Exhaled aerosols among PCR-confirmed SARS-CoV-2-infected children

The study investigates whether SARS-CoV-2-infected children and adolescents exhale higher concentrations of aerosol particles during normal breathing than uninfected peers and whether aerosol measurement could identify superspreaders. This work is motivated by evidence that airborne aerosol transmission is a major route for SARS-CoV-2 spread and reports that children, while capable of transmitting the virus, may be less infectious than adults. Biological factors such as lower ACE2 expression, differences in lung development and airway reopening dynamics, and activity-related aerosol generation inform the context. The research aims to clarify children’s role in transmission through quantitative breath aerosol measurements and to compare exhaled particle concentration and size distributions by infection status across pediatric age groups.

Prior literature establishes aerosols as a primary transmission route of SARS-CoV-2 and documents superspreading events driven by fine particles. Studies show interindividual variability and activity-dependent increases (e.g., speaking, singing). Most virus-laden particles are <5 µm, capable of deep lung deposition. Children generally experience milder COVID-19 and may have reduced susceptibility related to ACE2 expression and developmental factors; observational data suggest children are not primary drivers of transmission. Adult studies (e.g., Edwards et al.) reported increased exhaled aerosols with COVID-19 infection, age, and obesity, and identification of adult superspreaders exhaling >5,000 p/L. In pediatric cohorts measured earlier in the pandemic (e.g., Gutmann et al.), higher aerosol counts were seen in PCR-positive versus negative children, potentially influenced by variant (Delta) and disease severity. These mixed findings underscore the need for pediatric-specific aerosol data during the Omicron period.

Design: Monocentric prospective study of children/adolescents aged 2–17 years, grouped as 2–5, 6–11, and 12–17 years. Recruitment occurred Nov 2021–Apr 2022 via pediatric practices, schools, and sports clubs. Ethical approval: Ruhr-University Bochum (21-7365); DRKS registration (DRKS00028539). Informed consent obtained. Participants: SARS-CoV-2 PCR-positive and PCR-negative subjects; healthy controls were PCR-negative and free of acute URTI signs. Acute respiratory infection defined as cough, rhinitis, or fever within prior 72 h. Exclusion: inability to undergo measurement, understand study, or provide consent. Clinical data: demographics, BMI, comorbidities (cardiac/pulmonary), allergies, medications, COVID-19 vaccination, prior SARS-CoV-2 infection, physical fitness, tobacco exposure; symptom onset/timing captured for acutely infected. PCR testing for SARS-CoV-2 performed within 48 h of aerosol measurement; variant-specific PCR used in most participants. Aerosol measurement: Resp-Aer-Meter (Palas GmbH) using optical light scattering (Fidas system); detects particles ~145 nm–10 µm. Environmental aerosols minimized by HEPA-filtered inhalation and nose clip to enforce oral breathing. Protocol included leak test, 1-minute washout to clear environmental particles, followed by 60–90 s measurement of exhaled particles. Temperature and relative humidity of exhaled air recorded; integrated heating prevented condensation. Outputs included mean exhaled particle count per liter and size distribution. Endpoints: Primary—exhaled aerosol concentration (particles/L). Secondary—effects of age, sex, height, weight, BMI, symptoms, tobacco exposure, COVID-19 vaccination, prior infection; analysis of particle size distribution. Statistics: Analyses conducted in R 4.1. Log-transformed particle count served as outcome. Bivariate linear regressions examined each predictor; a common model with all predictors and infection status explored interactions. Predictors specific to SARS-CoV-2-positive patients (e.g., time since symptom onset) or highly collinear with infection status (e.g., respiratory symptoms) were excluded from the final multiple regression. An automated stepwise model selection (MASS::stepAIC) identified an optimized model minimizing AIC. Significance assessed via t-tests and p-values within linear models.

