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<p>Evidence linking secondhand tobacco exposures to childhood attention-deficit hyperactivity disorder (ADHD) risk has been reported, however, the causality of the relationship and potential biological pathways is unknown. We applied a two-step Mendelian randomisation (MR) analysis and Bayesian colocalization analysis to examine the causal relationship between smoking behaviours, secondhand tobacco-induced DNA methylation and childhood ADHD risk. The findings revealed causal positive connections between smoking behaviours of daily cigarette consumption (Odds ratio [OR]<sub>Inverse variance weighted (IVW)</sub>, 1.56 for per 1–SD increase; 95% CI: 1.17–2.09; <i>P</i> = 0.003), smoking cessation (OR<sub>IVW</sub>, 2.92 for per 1–SD increase; 95% CI: 1.65–5.17; <i>P</i> = 2.23 × 10<sup>− 4</sup>), smoking initiation (OR<sub>IVW</sub>, 3.01 for per 1–SD increase; 95% CI: 2.60–3.48; <i>P</i> = 6.41 × 10<sup>− 50</sup>) and the risk of childhood ADHD. On the contrary, age of initiation of regular smoking suggested a decreased risk with ADHD risk (OR<sub>IVW</sub>, 0.17 for per 1–SD increase; 95% CI: 0.06–0.47; <i>P</i> = 7.42 × 10<sup>− 4</sup>). Genetically predicted DNA methylation alterations related to secondhand tobacco exposure at cg23211703 [<i>PTPRF</i>], cg02772619, cg19716073 [<i>CACNG1</i>], and cg22500280 [<i>MAD1L1</i>] were associated with increased ADHD risk, whereas DNA methylation changes at cg03504834 [<i>FOXP2</i>], cg23666170 [<i>PLK1S1</i>], cg24476096 [<i>C1orf84/MED8</i>], cg12142869 [<i>OR10AD1</i>] and cg16572910 were related to decreased ADHD risk. Five CpG sites (cg23211703, cg03504834, cg02772619, cg12142869, and cg19716073) exhibited convincing colocalization evidence. This study provides evidence supporting a causal link between tobacco smoking, DNA methylation and childhood ADHD risk.</p>

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Early-life tobacco exposure elevating childhood attention-deficit hyperactivity disorder risk: a two-sample Mendelian randomisation analysis

  • 期刊论文

  • 发表日期：

    2026年4月7日

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  • Kelei Shang,
  • Chun Luo,
  • Xiaoguang Tan,
  • Menglei Xu,
  • Bin Li,
  • Houhong Wang,
  • Feng Cheng

摘要

Evidence linking secondhand tobacco exposures to childhood attention-deficit hyperactivity disorder (ADHD) risk has been reported, however, the causality of the relationship and potential biological pathways is unknown. We applied a two-step Mendelian randomisation (MR) analysis and Bayesian colocalization analysis to examine the causal relationship between smoking behaviours, secondhand tobacco-induced DNA methylation and childhood ADHD risk. The findings revealed causal positive connections between smoking behaviours of daily cigarette consumption (Odds ratio [OR]Inverse variance weighted (IVW), 1.56 for per 1–SD increase; 95% CI: 1.17–2.09; P = 0.003), smoking cessation (ORIVW, 2.92 for per 1–SD increase; 95% CI: 1.65–5.17; P = 2.23 × 10− 4), smoking initiation (ORIVW, 3.01 for per 1–SD increase; 95% CI: 2.60–3.48; P = 6.41 × 10− 50) and the risk of childhood ADHD. On the contrary, age of initiation of regular smoking suggested a decreased risk with ADHD risk (ORIVW, 0.17 for per 1–SD increase; 95% CI: 0.06–0.47; P = 7.42 × 10− 4). Genetically predicted DNA methylation alterations related to secondhand tobacco exposure at cg23211703 [PTPRF], cg02772619, cg19716073 [CACNG1], and cg22500280 [MAD1L1] were associated with increased ADHD risk, whereas DNA methylation changes at cg03504834 [FOXP2], cg23666170 [PLK1S1], cg24476096 [C1orf84/MED8], cg12142869 [OR10AD1] and cg16572910 were related to decreased ADHD risk. Five CpG sites (cg23211703, cg03504834, cg02772619, cg12142869, and cg19716073) exhibited convincing colocalization evidence. This study provides evidence supporting a causal link between tobacco smoking, DNA methylation and childhood ADHD risk.