Environmental Factors and ADHD Risk Research Paper

I. Introduction

Attention-Deficit/Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder characterized by persistent patterns of inattention, hyperactivity, and impulsivity, often impairing an individual’s daily functioning and quality of life (American Psychiatric Association, 2013). It is one of the most commonly diagnosed psychiatric disorders in childhood and adolescence, with a substantial impact extending into adulthood (Biederman, 2005). The prevalence of ADHD has been a subject of growing concern, with estimates suggesting that it affects approximately 5-10% of children worldwide (Polanczyk et al., 2015). While genetic factors have long been recognized as contributors to ADHD risk, there is increasing recognition that environmental factors also play a pivotal role in its etiology (Thapar et al., 2013). This research paper aims to investigate the multifaceted relationship between environmental factors and ADHD risk. The research problem addressed herein involves elucidating the specific environmental influences at various life stages that may contribute to the development of ADHD. By conducting a comprehensive examination of the existing literature, this study seeks to provide a clearer understanding of the mechanisms underlying this relationship and offer insights into potential avenues for prevention and intervention. In this pursuit, the following sections will navigate through the various environmental factors, mechanisms, case studies, and implications, contributing to a holistic comprehension of the intricate nexus between environmental factors and ADHD.

II. Literature Review

Overview of existing research on ADHD and its causes

The study of Attention-Deficit/Hyperactivity Disorder (ADHD) has been a subject of extensive research, shedding light on its multifaceted etiology. Historically, ADHD has been attributed primarily to genetic factors, as evidenced by familial aggregation and twin studies (Faraone et al., 2005). However, contemporary research has unveiled a more intricate picture, emphasizing the critical role of environmental factors in ADHD’s development and manifestation. To fully appreciate the complexity of ADHD’s etiology, it is essential to recognize that genetic predisposition alone does not provide a comprehensive understanding of this disorder.

Explanation of the multifactorial nature of ADHD

ADHD’s etiology is inherently multifactorial, encompassing a combination of genetic, neurobiological, environmental, and psychosocial elements (Franke et al., 2012). The intricate interplay among these factors underscores the need for a holistic approach to understanding the disorder. While genetic factors contribute significantly to ADHD risk, they do not operate in isolation. Rather, they interact with environmental influences, resulting in the heterogeneity observed in ADHD presentations and symptom severity (Thapar et al., 2013). Therefore, exploring the role of environmental factors is pivotal in comprehending ADHD’s etiological complexity.

Identification of genetic factors contributing to ADHD risk (briefly)

Genetic research has identified various susceptibility genes associated with ADHD, including genes related to neurotransmitter regulation (e.g., dopamine), neuronal growth, and synaptic plasticity (Faraone et al., 2015). These genetic factors are thought to increase an individual’s vulnerability to ADHD but do not solely account for its onset or severity. Genetic predisposition interacts dynamically with environmental factors, amplifying or mitigating the risk of developing ADHD.

Transition into the main focus on environmental factors

While genetic influences have been a cornerstone of ADHD research, recent attention has shifted toward environmental factors. Environmental factors encompass a wide range of prenatal, early childhood, school-age, and adolescence experiences that can impact an individual’s risk for ADHD. These factors include maternal smoking during pregnancy, exposure to environmental toxins, family environment, diet, academic stressors, and more. The following sections will delve into the intricate web of environmental factors and their potential influence on ADHD risk, highlighting the need to consider both genetic and environmental components when evaluating the etiology of this complex disorder.

III. Environmental Factors and ADHD

Attention-Deficit/Hyperactivity Disorder (ADHD) is a complex neurodevelopmental disorder influenced not only by genetic factors but also by a broad array of environmental influences. This section examines the multifaceted relationship between environmental factors and ADHD risk, categorizing them into distinct life stages: prenatal, early childhood, school-age, and adolescence.

Prenatal Factors

Maternal Smoking during Pregnancy: Maternal smoking during pregnancy has been consistently associated with an increased risk of ADHD in offspring (Langley et al., 2005). Nicotine exposure can disrupt fetal neurodevelopment, affecting the developing brain’s structure and function.

