Relative contributions of meteorological factors and atmospheric pollutants to childhood adenoid hypertrophy: A time-series study in Chongqing, China.

backgroundAdenoid hypertrophy significantly impacts children's health. While respiratory diseases are influenced by air pollution and meteorological factors, their effects on adenoid hypertrophy remain poorly understood.

objectiveTo quantify the effects of meteorological factors and air pollutants on childhood adenoid hypertrophy hospital visits.

methodsWe analyzed 236,438 hospital visits for childhood adenoid hypertrophy (2014-2019, 2023-2024) in children < 18 years in Chongqing, China (2922 observation days) using distributed lag nonlinear models. Environmental exposures were assigned at the district level based on monitoring stations nearest to each patient's residential district. We quantified associations using standardized regression coefficients and attributable disease burdens, examining non-linear exposure-response relationships and seasonal variability. Environmental exposures included six meteorological factors (temperature, atmospheric pressure, humidity, wind speed, sunshine duration, rainfall) and six air pollutants (PM2.5, PM10, NO₂, SO₂, CO, O₃).

resultsOzone demonstrated the largest model-based attributable burden, with an estimated 16,231 cases associated with IQR increases in exposure. Summer showed extraordinary disease concentration (79.5% of cases). These findings provide preliminary evidence for environmental associations with adenoid hypertrophy in subtropical basin settings, with ozone and summer season emerging as key factors.

conclusionThis time-series analysis identified strong environmental associations with childhood adenoid hypertrophy in a subtropical basin setting. Ozone demonstrated the largest model-based association with childhood adenoid hypertrophy hospital visits(16,231 attributable cases, 6.9% of burden), with extraordinary summer disease concentration (79.5% of cases). These findings provide important evidence linking environmental exposures to adenoid hypertrophy patterns, though causal confirmation through future studies would be needed before informing environmental health strategies in comparable subtropical basin regions.