Respiratory viruses continue to cause a substantial global burden of disease, resulting in millions of hospitalizations and considerable mortality each year (Organization WH, 2024; Sirota et al., 2025; Bender et al., 2024). Among the recognized transmission routes, airborne spread has gained increasing attention as a key contributor to the dissemination of these pathogens, especially in enclosed or poorly ventilated environments. The airborne route of transmission involves small virus-laden particles generated during routine expiratory activities, which can remain suspended in the air, travel over long distances, and deposit within the lower airways (Wang et al., 2021; Pöhlker et al., 2023).

However, respiratory particle generation is not a single, uniform process, but rather a complex and dynamic one that can be modulated by various physiological factors, such as airway structure, airflow dynamics, surface tension, and fluid rheology (Pöhlker et al., 2023; Bagheri et al., 2023; Johnson and Morawska, 2009; Almstrand et al., 2010; Roth et al., 2023; Edwards et al., 2004). In addition, different respiratory activities engage distinct regions of the airway, resulting in varied particle formation mechanisms and size distributions (Wang et al., 2021; Pöhlker et al., 2023; Kutter et al., 2018) (Figure 1). Fine respiratory particles (<5 μm) are primarily produced in the distal lung, where cyclic closure and reopening of small airways disrupts the airway lining fluid in the bronchioles and alveoli. Variations in tidal volume and breathing rate can further modulate this mechanism (Pöhlker et al., 2023; Bagheri et al., 2023; Johnson and Morawska, 2009; Almstrand et al., 2010; Bake et al., 2017; Morawska et al., 2009; Tinglev et al., 2016; Oldham and Moss, 2019). In more proximal regions, such as the larynx and oral cavity, particle generation is mainly driven by shear-induced fragmentation and fluid-film rupture caused by vocal fold oscillation, oral articulation, and increased airflow, typically resulting in larger particles (Pöhlker et al., 2023; Bagheri et al., 2023). Expulsive events such as coughing and sneezing commonly intensify these mechanisms, generating even broader particle size distributions (Pöhlker et al., 2023; Morawska et al., 2009; Zayas et al., 2012; Xie et al., 2009).

Importantly, transmission risk also depends on whether these exhaled particles contain infectious virus. Active infection at sites of particle generation, as discussed above, may contribute to viral presence in exhaled particles, although this relationship remains unconfirmed. Virus-specific factors, such as cellular tropism and strain specificity, along with host-related factors including immune competence and infection severity, likely further modulate virus presence (Wang et al., 2021; Puhach et al., 2023; Flerlage et al., 2021).

Despite growing understanding of the physiological mechanisms underlying respiratory particle formation and infection kinetics, considerable inter-individual variability in respiratory virus transmission persists, and its underlying drivers remain poorly understood. Epidemiological findings indicate that a small proportion of individuals contribute disproportionately to secondary transmission, highlighting the need to investigate host-specific drivers of transmission risk (Guo et al., 2023; Wegehaupt et al., 2023). Demographic factors (e.g., age, sex, body mass index), lifestyle factors (e.g., smoking status, physical activity), and infection-related factors (e.g., symptom onset, disease severity) have been associated with differences in airway characteristics, mucus properties, and viral shedding profiles (Lee et al., 2017; Dixon and Peters, 2018; Molgat-Seon et al., 2018; Schneider et al., 2021; Hussain-Alkhateeb et al., 2021; Marshall et al., 2020; Zanin et al., 2016; Sun et al., 2024; Li and Tang, 2021; Roman et al., 2016; Rathnayake et al., 2023; LoMauro and Aliverti, 2018). Through these effects, they may shape both the volume of particles produced and the likelihood that those particles carry infectious virus.

This systematic review synthesizes current evidence on the associations between host-related factors and both respiratory particle emission and the detection of virus in exhaled respiratory particles. Understanding how host factors influence both the generation and infectiousness of airborne particles can provide valuable proxies for transmission risk and offer insights into underlying physiological processes. By identifying individual-level determinants of airborne transmission, these findings aim to support risk assessment and guide public health strategies in clinical, occupational, and community settings, especially in preparation for future respiratory virus outbreaks.

The database searches yielded a total of 5,506 articles. After deduplication, 3,059 unique citations remained and were screened by title and abstract. Of these, 2,875 were excluded for not meeting the inclusion criteria. An additional six articles were excluded due to retrieval issues, leaving 178 studies for full-text review. Following full-text screening, 136 articles were excluded due to ineligible study designs, outcomes, article types, language, or duplication. Two more studies were added through reference list screening, resulting in 44 studies meeting the eligibility criteria and included in this systematic review. Of these, host factor associations with respiratory particle emission were examined in 34 studies. An additional 11 studies assessed viral presence in exhaled particles in relation to host factors; all of these were limited to influenza virus or SARS-CoV-2. One study contributed to both outcome categories and is therefore included in both counts (Viklund et al., 2022). A detailed overview of the database-specific search terms and corresponding results is provided in Supplementary Tables 1, 2. Detailed reviewer comments and final decisions from both the title/abstract and full-text screening stages are provided in Supplementary File 1. A PRISMA flow diagram is provided in Figure 2.

