Short-term black carbon exposure impairs mental health and DNA methylation signatures of mitochondrial carrier genes.
Evidence on short-term black carbon (BC) exposure on mental health and underlying mechanisms involving mitochondrial function remains limited. In the Guangxi Eco-Environmental Health and Aging Study with 2271 middle-aged and older adults, we addressed this knowledge gap and explored potential DNA methylation signatures involving mitochondrial regulatory genes. Short-term BC exposure was significantly associated with a 0.494-point and 0.348-point increase in PHQ-9 and GAD-7 scores, respectively, and higher odds of depression (odds ratio [OR] = 1.554, 95 %CI: 1.276-1.901) and anxiety (OR = 1.628, 95 %CI:1.330-1.999) symptoms. These adverse effects could be mitigated by good sleep quality, defined as the PSQI score < 7. In 573 participants with available DNA methylation data, we identified 113 CpG sites in mitochondrial regulatory genes significantly associated with 28-day BC exposure. Particularly, three and five sites were associated with PHQ-9 scores and depression symptoms, while 16 were associated with GAD-7 scores and five with anxiety symptoms, respectively. Mediation analysis revealed that three CpG sites mapped on SLC25A38, SLC25A37, and SLC25A35 mediated the impact of BC on depression, with mediation proportions ranging from approximately12.19 % to 24.84 %. Our findings suggest that short-term BC exposure may affect mental health outcomes through the epigenetic regulation of mitochondrial function, highlighting a potentially modifiable biological pathway linking environmental pollution to brain health.
Authors
Liu Liu, Luo Luo, Cai Cai, Wang Wang, Rong Rong, Mo Mo, Liang Liang, Ye Ye, Tang Tang, Niu Niu, Zhang Zhang, Luo Luo, Zhao Zhao, Guo Guo, Jiang Jiang, Li Li, Pang Pang, Qin Qin, Zhang Zhang, Gao Gao
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