Determination of Selected Perfluorocarboxylic Acids and Perfluorosulfonates in Human Serum. Int. J. Anal. Chem. 2020, 2020, 8878618. [Google Scholar] [CrossRef]
  52. Henn, B.C.; Bellinger, D.C.; Hopkins, M.R.; Coull, B.A.; Ettinger, A.S.; Jim, R.; Hatley, E.; Christiani, D.C.; Wright, R.O. Maternal and Cord Blood Manganese Concentrations and Early Childhood Neurodevelopment among Residents near a Mining-Impacted Superfund Site. Environ. Health Perspect. 2017, 125, 067020. [Google Scholar] [CrossRef] [PubMed]
  53. Gansler, D.A.; Varvaris, M.; Schretlen, D.J. The use of neuropsychological tests to assess intelligence. Clin. Neuropsychol. 2017, 31, 1073–1086. [Google Scholar] [CrossRef]
  54. Smelror, R.E.; Ueland, T. Cognitive functioning in early-onset psychosis. In Adolescent Psychosis; Elsevier: Amsterdam, The Netherlands, 2023; Volume 13, pp. 127–152. [Google Scholar]
  55. Chatham, C.H.; Taylor, K.I.; Charman, T.; D’Ardhuy, X.L.; Eule, E.; Fedele, A.; Hardan, A.Y.; Loth, E.; Murtagh, L.; Rubido, M.d.V.; et al. Adaptive behavior in autism: Minimal clinically important differences on the Vineland-II. Autism Res. 2018, 11, 270–283. [Google Scholar] [CrossRef]
  56. Burns, T.G.; King, T.Z.; Spencer, K.S. Mullen scales of early learning: The utility in assessing children diagnosed with autism spectrum disorders, cerebral palsy, and epilepsy. Appl. Neuropsychol. Child 2013, 2, 33–42. [Google Scholar] [CrossRef]
  57. Tsujii, N.; Usami, M.; Naya, N.; Tsuji, T.; Mishima, H.; Horie, J.; Fujiwara, M.; Iida, J. Efficacy and Safety of Medication for Attention-Deficit Hyperactivity Disorder in Children and Adolescents with Common Comorbidities: A Systematic Review. Neurol. Ther. 2021, 10, 499–522. [Google Scholar] [CrossRef] [PubMed]
  58. Biederman, J.; DiSalvo, M.; Vaudreuil, C.; Wozniak, J.; Uchida, M.; Woodworth, K.Y.; Green, A.; Farrell, A.; Faraone, S.V. The child behavior checklist can aid in characterizing suspected comorbid psychopathology in clinically referred youth with ADHD. J. Psychiatr. Res. 2021, 138, 477–484. [Google Scholar] [CrossRef]
  59. Goodman, C.V.; Till, C.; Green, R.; El-Sabbagh, J.; Arbuckle, T.E.; Hornung, R.; Lanphear, B.; Seguin, J.R.; Booij, L.; Fisher, M.; et al. Prenatal exposure to legacy PFAS and neurodevelopment in preschool-aged Canadian children: The MIREC cohort. Neurotoxicol. Teratol. 2023, 98, 107181. [Google Scholar] [CrossRef]
  60. Beck, I.H.; Bilenberg, N.; Möller, S.; Nielsen, F.; Grandjean, P.; Højsager, F.D.; Halldorsson, T.I.; Nielsen, C.; Jensen, T.K. Association Between Prenatal and Early Postnatal Exposure to Perfluoroalkyl Substances and IQ Score in 7-Year-Old Children From the Odense Child Cohort. Am. J. Epidemiol. 2023, 192, 1522–1535. [Google Scholar] [CrossRef] [PubMed]
  61. Vuong, A.M.; Webster, G.M.; Yolton, K.; Calafat, A.M.; Muckle, G.; Lanphear, B.P.; Chen, A. Prenatal exposure to per- and polyfluoroalkyl substances (PFAS) and neurobehavior in US children through 8 years of age: The HOME study. Environ. Res. 2021, 195, 110825. [Google Scholar] [CrossRef]
