高分子重金属絮凝剂对 Hg2+的捕集及性能

以含Hg^2 废水作为处理对象,研究了几个影响高分子重金属絮凝剂去除水中Hg^2 的因素,实验表明：(1)pH值对Hg^2 的去除率影响不大;(2)水中某些二价离子的存在不仅不会消耗高分子重金属絮凝剂的用量,而且会促进螯合体MHM-Hg^2 絮凝沉淀,Hg^2 的去除率在99％以上,而一价金属离子对处理效果影响不大;(3)Hg^2 和致浊物质会互相促进彼此的去除,浊度的去除率在98％以上,Hg^2 的去除率在99％以上;(4)高分子重金属絮凝剂对重金属离子具有选择性,可将部分重金属离子从其它离子中分离开、回收再利用．     

封闭垃圾填埋场通过地表向大气释放汞的测定

利用动力学通量箱及自动测汞仪联用技术,于2004年3月中旬对贵阳市的一座封闭生活垃圾填埋场汞通过地表向大气释放的过程进行了研究。3个采样点的汞释放通量日均值分别为559.1、88.2、53.6ng·m-2·h-1,汞释放通量强度与表层基质中的汞含量密切相关,该测定值高于世界背景地区通量的1~2个数量级,说明封闭垃圾填埋场也是大气汞的潜在来源。汞释放通量呈现明显的昼夜变化规律,白天较高并在午间前后达到最大,而夜间降至最低。气相因子中光照强度与汞的释放过程相关性最高,其次分别是气温、相对湿度、地温和风速。氧化态汞的光致还原作用是可能垃圾填埋场Hg0生成的主要途径,降雨初期能促进地表汞的释放。     

铅锌尾矿废弃地的化学性质研究

凡口铅锌尾矿废弃地的不同区位及不同深度的尾矿中铅锌含量存在着较大的差异 ,总锌为 70 3～ 19657mg/ kg、总铅 10 4 13～ 94 988mg/ kg。正常尾矿中 ,有效态锌含量达到 151.6～ 84 1.7mg/ kg,有效态铅含量很低 ( 0 .75～ 2 .50 mg/ kg) ,有机质、总氮、有效磷及速效钾等营养物质缺乏。当尾矿酸化后 ,p H降低 ,有效态 Pb、Zn含量升高 ,有效锌达到 175.8～ 2 82 8.0 mg/ kg,有效铅含量最高为 10 0 .0 mg/kg,而有机质、总氮和有效磷为零 ,使尾矿更加贫瘠。在尾矿库的边缘区位和尾矿表面的覆盖土壤区位 ,基质中营养物质含量增加 ,但是营养状况的改善又引起了有效态的 Pb、Zn含量升高。     

Determination of mercury and arsenic levels in fish caught in the Beheshtabad River,Chaharmahal and Bakhtiari Province,Iran

Mercury and arsenic pollution has been recognized as a potential environmental and public health problem for over 40 years. The major source of exposure to mercury for humans is the ingestion of fish. This study was conducted with the aim of determining the levels of mercury and arsenic in the muscles of four fish species caught in the Beheshtabad River and comparing the results with the maximum tolerance levels for mercury and arsenic. The samples of 90 fish were used for the determination of both the metals by graphite furnace atomic absorption spectrometry. The results showed that the concentrations ranged from 1.5 to 3.8 µg kg^?1 for mercury and from 35 to 70 µg kg^?1 for arsenic, with means of 2.7 ± 0.5 and 57 ± 12 µg kg^?1, respectively. Both mean levels were lower than the threshold limits acceptable by WHO standards.     

Urinary level of homovanillic acid and mercury in autistic children

Catecholamines and their metabolites affect children's nervous system. Dopamine is an important neurotransmitter in the brain. In the routine analysis for diagnostics of diseases, the dopamine metabolite homovanillic acid (HVA) is determined. Mercury is a neurotoxic agent and can cause different undesirable effects on the brain. In the present work a putative correlation between HVA, the main metabolite of dopamine, and mercury in urine of healthy and autistic children was studied. The level of HVA was higher in the urine of autistic children (14.5 ± 8.3 mg L^?1) compared to generally healthy children (4.4 ± 0.5 mg L^?1). The level of mercury in the urine of autistic children was lower (0.36 ± 0.24 µg L^?1) than in the urine of healthy children (2.1 ± 1.0 µg L^?1) showing that there is no correlation between HVA and mercury.     

