Nobili Cecilia, Riccò Matteo, Piglia Giulia, Manzoni Paolo
SCDU Pediatria e Neonatologia, Ospedale Degli Infermi, Dipartimento Materno-Infantile ASLBI, 13875 Ponderano, BI, Italy.
Postgraduate School of Pediatrics, University of Turin, 10126 Turin, TO, Italy.
Pathogens. 2025 Jul 14;14(7):690. doi: 10.3390/pathogens14070690.
Climate change and air pollution are reshaping viral circulation patterns and increasing host vulnerability, amplifying the burden of respiratory illness in early childhood. This narrative review synthesizes current evidence on how environmental exposures, particularly to nitrogen dioxide, ozone, and fine particulate matter, contribute to the incidence and severity of bronchiolitis, with a focus on biological mechanisms, epidemiological trends, and public health implications. Bronchiolitis remains one of the leading causes of hospitalization in infancy, with Respiratory Syncytial Virus (RSV) being responsible for the majority of severe cases. Airborne pollutants penetrate deep into the airways, triggering inflammation, compromising mucosal defenses, and impairing immune function, especially in infants with pre-existing vulnerabilities. These interactions can intensify the clinical course of viral infections and contribute to more severe disease presentations. Children in urban areas exposed to high levels of traffic-related emissions are disproportionately affected, underscoring the need for integrated public health interventions. These include stricter emission controls, urban design strategies to reduce exposure, and real-time health alerts during pollution peaks. Prevention strategies should also address indoor air quality and promote risk awareness among families and caregivers. Further research is needed to standardize exposure assessments, clarify dose-response relationships, and deepen our understanding of how pollution interacts with viral immunity. Bronchiolitis emerges as a sentinel condition at the crossroads of climate, environment, and pediatric health, highlighting the urgent need for collaboration across clinical medicine, epidemiology, and environmental science.
气候变化和空气污染正在重塑病毒传播模式，并增加宿主易感性，加重幼儿期呼吸道疾病负担。本叙述性综述综合了当前关于环境暴露，特别是二氧化氮、臭氧和细颗粒物暴露，如何导致细支气管炎发病率和严重程度的证据，重点关注生物学机制、流行病学趋势和公共卫生影响。细支气管炎仍然是婴儿期住院的主要原因之一，呼吸道合胞病毒（RSV）是大多数重症病例的病因。空气传播污染物深入呼吸道，引发炎症，损害黏膜防御功能，削弱免疫功能，尤其是对已有易感性的婴儿。这些相互作用会加剧病毒感染的临床病程，并导致更严重的疾病表现。暴露于高水平交通相关排放物的城市地区儿童受到的影响尤为严重，这凸显了综合公共卫生干预措施的必要性。这些措施包括更严格的排放控制、减少暴露的城市设计策略，以及在污染高峰期发布实时健康警报。预防策略还应关注室内空气质量，并提高家庭和照顾者的风险意识。需要进一步研究以规范暴露评估、阐明剂量反应关系，并加深我们对污染与病毒免疫相互作用的理解。细支气管炎在气候、环境和儿童健康的交叉点上成为一种警示性疾病，凸显了临床医学、流行病学和环境科学之间迫切需要开展合作。