This systematic review synthesizes evidence from 44 studies to elucidate if host determinants are associated with two critical aspects of airborne transmission: the generation of exhaled aerosol particles and the incorporation of infectious virus into those particles. Most host factor associations were reported for fine particles (<5 μm), reflecting both their abundance in exhaled respiratory particles and the methodological challenges inherent in assessing coarse particle fractions. Several host factors, including age, physical exercise, and active infection, emerged as consistent predictors of increased fine particle emission, whereas sex, BMI, and smoking yielded limited or inconsistent associations. Viral presence within these particles was most strongly linked to infection-related characteristics, particularly time since symptom onset and lower respiratory tract involvement, rather than demographic or lifestyle factors.

The host factor associations identified in this review may be explained by several underlying biophysical processes governing respiratory particle generation. As previously discussed, the cyclic closure and reopening of small airways in the distal lung is a primary mechanism contributing to the formation of fine particles (Figure 1). This process may vary across the lifespan. In younger individuals, ongoing alveolar development into early adulthood may limit the surface area available for particle formation, contributing to lower emission levels. In contrast, older adults exhibit reduced elastic recoil and increased airway collapsibility, which may enhance airway reopening and shear forces, thereby promoting increased fine particle generation (Roman et al., 2016; Thomas et al., 2019; Martins Rodrigues et al., 2021; Nikolić et al., 2018). Age-related changes in mucus composition may further influence fluid rheology and reduce surface tension thresholds, facilitating droplet fragmentation (Edwards et al., 2004; Hussain-Alkhateeb et al., 2021). Physical exercise also acts along this pathway by increasing tidal volume and airflow velocities, thereby amplifying shear forces and the frequency of airway reopening events. These mechanical stresses promote fragmentation of the airway surface liquid and enhance fine particle emission (Johnson and Morawska, 2009; Morawska et al., 2009; Archer et al., 2022; Harrison et al., 2023). However, systemic dehydration during intense exercise may reduce airway hydration, potentially limiting submicron particle production despite elevated ventilation (Marshall et al., 2020; Varga et al., 2022). A respiratory infection may similarly enhance particle output by increasing mucus production and airway surface liquid, or indirectly through elevated respiratory rates associated with shortness of breath (Li and Tang, 2021; Weston and Frieman, 2019). Positive correlation reported between viral load in clinical swabs and the quantity of fine respiratory particles may reflect immune-mediated effects on airway physiology, although this hypothesis requires further validation. One contradictory finding was reported, suggesting that changes in viscosity may reduce particle emissions during infection. However, the study was limited by its small sample size as well as the duration and volume of sampling (Viklund et al., 2022).

Host factors such as sex, BMI, and smoking were not consistently associated with fine particle emission. While it is known that these factors can influence respiratory tract physiology, their effects on particle generation may be indirect or context dependent. For example, the lack of sex differences may reflect comparable alveolar structure and lung function across sexes in adulthood (Molgat-Seon et al., 2018; LoMauro and Aliverti, 2018). Occasional findings, such as increased emission during nasal breathing or low-frequency phonation, suggest a minor role for proximal production mechanisms, although supporting evidence remains limited. Variable associations with BMI may relate to comorbid conditions such as asthma or COPD, which can affect airway reopening dynamics (Sun et al., 2024). Similarly, although smoking is known to alter the bronchial mucus barrier and increase mucus production, it does not appear to enhance fine particle formation (Rathnayake et al., 2023). One possible explanation, also noted in the context of infection (Viklund et al., 2022), is that increased viscosity may limit the fragmentation of the airway lining fluid, thereby reducing fine particle emission and potentially masking any effect of smoking, although this remains speculative (Edwards et al., 2004).

By contrast, viral loading of respiratory particles appears to depend more on infection biology than on the mechanics of particle generation. Findings regarding host factor associations were largely consistent across influenza virus and SARS-CoV-2, indicating similar patterns in viral load dynamics despite differences in virus type and variant. However, the lack of studies on other respiratory viruses constrains the generalizability of these observations. This limitation may relate to differences in tissue tropism, as seen with Omicron, which shows altered anatomical targeting compared to earlier variants and may contribute to virus-specific patterns of respiratory particle emission (Lai et al., 2023; Chatterjee et al., 2023).