Maternal Alcohol Consumption during Pregnancy: Prenatal alcohol exposure is a well-established risk factor for ADHD (O’Connor & Paley, 2009). It can lead to fetal alcohol spectrum disorders, which may include ADHD-like symptoms.

Exposure to Toxins and Pollutants during Pregnancy: Prenatal exposure to environmental toxins and pollutants, such as lead and pesticides, has been linked to ADHD risk (Braun et al., 2006). These substances can interfere with neurodevelopment and contribute to ADHD symptoms.

Premature Birth and Low Birth Weight: Premature birth and low birth weight are associated with an increased likelihood of ADHD (Indredavik et al., 2005). These factors may disrupt the development of neural pathways and brain structures.

Lead Exposure: Childhood lead exposure, often due to lead-based paint or contaminated soil, has been associated with ADHD (Nigg et al., 2008). Lead can impair cognitive and behavioral functioning, contributing to ADHD symptoms.

Early Childhood Factors

Nutrition and Diet: Diet quality, particularly the consumption of omega-3 fatty acids and certain micronutrients, has been linked to ADHD risk (Ríos-Hernández et al., 2017). Poor nutrition may affect brain development and function.

Parental Stress and Family Environment: High levels of parental stress and adverse family environments are associated with an increased risk of ADHD (Deault, 2010). Stressful family dynamics can impact a child’s emotional and cognitive development.

Exposure to Environmental Toxins (e.g., lead, pesticides): Continued exposure to environmental toxins during early childhood can exacerbate the risk of ADHD (Bouchard et al., 2010). Children are vulnerable to toxins present in their living environments.

Screen Time and Electronic Media Exposure: Excessive screen time and electronic media exposure during early childhood have been linked to ADHD-like symptoms (Swing et al., 2010). These activities may displace other essential developmental experiences.

School-Age Factors

Diet and Nutrition: Inadequate diet and nutritional deficiencies during school-age years can exacerbate ADHD symptoms (Millichap, 2012). Balanced nutrition is vital for optimal brain function.

School and Peer-Related Stressors: High academic and social stressors in school can contribute to the development and worsening of ADHD symptoms (DuPaul & Weyandt, 2006). Peer relationships and school environment play significant roles.

Neighborhood and Community Factors: Neighborhood characteristics, such as exposure to violence or socioeconomic disadvantage, can affect ADHD risk (Leventhal et al., 2015). These factors may contribute to chronic stress and emotional dysregulation.

Impact of Physical Activity and Outdoor Exposure: Lack of physical activity and limited outdoor exposure may exacerbate ADHD symptoms (Daley et al., 2006). Outdoor play and exercise can have positive effects on attention and impulse control.

Adolescence Factors

Continued Exposure to Environmental Toxins: Adolescents may continue to be exposed to environmental toxins, such as air pollution and heavy metals, which can exacerbate ADHD symptoms (Siddique et al., 2011). These toxins may have cumulative effects.

Substance Use and Abuse: Substance use, including alcohol and illicit drugs, is associated with increased ADHD risk (Wilens et al., 2007). Substance abuse can worsen ADHD symptoms and complicate treatment.

Sleep Disturbances: Adolescents with sleep disturbances, such as sleep deprivation or sleep disorders, may experience increased ADHD symptoms (Yoon et al., 2012). Poor sleep can impair cognitive functioning and emotional regulation.

Academic Pressures and Extracurricular Activities: High academic pressures and involvement in numerous extracurricular activities can contribute to ADHD symptomatology in adolescents (Langberg et al., 2008). Balancing academic and social demands is challenging for individuals with ADHD.

Understanding these diverse environmental factors and their contributions to ADHD risk is crucial for developing targeted prevention and intervention strategies that address the multifaceted nature of this disorder.

IV. Mechanisms of Environmental Influence

The relationship between environmental factors and the risk of Attention-Deficit/Hyperactivity Disorder (ADHD) is complex and multifaceted. Environmental influences can shape ADHD risk through various mechanisms that operate at different levels, encompassing neurobiological, epigenetic, and behavioral pathways. This section delves into these mechanisms, offering insights into how environmental factors may exert their impact on ADHD development.

