Chromosome damage in individuals exposed to heavy metals†

Testing the mutagenic activity of environmental pollutants has become an important area of modern environmental science and prophylactic medicine. The most suitable method for short‐term mutagenicity testing on man, at present, are chromosome studies on somatic cells of exposed individuals. Mutation types analyzed by such studies are of high practical relevance as indicator system of genetic damage induced in man under in vivo conditions. A rather large series of such studies has been dedicated to the action of heavy metals on individuals contacted with these metals under therapeutic, ecological or occupational conditions or by intoxication. Lead, cadmium, chromium, nickel, mercury, zinc and other metals as well as their compounds have been under study. Analyses of that kind, of course, are hampered by difficulties with the distinct estimation of the actual load as well as unclear conditions of exposition, e.g. simultaneous exposition to different metals.

Results obtained till now arouse some suspicion of a direct or indirect mutagenic activity in man by certain chromium and platinum compounds, arsenic, mercury, and combinations of lead with other heavy metals (cadmium, zinc, arsenic, antimony, etc.). Life style, above all smoking habits, well may act comutagenic. In most cases, however, mutagenic activity of metals and metal compounds apparently is clearly superposed by their toxic activity. In specific cases, chromosome studies also may contribute to discover sources of ecological exposition and to monitor occupational load by heavy metals.     

Cytotoxicity and cell membrane depolarization induced by aluminum oxide nanoparticles in human lung epithelial cells A549

The cytotoxicity of 13 and 22 nm aluminum oxide (Al₂O₃) nanoparticles was investigated in cultured human bronchoalveolar carcinoma-derived cells (A549) and compared with 20 nm CeO₂ and 40 nm TiO₂ nanoparticles as positive and negative control, respectively. Exposure to both Al₂O₃ nanoparticles for 24 h at 10 and 25 µg mL^?1 doses significantly decreased cell viability compared with control. However, the cytotoxicity of 13 and 22 nm Al₂O₃ nanoparticles had no difference at 5–25 µg mL^?1 dose range. The cytotoxicity of both Al₂O₃ nanoparticles were higher than negative control TiO₂ nanoparticles but lower than positive control CeO₂ nanoparticles (TiO₂ < Al₂O₃ < CeO₂). A real-time single cell imaging system was employed to study the cell membrane potential change caused by Al₂O₃ and CeO₂ nanoparticles using a membrane potential sensitive fluorescent probe DiBAC₄(3). Exposure to the 13 nm Al₂O₃ nanoparticles resulted in more significant depolarization than the 30 nm Al₂O₃ particles. On the other hand, the 20 nm CeO₂ particles, the most toxic, caused less significant depolarization than both the 13 and 22 nm Al₂O₃. Factors such as exposure duration, surface chemistry, and other mechanisms may contribute differently between cytotoxicity and membrane depolarization.     

雾霾期北京大气中多环芳烃污染特征及暴露风险评估

雾霾对我国尤其是华北平原地区造成了极大的困扰,其发生常以颗粒物浓度急剧增长为特征,给人群健康带来了极大的风险。为进一步阐释雾霾的形成过程及其健康效应,在冬季雾霾期对北京城区大气颗粒态及气态中18种多环芳烃(PAHs)进行了连续测定,同步监测颗粒物、痕量气体污染物以及气象参数的变化,并对PAHs的浓度、组成、气粒分配等大气行为以及其与气象因素的作用机制进行了探讨。北京城区大气气相和颗粒物相中ΣPAHs浓度分别为585 ng·m~(-3)和705 ng·m~(-3)。雾霾发生时,PM_(2.5)浓度升高了3.6倍,PAHs浓度升高了2.6倍,18种PAHs同系物的浓度均随PM_(2.5)的浓度线性增加,其线性相关性受PAHs来源以及氧化活性的影响;夜间较重质量数的PAHs相对比例增加,主要受日间交通源以及夜间燃烧源贡献强度影响。受颗粒物组成以及湿度的影响,雾霾天气下PAHs颗粒相分配率降低。进一步评估了北京城区人群的PAHs吸入健康效应,冬季雾霾频繁发生下其对人群癌症风险为6.2×10~(-5)。     

湖北农村燃柴和燃煤家庭大气多环芳烃污染特征和呼吸暴露风险

以具有致癌毒性的多环芳烃(polycyclic aromatic hydrocarbons,PAHs)为对象,本研究于2014年1月(冬季)在湖北恩施农村地区使用煤炭和薪柴的家庭中同步采集了室内外空气样品,分析了室内外空气中28种PAHs(∑PAH28)的浓度水平、成分谱和粒径分布,重点比较了不同燃料家庭的污染特征差异,并据此估算了暴露人群的健康风险。结果表明,在燃煤家庭,∑PAH28的室内和室外浓度分别是(507±449) ng·m~(-3)和(120±18) ng·m~(-3);而在燃柴家庭,其室内和室外∑PAH28浓度分别是(849±421) ng·m~(-3)和(268±44) ng·m~(-3)。受室内排放源影响,室内PAHs浓度显著高于室外,室内外∑PAH28浓度比值在2～13。颗粒态PAHs主要集中在细颗粒物上,PM1.0(空气动力学直径小于1.0μm)上的PAHs占到颗粒态PAHs的50%～80%。燃煤家庭的居民因PAHs呼吸暴露导致的终生致癌风险的中位数是1.8×10~(-5)(四分位距是1.2×10~(-5)～3.1×10~(-5)),使用薪柴的家庭人群暴露风险7.1×10~(-5)(6.5×10~(-5)～7.8×10~(-5))。无论是燃煤还是薪柴的家庭,居民因PAHs呼吸暴露导致的终生致癌风险均超过10-6的可接受风险水平,表明该地区的高浓度PAHs污染致使当地人群存在较高的致癌风险。     

