Noise, air pollution exposure and attention-deficit/hyperactivity disorder: a meta-analysis.

OBJECTIVE

This meta-analysis evaluated the associations between noise exposure, air pollutants, and attention-deficit/hyperactivity disorder (ADHD) in children, aiming to inform future prevention strategies.

METHODS

Studies were systematically retrieved from CNKI, Wanfang, PubMed, Web of Science, Embase, and the Cochrane Library, covering publications from inception to November 2025. Heterogeneity was assessed using Cochran's Q test and the I² statistic. Subgroup analyses, meta-regression, and sensitivity analyses were performed to evaluate the robustness of the findings.

RESULTS

Noise exposure was associated with a small increase in ADHD risk (odds ratio [OR] = 1.03, 95% confidence interval [CI]: 1.01-1.05), with stronger associations for childhood exposure, whereas prenatal exposure showed no significant effect. Given the modest effect size, this finding should be interpreted cautiously. Particulate matter (PM2.5 and PM10) was significantly associated with ADHD in continuous-exposure models-PM2.5 (OR = 1.32, 95% CI: 1.16-1.50) and PM10 (OR = 1.47, 95% CI: 1.15-1.87). In dichotomous models, PM2.5 was not significant, while PM10 remained positively associated (OR = 1.58, 95% CI: 1.11-2.26). Elevated nitrogen dioxide (NO2) exposure was also associated with a modest increase in ADHD risk (OR = 1.11, 95% CI: 1.02-1.20), whereas nitrogen oxides (NOx), ozone (O3), and sulfur dioxide (SO2) did not show significant associations.

CONCLUSIONS

Noise and several air pollutants (PM2.5, PM10, and NO2) were significantly associated with increased ADHD risk, particularly during childhood exposure. Other pollutants, including O3 and SO2, did not demonstrate significant effects. These findings suggest that environmental noise and several air pollutants may be associated with ADHD; however, some observed associations, particularly for noise and NO2, were modest in magnitude and should be interpreted cautiously. These results reflect observational associations rather than evidence of a strong or causal effect, while the evidence for some pollutants remains limited or inconclusive. Further research is needed to clarify pollutant-specific associations and the role of exposure timing.

SYSTEMATIC REVIEW REGISTRATION: https://www.crd.york.ac.uk/PROSPERO/view/CRD42024593274, identifier CRD42024593274; https://www.crd.york.ac.uk/PROSPERO/view/CRD42025632899, identifier CRD42025632899.