Urban Lifestyle and Climate-Driven Environmental Exposures: Immunological Consequences for Pediatric Respiratory Allergies

Abstract

Pediatric respiratory allergic diseases, including asthma and allergic rhinitis, are increasingly recognized as significant global health concerns, with rising prevalence rates linked to environmental changes driven by urbanization and climate change. This review explores the impact of climatic factors such as temperature fluctuations, shifting precipitation patterns, and dust storms on air pollution and its consequences on respiratory allergic diseases in children. Evidence suggests these environmental exposures increase allergen loads and profoundly influence immune system function. Air pollutants and airborne allergens promote Type 2 helper T-cell (Th2)-skewed responses, leading to elevated IgE production, eosinophilic inflammation, and airway hyperreactivity. Additionally, epithelial barrier dysfunction caused by oxidative stress triggers the release of alarmins such as thymic stromal lymphopoietin, interleukin-33 (IL-33), and IL-25, that activate innate lymphoid cells, and amplify allergic sensitization. Long-term exposure to pollutants also disrupts immune tolerance by impairing regulatory T-cell (Treg) activity and promoting persistent airway inflammation. This review highlights how these immunological pathways contribute to the severity and chronicity of allergic diseases in pediatric populations, with special attention to studies conducted in regions prone to dust storms. Understanding these mechanisms is critical for developing targeted public health strategies, improving air quality, and mitigating the health impacts of climate change on children.

Keywords: IgE; Th2 cells; climatic change; cytokines; lifestyle; pediatric respiratory allergy; urbanization.

Figure 1

The interplay between urbanization and climate change contributes to increased asthma incidence through environmental and lifestyle factors. Air pollution, biodiversity loss, and altered lifestyles, along with rising temperatures, extreme weather events, and meteorological changes, trigger immune system responses that lead to airway inflammation and asthma development. Pollutants and allergens damage respiratory epithelial cells, activating innate immune pathways (ILC2 and alarmins) and adaptive immune responses (dendritic cells and Th2 cytokines). This results in eosinophilic inflammation, mucus overproduction, and airway hyperresponsiveness, driving chronic asthma progression.