生物质灰结渣和腐蚀特性

针对目前生物质燃料燃烧过程中存在的灰结渣和受热面腐蚀问题,通过分析生物质灰的元素成分、矿物组成、理化特性及熔融特性等,探讨了灰结渣的形成过程和受热面腐蚀的机理。研究表明:生物质燃烧灰结渣的主要原因为碱金属硫酸盐及氯化物的形成降低了飞灰熔点,增加了飞灰的表面黏性,黏结在受热面表面形成结渣;此外,由于燃料中的氯化物在高温下参与氧化还原反应生成HCl和Cl₂,再与金属受热面发生化学反应,形成了受热面腐蚀。通过研究燃料成分、炉膛温度、过量空气系数、受热面材质等因素对结渣和受热面腐蚀的影响,得出可以采用生物质与煤混烧、加入添加剂、水洗及金属表面防腐等防治措施避免或减少结渣和腐蚀现象发生。     

Emission control for precursors causing acid rain (V): Improvement of acid soil with the bio-briquette combustion ash

The bio-briquette technique which mixes coal, biomass and sulfur fixation agent and bio-briquettes under 3-5 t/cm^2 line pressure has aroused people‘s attention in view of controlling the air pollution and the acid rain. In this paper, the physicochemical properties of bio-briquette and its ash were investigated. And the acid soil was improved by the bio-briquette combustion ash, which contained nutritive substances such as P, N, K and had the acid-neutralizing capacity(ANC). The pH, EC, effective nutrient elements(Ca, Mg, K, P and N), heavy metal elements(AI, Cu, Cd, Cr, Zn and Mn) and acid-neutralizing capacity change of ash-added soils within the range of 0-10%, were also studied. Specially, when 5% bio-briquette combustion ash was added to the tested soil, the content of the effective elements such as Ca, Mg and K rose by 100 times, ? times and twice, respectively. The total nitrogen also increased by about twice. The results showed the oxyanions such as that of AI, Cu, Cd, Cr, Zn and Mn were not potentially dangerous, because they were about the same as the averages of them in Chinese soil. It is shown that the ANC became stronger, though the ANC hardly increases in the ash-added soil. On the basis of the evaluation indices, it is concluded that the best mixture ratio is to add 2.5%--8% of the bio-briquette combustion ash to the tested soil.     

Leaching of arsenic from coal fly ashes 2. Arsenic pre‐leaching with sodium gluconate solution

The present study deals with the development of an efficient and reliable process for safe disposal of coal fly ash to remove arsenic that has been found to be the most easily leachable and hazardous heavy metal in coal fly ash. Pre‐leaching of fly ash prior to disposal by a natural chelating agent, sodium gluconate (SG), was proposed and studied. Several operational factors influencing arsenic leachability, such as concentration of SG solution, liquid to solid ratio, pH, length of leaching time and leaching temperature were examined. Arsenic was found to leach out substantially with SG, but almost no further release was observed from the ash pre‐leached by SG. After the pre‐leaching treatment, the desirable high buffering capacity of the ash was well sustained. SG solution was effectively regenerated by activated alumina adsorption so that it could be successfully reused for multiple leaching/adsorption cycles.     

In vitro genotoxicity of fly ash leachate in earthworm coelomocytes

Fly ash is the major coal combustion byproduct from thermal power plants. Considering its plant–nourishing constituents, its soil amendment in farmland is one of its promoted disposal methods. A substantial amount of heavy metals present in fly ash, which may leach out due to rainwater or irrigation water, may cause serious problem with long term use, especially to soil organisms. These metals may cause DNA damage through Reactive Oxygen Species (ROS) generation. In the present study, single cell gel electrophoresis [(SCGE) i.e., comet assay] was used to detect DNA damage in earthworm (Dichogaster curgensis) coelomocytes, following an in vitro exposure. Significant DNA damage was observed at the lowest concentration of fly ash leachate (6.25%) examined. DNA damage by all the tested concentrations (6.25%, 12.5%, 25%, 50%) differed significantly (p?<?0.001) from that of the negative control. Hence, long-term application of fly ash might prove harmful for earthworm populations.     

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.