Since the industrial revolution, air pollution has become a major problem causing several health problems involving the airways as well as the cardiovascular, reproductive, or neurological system. According to the WHO, about 3.6 million deaths every year are related to inhalation of polluted air, specifically due to pulmonary diseases. Polluted air first encounters the airways, which are a major human defense mechanism to reduce the risk of this aggressor. Air pollution consists of a mixture of potentially harmful compounds such as particulate matter, ozone, carbon monoxide, volatile organic compounds, and heavy metals, each having its own effects on the human body. In the last decades, a lot of research investigating the underlying risks and effects of air pollution and/or its specific compounds on the airways, has been performed, involving both in vivo and in vitro experiments. The goal of this review is to give an overview of the recent data on the effects of air pollution on healthy and diseased airways or models of airway disease, such as asthma or chronic obstructive pulmonary disease. Therefore, we focused on studies involving pollution and airway symptoms and/or damage both in mice and humans.

Purpose of review: The current review describes the role of different types of innate lymphoid cells (ILCs) in the pathogenesis of asthma inflammatory phenotypes by linking findings from murine asthma models with human studies. Novel treatment options are needed for patients with steroid-insensitive asthma. Strategies targeting ILCs, or their upstream or downstream molecules are emerging and discussed in this review. Recent findings: In eosinophilic asthma, ILCs, and especially type 2 ILCs (ILC2s), are activated by alarmins such as IL-33 upon allergen triggering of the airway epithelium. This initiates IL-5 and IL-13 production by ILC2, resulting in eosinophilic inflammation and airway hyperreactivity. Type 3 ILCs (ILC3s) have been shown to be implicated in obesity-induced asthma, via IL-1β production by macrophages, leading ILC3 and release of IL-17. ILC1s might play a role in severe asthma, but its role is currently less investigated. Summary: Several studies have revealed that ILC2s play a role in the induction of eosinophilic inflammation in allergic and nonallergic asthmatic patients mainly via IL-5, IL-13, IL-33 and thymic stromal lymphopoietin. Knowledge on the role of ILC3s and ILC1s in asthmatic patients is lagging behind. Further studies are needed to support the hypothesis that these other types of ILCs contribute to asthma pathogenesis, presumably in nonallergic asthma phenotypes.

Rationale: Participation in high-intensity exercise in early life might act as stressor to the airway barrier.Objectives: To investigate the effect of intense exercise and associated exposure to air pollution on the airway barrier in adolescent elite athletes compared with healthy controls and to study exercise-induced bronchoconstriction (EIB) in this population.Methods: Early-career elite athletes attending ‘Flemish-Elite-Sports-Schools’ (12–18 years) of 4 different sport disciplines (n=90) and control subjects (n=25) were recruited. Presence of EIB was tested by the eucapnic voluntary hyperventilation (EVH) test. Markers at mRNA and protein level; RNA-sequencing; carbon load in airway macrophages were studied on induced sputum samples.Results: 444 genes were differentially expressed in sputum from athletes compared with controls, which were related to inflammation and epithelial cell damage and sputum samples of athletes contained significantly more carbon loaded airway macrophages compared with controls (24%, 95% CI 20% to 36%, p<0.0004). Athletes had significantly higher substance P (13.3 pg/mL, 95% CI 2.0 to 19.2) and calprotectin (1237 ng/mL, 95% CI 531 to 2490) levels as well as IL-6, IL-8 and TNF-α mRNA levels compared with controls (p<0.05). The incidence of EIB in athletes was 9%. The maximal fall in forced expiratory volume in 1 s (%) after EVH test in athletes was significantly associated with prior PM₁₀and PM_2.5exposure.Conclusion: Early-career elite athletes showed increased markers of air pollution exposure, epithelial damage and airway inflammation compared with controls. Acute exposure to increased air pollution PM₁₀levels was linked to increased airway hyper-reactivity.Trial registration number: NCT03587675.

Although regular exercise-training improves immune/inflammatory status, the influence of air pollutants exposure during outdoor endurance training compared to a sedentary lifestyle has not yet been clarified. This study aimed to compare the immune/inflammatory responses in the airways of street runners and sedentary people after acute and chronic particulate matter (PM) exposure. Forty volunteers (street runners (RUN, n = 20); sedentary people (SED, n = 20)) were evaluated 1 (acute) and 10 (chronic) weeks after PM exposure. Cytokines [interferon (IFN)-γ, tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10, IL-13, and IL-17A] in nasal lavage fluid, salivary antibacterial peptides (lactoferrin (LTF), cathelicidin (LL-37), defensin-α 1–3), and secretory immunoglobulin A (SIgA), plasma club cell protein (CC16), and fractional exhaled nitric oxide (FeNO) were analyzed. After acute exposure, the RUN group showed lower levels of IL-13, IL-10, and FeNO, but higher defensin-α than the SED group. After chronic exposure, the RUN group showed elevation of IFN-γ, IL-10, IL-17A, and a decrease of FeNO levels, whereas the SED group showed elevation of TNF-α, IL-6, IL-10, and a decrease of IL-13 levels. Comparing these groups, the RUN group showed higher levels of SIgA and LTF, and lower FeNO levels than the SED group. In relation to the Th immune response analysis after acute and chronic PM exposure, the RUN group showed a pattern associated with Th1, while in the SED group, a Th2 pattern was found. Both groups showed also a Th17 immune response pattern. Our results allow us to suggest that the immune/inflammatory status of the respiratory tract after acute and chronic PM exposure was improved by the long-standing regular practice of outdoor endurance exercise compared to a sedentary lifestyle.