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Article Category: Review paper
Publicado en línea: 14 mar 2019
Páginas: 90 - 104
Recibido: 06 mar 2018
Aceptado: 27 jul 2018
DOI: https://doi.org/10.1515/ohs-2019-0010
© 2019 Faculty of Oceanography and Geography, University of Gdańsk, Poland
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Selected information on the use of arsenic compounds in human history (Bartrip 1992; Antman 2001; Hughes et al. 2011; Frith 2013; Radke et al. 2014; Wu et al. 2016; Akhtar et al. 2017; Bełdowski et al. 2018)
| Age/year | Application/Use |
|---|---|
| B.C. | The first application of arsenic compounds in ancient ti mes for the therapeuti c treatment as well as in combat (by Chinese, Egypti an, Indian, Rome) |
| 406–357 B.C. | Hippocrates presented the first medical reports on arsenic |
| 384–322 B.C. | Aristotle published a report on negati ve effects of arsenic |
| 82 B.C. | Consul Lucius Cornelius Sulla issued the Lex Cornelia outlawing arsenic poisoning |
| A.D. | The first in the history documented cases of arsenic poisoning involving Britannicus, Caesar Claudius |
| 55 A.D. | A documented report stating Britannicus’ death by arsenic poisoning (by the psychopathic murderer, emperor Nero, to secure his Roman throne) |
| 23-79 A.D. | First medical reports (by Pliny the Elder) in AD |
| 1250 A.D. | The official date of discovery (by Albertus Magnus) of arsenic |
| 8th | Jabir ibn Hayyan invented white arsenic |
| 15th | William Withering performed pharmacological experiments using arsenic |
| 1492–1503 | The Borgia pope (Alexander VI) murdered numerous cardinals by arsenic compounds |
| 17th–19th | An increase in the popularity of arsenical poisons (the apogee was reached in the 19th century) |
| 1640–1680 | Catherine Deshayes was sentenced to death for murdering (using arsenic) more than 2 000 infant victi ms |
| 17th | Teofania di Admo developed Aqua Tofana (one of the most famous arsenic poisons in world history) |
| 18–19th | Development of pigments based on As (Scheele’s Green, King’s yellow, Paris, or emerald green) for wallpapers |
| 1786 | Dr. Thomas Fowler invented arsenic solution for medical treatment |
| 1820 | The documented case of the murder of King George III of Great Britain |
| 1836 | The first test to detect arsenic in human body, developed by British chemist James Marsh |
| 1845 | Invention and application of Fowler’s solution for the treatment of leukemia |
| 1881 | Preparation (by LaCoste) of the first modern arsenical chemical weapon (called Dick) |
| 1871 | American explorer Charles Francis Hall became a victim of arsenic poisoning |
| 1880 | Pharmacological texts promoted arsenic compounds for treating skin and breast cancers |
| 1910 | The use of organoarsenic compounds in the treatment of pellagra, malaria and sleeping sickness |
| 1913–1939 | Synthesis and development of chemical weapons, including arsenic compounds: Adamsite, Lewisite, Clark I and Clark II |
| 1940 | Worldwide production of arsenic trioxide chromated copper arsenate (CCA) |
| 1942 | The U.S. Government established a limit standard for arsenic in drinking water at 50 μg l−1 |
| 1970 | Applicati\ on of arsenic trioxide (AsO) for the treatment of acute promyelocyti c leukemia; major production of arsenic chemical 23agents for wood protection |
| 1975 | EPA1 adopted a standard for arsenic in drinking water at 50 μg l−1 |
| 1993 | WHO2 recommends drinking water standard of 10 μg l−1 |
| 1995 | Dimethylarsinic acid, a tumor promoter in four rat organs |
| 2000 | U.S. FDA3 approves arsenic trioxide for leukemia chemotherapy |
| 2001 | EPA lowers the U.S. arsenic drinking water standard to 10 μg l−1 |
| 2002 | Arsenic (+3 Oxidation state) methyltransferase isolated in rat liver cytosol |
| Application of As in veterinary and occasionally in human medicine; the use of organoarsenicals in the production of pesticides, | |
