TY - JOUR
T1 - Corrigendum to “The association between organophosphate pesticide exposure and methylation of paraoxonase-1 in children with attention-deficit/hyperactivity disorder” [Environ. Int. 171 (2023) 107702] (Environment International (2023) 171, (S0160412022006298), (10.1016/j.envint.2022.107702))
AU - Chang, Chia Huang
AU - Subramani, Boopathi
AU - Yu, Ching Jung
AU - Du, Jung Chieh
AU - Chiou, Hsien Chih
AU - Hou, Jia Woei
AU - Yang, Winnie
AU - Chen, Chian-Feng
AU - Chen, Ying Sheue
AU - Hwang, Betau
AU - Chen, Mei Lien
N1 - Publisher Copyright:
© 2023 The Author(s)
PY - 2023
Y1 - 2023
N2 - The authors would like to include abstract and keywords, as they were missed during the production of the article. Abstract Exposure to organophosphate pesticides (OPPs) is ubiquitous and has been reported to interfere with neurodevelopment in children. OP compounds are metabolized by paraoxonase 1 (PON1), and interindividual differences in susceptibility to OP exposure are brought out by the genetic polymorphism and epigenetic modifications of PON1. DNA methylation is a common epigenetic modification that can regulate the expression of PON1. We have previously identified that PON1 single nucleotide polymorphisms are associated with OP levels and ADHD risk in children. This study aims to elucidate whether changes in PON1 DNA methylation levels due to OP exposure and genetic polymorphism could increase ADHD risk in children. A total of 181 children participated in this case-control study, including 85 children with ADHD and 96 children as control. We measured urinary concentrations of OP metabolites, dialkyl phosphate (DAP), including dimethyl alkylphosphate (DM) and diethyl alkylphosphate (DE) in children. The changes in DNA methylation levels in the proximal promoter region of PON1 were examined. The results showed that ADHD children had higher dimethyl phosphate (DMP) levels (238.95 nmol/g cre. vs. 164.83 nmol/g cre.; p-value, 0.01) and lower methylation levels (22 out of 25 CpG sites; p-value <0.05) than the control children. The mean methylation levels were 43.14 ± 11.44% for the ADHD group and 50.19 ± 13.74% for the control group (p-value <0.05). We observed a negative association between OP metabolites and mean methylation levels (β = -0.06, 95% CI = −0.09, −0.02). The mediation analysis showed a marginal significant mediation by PON1 methylation levels in the association between OPPs exposure and ADHD. These results imply that chronic sub-acute OPPs exposure could influence the PON1 methylation levels. This study expands our understanding of the relationship between exposure to OPPs, neurobehavior in children, and the role of PON1 DNA methylation and warrants further research. Keywords: Organophosphate exposure, paraoxonase-1, DNA methylation, attention-deficit/hyperactivity disorder.
AB - The authors would like to include abstract and keywords, as they were missed during the production of the article. Abstract Exposure to organophosphate pesticides (OPPs) is ubiquitous and has been reported to interfere with neurodevelopment in children. OP compounds are metabolized by paraoxonase 1 (PON1), and interindividual differences in susceptibility to OP exposure are brought out by the genetic polymorphism and epigenetic modifications of PON1. DNA methylation is a common epigenetic modification that can regulate the expression of PON1. We have previously identified that PON1 single nucleotide polymorphisms are associated with OP levels and ADHD risk in children. This study aims to elucidate whether changes in PON1 DNA methylation levels due to OP exposure and genetic polymorphism could increase ADHD risk in children. A total of 181 children participated in this case-control study, including 85 children with ADHD and 96 children as control. We measured urinary concentrations of OP metabolites, dialkyl phosphate (DAP), including dimethyl alkylphosphate (DM) and diethyl alkylphosphate (DE) in children. The changes in DNA methylation levels in the proximal promoter region of PON1 were examined. The results showed that ADHD children had higher dimethyl phosphate (DMP) levels (238.95 nmol/g cre. vs. 164.83 nmol/g cre.; p-value, 0.01) and lower methylation levels (22 out of 25 CpG sites; p-value <0.05) than the control children. The mean methylation levels were 43.14 ± 11.44% for the ADHD group and 50.19 ± 13.74% for the control group (p-value <0.05). We observed a negative association between OP metabolites and mean methylation levels (β = -0.06, 95% CI = −0.09, −0.02). The mediation analysis showed a marginal significant mediation by PON1 methylation levels in the association between OPPs exposure and ADHD. These results imply that chronic sub-acute OPPs exposure could influence the PON1 methylation levels. This study expands our understanding of the relationship between exposure to OPPs, neurobehavior in children, and the role of PON1 DNA methylation and warrants further research. Keywords: Organophosphate exposure, paraoxonase-1, DNA methylation, attention-deficit/hyperactivity disorder.
UR - http://www.scopus.com/inward/record.url?scp=85151444494&partnerID=8YFLogxK
U2 - 10.1016/j.envint.2023.107909
DO - 10.1016/j.envint.2023.107909
M3 - Comment/debate
C2 - 37003948
AN - SCOPUS:85151444494
SN - 0160-4120
JO - Environment International
JF - Environment International
M1 - 107909
ER -