PAHs’Dist ribution and Source Analysis in Surface Sediment s of the Meizhou Bay

[摘要]：2000 年10 月在湄洲湾海域6 个站位采集表层沉积物样,采用GC/ MS 法分析其多环芳烃的含量. 结果显示: 在这些沉积物样中,美国环保署优控的16 种多环芳烃的含量分布较为均匀,其范围为196. 7～299. 7 ng/ g ,平均值为 256. 1 ng/ g ;显著低于长江口、珠江口及其欧美主要港口表层沉积物中多环芳烃的含量. 对多环芳烃特征组分的比值 (菲/ 蒽比值,荧蒽/ 芘比值) 及16 种多环芳烃中四、五和六环总含量的百分比的分析表明:湄洲湾表层沉积物的多环 芳烃主要来源于燃料的高温燃烧.[Abstract]:The Meizhou Bay , located in the mid2east coast of Fujian , China , is a semi2enclosed narrow bay st retching deep into the inland with favorable hydrological circulation conditions. With the const ruction of port s , oil2refinery works and power indust ry in the coastal area ,PAHs’pollution is a potential environmental risk factor in this marine environment ,but no data of PAHs level in this marine environment were established before. The aim of this study is to examine PAHs’dist ribution in the surface sediment s and analyze their sources in the Meizhou Bay. The data showed that : PAHs’concent rations in the surface sediment s were f rom 196. 7 ～ 299. 7 ng/ g and average value was 256. 1 ng/ g. The result s revealed that PAHs’pollution in the sediment was similar. The result s also showed that sediment PAHs in the Meizhou Bay were much lower than those in the Pearl River Delta and the Yangtze River Delta and the major harbors in America and Aust ralia ; but higher than that in the surface sediment s of White Sea. Ratio values of specific PAH compounds such as phenanthrene/ anthracene and fluoranthene/ pyrene were calculated to evaluate the possible source of PAHs contamination in the surface sedi2 ment s of the Meizhou Bay ,the percentage of 4 + 5 + 6 rings of PAHs in total was also used to indicate PAHs’ possible sources. The result s suggested that the surface sediment s might mainly have pyrolytic input s of PAHs.国家自然科学基金(A20077023 ,C40106012) 资

Evaluation of the cytogenetic damage induced by the organophosphorous insecticide acephate

The organophosphorous insecticide acephate was tested for its ability to induce in vitro cytogenetic effect in human peripheral lymphocytes by using the chromosomal aberrations (CAs), sister chromatid exchange (SCE) and micronuclei (MN) assay. The level of nuclear DNA damage of acephate was evaluated by using the comet assay. Concentrations of 12.5, 25, 50, 100 and 200 μg mL−1 of acephate were used. All concentrations of acephate induced significant increase in the frequency of CAs and in the formation of MN dose dependently (r = 0.92 at 24 h, r = 0.95 at 48 h for CAs, r = 0.87 for MN). A significant increase was observed in induction of SCE at 50, 100 and 200 μg mL−1 concentrations during 24 h treatment and at all concentrations (except 12.5 μg mL−1) during 48 h treatment period in a dose-dependent manner (r = 0.84 at 24 h, r = 0.88 at 48 h). Acephate did not affect the replicative index and cytokinesis-block proliferation index (CBPI). However, it significantly decreased the mitotic index at all three highest concentrations (50, 100, 200 μg mL−1) for 24 h treatment and at all concentrations (except 12.5 μg mL−1) for 48 h treatment, dose-dependently (r = 0.94 at 24 h, r = 0.92 at 48 h). A significant increase in mean comet tail length was observed at 100 and 200 μg mL−1 concentrations compared with negative control in a concentration-dependent manner (r = 0.94). The mean comet tail intensity was significantly increased at only 200 μg mL−1 concentration. The present results indicate that acephate is a clastogenic, cytotoxic agent and it causes DNA damage at high concentrations in human lymphocytes in culture