| Present | herbicides and insecti cides; production of an arsenic by-product from smelti ng of copper, lead, cobalt, and gold ores; replacement of CCA by alternati ve reagents; a chemical weapons destruction program |
Selected examples of treatment technologies for arsenic compounds (Johnston & Heijnen 2001; U.S. EPA 2002; Nicomel et al. 2015; Reinsel 2015)
| Technology used | Description of the technology used |
|---|---|
| Technology for arsenic removal from water, wastewater and groundwater | |
| Oxidation | This method [e.g. air Oxidation by ozone; chemical oxidati on by gaseous chlorine, hypochlorite, permanganate, hydrogen peroxide, or potassium permanganate, and Fe(II), Mn(II)] is very effective in removing the pentavalent form of arsenic (arsenate) via arsenite to arsenate conversion. Oxidation must be coupled with a removal process such as coagulation, adsorptition or ion exchange. Oxidation is a very slow process, which can take hours or weeks to complete. An atmospheric oxygen, hypochlorite, and permanganate is the most commonly used technology indeveloping country. |
| Precipitation/Coprecipitation | This system is frequently used for the treatment of arsenic-contaminated drinking water and groundwater as well as wastewater originati ng from the metallurgical industry. This technology uses chemicals to transform dissolved contaminants into an insoluble solid or form another insoluble solid onto which dissolved contaminants are adsorbed. The solid is removed from the liquid phase by clarification or filtration. The method is associated with a simple operation system and the availability of sorbents, which in this case are ammonium sulfate, manganese sulfate, copper sulfate, sulfide, ferric salts (e.g. ferric chloride, sulfate and hydroxide), alum (aluminum hydroxide) and calcium hydroxide. The sulfide precipitation is the most widely used technology. |
| coagulation-Flocculation and filtration | It is based on the addition of a proper coagulant (alum, ferric chloride or ferric sulfate) to contaminated water. After that, the water is sti rred, allowed to settle, and filtered for best results. coagulation with ferric salts works best at pH below 8, while with alum – at a pH range of 6–7. The production of high amounts of arsenic-concentrated sludge is disadvantage of coagulation-flocculation, which requires a costly treatment of waste. Therefore, this process is not so common as the other methods. |
| Ion-Exchange Resins | The syntheti c materials (ion exchange resins) are applied to remove some compounds from water as well as for water softening. These resins mostly remove arsenate, therefore the raw water with arsenite should be oxidized first. The amount of water that can be treated is largely independent of arsenic concentration and pH. |
| Activated Alumina | This commercially available method is based on the use of acti vated alumina, which works better in slightly acidic environment (pH 5.5 to 6). For best results, raw water with arsenite should be oxidized before treatment. |
| Membrane methods | This method is based on the reverse osmosis and nanofiltration. For this purpose, synthetic membranes are used, which are water permeable but reject larger molecules, including arsenic, chloride, sulfate, nitrate and heavy metals. Reverse osmosis also effectively removes other constituents from water (e.g. organic carbon, salts, dissolved minerals, and color). This treatment process is relatively insensitive to pH. |
| Other technologies | They are less documented. Some of the technologies are sti ll under development, e.g. low-tech iron-coated sand and greensand, novel iron-based sorbents, aeration and sedimentation, and specially engineered syntheti c resins. |
| Technology for arsenic removal from soil/sediments and other waste | |
| Solidification/Stabilizatition | It physically binds or encloses contaminants within a stabilized mass and chemically reduces the hazard potenti al of waste by converti ng the contaminants into less soluble, mobile or toxic forms. |