The plausibility of a role for mercury in the etiology of autism: a cellular perspective

Autism is defined by a behavioral set of stereotypic and repetitious behavioral patterns in combination with social and communication deficits. There is emerging evidence supporting the hypothesis that autism may result from a combination of genetic susceptibility and exposure to environmental toxins at critical moments in development. Mercury (Hg) is recognized as a ubiquitous environmental neurotoxin and there is mounting evidence linking it to neurodevelopmental disorders, including autism. Of course, the evidence is not derived from experimental trials with humans but rather from methods focusing on biomarkers of Hg damage, measurements of Hg exposure, epidemiological data, and animal studies. For ethical reasons, controlled Hg exposure in humans will never be conducted. Therefore, to properly evaluate the Hg-autism etiological hypothesis, it is essential to first establish the biological plausibility of the hypothesis. This review examines the plausibility of Hg as the primary etiological agent driving the cellular mechanisms by which Hg-induced neurotoxicity may result in the physiological attributes of autism. Key areas of focus include: (1) route and cellular mechanisms of Hg exposure in autism; (2) current research and examples of possible genetic variables that are linked to both Hg sensitivity and autism; (3) the role Hg may play as an environmental toxin fueling the oxidative stress found in autism; (4) role of mitochondrial dysfunction; and (5) possible role of Hg in abnormal neuroexcitory and excitotoxity that may play a role in the immune dysregulation found in autism. Future research directions that would assist in addressing the gaps in our knowledge are proposed.     

Mercury exposure through diet in pregnant women and women of childbearing age

The study examined the stage of clean-up of the Port Lavaca bay sites in Texas, which were polluted during the early 1990's by effluent containing mercury (Hg) from a chloralkali plant. In addition to Hg intoxication through environmental contaminations, human exposure through dietary fish and other seafoods occurred. Bacteria converts inorganic Hg to alkyl organic compounds and subsequently the metal crosses the blood brain barrier thus exerting adverse effects on the fetal developing nervous system. In order to conduct a survey of dietary Hg exposure, blood was collected from pregnant women and those of childbearing age at routine clinic visits at each of three centers in South Texas cities (Galveston, Texas City, Port Lavaca/Victoria, TX). A questionnaire sought dietary and lifestyle information including consumption, sources of fish and other seafoods. A significant number of subjects (119 out of 175, 68%) ate fish caught locally. The blood Hg concentrations (µg?L^?1) range varied with the location of the study centers: City of Galveston 2.6–62; Texas City 2.8–111.8; and the Port Lavaca areas 3.02–126.7. The concentrations of blood Hg was directly proportional to the number of fish meals consumed for each species considered. Mean blood Hg concentrations for no fish meals per week were: Port Lavaca 4.5 (N?=?3), Galveston 4.3 (N?=?3), Texas City 3.5 (N?=?10). For >3 fish meals per week, the mean blood Hg concentrations were: Port Lavaca, 48.0 (N?=?53), Galveston 29.1 (N?=?35), Texas City, 36.1 (N?=?31). Data show that residues of Hg were still present in 1994 despite the clean-up efforts.     

