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<p>This Finnish population-nested case-control (FINPARK) study investigates the association between long-term exposure to six gaseous air pollutants and PD risk. Incident PD cases (<i>n</i> = 22,189) between 1996 and 2015 were identified from the Finnish medical reimbursement register maintained by the Finnish Social Security Institution. Age-, sex- and region-matched cases (<i>n</i> = 148,009) were identified from the Finnish population register. Time-weighted average air pollution exposure was modelled at the residential address for 16 years preceding the PD diagnosis. We observed a marginally increased risk for PD after higher levels of exposure to O<sub>3</sub> (OR 1.03, 95% CI 1.00-1.06 per IQR) for exposure 6–16 years before the index date. Inverse associations were observed for NO<sub>X</sub>, NO<sub>2</sub>, CO and SO<sub>2</sub>, potentially due to the strong negative correlation with O<sub>3</sub>. No association with NH<sub>3</sub> was observed. This may suggest a possible role of ozone in PD development even at low exposure levels, which requires further studies.</p>

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Long-term exposure to six gaseous air pollutants and risk of Parkinson’s Disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月31日

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  • Isabell Katharina Rumrich,
  • Antti Korhonen,
  • Lise Marie Frohn,
  • Camilla Geels,
  • Jørgen Brandt,
  • Sirpa Hartikainen,
  • Otto Hänninen,
  • Anna-Maija Tolppanen

摘要

This Finnish population-nested case-control (FINPARK) study investigates the association between long-term exposure to six gaseous air pollutants and PD risk. Incident PD cases (n = 22,189) between 1996 and 2015 were identified from the Finnish medical reimbursement register maintained by the Finnish Social Security Institution. Age-, sex- and region-matched cases (n = 148,009) were identified from the Finnish population register. Time-weighted average air pollution exposure was modelled at the residential address for 16 years preceding the PD diagnosis. We observed a marginally increased risk for PD after higher levels of exposure to O3 (OR 1.03, 95% CI 1.00-1.06 per IQR) for exposure 6–16 years before the index date. Inverse associations were observed for NOX, NO2, CO and SO2, potentially due to the strong negative correlation with O3. No association with NH3 was observed. This may suggest a possible role of ozone in PD development even at low exposure levels, which requires further studies.