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Whether inhaled particles that reach SA preferentially deposit to a particular sub-airway region is not entirely clear, but some studies have pointed to preferential deposition in more distal bronchiolar regions.

Toxicity attributable to particle surface area oxidative effects may therefore be exacerbated in regions of smaller particle deposition, including SA. Oxidative potential associated with inhaled particulates has been suggested as a mechanism by which inhaled material may cause toxicity particularly for anthropogenic environmental air pollutant particulates. Smaller particles have an increased surface area relative to their mass compared to larger size. In general, while there is substantial deposition of all particles in the nasal region upon inhalation, within the lower respiratory tract (lung), the SA region is consistently the primary site for the largest fraction of deposited particles. Due to airflow and structural differences within the respiratory tract, smaller ultrafine (<0.1 μm) and larger coarse (2.5–10 μm) particles preferentially deposit in nasal regions more than fine-sized particles. Similar findings have been observed for other fine-sized particles including those from tobacco smoke and inorganic dusts such as silica and asbestos, where concomitant SA disease is also observed. Within the human lung, it was observed that PM2.5 ambient air pollutant particles can accumulate in the SA, particularly in the distal bronchioles at up to 25 times greater doses than bronchial regions. Interestingly, ingestion of the Taiwanese plant Sauropus androgynus is also associated with bronchiolitis obliterans, with injury attributed to a yet unidentified chemical constituent. The systemic route of exposure to chemicals can also target SAs, for example, acute bronchiolitis associated with pharmaceutical exposures such as D-penicillamine and busulfan. Chemical-induced injury to SAs manifesting as bronchiolitis obliterans is also observed with inhalation of chemical vapours such as sulphur mustard and diacetyl. Indeed, fine-sized ambient air pollutant particle (0.1–2.5 μm in diameter ) levels are associated with increased SA resistance in asthmatic children and bronchiolitis in infants. Injury to this region has also been observed for other respiratory exposures including mineral dusts and diesel exhaust. The best characterized of these is tobacco smoking, where the SA is the primary site for early manifestations of lung injury and airway obstruction. Injury to human SA has been identified for many respiratory and systemic chemical and particulate exposures. We will also describe recent advances in single-cell sequencing of human airways, which have provided unprecedented details of cell phenotype, likely to impact airway chemical and particle injury. In this review, we will document the structural and cellular airway regional differences that are likely to influence airway susceptibility to injury, including the role of secretory club cells. Moreover, it is central to our understanding of SA disease aetiology and how interventional strategies for treatment may be developed. It is also important for the ability to develop appropriate models for toxicity testing. An understanding of why the SA are more susceptible to certain chemical and particle exposures than other airway regions is fundamental to our ability to identify hazardous materials, their properties, and accompanying exposure scenarios that compromise lung function. Currently, there is insufficient information in humans to make similar conclusions, prompting further necessary work in this area. Animal studies support the hypothesis that inherent cellular differences across the tracheobronchial tree, including metabolic CYP450 expression in the distal conducting airways, can influence SA susceptibility to injury. Susceptibility to injury can be attributed in part to structural features including airflow dynamics and tissue architecture, but recent evidence may indicate a more prominent role for cellular composition in directing toxicological responses.

They are susceptible to particle- and chemical-induced injury and play a major role in the development of airway disease such as COPD and asthma. Small airways (SA) in humans are commonly defined as those conducting airways <2 mm in diameter.

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