N 2 O as mediator of the associations of environmental exposure to POPs, mercury, and pollutants with infectious encephalitis: A mixture exposure and mediation approach
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Background Persistent environmental pollutants have become a significant concern in global environmental pollution. However, most studies overlook the harmful effects on diseases, particularly the chronic neurotoxicity, which remains undetermined. This study aims to determine the impact of major environmental factors on infectious encephalitis. Methods Our study investigated the correlation between persistent chemical pollutants (2005–2018) and reports and mortality cases of infectious encephalitis (Epidemic cerebrospinal meningitis and Encephalitis B). First, the quantile-based g computation (qgcomp) statistical method was used to analyze the correlation of different chemical pollutants. Next, the Bayesian Kernel Machine Regression-Causal Mediation Analysis (BKMR-CMA) method was applied to explore the mediating effect of greenhouse gases between persistent chemical pollution mixtures and the incidence and mortality of infectious encephalitis. Finally, the Lasso regression method was used to assess the sensitivity of different age groups of encephalitis patients to the risks of different chemical pollutants. Results The overall incidence of infectious encephalitis shows a declining trend. In the qgcomp model, it shows that OC, NH 3 , PM 10 , CO 2 bio, and PCB have a positive risk effect on epidemic cerebrospinal meningitis reports and deaths. CH 4 and N 2 O have a positive risk effect on encephalitis B reports and deaths, both showing a positive exposure combined intervention level. In the BKMR-CMA model, for epidemic cerebrospinal meningitis report cases, N 2 O mediates at the 10% and 90% levels, and the direct effect risk of the controlled chemical pollution mixture shows a trend of first decreasing and then increasing. Among them, PCB and OC exhibit a positive risk effect at all levels. For epidemic cerebrospinal meningitis death cases, N 2 O mediates at the 10% and 90% levels, and the direct effect risk of the controlled chemical pollution mixture shows a downward trend, with PCB and NMVOC exhibiting a positive risk effect at all levels. For encephalitis B reports and death cases, N 2 O mediates at the 10% and 90% levels, and the direct effect risk of the controlled chemical pollution mixture shows a trend of first decreasing and then increasing, with CH 4 and HCB exhibiting a positive risk effect at all levels. The mediating effect of N 2 O is concentrated in encephalitis B reports and deaths, where the control direct effects (CDE) of the CH 4 , N 2 O, and HCB chemical pollutant model were assessed at three different quantiles. The CDEs at the 10%, 50%, and 75% quantiles were 757.37 (95% CI: 85.36, 1580.16), 872.86 (95% CI: 215.66, 1706.86), and 894.98 (95% CI: 209.22, 1726.33), respectively. The death effects were 31.31 (95% CI: -0.05, 66.40), 36.76 (95% CI: 8.62, 71.13), and 38.06 (95% CI: 8.46, 75.09). Main sensitive factors for epidemic cerebrospinal meningitis in the 0–10 years group were OC and CO 2 bio, for encephalitis B in the 0–10 years group were N 2 O, and for encephalitis B in the 19–50 years group was CH 4 . Conclusions We found that most persistent chemical pollutants in the air increase the risk of neurotoxicity-related morbidity and mortality. Among them, epidemic cerebrospinal meningitis is primarily driven by PCB and OC, while encephalitis B is mainly driven by CH 4 and HCB. The greenhouse gas N 2 O may play a mediating role between chemical pollutant exposure and the outcomes of infectious encephalitis. In the future, identifying the mechanisms of chemical mixtures can better support the causal relationship between air pollution and neurotoxicity.
