Because the developing brain of a child is vulnerable to environmental toxins, even very low concentration of neurotoxin can affect children’s neurodevelopment. Lead is a neurotoxic heavy metal which has the harmful effect on the striatal-frontal circuit of brain. This area of the brain is known to be closely related to attention deficit hyperactivity disorder (ADHD) pathophysiology. The primary objective of the present study was to investigate whether elevated blood lead concentration is a risk factor for ADHD. The secondary objective was to examine the association between blood lead concentration and symptom severity. We conducted a frequency-matched, hospital-based case-control study with 114 medically diagnosed ADHD cases and 114 controls. The participants were matched for age and sex. The diagnoses of ADHD were assessed with semi-structured diagnostic interviews. The participants completed the continuous performance test (CPT), and their parents completed the ADHD-rating scale (ADHD-RS). Blood lead concentrations were measured by using graphite furnace atomic absorption spectrometry featuring Zeeman background correction. Children with ADHD exhibited blood lead concentrations that were significantly higher than those of the controls ( 1.90 ± 086 μg/dℓ vs. 1.59 ± 0.68 μg/dℓ, p = 0.003). The log transformed total blood lead concentration was associated with a higher risk of ADHD (OR: 1.60, 95 % CI: 1.04–2.45, p < 0.05). The analysis also revealed that the children with blood lead concentrations above 2.30 μg/dℓ were at a 2.5–fold (95 % CI: 1.09–5.87, p < 0.05) greater risk of having ADHD. After adjusting for covariates, our multivariate regression models indicated that blood lead concentrations were not significantly associated with ADHD-RS or CPT profiles among the ADHD cases. Even low blood lead concentrations are a risk factor for ADHD in children. This study warrants primary prevention policies to reduce the environmental lead burden. Future studies may be required to ascertain the effects of lead on symptom severity in ADHD.

Woo Jin Kim, Young Rong Bang, Je-Wook Kang, Jae Ho Yoo, Seong Hwan Kim, and Jae Hong Park. J Korean Acad Child Adolesc Psychiatry 2020;31:154-60. https://doi.org/10.5765/jkacap.200014

강제욱, et al. J Korean Neuropsychiatr Assoc. 2022 Nov;61(4):317-324. https://doi.org/10.4306/jknpa.2022.61.4.317

Background and Objectives: Most genetic studies have focused on catecholamine system genes to identify etiology in attention-deficit/hyperactivity disorder (ADHD), and there is growing evidence that the interaction of several genes may synergistically or antagonistically affect disease outcomes. We investigated the interaction between the alpha-2 adrenergic receptor (ADRA2A) and its transporter (SLC6A2) to determine the etiology and treatment outcomes for ADHD. Materials and Methods: Children with ADHD (age 8.3 ± 2.0 y, 72 boys and 11 girls) were assessed using the Kiddie Schedule for Affective Disorders-Present and Lifetime (K-SASD-PL), ADHD rating scale-IV (ARS), Clinical Global Impressions-Improvement (CGI-I), and Clinical Global Impressions-Severity (CGI-S) scales. Neuropsychological assessments were performed using a continuous performance test (CPT). Methylphenidate was titrated based on the CGI-I and CGI-S scales for 8 weeks. We assessed two polymorphisms, ADRA2A rs553668 and SLC6A2 rs998424, for their association with disease outcomes. Results: The ADRA2A polymorphism had a significant effect on visual/auditory commission errors in the CPT. The CC genotype for ADRA2A combined with the GG genotype for SLC6A2 showed more commission errors than the other combinations of genotypes. Treatment outcome assessment using the CGI-S showed that the SLC6A2 GG genotype had more favorable treatment outcome (p < 0.05) and significant gene × dose interaction on ARS score across 8 weeks (p < 0.01). Conclusions: Our findings provide preliminary evidence for the effect of ADR2A and SLC6A2 gene–gene interactions on the attention system and treatment response in children with ADHD. Although these findings require future replication, our study contributes to the understanding of the genetic basis of ADHD.