Environmental Health and Preventive Medicine
Online ISSN : 1347-4715
Print ISSN : 1342-078X
ISSN-L : 1342-078X
The increased risk of exposure to fine particulate matter for depression incidence is mediated by elevated TNF-R1: the Healthy Aging Longitudinal Study
Ta-Yuan ChangTing-Yu ZhuangYun-Chieh YangChih-Cheng HsuWan-Ju Cheng
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2025 Volume 30 Pages 49

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Abstract

Background: Depression among older adults is an important public health issue, and air and noise pollution have been found to contribute to exacerbation of depressive symptoms. This study examined the association of exposure to air and noise pollutants with clinically-newly-diagnosed depressive disorder. The mediating role of individual pro-inflammatory markers was explored.

Methods: We linked National Health Insurance claim data with 2998 healthy community-dwellers aged 55 and above who participated in the Healthy Aging Longitudinal Study between 2009 and 2013. Newly diagnosed depressive disorder was identified using diagnostic codes from the medical claim data. Pollutants were estimated using nationwide land use regression, including PM2.5 and PM10, carbon monoxide, ozone, nitrogen dioxide, sulfur dioxide, and road traffic noise. Cox proportional hazard models were employed to examine the association between pollutants and newly developed depressive disorders. The mediating effect of serum pro-inflammatory biomarkers on the relationship was examined.

Results: Among the 2998 participants, 209 had newly diagnosed depressive disorders. In adjusted Cox proportional hazard models, one interquartile range increase in PM2.5 (8.53 µg/m3) was associated with a 17.5% increased hazard of developing depressive disorders. Other air pollutants and road traffic noise were not linearly associated with depressive disorder incidence. Levels of serum tumor necrosis factor receptor 1 mediated the relationship between PM2.5 and survival time to newly onset depressive disorder.

Conclusion: PM2.5 is related to an increased risk of newly developed depressive disorder among middle-aged and older adults, and the association is partially mediated by the pro-inflammatory marker TNF-R1.

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