Effects of Maternal Air Pollution on Offspring's Immune Health and Asthma Risk: The Role of Dietary Management

Breathing clean air is essential for maintaining human health. Air pollution, which can be divided into ambient-air-pollution (AAP) and household-air-pollution (HAP), has become one of the leading global risk factors for disease. A growing body of evidence links both AAP and HAP to increased prevalence of various health problems, including allergic-asthma. Chapter 1 of this thesis introduced the health effects of air-pollution, focusing on exposure during pregnancy and its impact on early-life immune and respiratory development. It also highlighted the potential role of the gut–lung axis and the benefits of dietary interventions such as probiotics and prebiotics. Given the global rise in air-pollution, this thesis aimed to investigate the adverse effects of exposure to common indoor air pollutants, particularly cigarette-smoke, the most prevalent source of indoor pollution, and its possible transgenerational consequences involving the gut–lung axis. Chapter 2 presented a review of the impact of air pollutants on gastrointestinal and respiratory health, emphasizing the bidirectional communication between these systems, known as the gut–lung axis. Through microbial metabolites, immune mediators, and lipid signaling, these organs influence each other’s homeostasis and inflammation. The potential of probiotics, prebiotics, and their combinations (synbiotics) to counteract air pollution–induced inflammation and oxidative stress was discussed. By improving microbiota composition and metabolic activity, synbiotics may strengthen mucosal barriers and activate anti-inflammatory pathways. Although human studies remain limited, current evidence suggests promising benefits for both the gastrointestinal and respiratory systems. Chapter 3 examined how exposure to cigarette-smoke during pregnancy and lactation affects maternal immune responses using a murine model. Cigarette smoke exposure during this critical period led to an increased accumulation of inflammatory cells, particularly neutrophils, in the lungs of pregnant mice. Transcriptomic analysis revealed that neutrophil chemotaxis was the most enriched pathway in exposed pregnant dams. Cigarette-smoke also altered gut microbiota composition, reducing diversity and short-chain fatty acid levels, suggesting a disturbed gut–lung interaction. Building on these findings, Chapter 4 explored whether postnatal synbiotic supplementation (a combination of GOS/FOS/2-FL and Bifidobacterium breve M-16V) could mitigate allergic asthma in offspring exposed to maternal cigarette-smoke. Using a house-dust-mite asthma model, results showed that synbiotics reduced lung resistance, eosinophil counts, and serum IgE and IgG1 levels. They also restored beneficial gut bacteria such as Bifidobacterium and Akkermansia, indicating a role in rebalancing the microbiota and attenuating allergic inflammation. Chapter 5 further investigated intergenerational effects by studying influenza vaccine responses in offspring of cigarette-smoke–exposed dams. Despite maternal exposure, offspring showed normal vaccine-specific antibody production and delayed-type hypersensitivity responses, though a higher frequency of activated Th2 cells was observed, suggesting a subtle immune skewing without impairing vaccine efficacy. Finally, Chapter 6 summarized the key findings: maternal cigarette smoke exposure adversely affects lung and gut health in mothers, alters offspring immune development, and increases allergic susceptibility. However, nutritional intervention with synbiotics can counteract these effects by improving microbial balance and reducing inflammation. Overall, this thesis underscores the detrimental impact of maternal air pollution exposure on both mothers and offspring and highlights synbiotics as a promising preventive strategy to protect immune and respiratory health.