Neurobiological Pathways

1. Neurodevelopmental Disruption: Environmental factors, such as prenatal exposure to toxins or maternal smoking, can disrupt the normal development of the fetal brain. These disruptions may lead to alterations in brain structures and functions implicated in ADHD, such as the prefrontal cortex, basal ganglia, and dopamine systems (Braun et al., 2006). Consequently, compromised neural pathways can result in attentional and executive function deficits characteristic of ADHD.
2. Neurotransmitter Dysregulation: Certain environmental toxins, like lead or pesticides, can interfere with neurotransmitter systems, particularly the dopamine and norepinephrine pathways (Nigg et al., 2008). Dysregulation of these systems is a central feature of ADHD. Neurotransmitter imbalances may impair signal transmission within the brain, contributing to symptoms like inattention and hyperactivity.
3. Neuroinflammation: Environmental factors, such as exposure to air pollution or chronic stress, can trigger neuroinflammatory responses (Calderón-Garcidueñas et al., 2008). Neuroinflammation may alter neural connectivity and function, potentially influencing ADHD risk. It can lead to neurocognitive impairments and emotional dysregulation, hallmark features of the disorder.
4. Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysregulation: Chronic stress during early childhood or adolescence can dysregulate the HPA axis, leading to altered cortisol secretion patterns (Lupien et al., 2009). HPA axis dysregulation has been linked to emotional dysregulation and impaired executive functioning, which are prominent in ADHD.

Epigenetic Pathways

1. DNA Methylation: Environmental factors can induce epigenetic modifications, such as DNA methylation, which can alter gene expression patterns associated with ADHD susceptibility (Rijlaarsdam et al., 2017). For instance, maternal smoking during pregnancy can lead to differential DNA methylation in genes related to neurodevelopment, potentially increasing ADHD risk in offspring.
2. Histone Modifications: Environmental influences can also impact histone modifications, influencing chromatin structure and gene expression. Epigenetic changes in key genes implicated in ADHD, including those involved in dopamine regulation and neural plasticity, may contribute to the disorder’s development (van Mil et al., 2014).
3. MicroRNA Regulation: MicroRNAs, small RNA molecules that regulate gene expression, can be influenced by environmental factors. Dysregulation of microRNA networks has been associated with ADHD-related molecular pathways, suggesting a potential epigenetic link between environmental exposures and ADHD susceptibility (Perroud et al., 2018).

Behavioral Pathways

1. Stress and Coping Mechanisms: Adverse environmental conditions, such as exposure to violence or family stress, can lead to maladaptive stress responses and coping mechanisms in children (Evans, 2003). These responses may include impulsive behaviors and emotional dysregulation, which are core features of ADHD.
2. Dietary Patterns: Nutritional factors, including diet quality and specific nutrient intake, can influence behavior and cognitive functioning (Millichap, 2012). Poor nutrition may lead to fluctuations in blood sugar levels, affecting attention and impulse control in individuals with ADHD.
3. Sedentary Lifestyle: Excessive screen time and reduced physical activity, common in modern childhood, can impact brain development and cognitive functioning (Daley et al., 2006). Sedentary behavior may exacerbate ADHD symptoms by reducing opportunities for self-regulation through physical activity.
4. Sleep Disturbances: Environmental factors that disrupt sleep, such as inadequate sleep hygiene or sleep disorders, can impair attention, mood regulation, and impulse control (Yoon et al., 2012). Sleep disturbances may exacerbate ADHD symptoms, further compromising cognitive and emotional functioning.

Understanding these mechanisms is essential for comprehending how environmental factors contribute to ADHD risk and symptomatology. It underscores the dynamic interplay between genes and the environment, highlighting the role of gene-environment interactions in the disorder’s etiology. Additionally, recognizing these mechanisms provides insight into potential targets for intervention and prevention strategies that can mitigate ADHD risk and improve outcomes for affected individuals. Further research in this area is crucial for a more comprehensive understanding of ADHD’s complex etiology and the development of effective therapeutic approaches.

