Abstract
The purpose of our study was to test the hypothesis that prenatal tobacco smoking exposure (PSE) could modulate the association of genetic variants with ADHD. A community based case-control study was conducted among Chinese children and 168 ADHD patients and 233 controls were recruited by using combination diagnosis of DSM-IV, SNAP-IV and semi-structured clinical interview. Logistic regression analysis was performed to estimate the effect of prenatal tobacco smoking exposure and genotype frequencies on ADHD susceptibility individually by adjustment for potential confounders. Multiplicative and additive interaction analysis were performed to evaluate the interactions between risk genes and PSE with regard to ADHD. Prenatal tobacco smoke exposure was a significant risk factor of ADHD even after adjusted for other potential confounders. ADRA2A rs553668, DRD2 rs1124491 and SLC6A4 rs6354 were identified to be associated with ADHD. A significant multiplicative and additive gene-environment interactions were observed between the PSE and the ADRA2A rs553668 in relation to ADHD and ADHD-ODD. The risk of the genetic variants in ADHD was increased significantly if the child had prenatal tobacco exposure. The genetic risk for ADHD could be influenced by the presence of environmental risks. The environmental and the genetic risks are not distinct to each other. More gene-environment interaction studies were needed to reveal the etiology of ADHD.
Highlights
The purpose of our study was to test the hypothesis that prenatal tobacco smoking exposure (PSE) could modulate the association of genetic variants with Attention-deficit/hyperactivity disorder (ADHD)
A community based case-control study was conducted among Chinese children and 168 ADHD patients and 233 controls were recruited by using combination diagnosis of DSM-IV, SNAP-IV and semi-structured clinical interview
Large numbers of studies demonstrated a relationship between maternal smoking exposure during pregnancy and ADHD, most of previous studies have investigated the effect of smoking exposure only and there were few studies on gene–environment interactions which were more likely to play the real role in the etiology of ADHD21
Summary
The purpose of our study was to test the hypothesis that prenatal tobacco smoking exposure (PSE) could modulate the association of genetic variants with ADHD. Logistic regression analysis was performed to estimate the effect of prenatal tobacco smoking exposure and genotype frequencies on ADHD susceptibility individually by adjustment for potential confounders. Prenatal tobacco smoke exposure was a significant risk factor of ADHD even after adjusted for other potential confounders. The risk of the genetic variants in ADHD was increased significantly if the child had prenatal tobacco exposure. With regard to prenatal smoking, it is constantly identified to be a risk factor for offspring hyperactivity symptom and ADHD14,17–19. Evidence from epidemiological researches suggests that maternal cigarette smoking and environmental tobacco exposure during pregnancy are all in association with high risk of ADHD. Large numbers of studies demonstrated a relationship between maternal smoking exposure during pregnancy and ADHD, most of previous studies have investigated the effect of smoking exposure only and there were few studies on gene–environment interactions which were more likely to play the real role in the etiology of ADHD21
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