Nitrogen-containing organic compounds (NOCs) are important constituents of fine particulate matter emitted from household solid-fuel combustion, yet their personal-exposure characteristics and potential biological relevance remain insufficiently understood. We conducted an exploratory cross-sectional study among 15 rural homemakers, including 12 solid-fuel users and three electric-heating controls. Personal breathing-zone PM2.5 and PM0.25 samples were collected during two consecutive 24-h periods, and six classes of filter-collected PM-associated NOCs were quantified. Urinary inflammatory and oxidative-stress-related biomarkers and a targeted panel of 62 amino-acid-related metabolites were also analyzed. Personal exposure concentrations of the measured NOC classes were substantially higher in solid-fuel households than in electric-heating households, with particularly pronounced differences in free amino acids (FAAs) and C6-C20 alkyl nitriles. Urea dominated the total measured NOC mass, whereas FAAs constituted the largest non-urea fraction in the solid-fuel group. Correlation and exploratory mixture-response analyses indicated that FAAs and alkyl nitriles were the NOC classes most consistently associated with urinary C-reactive protein and vascular endothelial growth factor. Targeted urinary amino-acid profiling identified lower urinary concentrations of 4-hydroxyphenyllactic acid and methylguanidine in solid-fuel users based on nominal criteria, together with a borderline reduction in serotonin. Exploratory KEGG analysis further organized the measured metabolites into broad amino-acid-related biochemical categories, but was not interpreted as evidence of pathway activation or impairment. Overall, household solid-fuel use was associated with an NOC-rich personal PM exposure profile and selected urinary biomarker and targeted amino-acid-related patterns. Given the small and imbalanced sample and cross-sectional design, these findings should be interpreted as hypothesis-generating associations rather than confirmed biomarkers, causal effects, or mechanistic evidence.
Microplastics (MPs) pollution represents a pressing global environmental challenge, with studies increasingly highlighting their associated health risks. Although MPs have been detected in human lung tissues, the majority of existing research has concentrated on their physicochemical characteristics, environmental distribution and pulmonary health risks. Consequently, our understanding of the specific biological targets and effective intervention strategies against these risks remains limited. To identify therapeutic targets, we screened for pulmonary differential metabolites between normal mice and mice exposed to airborne MPs, derived from dust fall of 10 cities in China. Proteomics results showed adenosine 5'-monophosphate-activated protein kinase (AMPK) signalling pathway was one of critical targets. Through molecular docking and molecular dynamics stimulation, honokiol (HNK) was selected as therapeutic drug to regulate AMPK. In vitro results demonstrated that HNK significantly ameliorated autophagy inhibition in RAW264.7 cell, and alleviated mitochondrial dysfunction in BEAS-2B cell. Drug mechanism research revealed that HNK activated autophagy via the AMPK/mammalian target of rapamycin (AMPK/mTOR) pathway, and promoted mitophagy through the AMPK/E3 ubiquitin protein ligase parkin (AMPK/Parkin) pathway, thereby restoring mitochondrial function. Further targeted energy metabolomics analysis illustrated that HNK regulated the guanosine triphosphate to guanosine diphosphate (GTP/GDP) ratio, adenosine triphosphate (ATP) production, and nucleotide metabolism. These functions accelerated the restoration of autophagic flux, mitophagy reactivation and DNA repair. In conclusion, HNK effectively alleviates airborne MPs-induced autophagy inhibition, mitochondrial dysfunction and energy metabolism disorder via AMPK signalling, providing a promising intervention strategy for pulmonary injury caused by airborne MPs.