A method was developed for determination of thirteen amines including seven aliphatic amines, two heterocyclic amines and four aromatic amines in atmospheric particulate matter (PM) by gas chromatography-mass spectrometry (GC-MS). Samples were ultrasonically extracted with ultra-pure water and derivatized with benzenesulfonyl chloride (BSC) under alkaline conditions. The derivatives were extracted with dichloromethane and then detected by GC-MS using DB-5MS chromatographic column. The method detection limit (S/N=3) and quantitation limit (S/N=10) were 0.00008-0.017 μg/mL and 0.00026-0.0565 μg/mL respectively, and the correlation coefficients were 0.9903-0.9996, which indicated that the standard curve had good linear correlation. In addition, the relative standard deviation was less than 30％ and the average recovery was 54.4％-159.7％ except for methylamine and benzylamine at spiked level of 1.0 μg/mL, showing high precision and accuracy. 9 kinds of amines were detected in the PM2.5 samples collected in Guangzhou city by this method, among which dimethylamine and butylamine accounted for 90％ of the total nine amines, which indicated that they were primary amines in PM2.5; while propylamine exhibited the lowest level in PM2.5 with the concentration less than 1.0 ng/m3.

Aristolochic acids (AAs) have long been considered as a potent carcinogen due to its nephrotoxicity. Aristolochic acid I (AAI) reacts with DNA to form covalent aristolactam (AL)-DNA adducts, leading to subsequent A to T transversion mutation, commonly referred as AA mutational signature. Previous research inferred that AAs were widely implicated in liver cancer throughout Asia. In this study, we explored whether AAs exposure was the main cause of liver cancer in the context of HBV infection in mainland China. Totally 1256 liver cancer samples were randomly retrieved from 3 medical centers and a refined bioanalytical method was used to detect AAI-DNA adducts. 5.10% of these samples could be identified as AAI positive exposure. Whole genome sequencing suggested 8.41% of 107 liver cancer patients exhibited the dominant AA mutational signature, indicating a relatively low overall AAI exposure rate. In animal models, long-term administration of AAI barely increased liver tumorigenesis in adult mice, opposite from its tumor-inducing role when subjected to infant mice. Furthermore, AAI induced dose-dependent accumulation of AA-DNA adduct in target organs in adult mice, with the most detected in kidney instead of liver. Taken together, our data indicate that AA exposure was not the major threat of liver cancer in adulthood.