  62. Wang, H.; Luo, F.; Zhang, Y.; Yang, X.; Zhang, S.; Zhang, J.; Tian, Y.; Zheng, L. Prenatal exposure to perfluoroalkyl substances and child intelligence quotient: Evidence from the Shanghai birth cohort. Environ. Int. 2023, 174, 107912. [Google Scholar] [CrossRef]
  63. Liew, Z.; Ritz, B.; Bach, C.C.; Asarnow, R.F.; Bech, B.H.; Nohr, E.A.; Bossi, R.; Henriksen, T.B.; Bonefeld-Jørgensen, E.C.; Olsen, J. Prenatal Exposure to Perfluoroalkyl Substances and IQ Scores at Age 5; a Study in the Danish National Birth Cohort. Environ. Health Perspect. 2018, 126, 067004. [Google Scholar] [CrossRef] [PubMed]
  64. Wang, Y.; Rogan, W.J.; Chen, H.-Y.; Chen, P.-C.; Su, P.-H.; Chen, H.-Y.; Wang, S.-L. Prenatal exposure to perfluroalkyl substances and children’‘s’ IQ: The Taiwan maternal and infant cohort study. Int. J. Hyg. Environ. Health 2015, 218, 639–644. [Google Scholar] [CrossRef]
  65. Harris, M.H.; Oken, E.; Rifas-Shiman, S.L.; Calafat, A.M.; Ye, X.; Bellinger, D.C.; Webster, T.F.; White, R.F.; Sagiv, S.K. Prenatal and childhood exposure to per- and polyfluoroalkyl substances (PFASs) and child cognition. Environ. Int. 2018, 115, 358–369. [Google Scholar] [CrossRef] [PubMed]
  66. Skogheim, T.S.; Villanger, G.D.; Weyde, K.V.F.; Engel, S.M.; Surén, P.; Øie, M.G.; Skogan, A.H.; Biele, G.; Zeiner, P.; Øvergaard, K.R.; et al. Prenatal exposure to perfluoroalkyl substances and associations with symptoms of attention-deficit/hyperactivity disorder and cognitive functions in preschool children. Int. J. Hyg. Environ. Health 2020, 223, 80–92. [Google Scholar] [CrossRef]
  67. Zhang, B.; Wang, Z.; Zhang, J.; Dai, Y.; Ding, J.; Guo, J.; Qi, X.; Wu, C.; Zhou, Z. Prenatal exposure to per- and polyfluoroalkyl substances, fetal thyroid function, and intelligence quotient at 7 years of age: Findings from the Sheyang Mini Birth Cohort Study. Environ. Int. 2024, 187, 108720. [Google Scholar] [CrossRef] [PubMed]
  68. Bünger, A.; Grieder, S.; Schweizer, F.; Grob, A. The comparability of intelligence test results: Group- and individual-level comparisons of seven intelligence tests. J. Sch. Psychol. 2021, 88, 101–117. [Google Scholar] [CrossRef] [PubMed]
  69. Vuong, A.M.; Yolton, K.; Xie, C.; Dietrich, K.N.; Braun, J.M.; Webster, G.M.; Calafat, A.M.; Lanphear, B.P.; Chen, A. Prenatal and childhood exposure to poly- and perfluoroalkyl substances (PFAS) and cognitive development in children at age 8 years. Environ. Res. 2019, 172, 242–248. [Google Scholar] [CrossRef]
  70. Forns, J.; Verner, M.-A.; Iszatt, N.; Nowack, N.; Bach, C.C.; Vrijheid, M.; Costa, O.; Andiarena, A.; Sovcikova, E.; Høyer, B.B.; et al. Early Life Exposure to Perfluoroalkyl Substances (PFAS) and ADHD: A Meta-Analysis of Nine European Population-Based Studies. Environ. Health Perspect. 2020, 128, 57002. [Google Scholar] [CrossRef]