• Cohort: 250 participants; 105 PCR-positive, 145 PCR-negative. Variant testing conducted in 89 (≈85%) of positives; all were Omicron. Median age: 9 years (IQR 7–11). Sex: 49.6% female, 50.4% male. Median BMI: 17.96 (positive) vs 16.46 (negative). - Symptoms: 81.9% of PCR-positive had symptoms. - Overall exhaled particle counts: Median 79.55 p/L (IQR 44.55–141.15). - By infection status: Median 82.72 p/L (IQR 44.55–149.52) in PCR-positive vs 79.55 p/L (IQR 44.55–136.78) in PCR-negative; no significant difference in bivariate model (t = 0.82, p = 0.415). - Multiple regression (optimized model): SARS-CoV-2 status became a significant predictor when adjusting for age, BMI, COVID-19 vaccination, and prior infection (t ≈ 2.81, p = 0.005). - Age: No significant effect overall (bivariate t = 1.18, p = 0.24; optimized model t = −1.68, p = 0.094), with a tendency for higher counts in older children (2–5 years: 79.54 p/L; 6–11: 77.96 p/L; 12–17: 98.63 p/L). - COVID-19 vaccination: Strongly associated with higher exhaled particle counts; vaccinated median 133 p/L vs unvaccinated 74.8 p/L; highly significant in bivariate and optimized models (p < 0.001). - Prior SARS-CoV-2 infection: Not significant in bivariate analysis (t = 1.4, p = 0.163) but significant in the adjusted model (t = 2.26, p = 0.025). - Non-significant factors: sex (p = 0.263), cough (p = 0.934), rhinitis (p = 0.472), sore throat (p = 0.423), fever (p = 0.343), allergies (p = 0.31), tobacco exposure (p = 0.332), comorbidities (p = 0.605). - Particle size distribution: Significant difference between PCR-positive and PCR-negative (p = 0.041). Median particle size 0.21 µm in both groups; distribution narrower in PCR-positive. Most particles were <0.5 µm. - Superspreaders: None identified among infected children; no child exceeded 595 p/L, far below adult superspreader thresholds (>5,000 p/L) reported in other studies.

The study directly addresses whether infected children exhale more aerosol particles than uninfected peers and whether superspreaders can be identified via passive breathing measurements. Bivariate analyses showed no difference by infection status, while multivariable modeling suggested a modest association when adjusting for age, BMI, vaccination, and prior infection. However, absolute particle counts were low, and no superspreaders were detected, indicating that pediatric infection does not manifest as markedly elevated aerosol emissions during quiet breathing. Findings align with epidemiological observations that children are less likely to drive transmission compared to adults and suggest physiological underpinnings (lung development, fewer alveoli/terminal bronchioles, lower minute ventilation) that may reduce aerosol generation. Compared with adult studies reporting higher emissions and superspreaders, this pediatric cohort—predominantly infected with Omicron—showed lower counts, supporting the hypothesis that variant biology and lower lung involvement with Omicron may reduce deep-lung aerosol formation. The unexpected association between vaccination and higher aerosol counts lacks a clear mechanistic explanation and warrants further investigation. Overall, exhaled aerosol measurement during resting breathing appears unsuitable for infection screening or superspreader detection in children and adolescents.

Exhaled aerosol particle counts in children and adolescents are generally low and do not differ meaningfully between SARS-CoV-2 PCR-positive and PCR-negative participants in unadjusted analyses; no superspreaders were identified. While infection status reached significance in an adjusted model, the clinical utility of aerosol measurements for identifying infected children or interrupting transmission chains is limited. The study contributes pediatric-specific data using standardized measurement methods during an Omicron-dominant period and highlights potential influences of age, prior infection, and vaccination. Future research should include longitudinal measurements across infection timelines, variant-specific and severity-stratified cohorts (including hospitalized patients), controlled environmental conditions, assessment of exhaled viral RNA/viability, and mechanistic studies to explain the vaccination-associated increase in exhaled particle counts.

• Cohort predominantly mildly ill, nonhospitalized participants; findings may not generalize to severe pediatric COVID-19. - Up to 48-hour interval between PCR testing and aerosol measurement could introduce misclassification or temporal variability. - No testing for other respiratory pathogens; co-infections could confound aerosol production. - Cross-sectional design without longitudinal follow-up; dynamics over the course of infection not captured. - Environmental conditions (humidity, season, ambient aerosols) were not controlled and may influence measurements. - Compliance and breathing technique variability, particularly in younger children, may affect measurement accuracy. - Variant distribution skewed to Omicron; results may not generalize to other variants (e.g., Delta). - No PCR or viral culture performed on exhaled aerosol samples to assess viral content/viability. - Vaccination timing relative to measurement was not recorded, limiting interpretation of vaccination effects.