Personal exposure to fine particulate matter and renal function in children: A panel study
2020
Liu, Miao | Guo, Wenting | Cai, Yunyao | Yang, Huihua | Li, Wenze | Yang, Liangle | Lai, Xuefeng | Fang, Qin | Ma, Lin | Zhu, Rui | Zhang, Xiaomin
There is a lack of evidence regarding the association of short-term exposure to fine particulate matter (PM₂.₅) with renal function in children and its underlying mechanism. We included 105 children aged 4–13 years from a panel study conducted in Wuhan, China with up to 3 repeated visits across 3 seasons from October 9, 2017 to June 1, 2018. We measured personal real-time PM₂.₅ exposure concentration continuously for 72 h preceding each round of health examinations that included serum creatinine and cytokines. Linear mixed-effects models were performed to estimate the effects of PM₂.₅ on estimated glomerular filtration rate (eGFR) over various lag times, and a mediation analysis was applied for the role of cytokines in association between PM₂.₅ and eGFR. Results showed that personal exposure to PM₂.₅ was dose-responsive related to decreased eGFR within lag 2 days. The effect was the strongest at lag 0 day with estimation of −1.69% [95% confidence interval (CI): -2.27%, −1.10%] in eGFR by a 10-μg/m³ increase in PM₂.₅, and reached peak at lag 3 h, then declined over time. Such inverse relationships were more evident among children aged 4–6 years, or boys or those who lived proximity to major roadways <300 m. Notably, eGFR still held on to decrease even when PM₂.₅ was below Class II Chinese ambient air quality standard at lag 0 day. Moreover, the effect of PM₂.₅ on eGFR was significantly reduced in children with high and medium levels of serum chemokine ligand 27 (CCL27), but not in those with low CCL27. Furthermore, CCL27 was positively relevant to PM₂.₅, and mediated proportion of CCL27 ranged from 3.75% to 6.61% in relations between PM₂.₅ and decreased eGFR over various lag times. In summary, short-term PM₂.₅ exposure might be dose-responsive associated with reduced eGFR whereby a mechanism partly involving CCL27 among healthy children.
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