Liver and renal lesions in mercury-contaminated narwhals (Monodon monoceros) from North West Greenland

Narwhals (Monodon monoceros) from North West Greenland are known to bioaccumulate mercury (Hg) in tissues and internal organs. This is postulated to be a health concern and therefore studies were undertaken to conduct a screening study of Hg concentrations and histopathology of liver and renal tissues in a total of 12 specimens. The sample consisted of two sub-adults (one male, one female) and 10 adult (six males, four females) collected in Qaanaaq (Thule) 2010. In liver, Hg mean ± SD was 11.88 ± 10.47 μg/g ww (range: 0.39?31.8 μg/g ww) while the concentrations in kidneys were 1.85 ± 1.20 μg/g ww (range: 0.41?4.03 μg/g ww). There was no marked difference in Hg concentrations between males and females while sub-adults had significantly lower concentrations. The histological examinations of renal tissue showed glomerular capillary dilatation and basement membrane thickening, dilatation, and hyalinization of Bowman's space/capsule and tubular lesions with hyaline casts accompanied by interstitial fibrosis in the kidneys. In liver tissue, portal cell infiltrates and fibrosis, bile duct proliferation, lipid-filled Ito cells, and steatosis were found. There was no marked difference in histological prevalence between males and females and in Hg concentrations in individuals with or without lesions. Four of seven renal lesions and one liver lesion were found in the two sub-adult whales. Based upon these findings, as well as the nature of the lesions, evidence suggests that histopathological alterations were a result of age but that Hg might be an aggravating co-factor in development of renal lesions in particular.     

Thimerosal in childhood vaccines contributes to accumulating mercury toxicity in the kidney

Mercury (Hg) is a hazardous chemical that accumulates in many cells and tissues, thereby producing toxicity. The kidney is a key target organ for Hg accumulation and toxicity. The contributing factors to Hg accumulation in humans include: (1) elemental and inorganic Hg exposure, often occurring by inhalation of Hg vapors; (2) exposure to methyl Hg (meHg), for example, through contaminated seafood; and (3) exposure to ethyl mercury (etHg) via thimerosal-containing vaccines. Systematic investigations on the toxic effects of etHg/thimerosal on the nervous system were carried out, and etHg/thimerosal emerged as a possible risk factor for autism and other neurodevelopmental disorders. There is, however, little known about the mechanisms and molecular interactions underlying toxicity of etHg/thimerosal in the kidney, which is the focus of the current review. Susceptible populations such as infants, pregnant women, and the elderly are exposed to etHg through thimerosal-containing vaccines, and in-depth study of the potential adverse effects on the kidney is needed. In general, toxicity occurring in association with different forms of Hg is related to: intracellular thiol metabolism and oxidative stress reactions; mitochondrial function; intracellular distribution and build-up of calcium; apoptosis; expression of stress proteins; and also interaction with the cytoskeleton. Available evidence for the etHg-induced toxicity in the kidney was examined, and the main mechanisms and molecular interactions of cytotoxicity of etHg/thimerosal exposure in kidney described. Such accumulating knowledge may help to indicate molecular pathways that, if modulated, may better handle Hg-mediated toxicity.     

Mercuric chloride effects on adult rat oval cells-induced apoptosis

In the present investigation, the toxicity of mercuric chloride (HgCl₂) was evaluated in adult oval cells isolated from rat utilizing the 2-acetylaminofluorene/partial hepatectomy technique. Isolated oval cells were incubated with 5 μM of HgCl₂ for 8 hr to elucidate in vitro cytotoxic responses. Recently, autophagic cell death was found in rat hepatocytes in vitro within 30 min of incubation with 5 μM of mercury (Hg) which triggered apoptosis and necroptosis in a time-dependent manner. Nuclear degradation occurred within 30 min of incubation and progressed with time until 8 hr. Apoptosis evidenced by activation of caspase-dependent pathway between 30 min to 8 hr of incubation was mediated via interchange of death domain signaling pathways. Receptor-interacting protein played a positive role to modulate the death domain receptors in the scenario of apoptotic death of oval cells until 6 hr. Autophagic marker proteins ATG12 and LC3B exerted a significant role in triggering apoptosis in 5 μM Hg-treated oval cells. No apparent expression of apoptosis-inducing-factor (AIF) and HMGB1 indicated absence of caspase-independent apoptosis and necrosis in the rat oval cells between 30 min and 8 hr. Thus a low concentration of Hg modulates programmed cell death in adult rat oval cells by altering expression of proteins involved in the molecular mechanisms of cellular functions.