V. Case Studies and Research Findings

This section presents key studies that have explored the association between specific environmental factors and the risk of Attention-Deficit/Hyperactivity Disorder (ADHD). Each study offers valuable insights into the intricate relationship between environmental exposures and ADHD risk, shedding light on various methodologies and their limitations.

Prenatal Factors

Maternal Smoking during Pregnancy

One seminal study by Thapar et al. (2009) investigated the impact of maternal smoking during pregnancy on ADHD risk. This large-scale longitudinal study followed children from birth to age 7 and found a significant association between maternal smoking during pregnancy and an increased risk of ADHD diagnosis. However, the study faced challenges in accurately measuring smoking exposure, as reliance on self-reported data from mothers may introduce recall bias.

Exposure to Toxins and Pollutants during Pregnancy

Grandjean et al. (2018) conducted a comprehensive meta-analysis examining the effects of prenatal exposure to environmental toxins and pollutants on ADHD risk. Their findings indicated that exposure to lead, mercury, and polychlorinated biphenyls (PCBs) was associated with an elevated risk of ADHD. This study’s strength lies in its synthesis of multiple studies, providing robust evidence. Nonetheless, the complexity of pollutant interactions and variations in exposure levels across different regions pose challenges in interpreting the specific role of each toxin.

Early Childhood Factors

Nutrition and Diet

Millichap and Yee (2012) conducted a review of dietary interventions for ADHD. They found that a diet rich in omega-3 fatty acids and essential nutrients could have a positive impact on ADHD symptoms. However, the study highlighted the heterogeneity of dietary interventions and the need for more controlled trials to establish causal relationships.

Exposure to Environmental Toxins (e.g., lead, pesticides)

Froehlich et al. (2009) conducted a case-control study examining the association between lead exposure and ADHD risk. Their results showed a significant association between elevated blood lead levels in children and an increased risk of ADHD. The study was valuable in demonstrating a dose-response relationship between lead exposure and ADHD severity. Nevertheless, it was limited by its cross-sectional design, which precluded the establishment of causality.

School-Age Factors

School and Peer-Related Stressors

A longitudinal study by Owens et al. (2017) investigated the role of school-related stressors in the development of ADHD symptoms. They found that high levels of academic stress, peer victimization, and school discipline problems were associated with an increased likelihood of developing ADHD symptoms over time. The study’s prospective design provided valuable insights into the temporal relationship between stressors and ADHD symptoms. However, it relied on self-report measures, which may be influenced by reporting biases.

Impact of Physical Activity and Outdoor Exposure

A randomized controlled trial by Tantillo et al. (2013) assessed the effects of an outdoor adventure program on children with ADHD. The study demonstrated that participation in outdoor activities improved attention and executive functioning in children with ADHD. This research contributed to understanding the potential benefits of physical activity and outdoor exposure in ADHD management. However, the study’s generalizability may be limited to specific populations and settings.

Adolescence Factors

Substance Use and Abuse

Molina et al. (2007) conducted a longitudinal study to examine the relationship between substance use and ADHD symptoms during adolescence. They found that substance use significantly exacerbated ADHD symptoms and impaired functional outcomes. This study emphasized the importance of considering comorbidities and their impact on ADHD outcomes. However, it relied on self-reported substance use data, which may be subject to underreporting.

Sleep Disturbances

Langberg et al. (2016) conducted a cross-sectional study examining the prevalence of sleep disturbances in adolescents with ADHD and their impact on ADHD symptom severity. The study revealed a high prevalence of sleep disturbances among adolescents with ADHD and a significant association between poor sleep and greater ADHD symptom severity. This research highlighted the need for comprehensive ADHD assessments that include consideration of sleep patterns. However, the study’s cross-sectional design limited the establishment of causality.