  71. Dalsager, L.; Jensen, T.K.; Nielsen, F.; Grandjean, P.; Bilenberg, N.; Andersen, H.R. No association between maternal and child PFAS concentrations and repeated measures of ADHD symptoms at age 2(1/2) and 5 years in children from the Odense Child Cohort. Neurotoxicol. Teratol. 2021, 88, 107031. [Google Scholar] [CrossRef]
  72. Kim, J.I.; Kim, B.-N.; Lee, Y.A.; Shin, C.H.; Hong, Y.-C.; Døssing, L.D.; Hildebrandt, G.; Lim, Y.-H. Association between early-childhood exposure to perfluoroalkyl substances and ADHD symptoms: A prospective cohort study. Sci. Total Environ. 2023, 879, 163081. [Google Scholar] [CrossRef] [PubMed]
  73. Liew, Z.; Ritz, B.; von Ehrenstein, O.S.; Bech, B.H.; Nohr, E.A.; Fei, C.; Bossi, R.; Henriksen, T.B.; Bonefeld-Jørgensen, E.C.; Olsen, J. Attention deficit/hyperactivity disorder and childhood autism in association with prenatal exposure to perfluoroalkyl substances: A nested case-control study in the Danish National Birth Cohort. Environ. Health Perspect. 2015, 123, 367–373. [Google Scholar] [CrossRef] [PubMed]
  74. Skogheim, T.S.; Weyde, K.V.F.; Aase, H.; Engel, S.M.; Surén, P.; Øie, M.G.; Biele, G.; Reichborn-Kjennerud, T.; Brantsæter, A.L.; Haug, L.S.; et al. Prenatal exposure to per- and polyfluoroalkyl substances (PFAS) and associations with attention-deficit/hyperactivity disorder and autism spectrum disorder in children. Environ. Res. 2021, 202, 111692. [Google Scholar] [CrossRef] [PubMed]
  75. Itoh, S.; Yamazaki, K.; Suyama, S.; Ikeda-Araki, A.; Miyashita, C.; Bamai, Y.A.; Kobayashi, S.; Masuda, H.; Yamaguchi, T.; Goudarzi, H.; et al. The association between prenatal perfluoroalkyl substance exposure and symptoms of attention-deficit/hyperactivity disorder in 8-year-old children and the mediating role of thyroid hormones in the Hokkaido study. Environ. Int. 2022, 159, 107026. [Google Scholar] [CrossRef] [PubMed]
  76. Quaak, I.; De Cock, M.; De Boer, M.; Lamoree, P.; Leonards, P.; Van de Bor, M. Prenatal Exposure to Perfluoroalkyl Substances and Behavioral Development in Children. Int. J. Environ. Res. Public. Health 2016, 13, 511. [Google Scholar] [CrossRef]
  77. Oh, J.; Bennett, D.H.; Calafat, A.M.; Tancredi, D.; Roa, D.L.; Schmidt, R.J.; Hertz-Picciotto, I.; Shin, H.-M. Prenatal exposure to per- and polyfluoroalkyl substances in association with autism spectrum disorder in the MARBLES study. Environ. Int. 2021, 147, 106328. [Google Scholar] [CrossRef]
  78. Choi, J.W.; Oh, J.; Bennett, D.H.; Calafat, A.M.; Schmidt, R.J.; Shin, H.-M. Prenatal exposure to per- and polyfluoroalkyl substances and child behavioral problems. Environ. Res. 2024, 251 Pt 1, 118511. [Google Scholar] [CrossRef]
  79. Shin, H.-M.; Bennett, D.H.; Calafat, A.M.; Tancredi, D.; Hertz-Picciotto, I. Modeled prenatal exposure to per- and polyfluoroalkyl substances in association with child autism spectrum disorder: A case-control study. Environ. Res. 2020, 186, 109514. [Google Scholar] [CrossRef]
