As an emerging and pervasive environmental pollutant, airborne microplastics (MPs) have attracted increasing attention due to their potential health impacts following inhalation exposure. Owing to their small size, diverse physicochemical properties, and aerodynamic behavior, MPs can deposit along the entire respiratory tract, including the nasal cavity, conducting airways, and alveolar regions. Accumulating evidence suggests that such deposition may profoundly affect epithelial barrier integrity, local immune regulation, and host susceptibility to respiratory allergic diseases. However, current knowledge remains fragmented, and a comprehensive synthesis of detection methodologies, exposure characteristics, and biological mechanisms is still lacking. This review systematically summarizes recent advances in airborne MP sampling, identification, and exposure assessment, with an emphasis on analytical techniques applicable to respiratory exposure scenarios. We further integrate experimental, epidemiological, and mechanistic studies to evaluate the differential effects of MP characteristics—such as polymer composition, particle size, shape, and surface chemistry—on the initiation and exacerbation of respiratory allergic disorders, including allergic rhinitis and asthma. Emerging evidence indicates that inhaled MPs can compromise airway epithelial structure and function by disrupting tight junctions, impairing mucociliary clearance, and weakening mucosal barrier defenses. These alterations facilitate allergen penetration and enhance antigen uptake and presentation, thereby promoting sensitization and skewing adaptive immune responses toward a Th2-dominant phenotype. At the molecular level, MPs have been shown to induce oxidative stress in epithelial and immune cells, leading to the activation of key inflammatory pathways, including NF-κB signaling and NLRP3 inflammasome assembly, which collectively sustain chronic airway inflammation. Alveolar macrophages, which play a pivotal role in particle clearance and immune homeostasis, appear particularly susceptible to MP exposure. MPs may impair macrophage phagocytic function, induce aberrant cytokine production, and drive macrophage polarization toward an M1-like phenotype, thereby amplifying allergic inflammation and disrupting immune resolution. In addition, growing evidence suggests that MPs can act as carriers for environmental allergens and chemical additives, further enhancing their adjuvant-like effects in allergic sensitization. Beyond direct cellular effects, MPs may also alter the composition and function of the nasal and airway microbiota, creating a pro-allergic microenvironment that increases host vulnerability to immune dysregulation. Such microbiome perturbations represent an emerging dimension of MP-related respiratory toxicity that warrants further investigation. Collectively, the findings summarized in this review highlight airborne MPs as biologically active inhalation pollutants with the capacity to modulate epithelial barriers, immune responses, and microbial ecosystems in ways that favor the development and progression of respiratory allergic diseases. Future research integrating exposure science, immunotoxicology, and microbiome-based approaches will be critical for elucidating causal pathways. In particular, the establishment of standardized exposure metrics, clarification of dose–response relationships, and development of physiologically relevant inhalation models are essential for robust risk assessment and for informing evidence-based prevention strategies and clinical interventions targeting MP-associated respiratory allergy.
Xu et al. (Thu,) studied this question.