These case studies and research findings collectively underscore the diverse environmental influences on ADHD risk across different life stages. They provide critical insights into the complex interplay between environmental exposures and ADHD development. However, it is essential to acknowledge the limitations inherent in each study, such as recall bias, reliance on self-report data, and difficulties in establishing causality. Further research is needed to elucidate the precise mechanisms through which these environmental factors influence ADHD and to develop more effective prevention and intervention strategies tailored to individuals at risk.

VI. Discussion

The synthesis of evidence presented in the previous sections underscores the intricate relationship between environmental factors and the risk of Attention-Deficit/Hyperactivity Disorder (ADHD). This discussion aims to evaluate the strength of the association between environmental factors and ADHD risk and to consider the implications of these findings for prevention and intervention strategies.

Strength of the Association between Environmental Factors and ADHD Risk

The evidence reviewed reveals a compelling association between environmental factors and ADHD risk across various life stages. Prenatal factors, such as maternal smoking, alcohol consumption, and exposure to toxins, exhibit consistent links with increased ADHD risk (Langley et al., 2005; O’Connor & Paley, 2009; Braun et al., 2006). Early childhood factors, including nutrition, family environment, and exposure to environmental toxins, also demonstrate significant associations with ADHD (Ríos-Hernández et al., 2017; Deault, 2010; Bouchard et al., 2010). School-age and adolescence factors, such as academic stressors, physical activity, substance use, and sleep disturbances, further contribute to the complexity of ADHD etiology (Owens et al., 2017; Daley et al., 2006; Molina et al., 2007; Langberg et al., 2016).

However, it is crucial to recognize that the strength of these associations varies depending on the specific environmental factor, the timing of exposure, and individual susceptibility. While some factors, like maternal smoking during pregnancy and lead exposure, exhibit relatively strong links to ADHD risk, others, such as dietary patterns and screen time, may have more moderate or context-dependent associations. Additionally, the multifactorial nature of ADHD suggests that no single environmental factor operates in isolation. Gene-environment interactions further complicate the assessment of the strength of these associations. Therefore, a comprehensive understanding of ADHD etiology requires considering the cumulative impact of multiple environmental factors and their interactions with genetic predispositions.

Implications for Prevention and Intervention Strategies

The insights gained from the examination of environmental factors in ADHD risk have several implications for prevention and intervention strategies:

1. Prenatal Care and Education: Early interventions should focus on educating expectant mothers about the risks associated with maternal smoking and alcohol consumption during pregnancy. Healthcare providers can play a pivotal role in identifying at-risk mothers and providing guidance on smoking cessation and alcohol abstinence (Thapar et al., 2009).
2. Environmental Regulation and Public Policy: Policy measures aimed at reducing exposure to environmental toxins, such as lead and pesticides, are crucial in minimizing their impact on ADHD risk (Froehlich et al., 2009). Stricter regulations on lead paint and pesticide use can help protect children from harmful exposures.
3. Nutritional Interventions: Dietary interventions that promote balanced nutrition and supplementation of essential nutrients, particularly omega-3 fatty acids, may benefit children with ADHD (Millichap and Yee, 2012). Promoting healthy eating habits and addressing dietary deficiencies can be integral components of ADHD management.
4. Stress Reduction and Coping Skills: Schools and families can implement stress reduction programs and teach coping skills to children facing academic and peer-related stressors (Owens et al., 2017). This can help mitigate the impact of chronic stress on ADHD symptomatology.
5. Physical Activity and Outdoor Exposure: Encouraging physical activity and outdoor play can be an effective strategy to improve attention and impulse control in children with ADHD (Tantillo et al., 2013). Incorporating outdoor activities into educational settings may also be beneficial.
6. Early Identification and Intervention: Identifying ADHD symptoms early and providing evidence-based interventions, including behavioral therapy and, in some cases, medication, can mitigate the impact of environmental risk factors (American Academy of Pediatrics, 2019). Timely interventions can enhance the child’s coping mechanisms and academic performance.
7. Parental Education and Support: Parents should be educated about the potential impact of environmental factors on ADHD risk. Support groups and parenting programs can help families navigate the challenges associated with environmental risk factors and ADHD management (Deault, 2010).
8. Comprehensive Assessment: Healthcare providers and educators should conduct comprehensive assessments of children with ADHD, including evaluations of sleep patterns, substance use, and nutritional habits (Langberg et al., 2016). Identifying and addressing comorbid conditions and lifestyle factors can improve treatment outcomes.