  80. Lyall, K.; Yau, V.M.; Hansen, R.; Kharrazi, M.; Yoshida, C.K.; Calafat, A.M.; Windham, G.; Croen, L.A. Prenatal Maternal Serum Concentrations of Per- and Polyfluoroalkyl Substances in Association with Autism Spectrum Disorder and Intellectual Disability. Environ. Health Perspect. 2018, 126, 017001. [Google Scholar] [CrossRef]
  81. Hoadley, L.; Watters, M.; Rogers, R.; Werner, L.S.; Markiewicz, K.V.; Forrester, T.; McLanahan, E.D. Public health evaluation of PFAS exposures and breastfeeding: A systematic literature review. Toxicol. Sci. 2023, 194, 121–137. [Google Scholar] [CrossRef]
  82. Mamsen, L.S.; Björvang, R.D.; Mucs, D.; Vinnars, M.-T.; Papadogiannakis, N.; Lindh, C.H.; Andersen, C.Y.; Damdimopoulou, P. Concentrations of perfluoroalkyl substances (PFASs) in human embryonic and fetal organs from first, second, and third trimester pregnancies. Environ. Int. 2019, 124, 482–492. [Google Scholar] [CrossRef] [PubMed]
  83. Hanssen, L.; Dudarev, A.A.; Huber, S.; Odland, J.; Nieboer, E.; Sandanger, T.M. Partition of perfluoroalkyl substances (PFASs) in whole blood and plasma, assessed in maternal and umbilical cord samples from inhabitants of arctic Russia and Uzbekistan. Sci. Total Environ. 2013, 447, 430–437. [Google Scholar] [CrossRef]
  84. Chen, F.; Yin, S.; Kelly, B.C.; Liu, W. Isomer-Specific Transplacental Transfer of Perfluoroalkyl Acids: Results from a Survey of Paired Maternal, Cord Sera, and Placentas. Environ. Sci. Technol. 2017, 51, 5756–5763. [Google Scholar] [CrossRef] [PubMed]
  85. Macheka-Tendenguwo, L.R.; Olowoyo, J.O.; Mugivhisa, L.L.; Abafe, O.A. Per- and polyfluoroalkyl substances in human breast milk and current analytical methods. Environ. Sci. Pollut. Res. Int. 2018, 25, 36064–36086. [Google Scholar] [CrossRef]
  86. Timmermann, A.; Avenbuan, O.N.; Romano, M.E.; Braun, J.M.; Tolstrup, J.S.; Vandenberg, L.N.; Fenton, S.E. Per- and Polyfluoroalkyl Substances and Breastfeeding as a Vulnerable Function: A Systematic Review of Epidemiological Studies. Toxics 2023, 11, 325. [Google Scholar] [CrossRef] [PubMed]
  87. Jian, J.-M.; Chen, D.; Han, F.-J.; Guo, Y.; Zeng, L.; Lu, X.; Wang, F. A short review on human exposure to and tissue distribution of per- and polyfluoroalkyl substances (PFASs). Sci. Total Environ. 2018, 636, 1058–1069. [Google Scholar] [CrossRef] [PubMed]
  88. Ragnarsdottir, O.; Abdallah, M.A.; Harrad, S. Dermal uptake: An important pathway of human exposure to perfluoroalkyl substances? Environ. Pollut. 2022, 307, 119478. [Google Scholar] [CrossRef] [PubMed]
  89. Lin, C.-Y.; Lin, L.-Y.; Wen, T.-W.; Lien, G.-W.; Chien, K.-L.; Hsu, S.H.; Liao, C.-C.; Sung, F.-C.; Chen, P.-C.; Su, T.-C. Association between levels of serum perfluorooctane sulfate and carotid artery intima-media thickness in adolescents and young adults. Int. J. Cardiol. 2013, 168, 3309–3316. [Google Scholar] [CrossRef]
