Cyanide-main.zip
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The Aurul disaster in late January 2000was by no means the only recent accident in a Romanian mine. Only one weeklater, the Remin SA company in Baia Mare released cyanide-contaminatedwater to the Lapus river, which flows into the Somes (Szamos), a tributaryof the Tisza. The Romplumb SA metal processing works in Baia Mare are alsoa source of frequent heavy metal and toxic releases to the Lapus. Six weeksafter the cyanide disaster, a dam burst in the lead and zinc mine in BaiaBorsa, releasing 20,000 tonnes of toxic sludge into another tributary ofthe Tisza, the Viseu (Visó). In one of the four Remin mines in Borsa, adam had already once burst with severe consequences in 1997.
In late December 1999, several thousandcubic metres of cyanide-contaminated effluent were released from the Baiade Aries mine into the Aries river, which subsequently flowed into theMures (Maros) tributary of the Tisza. The Industria Sârmei metal processingcombine in Câmpia Turzii discharges all of its effluents into the Aries.A further cyanide disaster may well be caused by the tailing ponds of thegold mines in Brad, Abrud and Zlatna. The latest accident to happen inBrad was in May 1998, when the Tisza tributary Crisul Alb (Fehér Körös)was contaminated severely with cyanides and heavy metals. The uranium minesnear Brad are a further threat to this river. In Zlatna, the Ampelum noble-metalprocessing combine released sulphur oxides in February 1998, devastating47 thousand hectares of farmland and 193 km of river landscape. Metal smeltersaround Hunedoara pollute the Mures (Maros) on a regular basis. In Tirnaveni,an accident in the Bicapa combine in December 1999 caused chromium levelsto rise to 20 times the permissible values; the poison reached the Mures.In Slovakia, too, magnesite and other ore mines operate on the Tisza tributaryHórnad (Hernád) near Kosice; here, again, there are reports of heavy metallevels in excess of permissible values in the river's water. A cyanidepollution incident was reported in February 2000 from the Slovakian partof the Bodrog plain (Bodrog Köz). Little is currently known about the operationsof the Ukrainian gold mine in Muzhievsk. Should a disaster happen here,this would have major impacts upon the Tisza river.
CountermeasuresBefore cyanide antidote can be administered, the patient must be removed from the cyanide-laden area, clothing removed, and skin washed with soap and water. If cyanide salts have been ingested, activated charcoal may prevent absorption from the gastrointestinal tract.
RecoveryAlthough recovery from a chemical attack is rare, victims may survive sub-lethal exposures, whether from ingestion, smoke inhalation, or exposure to cyanide-containing industrial products. Patients who are treated successfully for cyanide poisoning should be observed for development of long-term neuropsychiatric symptoms that are similar to symptoms experienced by survivors of cardiac arrest or carbon monoxide poisoning.
Cyanide poisoning may result from different exposures: residential fires, industrial accidents, drug and plant intoxication. Clinical features include coma, respiratory arrest and cardiovascular collapse. The biological hallmark is lactic acidosis. A plasma lactate concentration > or = 10 mmol/L in fire victims without severe burns and > or = 8 mmol/L in pure cyanide poisoned patients is a sensitive and specific indicator of cyanide intoxication. Many antidotes are available and efficient. However, therapeutic strategies are still debated. Our objective was to compare conventional treatments to hydroxocobalamin. This article reviews the literature on cyanide poisoning treatment. Conventional treatment of cyanide poisoning includes decontamination, supportive and specific treatment. Decontamination should be adapted to the route of poisoning and never postpone supportive treatment. Basic life support includes immediate administration of high flow of oxygen, airway protection and cardiopulmonary resuscitation. Advanced life support includes mechanical ventilation, catecholamine and sodium bicarbonate infusion. Supportive treatment is efficient but does not modify the time course or the body burden of cyanide. Numerous antidotes are available. Oxygen counteracts efficiently cyanide action at the mitochondrial level. Sodium thiosulfate, methemoglobin forming agents and cobalt compounds act efficiently by complexing or transforming cyanide into non-toxic stable derivatives. However, regarding the main clinical condition of cyanide poisoning, i.e. smoke inhalation, we should take into account not only the efficiency of antidotes but also their safety. Sodium thiosulfate is both efficient and safe, but acts with delay. Methemoglobin-forming agents are potent, but due to the transformation of hemoglobin into methemoglobin, they impair tissue delivery of oxygen. Experimental data showed increased mortality in carbon monoxide- and cyanide-poisoned rats treated with these agents. Cobalt EDTA and hydroxocobalamin are efficient and act immediately. Cobalt EDTA is more potent on a molar basis; however, numerous side effects limit its use to evidenced cyanide poisoning. In a prospective study, hydroxocobalamin appeared safe in fire victims with or without cyanide poisoning. The only reported side effect was a red coloration of skin and urine. In conclusion, antidotes are beneficial in cyanide poisoning. In suspected cyanide-poisoned patients, we recommend the use of hydroxocobalamin as first-line antidote, owing to its safety. In massive cyanide poisoning, due to the limited potency of hydroxocobalamin, continuous infusion of sodium thiosulfate should be associated.
