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Characterization of the typical petroleum pollutants, polycyclic aromatic hydrocarbons (PAHs) and n-alkanes, and indigenous microbial community structure and function in historically contaminated soil at petrol stations is critical. Five soil samples were collected from a petrol station in Beijing, China. The concentrations of 16 PAHs and 31 n-alkanes were measured by gas chromatography-mass spectrometry. The total concentrations of PAHs and n-alkanes ranged from 973 ± 55 to 2667 ± 183 μg/kg and 6.40 ± 0.38 to 8.65 ± 0.59 mg/kg (dry weight), respectively, which increased with depth. According to the observed molecular indices, PAHs and n-alkanes originated mostly from petroleum-related sources. The levels of ΣPAHs and the total toxic benzo[a]pyrene equivalent (ranging from 6.41 to 72.54 μg/kg) might exert adverse biological effects. Shotgun metagenomic sequencing was employed to investigate the indigenous microbial community structure and function. The results revealed that Proteobacteria and Actinobacteria were the most abundant phyla, and Nocardioides and Microbacterium were the important genera. Based on COG and KEGG annotations, the highly abundant functional classes were identified, and these functions were involved in allowing microorganisms to adapt to the pressure from contaminants. Five petroleum hydrocarbon degradation-related genes were annotated, revealing the distribution of degrading microorganisms. This work facilitates the understanding of the composition, source, and potential ecological impacts of residual PAHs and n-alkanes in historically contaminated soil.
相似文献To examine pesticide mixture toxicity to aqueous organisms, we assessed the single and combined toxicities of thiamethoxam and other four pesticides (chlorpyrifos, beta-cypermethrin, tetraconazole, and azoxystrobin) to the rare minnow (Gobiocypris rarus). Data from 96-h semi-static toxicity assays of various developmental phases (embryonic, larval, juvenile, and adult phases) showed that beta-cypermethrin, chlorpyrifos, and azoxystrobin had the highest toxicities to G. rarus, and their LC50 values ranged from 0.0031 to 0.86 mg a.i. L?1, from 0.016 to 6.38 mg a.i. L?1, and from 0.39 to 1.08 mg a.i. L?1, respectively. Tetraconazole displayed a comparatively high toxicity, and its LC50 values ranged from 3.48 to 16.73 mg a.i. L?1. By contrast, thiamethoxam exhibited the lowest toxic effect with LC50 values ranging from 37.85 to 351.9 mg a.i. L?1. Rare minnow larvae were more sensitive than embryos to all the pesticides tested. Our data showed that a pesticide mixture of thiamethoxam–tetraconazole elicited synergetic toxicity to G. rarus. Moreover, pesticide mixtures containing beta-cypermethrin in combination with chlorpyrifos or tetraconazole also had synergetic toxicities to fish. The majority of pesticides are presumed to have additive toxicity, while our data emphasized that the concurrent existence of some chemicals in the aqueous circumstance could cause synergetic toxic effect, leading to severe loss to the aqueous environments in comparison with their single toxicities. Thence, the synergetic impacts of chemical mixtures should be considered when assessing the ecological risk of chemicals.
相似文献Polycyclic aromatic hydrocarbon (PAH) exposure and genetic susceptibility were conductive to genotoxic effects including gene damage, which can increase mutational probability. We aimed to explore the dose-effect associations of PAH exposure with damage of exons of epidermal growth factor receptor (EGFR) and breast cancer susceptibility gene 1 (BRCA1), as well as their associations whether modified by Flap endonuclease 1 (FEN1) genotype. Two hundred eighty-eight coke oven male workers were recruited, and we detected the concentration of 1-hydroxypyrene (1-OH-pyr) as PAH exposure biomarker in urine and examined base modification in exons of EGFR and BRCA1 respectively, and genotyped FEN1 rs174538 polymorphism in plasma. We found that the damage indexes of exon 19 and 21 of EGFR (EGFR-19 and EGFR-21) were both significantly associated with increased urinary 1-OH-pyr (both Ptrend < 0.001). The levels of urinary 1-OH-pyr were both significantly associated with increased EGFR-19 and EGFR-21 in both smokers and nonsmokers (both P < 0.001). Additionally, we observed that the urinary 1-OH-pyr concentrations were linearly associated with both EGFR-19 and EGFR-21 only in rs174538 GA+AA genotype carriers (both P < 0.001). Moreover, FEN1rs rs174538 showed modifying effects on the associations of urinary 1-OH-pyr with EGFR-19 and EGFR-21 (both Pinteraction < 0.05). Our findings revealed the linear dose-effect association between exon damage of EGFR and PAH exposure and highlight differences in genetic contributions to exon damage and have the potential to identify at-risk subpopulations who are susceptible to adverse health effects induced by PAH exposure.
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