  90. Grandjean, P.; Andersen, E.W.; Budtz-Jørgensen, E.; Nielsen, F.; Mølbak, K.; Weihe, P.; Heilmann, C. Serum vaccine antibody concentrations in children exposed to perfluorinated compounds. JAMA 2012, 307, 391–397. [Google Scholar] [CrossRef]
  91. Granum, B.; Haug, L.S.; Namork, E.; Stølevik, S.B.; Thomsen, C.; Aaberge, I.S.; van Loveren, H.; Løvik, M.; Nygaard, U.C. Pre-natal exposure to perfluoroalkyl substances may be associated with altered vaccine antibody levels and immune-related health outcomes in early childhood. J. Immunotoxicol. 2013, 10, 373–379. [Google Scholar] [CrossRef]
  92. White, S.S.; Stanko, J.P.; Kato, K.; Calafat, A.M.; Hines, E.P.; Fenton, S.E. Gestational and chronic low-dose PFOA exposures and mammary gland growth and differentiation in three generations of CD-1 mice. Environ. Health Perspect. 2011, 119, 1070–1076. [Google Scholar] [CrossRef] [PubMed]
  93. Yang, C.; Tan, Y.S.; Harkema, J.R.; Haslam, S.Z. Differential effects of peripubertal exposure to perfluorooctanoic acid on mammary gland development in C57Bl/6 and Balb/c mouse strains. Reprod. Toxicol. 2009, 27, 299–306. [Google Scholar] [CrossRef] [PubMed]
  94. Lopez-Espinosa, M.-J.; Mondal, D.; Armstrong, B.; Bloom, M.S.; Fletcher, T. Thyroid function and perfluoroalkyl acids in children living near a chemical plant. Environ. Health Perspect. 2012, 120, 1036–1041. [Google Scholar] [CrossRef]
  95. Tsai, M.-S.; Lin, C.-C.; Chen, M.-H.; Hsieh, W.-S.; Chen, P.-C. Perfluoroalkyl substances and thyroid hormones in cord blood. Environ. Pollut. 2017, 222, 543–548. [Google Scholar] [CrossRef]
  96. Lin, C.-Y.; Wen, L.-L.; Lin, L.-Y.; Wen, T.-W.; Lien, G.-W.; Hsu, S.H.; Chien, K.-L.; Liao, C.-C.; Sung, F.-C.; Chen, P.-C.; et al. The associations between serum perfluorinated chemicals and thyroid function in adolescents and young adults. J. Hazard. Mater. 2013, 244–245, 637–644. [Google Scholar] [CrossRef] [PubMed]
  97. Kataria, A.; Trachtman, H.; Malaga-Dieguez, L.; Trasande, L. Association between perfluoroalkyl acids and kidney function in a cross-sectional study of adolescents. Environ. Health 2015, 14, 89. [Google Scholar] [CrossRef]
  98. Qin, X.-D.; Qian, Z.; Vaughn, M.G.; Huang, J.; Ward, P.; Zeng, X.-W.; Zhou, Y.; Zhu, Y.; Yuan, P.; Li, M.; et al. Positive associations of serum perfluoroalkyl substances with uric acid and hyperuricemia in children from Taiwan. Environ. Pollut. 2016, 212, 519–524. [Google Scholar] [CrossRef] [PubMed]
  99. Fei, C.; McLaughlin, J.K.; Lipworth, L.; Olsen, J. Prenatal exposure to perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS) and maternally reported developmental milestones in infancy. Environ. Health Perspect. 2008, 116, 1391–1395. [Google Scholar] [CrossRef]
  100. Goudarzi, H.; Nakajima, S.; Ikeno, T.; Sasaki, S.; Kobayashi, S.; Miyashita, C.; Ito, S.; Araki, A.; Nakazawa, H.; Kishi, R. Prenatal exposure to perfluorinated chemicals and neurodevelopment in early infancy: The Hokkaido Study. Sci. Total Environ. 2016, 541, 1002–1010. [Google Scholar] [CrossRef]
