Environmental Noise and Childhood Asthma: A Hypothesis-Generating Review of Potential Neuro-Immune Mechanisms

Childhood asthma is a heterogeneous prevalent chronic airway disease in paediatrics worldwide. It not only directly impairs the cardiopulmonary development, sleep rhythms and social skills of school-aged children, but also significantly increases the burden of medical care on families and the pressure on public health prevention and control. Environmental noise is a significant risk factor for allergic diseases, but its pathogenicity is not solely due to physical stimulation. Rather, it acts as a systemic stressor, reshaping the body's pathological microenvironment through potential indirect pathways. Given the current lack of direct clinical evidence, this article conducts a hypothesis-generating review of the potential neuro-immune mechanisms by which noise may induce or exacerbate childhood asthma. At the immune-inflammatory level, noise disrupts immune homeostasis, facilitates T-helper type 2 (Th2) inflammation, disrupts the airway epithelial barrier through systemic oxidative stress, activates chemokine networks to mediate immune cell recruitment and drives non-Th2 inflammation. At the neuroendocrine level, noise leads to autonomic imbalance and receptor remodelling, triggering vagal rebound; simultaneously, it induces central sensitisation through the 'lung-brain axis', triggering substance P-mediated neurogenic inflammation; and it disrupts sleep rhythms, triggering airway hyperresponsiveness during the nocturnal vagal hypertonic period. Elucidating these two potential mechanisms provides a new theoretical basis for neuro-immune-targeted interventions, psychosomatic treatment and acoustic environment optimisation for childhood asthma.