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Peer-reviewedCC BY 4.0Public Health Challenges

Ambient Air Pollution and Kawasaki Disease: A Systematic Review and Meta‐Analysis of Epidemiological Evidence

  • Amogh Verma1
  • Ranjana Sah2
  • Pratima Pandey3
  • Asif Jan4,5,6
  • Daniel Dubwa7
7 affiliations
  1. 1Department of Internal Medicine Rama Medical College Hospital and Research Centre Hapur Uttar Pradesh India
  2. 2Dr. D. Y. Patil Medical College Hospital and Research Centre Dr. D. Y. Patil Vidyapeeth (Deemed‐to‐be‐University) Pune Maharashtra India
  3. 3Department of Pharmacy Practice National Institute of Pharmaceutical Education and Research S.A.S Nagar Punjab India
  4. 4Department of Pharmacy University of Peshawar Peshawar Khyber Pakhtunkhwa Pakistan
  5. 5Saidu Group of Teaching Hospitals Saidu Sharif, Swat Khyber Pakhtunkhwa Pakistan
  6. 6District Headquarter Hospital Charsadda Charsadda Khyber Pakhtunkhwa Pakistan
  7. 7Department of Pharmacy Makerere University Kampala Uganda
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Abstract

Background: Kawasaki disease (KD) is a childhood vasculitis with a multifactorial etiology involving genetic susceptibility and environmental influences. Ambient air pollution has been proposed as a potential environmental trigger, but epidemiological findings have been inconsistent across pollutants, populations, and exposure periods. This systematic review and meta‐analysis aimed to synthesize the association between ambient air pollution and KD.

Methods: PubMed, Embase, and Web of Science were searched from database inception through December 29, 2024, for observational studies evaluating associations between ambient air pollutants and KD. Multivariable‐adjusted estimates were preferentially used for quantitative synthesis. Hazard ratios and odds ratios were interpreted as relative risks, and estimates were standardized to a 10 µg/m3 increase in pollutant concentration where applicable. Random‐effects models were used to obtain pooled relative risks, with heterogeneity assessed using I 2 statistics.

Results: Thirteen studies met the inclusion criteria. The studies included diverse epidemiological designs and were predominantly conducted in Asian populations, with additional studies from North America and Italy. Across the quantitative synthesis, no statistically significant association was observed between a standardized 10 µg/m3 increase in individual pollutants and KD occurrence. The pooled relative risks were 1.00 (95% confidence interval [CI], 0.985–1.016) for PM2.5, 1.00 (95% CI, 0.983–1.022) for PM10, 1.008 (95% CI, 0.966–1.051) for SO2, 0.99 (95% CI, 0.989–1.009) for NO2, and 1.013 (95% CI, 0.981–1.046) for O3 and CO. For PM2.5, between‐study heterogeneity was moderate (I 2 = 43.8%), whereas Egger's test showed no evidence of significant publication bias (p = 0.2703).

Conclusion: Current evidence does not demonstrate a statistically significant overall association between ambient air pollution and KD. However, associations may vary by pollutant, exposure timing, geographical setting, and meteorological conditions. Future studies should use standardized exposure windows and account for key meteorological factors to clarify these potential context‐specific associations.

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Cite

BibTeXRIS
BibTeX
@article{verma2026ambient,
  title = {{Ambient Air Pollution and Kawasaki Disease: A Systematic Review and Meta‐Analysis of Epidemiological Evidence}},
  author = {Amogh Verma and Ranjana Sah and Pratima Pandey and Asif Jan and Daniel Dubwa},
  journal = {Public Health Challenges},
  year = {2026},
  month = nov,
  doi = {10.1002/puh2.70448},
  url = {https://doi.org/10.1002/puh2.70448},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Ambient Air Pollution and Kawasaki Disease: A Systematic Review and Meta‐Analysis of Epidemiological Evidence
AU  - Amogh Verma
AU  - Ranjana Sah
AU  - Pratima Pandey
AU  - Asif Jan
AU  - Daniel Dubwa
PY  - 2026
DA  - 2026/11/07
JO  - Public Health Challenges
DO  - 10.1002/puh2.70448
UR  - https://doi.org/10.1002/puh2.70448
AB  - Background: Kawasaki disease (KD) is a childhood vasculitis with a multifactorial etiology involving genetic susceptibility and environmental influences. Ambient air pollution has been proposed as a potential environmental trigger, but epidemiological findings have been inconsistent across pollutants, populations, and exposure periods. This systematic review and meta‐analysis aimed to synthesize the association between ambient air pollution and KD.  Methods: PubMed, Embase, and Web of Science were searched from database inception through December 29, 2024, for observational studies evaluating associations between ambient air pollutants and KD. Multivariable‐adjusted estimates were preferentially used for quantitative synthesis. Hazard ratios and odds ratios were interpreted as relative risks, and estimates were standardized to a 10 µg/m3 increase in pollutant concentration where applicable. Random‐effects models were used to obtain pooled relative risks, with heterogeneity assessed using I 2 statistics.  Results: Thirteen studies met the inclusion criteria. The studies included diverse epidemiological designs and were predominantly conducted in Asian populations, with additional studies from North America and Italy. Across the quantitative synthesis, no statistically significant association was observed between a standardized 10 µg/m3 increase in individual pollutants and KD occurrence. The pooled relative risks were 1.00 (95% confidence interval [CI], 0.985–1.016) for PM2.5, 1.00 (95% CI, 0.983–1.022) for PM10, 1.008 (95% CI, 0.966–1.051) for SO2, 0.99 (95% CI, 0.989–1.009) for NO2, and 1.013 (95% CI, 0.981–1.046) for O3 and CO. For PM2.5, between‐study heterogeneity was moderate (I 2 = 43.8%), whereas Egger's test showed no evidence of significant publication bias (p = 0.2703).  Conclusion: Current evidence does not demonstrate a statistically significant overall association between ambient air pollution and KD. However, associations may vary by pollutant, exposure timing, geographical setting, and meteorological conditions. Future studies should use standardized exposure windows and account for key meteorological factors to clarify these potential context‐specific associations.
SN  - 2769-2450
ER  -