Background <p>Urinary tract infection (UTI) is among the most common bacterial infections in children and can lead to both acute and chronic complications. Although fine particulate matter (PM<sub>2.5</sub>) is a known risk factor for cardiovascular, respiratory, and renal diseases, its role in pediatric urinary tract infections remains unclear; therefore, we examined the association between long-term PM<sub>2.5</sub> exposure and UTI incidence in children using a nationwide longitudinal cohort.</p> Methods <p>We analyzed data from 395,032 children aged 0–19 years in the National Health Insurance Service–National Sample Cohort from 2002 to 2019. Annual average PM<sub>2.5</sub> exposure was estimated at 1 km<sup>2</sup> resolution using validated machine-learning ensemble models and assigned to residential districts. UTI and antibiotic-treated UTI were identified using ICD-10 codes and prescription records. Cox proportional-hazards models with time-varying exposures and covariates were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). Subgroup and sensitivity analyses were conducted to assess effect modification and robustness.</p> Results <p>During follow-up, 28,129 UTI and 14,128 antibiotic-treated UTI cases occurred. A 5&#xa0;µg/m<sup>3</sup> increase in annual PM<sub>2.5</sub> was associated with a higher risk of UTI (HR: 1.05, 95% CI: 1.02–1.08) and antibiotic-treated UTI (HR: 1.07, 95% CI: 1.03–1.11). The association between PM<sub>2.5</sub> exposure and UTI risk was stronger among children living in rural areas. Our findings were consistent in sensitivity analyses, with 1-year lag exposure showing stronger associations.</p> Conclusion <p>Long-term exposure to PM<sub>2.5</sub> was associated with an increased risk of both UTI and antibiotic-treated UTI in children. These findings suggest that air pollution may contribute to pediatric UTI risk through mechanisms involving systemic inflammation, oxidative stress, and immune dysregulation.</p>

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Association between long-term PM2.5 exposure and risk of urinary tract infection in children: a nationwide longitudinal cohort study

  • Jung Eun Choi,
  • Hyemin Jang,
  • Whanhee Lee,
  • Jongmin Oh,
  • Hae Soon Kim,
  • Ji Hyen Lee,
  • Jung Won Lee,
  • Eunhee Ha

摘要

Background

Urinary tract infection (UTI) is among the most common bacterial infections in children and can lead to both acute and chronic complications. Although fine particulate matter (PM2.5) is a known risk factor for cardiovascular, respiratory, and renal diseases, its role in pediatric urinary tract infections remains unclear; therefore, we examined the association between long-term PM2.5 exposure and UTI incidence in children using a nationwide longitudinal cohort.

Methods

We analyzed data from 395,032 children aged 0–19 years in the National Health Insurance Service–National Sample Cohort from 2002 to 2019. Annual average PM2.5 exposure was estimated at 1 km2 resolution using validated machine-learning ensemble models and assigned to residential districts. UTI and antibiotic-treated UTI were identified using ICD-10 codes and prescription records. Cox proportional-hazards models with time-varying exposures and covariates were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). Subgroup and sensitivity analyses were conducted to assess effect modification and robustness.

Results

During follow-up, 28,129 UTI and 14,128 antibiotic-treated UTI cases occurred. A 5 µg/m3 increase in annual PM2.5 was associated with a higher risk of UTI (HR: 1.05, 95% CI: 1.02–1.08) and antibiotic-treated UTI (HR: 1.07, 95% CI: 1.03–1.11). The association between PM2.5 exposure and UTI risk was stronger among children living in rural areas. Our findings were consistent in sensitivity analyses, with 1-year lag exposure showing stronger associations.

Conclusion

Long-term exposure to PM2.5 was associated with an increased risk of both UTI and antibiotic-treated UTI in children. These findings suggest that air pollution may contribute to pediatric UTI risk through mechanisms involving systemic inflammation, oxidative stress, and immune dysregulation.