Viral replication is reported to peak during the early phase of infection, likely contributing to a higher probability that exhaled particles contain infectious virus (Puhach et al., 2023; Chen et al., 2021). This aligns with consistent findings of a temporal decline in exhaled viral load as time since symptom onset increases. However, more severe infections can result in prolonged viral loads in the lower respiratory tract, potentially explaining the absence of a temporal decline in some studies (Puhach et al., 2023; Lim et al., 2021). The anatomical focus of infection appears to also influence the likelihood of detecting virus in exhaled particles. Specifically, associations between viral load in particles and lower respiratory tract symptoms were more frequently observed than with upper respiratory symptoms, which suggest independent mechanisms. This is consistent with studies reporting that especially involvement of the lower respiratory tract increases the likelihood of virus presence in exhaled particles (de Mesquita et al., 2021; Yan et al., 2018; Lindsley et al., 2016). Inconsistent correlations between swab-based viral load and exhaled viral particles underscore this anatomical disconnect. Notably, studies focusing specifically on coughing, which generates high-velocity shear-driven emissions, have demonstrated stronger correlations with upper airway viral load, suggesting that these clinical parameters may be more closely linked to proximal particle generation mechanisms (Lindsley et al., 2010; de Mesquita et al., 2021; Yan et al., 2018).

Demographic and lifestyle host factors did not consistently account for the presence of virus in exhaled particles. Although age was frequently associated with increased fine particle emission, it was less informative in identifying individuals likely to shed infectious virus. This may be attributed to the predominance of studies involving mildly symptomatic or outpatient populations, in whom minimal lower respiratory tract involvement may limit the generation of virus-laden particles from distal airways. However, a few studies did report positive associations for age and BMI, which may suggest potential links. Other physiological processes, particularly differences in immune response such as impaired immune clearance associated with advancing age or elevated BMI, could contribute to these associations (Flerlage et al., 2021; Schneider et al., 2021).

It is important to note that most reported associations between host factors and the presence of respiratory viruses are based on detection of genomic material rather than replication-competent virus. This detection shows that viral material can be present even in small particles, but infectious virus is less often recovered in the current evidence base. Therefore, RNA-based findings should be regarded as indicators of viral shedding rather than direct proof of infectiousness.

A limited number of studies assessed host factor associations with coarse particle emission. However, the findings suggest that the effects of age and physical exercise were weaker for coarse particles than for fine particles. The limited evidence likely reflects methodological constraints: sampling interfaces such as masks and tubing may reduce capture of larger particles due to impaction losses and flow restrictions, while dehydration and shrinkage may further bias size classification (Pöhlker et al., 2023; Bagheri et al., 2023; Edwards et al., 2004). Beyond particle size bias, other methodological constraints were common across studies. The majority were cross-sectional and conducted at a single time point, limiting the ability to capture dynamic changes in respiratory particle output or viral shedding over time. Few studies accounted for individual-level factors such as hydration status, which may influence particle generation (Gregson et al., 2021; Rawat et al., 2023; Oh et al., 2024). Heterogeneity in instrumentation and study protocols introduced variability across findings, making it difficult to isolate the absolute effect of host factors (Hu et al., 2024; Verreault et al., 2008). Symptom classification often relied on self-reported data, introducing potential misclassification.

Despite methodological variability, the inclusion of diverse study designs strengthens the overall conclusions of this review. Studies maintained internal consistency in sampling and analysis, allowing meaningful comparisons within cohorts. By evaluating both respiratory particle emission and viral presence, this review provides an integrated perspective on host-related determinants of airborne transmission. The findings suggest that certain host characteristics, particularly when considered in combination, may serve as practical indicators of infectiousness. Individuals with increased particle emission and a greater likelihood of virus presence, such as older adults in the early phase of infection or those with lower respiratory involvement, may benefit from targeted mitigation strategies. Future studies should examine the combined impact of host factors on viable viruses in respiratory particles, explore less-studied variables such as the effect of physical exercise, and include a broader range of respiratory pathogens. In parallel, investigating the underlying generation mechanisms that drive these associations may clarify causal pathways and strengthen mechanistic understanding. The adoption of standardized measurement approaches that include the coarse particle range, along with expanded clinical characterization in longitudinal studies, will be essential for improving data comparability and strengthening outbreak preparedness.

This systematic review highlights that host factors influence airborne transmission through two distinct mechanisms: airway biomechanics driving particle generation and infection biology determining viral presence in exhaled particles. Older age, physical exercise, and active respiratory infections were consistently associated with increased fine respiratory particle emission, whereas other variables, including sex, BMI, and smoking, showed no consistent associations or were insufficiently studied. Viral presence in respiratory particles was more closely linked to time since symptom onset and anatomical site rather than individual demographic or lifestyle factors. No single host factor explained both increased particle emission and viral presence, but combinations such as older age with lower respiratory involvement may better indicate transmission potential. Current evidence remains constrained by methodological heterogeneity, a predominant focus on SARS-CoV-2 and influenza, and reliance on genomic detection rather than viral viability. Closing these gaps will be essential not only for refining risk assessment and guiding targeted interventions, but also for strengthening outbreak preparedness and improving infection control strategies.