  101. Stein, C.R.; Savitz, D.A.; Bellinger, D.C. Perfluorooctanoate and neuropsychological outcomes in children. Epidemiology 2013, 24, 590–599. [Google Scholar] [CrossRef]
  102. Parenti, I.; Rabaneda, L.G.; Schoen, H.; Novarino, G. Neurodevelopmental Disorders: From Genetics to Functional Pathways. Trends Neurosci. 2020, 43, 608–621. [Google Scholar] [CrossRef] [PubMed]
  103. Antolini, G.; Colizzi, M. Where Do Neurodevelopmental Disorders Go? Casting the Eye Away from Childhood towards Adulthood. Healthcare 2023, 11, 1015. [Google Scholar] [CrossRef]
  104. Bragg, M.; Chavarro, J.E.; Hamra, G.B.; Hart, J.E.; Tabb, L.P.; Weisskopf, M.G.; Volk, H.E.; Lyall, K. Prenatal Diet as a Modifier of Environmental Risk Factors for Autism and Related Neurodevelopmental Outcomes. Curr. Environ. Health Rep. 2022, 9, 324–338. [Google Scholar] [CrossRef] [PubMed]
  105. Brabhukumr, A.; Malhi, P.; Ravindra, K.; Lakshmi, P. Exposure to household air pollution during first 3 years of life and IQ level among 6–8-year-old children in India- A cross-sectional study. Sci. Total Environ. 2020, 709, 135110. [Google Scholar] [CrossRef]
  106. Carroll, J.B. Psychometrics, intelligence, and public perception. Intelligence 1997, 24, 25–52. [Google Scholar] [CrossRef]
  107. Iqubal, A.; Ahmed, M.; Ahmad, S.; Sahoo, C.R.; Iqubal, M.K.; Haque, S.E. Environmental neurotoxic pollutants: Review. Environ. Sci. Pollut. Res. 2020, 27, 41175–41198. [Google Scholar] [CrossRef]
  108. Thapar, A.; Cooper, M. Attention deficit hyperactivity disorder. Lancet 2016, 387, 1240–1250. [Google Scholar] [CrossRef] [PubMed]
  109. Koutsoklenis, A.; Honkasilta, J. ADHD in the DSM-5-TR: What has changed and what has not. Front. Psychiatry 2022, 13, 1064141. [Google Scholar] [CrossRef]
  110. Association, A.P. Diagnostic and Statistical Manual of Mental Disorders; American Psychiatric Association: Washington, DC, USA, 2000. [Google Scholar]
  111. Wang, L.; Wang, B.; Wu, C.; Wang, J.; Sun, M. Autism Spectrum Disorder: Neurodevelopmental Risk Factors, Biological Mechanism, and Precision Therapy. Int. J. Mol. Sci. 2023, 24, 1819. [Google Scholar] [CrossRef]
  112. Hirota, T.; King, B.H. Autism Spectrum Disorder: A Review. JAMA 2023, 329, 157–168. [Google Scholar] [CrossRef]
  113. Rosen, T.E.; Mazefsky, C.A.; Vasa, R.A.; Lerner, M.D. Co-occurring psychiatric conditions in autism spectrum disorder. Int. Rev. Psychiatry 2018, 30, 40–61. [Google Scholar] [CrossRef] [PubMed]
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Article Metrics

Citations

Article Access Statistics

Journal Statistics
Multiple requests from the same IP address are counted as one view.
Download PDF
Advancements on Ultrasonic Degradation of Per- and Polyfluoroalkyl Substances (PFAS): Toward Hybrid Approaches
Previous
Low Concentrations of Biochar Improve Germination and Seedling Development in the Threatened Arable Weed Centaurea cyanus
Next