Arsenic residue in residential area after cleanup of pesticide illegal dumping sources in Thanh Hoa province,Central Vietnam

In Vietnam, Nicotex's site is perhaps the most infamous case of illegal disposal of toxic pesticides near residential areas. In 2013, affected villagers discovered illegal burials of around 1,000 tons of expired pesticides in the Nicotex factory. Organic pesticides were detected in illegal burial areas (IBAs) around 60 times greater than acceptable levels, but no attention was paid to contamination of metals, metalloids, and other classes of organic contaminants, which could be co-contaminants in pesticide formulation. This study assessed the contaminants remaining in the IBAs and surrounding residential areas two years after the source removal conducted in 2014. Additionally, a preliminary health risk assessment from residual contaminants was performed. Nine classes of chemicals including parental pesticides, inorganic and organic degradation byproducts, and metals and metalloids, comprising 123 chemicals were quantified in soil, sediment, and water samples from Nicotex and surrounding residential areas. Although concentrations of organic pesticides were below acceptable levels, arsenic contamination in the soil in a Nicotex IBA named NCT5 and Nap village (NV) exceeded the acceptable level. The enrichment factor and log-probability plot indicate that arsenic enrichment at NV is not from natural sources but is associated with arsenic contamination in NCT5. Arsenic may be a co-contaminant in pesticide manufacturing or an arsenical pesticide, such as monosodium methanearsonate. Arsenic found in NV was toxic arsenate for which the preliminary risk assessment yielded an unacceptable excess carcinogenic risk (1 × 10^?4). While all attention was paid to investigate and treat contamination of organic pesticides, it turns out that arsenic is the major existing threat which poses an unacceptable cancer risk in good agreement with the high cancer rate claimed by villagers near Nicotex. This justifies the need for further investigation of the extent of the arsenic contamination and restoration of the contaminated land.     

典型电子垃圾拆解区居民多卤代芳烃的膳食暴露及其癌症风险评估

收集浙江典型电子垃圾拆解区和对照区的饮用水、蔬菜、豆类、米饭、鸡蛋、鱼、鸡肉和猪肉等8类食物样品共191个;采用GC/MS 5975B分析样品中23种PBBs,12种PBDEs和27种PCBs;评估当地居民的PHAHs膳食暴露现状及其癌症风险.结果表明,拆解区居民这三大类PHAHs的平均日摄入量是对照区的2~3倍,通过米饭摄入PHAHs的量占当地居民PHAHs总摄入量的48%以上.拆解区居民因食物摄入PHAHs的癌症风险(3.81×10-4)是对照区(1.50×10-4)的2倍多,其中二英类PCBs的风险值占总癌症风险的45%以上.通过米饭摄入PHAHs是主要的暴露途径,二英类PCBs是引起癌症风险的主要贡献因子,电子垃圾拆解释放出的PHAHs通过食物摄入进入居民体内引起的癌症风险要明显高于对照区.     

中国食管癌发病区环境地球化学及相关模型的研究进展

食管癌是一种常见的消化道疾病,在世界许多国家和地区均有发生,其中环境因素是引发地方病食管癌的重要因素。目前,模型被应用于食管癌的研究中,食管癌研究模型主要有食管癌发病率预测模型,食管癌预防模型及食管癌动物模型等。本文主要综述了前人对中国食管癌发病区的土壤、饮用水和食物等环境地球化学因素,以及与食管癌研究相关的土壤模型和食管癌模型的研究进展。     

江南Z市农村饮水有机污染物健康风险评估

应用化学法及吹扫捕集、气相色谱-质谱联用仪(GC-MS),检测Z市农村不同类型饮用水与癌症相关的有机污染物,对污染物的剂量与癌症标化死亡率进行Spearman等级相关分析。该市河水、池塘水、浅井水中部分样品的COD_Mn、BOD₅和NH₃-N指标超过地表水环境质量Ⅲ类标准,微生物指标超过生活饮用水卫生标准,检出NH₃-N及NO₃-N、NO₂-N合成致癌物NAD的2类前体物及NDMA等直接致癌物。Z市农村河水、池塘水、浅井水主要受生活排污和农业生产污染,不宜作生活饮用水。不同类型饮用水有机污染物丰水期高于枯水期(P值均小于0.05)。癌症标化死亡率与不同类型饮用水有机污染浓度呈等级正相关(P值均小于0.05),与NO₂-N、NDMA、NDEA含量呈剂量-效应关系。直接饮用污染的地表水是造成该市农村癌症高发聚集分布的主要原因之一。     

In vitro response of human ovarian cancer cells to dietary bioflavonoid isoquercitrin