In conclusion, the evidence reviewed in this paper underscores the significant role of environmental factors in ADHD risk. While the strength of these associations varies, the multifactorial nature of ADHD suggests that a comprehensive approach is necessary for understanding its etiology and developing effective prevention and intervention strategies. By addressing environmental influences in tandem with genetic predispositions, healthcare providers, educators, and policymakers can work collaboratively to reduce the burden of ADHD and improve the lives of individuals affected by this complex disorder. Further research is essential to refine our understanding of specific environmental factors, their mechanisms of influence, and their interactions with genetic vulnerabilities.

VII. Conclusion

This research paper has delved into the complex interplay between environmental factors and the risk of Attention-Deficit/Hyperactivity Disorder (ADHD). As we conclude, it is crucial to summarize the main findings, emphasize the significance of understanding environmental factors in ADHD risk, suggest future research directions, and offer practical recommendations for parents, educators, and policymakers.

Main Findings

The main findings of this research paper can be distilled into several key points:

• Environmental factors play a pivotal role in ADHD risk across various life stages, including prenatal, early childhood, school-age, and adolescence.
• Specific environmental factors, such as maternal smoking during pregnancy, lead exposure, academic stressors, and substance use, have been consistently associated with an increased risk of ADHD.
• Mechanisms through which environmental influences operate encompass neurobiological, epigenetic, and behavioral pathways, highlighting the complexity of ADHD etiology.
• The strength of associations between environmental factors and ADHD risk varies depending on factors such as timing of exposure, individual susceptibility, and gene-environment interactions.
• Preventive and intervention strategies should consider the multifaceted nature of ADHD etiology, addressing both genetic and environmental components.

Significance of Understanding Environmental Factors in ADHD Risk

Understanding the role of environmental factors in ADHD risk holds profound implications:

• It allows for a more comprehensive understanding of ADHD’s complex etiology, moving beyond the historical emphasis on genetic factors alone.
• It provides opportunities for early identification of at-risk individuals and targeted interventions to mitigate ADHD risk.
• It underscores the importance of environmental regulation and public policy measures aimed at reducing exposure to toxins and promoting healthy lifestyles.
• It empowers parents, educators, and healthcare providers with knowledge to implement evidence-based strategies for ADHD prevention and management.

Future Research Directions

To advance our understanding of environmental factors in ADHD risk, future research should focus on:

• Exploring gene-environment interactions to identify genetic markers that modulate the impact of environmental exposures on ADHD risk.
• Conducting longitudinal studies to assess the long-term effects of early environmental influences on ADHD outcomes into adulthood.
• Investigating the role of additional environmental factors, such as dietary additives, prenatal stress, and social determinants of health, in ADHD risk.
• Expanding research into potential sex-specific differences in how environmental factors influence ADHD risk.
• Examining the effectiveness of preventive interventions and early-life interventions aimed at reducing environmental risk factors associated with ADHD.

Practical Recommendations

For parents, educators, and policymakers, practical recommendations include:

• Promoting maternal health and education about the risks of maternal smoking and alcohol consumption during pregnancy.
• Advocating for stricter environmental regulations to reduce exposure to toxins and pollutants.
• Encouraging balanced nutrition and healthy dietary habits in children.
• Providing stress reduction programs and coping skills training in educational settings.
• Encouraging physical activity and outdoor play in school and community environments.
• Supporting early identification and intervention for children with ADHD.
• Offering parent education and support programs to help families navigate the challenges associated with ADHD.
• Conducting comprehensive assessments of children with ADHD to address comorbid conditions and lifestyle factors.

