Peer-reviewed article
Environmental Noise and Childhood Asthma: A Hypothesis-Generating Review of Potential Neuro-Immune Mechanisms.
Jing N, Zhang F, Zhao N, Xu X, Wang Y et al. ·
Summary
Written by AI, not yet AICS's view · claude-haiku-4-5-20251001This review article examines how environmental noise may contribute to childhood asthma through neuro-immune mechanisms. The authors propose that noise acts as a systemic stressor affecting both immune-inflammatory responses and neuroendocrine function, potentially triggering or worsening asthma in children. The review identifies specific pathways including Th2 inflammation, oxidative stress, autonomic imbalance, and disrupted sleep patterns as potential mechanisms. The findings suggest that understanding these mechanisms could lead to new interventions targeting the neuro-immune system and acoustic environment improvements for children with asthma.
Key points
- Childhood asthma is a heterogeneous chronic airway disease affecting cardiopulmonary development, sleep rhythms and social skills in school-aged children
- Environmental noise disrupts immune homeostasis and facilitates T-helper type 2 (Th2) inflammation
- Noise leads to autonomic imbalance and triggers vagal rebound through neuroendocrine pathways
- Sleep disruption from noise can trigger airway hyperresponsiveness during nocturnal periods
- Understanding neuro-immune mechanisms provides a basis for neuro-immune-targeted interventions and acoustic environment optimization
Limitations
This is a hypothesis-generating review without direct clinical evidence. The document presents theoretical mechanisms and proposed pathways rather than empirical findings from studies with measured outcomes, so it cannot provide evidence about what interventions actually work or the magnitude of noise's impact on asthma incidence.
Abstract
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.