| Vitrification | High temperature treatment that reduces the mobility of metals by incorporati ng them into a chemically durable, leach-resistant, vitreous mass. The process reduces the concentration of compounds in soil and waste. |
| Soil Washing/Acid Extraction | The ex situ technology that uses the behavior of some contaminants to preferenti ally adsorb onto fine soil/sediment fractions. The soil/sediment is suspended in a wash solution and the fines are separated from the suspension, thereby reducing the contaminant concentration in the remaining soil. |
| Biological treatment | It involves the use of microorganisms that act directly on contaminant species or create ambient conditions that cause the contaminant to leach from soil/sediment or precipitate/co-precipitate from water. |
| Electrokinetic treatment | The usage of current and electrodes for soil/sediment. The current is applied to soil to mobilize contaminants in the form of charged species. Contaminants arriving at the electrodes can be removed by electroplati ng or electrodeposition, precipitation or co-precipitation, adsorption, complexing with ion-exchange resins, or by pumping water (or other fluid) near the electrode. |
| Phytoremediation | It involves the use of plants to degrade, extract, contain, or immobilize contaminants in soil, sediment and groundwater. |
| In situ soil flushing | It extracts organic and inorganic contaminants from soil/sediment by using water, a solution of chemicals in water, or an organic extractant, without excavati ng the contaminated material itself. The solution is injected into or sprayed onto the area of contamination, causing the contaminants to become mobilized by dissolution or emulsification. After passing through the contamination zone, the contaminant-bearing flushing solution is collected and pumped to the surface for treatment, discharge or reinjection. |
Total arsenic concentration values in environmental samples from selected worldwide localities
| Country | Area | Concentration | Units | References | |
|---|---|---|---|---|---|
| Water | |||||
| Spain | Tinto River estuary | < 2.00–4.90 | μg l-1 | ||
| Finland | Vörå River estuary | 12.10–17.00 | mgl-1 | ||
| India | Mahanadi estuary | 8.0 ±3.7 | μg l-1 | ||
| South Korea | Taehwa estuary | 2.3 (AsIII), 94(AsV) | μg l1 | ||
| France | Gironde estuary | 5.3 | μg l1 | ||
| Italy (Alps - Adriatic Sea) | Po River | n.d.–20.0 | μg l-1 | ||
| Bangladesh | Karnaphuli River | 13.31–41.53 | μg l-1 | ||
| Vietnam | Red River Basin | <1.00 | μg l-1 | ||
| Brazil | Carmo River | 36.70–68.30 | μg l-1 | Varejão et al. 2011 | |
| Poland | Wieprza River | <2.00 | μg l-1 | ||
| India | Ganga–Brahmaputra river system | up to 128 | μg l-1 | Chetia et al. 2011 | |
| Spain | Anllóns River | 0.98 | μg l-1 | ||
| 9.45 ± 1.93 surface | |||||
| China | Caohai Lake | 9.84 ±2.37 bottom | μg l-1 | ||
| 6.68 ± 1.72 surface | |||||
| China | Waihai Lake | 6.72 ± 1.64 bottom | μg l-1 | ||
| Argentina | Chasicó Lake | 0.195–0.315 (wet period) 0.058–0.413 (dry period) |
mg l-1 | ||
| Pakistan | Mancharl Lake | 35–157 | μg l-1 | ||
| Coastal waters around Tallin | < 0.1-1.75 | ||||
| Baltic Sea | Kakumäe region | 2.12 ±0.03 | μg l-1 | ||
| 0.05–0.19 (As(III)) | |||||
| Baltic Sea | Arkona Basin | 0.49–1.10 (As(III) + As(V)) | μg l-1 | ||
| < 0.001–0.28 (As(III)) | |||||
| Baltic Sea | Bornholm Basin | 0.58–1.04 As(III) + As(V)) | μg l-1 | ||
| < 0.001–0.54 (As(III)) | |||||
| Baltic Sea | Eastern Gotland Basin | 0.52–1.10 As(III) + As(V))0.02–0.61 (As(III)) | μg l-1 | ||
| Baltic Sea | Western Gotland Basin | 0.49–0.99 As(III) + As(V)) | μg l -11 | ||
| 0.59A | |||||
| 0.76B | |||||
| Baltic Sea* | Bornholm | 0.63C | μg l-1 | ||
| 0.55D | |||||
| Sediments | |||||
| Bangladesh | Karnaphuli River | 11.56–35.48 | μg g-1 d.w. | ||
| China | Yangtze estuary | 7.86 ±2.63 | μg g-1 | ||