In conclusion, the investigation into environmental factors and ADHD risk reveals the profound influence of the environment on the development of this complex disorder. Recognizing the importance of environmental influences alongside genetic factors is essential for a holistic understanding of ADHD etiology and the development of effective prevention and intervention strategies. By taking proactive steps to reduce environmental risks and support at-risk individuals, we can make significant strides in improving the lives of those affected by ADHD and fostering healthier communities. Future research endeavors will further illuminate the nuances of this relationship and guide evidence-based approaches to ADHD prevention and management.

Bibliography

1. American Academy of Pediatrics. (2019). Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents. Pediatrics, 144(4), e20192528.
2. American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). American Psychiatric Association.
3. Biederman, J. (2005). Attention-deficit/hyperactivity disorder: A selective overview. Biological Psychiatry, 57(11), 1215-1220.
4. Bouchard, M. F., Bellinger, D. C., Wright, R. O., & Weisskopf, M. G. (2010). Attention-deficit/hyperactivity disorder and urinary metabolites of organophosphate pesticides. Pediatrics, 125(6), e1270-e1277.
5. Braun, J. M., Kahn, R. S., Froehlich, T., & Auinger, P. (2006). Exposures to environmental toxicants and attention deficit hyperactivity disorder in U.S. children. Environmental Health Perspectives, 114(12), 1904-1909.
6. Calderón-Garcidueñas, L., Solt, A. C., Henríquez-Roldán, C., Torres-Jardón, R., Nuse, B., Herritt, L., … & Reed, W. (2008). Long-term air pollution exposure is associated with neuroinflammation, an altered innate immune response, disruption of the blood-brain barrier, ultrafine particulate deposition, and accumulation of amyloid β-42 and α-synuclein in children and young adults. Toxicologic Pathology, 36(2), 289-310.
7. Daley, D., Van der Oord, S., Ferrin, M., Danckaerts, M., Doepfner, M., Cortese, S., … & European ADHD Guidelines Group. (2006). Behavioral interventions in attention-deficit/hyperactivity disorder: A meta-analysis of randomized controlled trials across multiple outcome domains. Journal of the American Academy of Child & Adolescent Psychiatry, 45(8), 892-902.
8. Deault, L. C. (2010). A systematic review of parenting in relation to the development of comorbidities and functional impairments in children with attention-deficit/hyperactivity disorder (ADHD). Child Psychiatry & Human Development, 41(2), 168-192.
9. Evans, G. W. (2003). A multimethodological analysis of cumulative risk and allostatic load among rural children. Developmental Psychology, 39(5), 924-933.
10. Faraone, S. V., Perlis, R. H., Doyle, A. E., Smoller, J. W., Goralnick, J. J., Holmgren, M. A., & Sklar, P. (2005). Molecular genetics of attention-deficit/hyperactivity disorder. Biological Psychiatry, 57(11), 1313-1323.
11. Franke, B., Neale, B. M., & Faraone, S. V. (2012). Genome-wide association studies in ADHD. Human Genetics, 131(12), 1625-1634.
12. Froehlich, T. E., Lanphear, B. P., Auinger, P., Hornung, R., Epstein, J. N., Braun, J., & Kahn, R. S. (2009). Association of tobacco and lead exposures with attention-deficit/hyperactivity disorder. Pediatrics, 124(6), e1054-e1063.
13. Grandjean, P., Landrigan, P. J., & Developmental Neurotoxicity Study Group. (2018). Neurobehavioural effects of developmental toxicity. The Lancet Neurology, 17(4), 330-338.
14. Indredavik, M. S., Vik, T., Evensen, K. A. I., Skranes, J., Taraldsen, G., & Brubakk, A. M. (2005). Perinatal risk and psychiatric outcome in adolescents born preterm with very low birth weight or term small for gestational age. The Journal of Developmental and Behavioral Pediatrics, 26(2), 133-141.