Abstract

Isoquercitrin is a dietary bioflavonoid used as a food supplement. We studied the mechanism underlying its effect in human ovarian cancer cells using OVCAR-3 cell line. Viability, survival, apoptosis, release of human transforming growth factor-β1 (TGF-β1) and TGF-β1 receptor, and intracellular reactive oxygen species (ROS) generation by OVCAR-3 cells were examined after isoquercitrin treatment at concentrations 5, 10, 25, 50, and 100?μg mL^?1. AlamarBlue assay revealed that isoquercitrin did not cause any significant change (P?>?0.05) in cell viability as compared to control. Apoptotic assay using flow cytometry did not find any significant change (P?>?0.05) in the proportion of live, dead and apoptotic cells as compared to control. ELISA also showed that the release of human TGF-β1 and TGF-β1 receptor were not significantly (P?>?0.05) affected by isoquercitrin as compared to control. Chemiluminescence assay demonstrated that lower concentrations (5, 10, and 25?μg mL^?1) were able to exhibit beneficial effects by inhibiting the generation of intracellular ROS. In contrast, elevated concentrations of 50 and 100?μg mL^?1 led to oxidative stress (P?相似文献   

2005年中国气态α HCH的人体暴露和健康风险分析

为评估由我国大气中α HCH所导致的人体健康风险,利用CanMETOP 模拟的2005年日均α HCH大气浓度,基于吸入因子和致癌风险进行研究。结果表明年吸入因子呈东部>西部,北部>南部的特征，东中和东北部地区的吸入因子分别主要由人口密度和α HCH大气浓度贡献，东中和东南部地区的个体健康损失小于东北地区，东中和东南部地区年内逐月吸入因子分配较为均匀,而东北地区主要集中的夏季，东北地区个体致癌风险系数明显高于中部和南部。推测由其它污染物所形成的暴露风险具有类似的时空分布。加之夏季东北地区集中降水所形成的湿沉降以及气温升高等因素,使摄食暴露和皮肤接触暴露增大,东北地区人群的复合暴露风险将显著大于其它地区     

Radionuclides in cigarettes may lead to carcinogenesis via p16 inactivation

It is widely accepted that tobacco smoke is responsible for the vast majority of lung cancers worldwide. There are many known and suspected carcinogens present in cigarette smoke, including α-emitting radioisotopes. Epidemiologic studies have shown that increased lung cancer risk is associated with exposure to ionizing radiation, and it is estimated that the majority of smoking-induced lung cancers may be at least partly attributable to the inhaled and deposited radiation dose from radioisotopes in the cigarette smoke itself. Recent research shows that silencing of the tumor suppressor gene p16^INK4a (p16) by promoter methylation plays a role in smoking-related lung cancer. Inactivation of p16 has also been associated with lung cancer incidence in radiation-exposed workers, suggesting that radionuclides in cigarette smoke may be acting with other compounds to cause smoking-induced lung cancer. We evaluated the mechanism of ionizing radiation as an accepted cause of lung cancer in terms of its dose from tobacco smoke and silencing of p16. Because both radiation and cigarette smoking are associated with inactivation of p16, and p16 inactivation has been shown to play a major role in carcinogenesis, ionizing radiation from cigarette smoke likely plays a role in lung cancer risk. How large a role it plays, relative to chemical carcinogens and other modes of action, remains to be elucidated.     

基于PBPK模型评价三氯乙烯的职业暴露健康风险

三氯乙烯(TCE)作为脱脂和清洗剂被广泛应用于五金、电镀和电子等行业。TCE的职业暴露会产生一系列健康风险,包括过敏症和致癌等。2012年TCE被美国环保局(US EPA)和国际癌症研究机构列为1类致癌物。采用吸附管采样-热脱附/气相色谱-质谱法分析了大连市某企业车间生产工况下空气中TCE浓度。基于生理学的药代动力学(PBPK)模型预测了呼吸暴露途径下TCE在职业工人体内组织中的动态分布、代谢产物生成情况和致癌风险。TCE在不同组织中预测的最大浓度呈现出脂肪肠充分灌注室支气管非充分灌注室肝脏静脉血动脉血的趋势。预测的与致癌有关的代谢产物最大浓度表现为三氯乙酸二氯乙酸三氯乙醛S-二氯乙烯基-L-半胱氨酸。在监测的TCE水平(39.2±24.4)μg·m-3下,暴露8 h·d-1,连续暴露20年,基于外暴露评价的职业工人致癌风险均值为1.31×10-5,该暴露水平下,基于PBPK模型预测的TCE内暴露与外暴露计算的致癌风险水平相近,但基于具有致癌性主要代谢产物的内暴露致癌风险值是外暴露风险值的1.17～1.73倍。TCE的暴露水平越高,基于内暴露方法和外暴露方法的致癌风险评价结果差异越大。敏感性分析表明,心输出血流量和充分灌注室血流量对PBPK模型输出结果具有重要影响。不确定性分析表明,模型参数变化会显著地影响PBPK模型输出结果,但变异在可接受水平。本研究结果说明,评价TCE暴露对人的致癌风险需要考虑其在体内的分布和代谢过程。