Abstract:
Background: Persistent chemical 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. Infectious encephalitis is a severe public health issue, and its prevalence and transmission exhibit significant seasonal characteristics. Previous studies have found that meteorological conditions are associated with an increased risk. However, other environmental factors, such as chemical pollutants, that may affect its effects have not been identified. This study aims to determine the impact of major environmental factors on infectious encephalitis.
Objective: Our study investigated the correlation between persistent chemical pollutants and cases of infectious encephalitis. Qgcomp method was first used to analyze the correlation of chemical pollutants. BKMR-CMA was then applied to explore mediating role of greenhouse gases in relationship between persistent chemical pollutant mixtures and incidence and death of infectious encephalitis. Finally, Lasso regression was used to assess sensitivity of different age groups of encephalitis patients to risks of various chemical pollutants.
Results: In China, the overall incidence of infectious encephalitis shows a declining trend. Among them, epidemic cerebrospinal meningitis reports and deaths are concentrated in the winter and spring seasons, with the affected population primarily in the 0-10 years and 19-50 years age groups. Encephalitis B reports and deaths are concentrated in the summer and autumn seasons, with the affected population primarily in the 0-10 years and 50 years and older age groups. In the qgcomp model, it shows that OC, NH3, PM10, CO2bio, and PCB have a positive risk effect on epidemic cerebrospinal meningitis reports and deaths. CH4 and N2O 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, N2O 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, N2O 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, N2O 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 CH4 and HCB exhibiting a positive risk effect at all levels. The mediating effect of N2O is concentrated in encephalitis B reports and deaths, where the control direct effects (CDE) of the CH4, N2O, 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). In different age groups, the main sensitive factors for epidemic cerebrospinal meningitis in the 0-10 years group were OC and CO2bio, for encephalitis B in the 0-10 years group were N2O, and for encephalitis B in the 19-50 years group was CH4.
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 CH4 and HCB. The greenhouse gas N2O may play a mediating role between chemical pollutant exposure and the outcomes of infectious encephalitis. The correlation between environmental chemical factors and infectious encephalitis varies significantly across different age groups. In the future, identifying the mechanisms of chemical mixtures can better support the causal relationship between air pollution and neurotoxicity, thus confirming the need to reduce exposure in sensitive populations.
Biography:
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