Doctors can test urine for "thiocyanate" shortly after exposure to cyanide. Blood levels of cyanide can indicate recent exposure. Cigarette smokers generally have higher levels of cyanide-related compounds in their bodies than do nonsmokers.
According to the Cyanide Poisoning Treatment Coalition (CPTC), exposure to hydrogen cyanide in building fires is the leading cause of cyanide poisoning. The CPTC is a non-profit organization made up of individuals and groups. Members of the coalition all have direct involvement with the identification and treatment of cyanide exposure. Their mission is, "To foster a rational approach to the diagnosis and treatment of cyanide poisoning through research, advocacy and education, thereby reducing the morbidity/mortality from cyanide-related causes." At present, there are few resources available to increase awareness of the risk of exposure to cyanide. The CPTC hopes to become an important source of information concerning cyanide poisoning and an advocate towards improvement of early recognition and appropriate treatment.
When two species co-exist, heterospecific metabolites are important cues for neighbour detection and subsequently trigger complex plant response strategies [5, 9]. Cyanide commonly occurs in over 3000 plant species, including important crop plants, such as maize, wheat and cassava [24, 25]. Exposure to cyanide can shorten plant embryo dormancy and induce ET production in seedlings [26, 27]. In modern intensive agro-ecosystems, cyanide-containing crops are intercropped with legumes (intercropping: a farming practice involving two or more crop species or genotypes growing together and coexisting for a period of time [28, 29]), but very few studies have focused on the chemical linkage between cyanide-containing plants and legumes [28,29,30]. Whether cyanide from cyanide-rich plants act as a chemical cue to influence ET signalling in non-cyanide-containing plants remains to be uncovered.
Acera et al. [44] reported that some soil microorganisms have the potential to transform cyanide to amino acids (such as β-cyanoalanine), which may be further metabolized to ET [13]. To eliminate the interference of soil microorganisms on ET production, quantitative real-time PCR (qRT-PCR) was used to track gene expression related to 1-aminocyclopropane-1-carboxylic acid synthase (ACS) and 1-aminocyclopropane-1-carboxlic acid oxidase (ACO). The expression of the AhACS1, AhACO1 and AhACO2 transcripts, which probably encode peanut ACS and ACO proteins, was significantly higher in the intercropped and cyanide-treated peanut roots (Pip and CNp) (Fig. 2e, f). Similar differences were found between the cyanide addition treatments and the control in the hydroponic experiments (Fig. S2 in Additional file 1). When plant species co-exist, heterospecific compounds become chemical cues for focal plants to recognize competitors [45]. Here, cyanide from neighbouring cassava was shown to activate the peanut ET production in response to the neighbour belowground.
Cliffs Burns Harbor (Cleveland-Cliffs) has agreed to resolve alleged violations of the Clean Water Act (CWA) and other laws, for an August 2019 discharge of ammonia and cyanide-laden wastewater into the East Branch of the Little Calumet River. The discharge, which led to fish kills in the river, also caused beach closures along the Indiana Dunes National Lakeshore. Cleveland-Cliffs is undertaking substantial measures to improve its wastewater system at its steel manufacturing and finishing facility in Burns Harbor, Indiana.
The ecological exposure assessment for cyanides focuses on potential releases of free cyanide from three main sectors of activity: metal mining, iron and steel manufacturing, and application of ferrocyanide-containing road salts. When available, measurements of CNWAD and CNFree were considered in addition to measurements of CNT for the ecological exposure characterization. Approximately 40% of measured concentrations of total cyanide (CNT) in samples collected in areas receiving metal mining effluent exceeded the PNEC. Average yearly releases of cyanides from integrated steel mills were calculated using loadings reported to a provincial government and it was determined that releases from two facilities could exceed the PNEC. Finally, concentrations of CNT and CNWAD in the environment receiving runoff from parking lots and highways where ferrocyanide-containing road salts were applied were determined to be sufficiently elevated to have the potential to cause chronic adverse effects to organisms. 781b155fdc