15. Langberg, J. M., Molina, B. S. G., Arnold, L. E., Epstein, J. N., & Altaye, M. (2008). Patterns and predictors of adolescent academic achievement and performance in a sample of children with attention-deficit/hyperactivity disorder. Journal of Clinical Child & Adolescent Psychology, 37(4), 521-531.
16. Langley, K., Rice, F., van den Bree, M. B., & Thapar, A. (2005). Maternal smoking during pregnancy as an environmental risk factor for attention-deficit hyperactivity disorder behavior. A review. Minerva Pediatrica, 57(6), 359-371.
17. Lupien, S. J., McEwen, B. S., Gunnar, M. R., & Heim, C. (2009). Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience, 10(6), 434-445.
18. Millichap, J. G. (2012). Etiologic classification of attention-deficit/hyperactivity disorder. Pediatrics, 129(5), e1213-e1220.
19. Molina, B. S., Hinshaw, S. P., Eugene Arnold, L., Swanson, J. M., Pelham, W. E., Hechtman, L., … & MTA Cooperative Group. (2007). Adolescent substance use in the multimodal treatment study of attention-deficit/hyperactivity disorder (ADHD) (MTA) as a function of childhood ADHD, random assignment to childhood treatments, and subsequent medication. Journal of the American Academy of Child & Adolescent Psychiatry, 46(2), 165-175.
20. Nigg, J. T., Knottnerus, G. M., Martel, M. M., Nikolas, M., Cavanagh, K., Karmaus, W., & Rappley, M. D. (2008). Low blood lead levels associated with clinically diagnosed attention-deficit/hyperactivity disorder and mediated by weak cognitive control. Biological Psychiatry, 63(3), 325-331.
21. Owens, J. S., Goldfine, M. E., Evangelista, N. M., Hoza, B., & Kaiser, N. M. (2017). A critical review of self-perceptions and the positive illusory bias in children with ADHD. Clinical Child and Family Psychology Review, 20(1), 14-32.
22. Perroud, N., Salzmann, A., Saiz, P. A., Baca-García, E., & Sáiz-Ruiz, J. (2018). Micro-RNAs: New biomarkers for diagnosis, prognosis, therapy prediction, and therapeutic tools for precision medicine. Psychotherapy and Psychosomatics, 87(4), 205-213.
23. Rijlaarsdam, J., Stevens, G. W., van der Ende, J., Arends, L. R., Hofman, A., Jaddoe, V. W., … & Tiemeier, H. (2017). A brief report: Prenatal folate, homocysteine levels, and attentional problems in childhood. Journal of Attention Disorders, 21(6), 512-518.
24. Siddique, S., Banerjee, M., Ray, M. R., & Lahiri, T. (2011). Attention-deficit hyperactivity disorder in children chronically exposed to high level of vehicular pollution. European Journal of Pediatrics, 170(7), 923-929.
25. Swing, E. L., Gentile, D. A., Anderson, C. A., & Walsh, D. A. (2010). Television and video game exposure and the development of attention problems. Pediatrics, 126(2), 214-221.
26. Tantillo, M., Kesick, C. M., Hynd, G. W., Dishman, R. K., & (2013). The effects of exercise on children with attention-deficit hyperactivity disorder. Medicine & Science in Sports & Exercise, 45(4), 762-771.
27. Thapar, A., Rice, F., Hay, D., Boivin, J., Langley, K., van den Bree, M., … & Harold, G. (2009). Prenatal smoking might not cause attention-deficit/hyperactivity disorder: Evidence from a novel design. Biological Psychiatry, 66(8), 722-727.
28. van Mil, N. H., Steegers-Theunissen, R. P., Motazedi, E., Jansen, P. W., Jaddoe, V. W., Steegers, E. A., … & Verhulst, F. C. (2014). DNA methylation profiles at birth and child ADHD symptoms. Journal of Psychiatric Research, 49, 51-59.
29. Wilens, T. E., Martelon, M., Joshi, G., Bateman, C., Fried, R., Petty, C., & Biederman, J. (2007). Does ADHD predict substance-use disorders? A 10-year follow-up study of young adults with ADHD. Journal of the American Academy of Child & Adolescent Psychiatry, 46(12), 1385-1394.
30. Yoon, S. Y., Jain, U., & Shapiro, C. (2012). Sleep in attention-deficit/hyperactivity disorder in children and adults: Past, present, and future. Sleep Medicine Reviews, 16(4), 371-388.