| Spain | Anllóns River | 106 | μg g-1 | ||
| India | Mahanadi estuary | 2.1 | μg g-1 | ||
| Slovenia | Valenjsko Lake | 9.69 ±3.68 | μg g-1 d.w. | Petkovšsek et al. 2011 | |
| Slovenia | Družmirsko Lake | 8.12 ±2.55 | μg g-1 d.w. | Petkovšsek et al. 2011 | |
| Slovenia | Škalsko Lake | 7.51 ±2.30 | μg g-1 d.w. | Petkovšsek et al. 2011 | |
| Baltic Sea | Bothnian Sea | 167–216 | μg g-1 | Uścinowicz 2011 | |
| Baltic Sea | Gdańsk Deep | 15.5 | μg g-1 | ||
| Baltic Sea | Gulf of Gdańsk | 9.8 | μg g-1 | ||
| Baltic Sea | Lithuanian EEZ | 6.2 | μg g-1 | ||
| Baltic Sea | Gulf of Finland (Estonia) | 15.80–27.70 | μg g-1 d.w. | ||
| Baltic Sea* | Bornholm Deep | 17.0 | μg g-1 | Bełdowski et al. 2016a | |
| Baltic Sea* | Gotland Deep | 13.3 | μg g-1 | ||
| Baltic Sea | Southern Baltic Sea | < 5–29 | μg g-1 | Uścinowicz 2011 | |
| Tunisia | Mediterranean Sea | 13.11–36.00 | μg g-1 d.w. | ||
| Croatia | West Istria Sea | 8.12–23.44 | μg g-1 d.w. | ||
| Iran | Southern Caspian Sea | 8–17 | μg g-1 d.w. | ||
Selected symptoms of arsenic poisoning (Das et al. 1980; Sanders 1986; Eisler 1988; Gomez-Caminero et al. 2001; UKMPA 2001; Kumari et al. 2016)
| Living organisms | Standard measure of toxicity | Poisoning symptoms |
|---|---|---|
| Fish | LC50 varies from 5.5 to 91 mg As I-1 and depends on individual species. | Acute exposure: It may cause behavioral and hematological changes, lethal effects, internal damage of organs (liver and kidney, gills, gonads, brain), skin problem, shock, breathing problem, decrease in orientation. |
| Chronic poisoning may occur at 1 μg I-1 | Chronic reproduction poisoning and development triggers problems of young with fish, changes in enzymes and DNA structure, death, permanent degradation of the gastrointestinal tract and circulatory system. | |
| Marine mammals, seabirds and sea turtles | Acute exposure creates gastroenteritis, shock, breathing problems, decrease in orientation, degenerative changes in liver, and kidney, gills, gonads and brain, muscular incoordination, debility, slowness, jerkiness, hyperactivity, drooping eyelid, huddled position, unkempt appearance, loss of righting reflex, immobility, seizures, loss of hearing, dermatitis, blindness | |
| Symptoms occur within a few hours and deaths within 1 to 6 days. Death or malformations have been documented after single oral doses of 2.5 to -1 33 mg As kgbody weight, chronic doses of 1 to 10 mg As kg-1 body weight, and at dietary levels > 5 and < 50 mg As kgdiet. -1 | Chronic poisoning is responsible for effects on reproduction, changes in the immune system, destruction of enzymes (e.g. glutathione-S-transferase), changes in cellular detoxification, receptor damage, cancer, chromosomal damage, birth defects, death | |
| Bottom organisms (e.g. mussels, snails, cephalopods) | 48 h LC/EC50 values range from 0.68 to 73.5 mg I-1 -1 for trivalent arsenic and from 3.6 to 49.6 mg As Ifor pentavalent arsenic. | Acute exposure: It can cause dermal effects, decrease in orientation, lethal effects and destruction of organs
Chronic poisoning causes mutations, population decline, increase in mortality |
| Zooplankton (e.g. rotifers, copepods and cladocerans, diatoms) | Concentration of 4 mg As (III) I-1 reduction in po- pulation. | Acute exposure: lethal effects, shock, degradation |
| 48 h EC50 is 326 μg I-1 |
Chronic poisoning: Population decline (4 mg As I-1), reduction in the number of young individuals, intraspecific mutations, increased mortality, reduced immunity | |
| Phytoplankton (e.g. algae, blue-green algae) | EC50 from 0.007 to > 2.0 mg I-1. EQS was established at 25 μg l -1 |
Acute exposure is associated with dermal effects, population decline, lethal effects |
| Chronic poisoning is responsible for inhibition of the growth as well as blocking of phosphate uptake, inhibition of cell multiplication (at 3.5 mg As(V) I-1), change in species composition, population decline and increase in mortality |