Polycyclic aromatic hydrocarbons in urban soils of Beijing: status, sources, distribution and potential risk

We studied the source, concentration, spatial distribution and health risk of 16 polycyclic aromatic hydrocarbons (PAHs) in urban soils of Beijing. The total mass concentration of 16 PAHs ranged from 93 to 13 141 μg kg⁻¹ with a mean of 1228 μg kg⁻¹. The contour map of soil PAH concentrations showed that the industrial zone, the historical Hutong district and the university district of Beijing have significantly higher concentrations than those in remainder of the city. The results of sources identification suggested that the primary sources of PAHs were vehicle exhaust and coal combustion and the secondary source was the atmospheric deposition of long-range transported PAHs. The incremental lifetime cancer risks (ILCRs) of exposing to PAHs in the urban soils of Beijing for adult were 1.77 × 10⁻⁶ and 2.48 × 10⁻⁵, respectively under normal and extreme conditions. For child, they were 8.87 × 10⁻⁷ and 6.72 × 10⁻⁶, respectively under normal and extreme conditions.     

大连市肿瘤发生率与居民血硒水平的研究

采用新极谱法测定大连市健康居民３００例和癌症患者５０例全血的硒含量,分别为１４６．５±５１．０μｇ／Ｌ（１４８．１±５０．２μｇ／Ｌ和１４４．７±５１．９μｇ／Ｌ）和１２２．７±５５．９μｇ／Ｌ是正态分布类型,均小于我国低硒地区１６０μｇ／Ｌ是     

广西扶绥肝癌高发与饮水水质关系的研究

广西扶绥是我国肝癌高发县之一，病区居民主要饮有机污染严重的塘水，塘水中的有机污染指标和某些有机组分均很高，而且与死亡率呈显的正相关关系。而石灰岩层中的深井水则相反，水质好，死亡率很低。测试结果表明，塘水中存在亚硝胺类化合物，它们与死亡率有较好的平行关系。用这类塘水进行人体外周血淋巴细胞微核试验和细胞染色体畸变试验，证明其中有致突变的化学物质。通过换水可阻截水中有害有机物和致癌物进入人体，以达到增     

<Emphasis Type="Bold">Chronodisruption and cancer</Emphasis>

Research into health effects of chronodisruption (CD), a relevant disturbance of the circadian organization of physiology, endocrinology, metabolism and behaviour, is evolving at a rapid pace. With regard to malignancies, our synthesis of key experiments indicates that CD can play a causal role for cancer growth and tumor progression in animals. Moreover, our meta-analyses of 30 epidemiological studies evince that flight personnel and shift workers exposed to chronodisruption may have increased breast and prostate cancer risks: summary relative risks (RRs) for investigations of flight personnel and of shift workers suggested a 70 and 40% increase in the risk of breast cancer, respectively, and excess relative risks of prostate cancer in nine studies in flight personnel (40%) and in two studies in male shift workers. There was a remarkable indication of homogeneity of results from the individual studies that contribute to the average statistics. However, in view of doubts about whether the differing assessments of CD can really be regarded as valid reflections of the same causative phenomenon and the lack of control of covariates in the majority of studies, it is premature to conclude that the risk observations reflect a real, rather than spurious, association with CD. The challenge for future epidemiological investigations of the biologically plausible links between chronodisruption and human cancers is to conduct studies which appreciate details of transmeridian travelling, of shift work and of covariates for the development of the diseases.     

不同粒径的大气细颗粒物对A549细胞的毒性研究

研究了不同粒径的大气细颗粒物对人肺癌上皮细胞A549的生物学效应,探讨了大气中细颗粒物粒径与细胞毒性的关系。采集杭州市大气中不同粒径的细颗粒物,制备成不同粒径的颗粒物总悬浮液,将A549细胞暴露于该制备液24 h后,测定细胞活力(MTT法)和培养液上清液中的LDH含量;并选择最佳浓度为后续暴露剂量,测定ROS生成量,评价不同粒径大气细颗粒物对细胞损伤效应。此外,还采用RTPCR测定凋亡基因P50、BAX、BCL-2表达情况。不同粒径的细颗粒物均显著抑制A549细胞活力,LDH显著增多,并存在剂量-效应关系;最佳染毒质量浓度为10μg/m L;ROS的生成量和各个凋亡基因的mRNA表达量均高于对照组。大气中不同粒径的细颗粒物均能对A549细胞产生毒性,并且随粒径增加,颗粒物对细胞的毒性呈降低趋势。     

Arsenic in Drinking Water and Bladder Cancer: Comparison between Studies Based on Cancer Registry and Death Certificates

Associations between arsenic in drinking water and bladder cancer in an area along the southwest coast of Taiwan have been documented for decades. Several ecologic studies were conducted to assess the dose-response relationships. Some of them used the National Cancer Registry Program to identify cancer cases, and some used death certificates. Whereas the cancer registry collects information on all patients no matter if they died of bladder cancer or not, the case ascertainment might be incomplete due to the fact that reporting of cases is not mandatory. Reporting of death, on the other hand, is strictly enforced by law, but patients who did not die of bladder cancer might not be identified. In order to assess the problems with both approaches, we conducted a study using both case identification mechanisms. A total of 243 townships with measurements of arsenic in drinking water were included in the analysis of cancer registry data, and death certificates were collected from 10 of those townships. In both analyses, the same measurements of arsenic made by the mercuric bromide stain method were adopted. Due to limitation of the method, all levels below 0.04mg L^–1 were combined as a single exposure category. The results were very much alike; both approaches detected statistically significant associations between high arsenic levels in drinking water (above 0.64mg L^–1) and occurrence of bladder cancer but did not find such associations for arsenic exposures at lower levels.