Carbon Disulphide : a brief introduction

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Carbon Disulphide: History, exposure and Effects.

Background
This paper is a brief review of the Study on Carbon disulphide, it discusses the historical background of this toxic chemical, the sources, current decline in usage and the physiological effects (acute and chronic).

October 2015


2.0 Literature
2.1 Historical Background
source.25
Carbon disulphide was first observed (accidentally) in the year 1796 by a German Chemist Lampadius, He observed the liquid product (carbon disulphide) when he mixed iron pyrites (FeS2) and charcoal.1 since its accidental discovery CS2 has since been used for a lot of processes. In the 1940s the Scottish surgeon tested Carbon disulphide for its Narcotics-anesthetic effects. Even though CS2 was shown to have strong anesthetic properties, its use was discontinued because it caused hallucinations, headaches and nausea.1 the widespread use of carbon disulphide in the industry is evidenced by its strong solvent properties. Products such as lacquers, fats, camphor and matches have been produced in the past using CS2 as a solvent.1

2.1.1 CS2 from Nature
Various natural sources have been responsible for considerable amount of CS2 in the environment, the largest Biogenic sources tends to be soils, marshes and coastal regions.2 the production of CS2 arises as a result of metabolic processes involving plants and animals.2 It is estimated that up to 2280 tonnes of CS2 per year could be released from the weathering of Sulphide (S2-) containing minerals globally.2 Even though the estimates still leaves much to be desired, at least 40% of CS2 releases and over 80% are a result of Natural Processes/biological activity.2
2.1.2 Anthropogenic sources
Man has also contributed a fair share of the world's carbon disulphide supply. The anthropogenic sources of CS2 arise as a result of using CS2 as a solvent of choice in the production of viscose rayon and cellophane.2 CS2 gets into the atmosphere through these processes because it is not bound to the product.2 If about 75% of the world's production of about 1million tonnes are used for these processes, then some 700,000 tonnes may be released annually.2
2.1.3 Decline in the Use of CS2
Industrial emissions of CS2 to the atmosphere have declined as textile manufacturing has shifted from the US to Asia, and the use of CS2 in carbon tetrachloride production has been phased out.3 there has been a decline in the amount of Carbon disulphide produced through anthropogenic sources worldwide. This is due to the discontinued use of carbon disulphide in many processes as depicted in the following works. Global production of CS2 has seen a steady decline from 1.025million tonnes in 1984 to 0.9million tonnes in 1990.4 US production amounted to about 143 Kilotonnes in 1985 alone.5 Production from the United Kingdom before 1992 was estimated to fall between 25 to 35 kilotonnes.6 In the year 1996, Canada's production of CS2 accounted for 3.1 kilotonnes of their Commercial production.7 It has been reported that Canadian domestic production has witnessed a steady fall from the 25 kilotonnes in 1976 to the 10.9 kilotonnes estimated in 1993, The closure of many rayon and cellulose fibre industry in Canada has been fingered as the cause of the observed fall in the CS2 level. This is due to the fact that these industries are major users of CS2.8

2.2 Toxicokinetics
CS2 is absorbed via the skin and respiratory tract (gaseous nature supports the exposure to CS2 through the lungs). The absorption is mainly diffusion dependent, this shows the absence of binding for absorption. Respiratory absorption is proportional to the CS2 in the air.12 once absorbed CS2 accumulates twice as much in red blood cells compared to the plasma. CO and CO2 have been identified as common metabolites of CS213-14, CS2 is rapidly dissipated in fat rich tissues and organs compared to persistence in the blood stream. Some metabolites like thiourea and Mercaptothioaxolinone has also been observed in human urine after CS2 exposure.14

2.3 General Toxicity
CS2 exposure usually gives both acute and chronic effects. CS2 is a systemic toxicant, and it exhibits a wide range of toxicodynamic effects, these include neuropsychiatric, cardiovascular, ocular, gastrointestinal, endocrine, and reproductive disorders, many of these disorders have been observed in workers exposed9-11.

Some hypothesis have been proposed to explain the toxic action of CS2.15
Chelation by metabolites of various trace metals essential for enzyme function: CS2 acts as a ligand in the body and it chelates many important metal ions necessary for normal body functions, this leads to a reduction in the bioavailability of the metal and also speciation of the metal that may lead to other metabolic pathways that may be toxic or not.
Enzyme inhibition: CS2 can also act by inhibiting enzyme action, thus prompting massive biochemical changes in the body.
Disturbance of vitamin metabolism, especially of B6 and Nicotinic acid
Disturbance of catecholamine metabolism: the catecholamines are important amino acid derivatives, mostly derived from the amino acid tyrosine and phenylalanine. Examples include epinephrine, norepinephrine, dopamine; they are important hormones and secretions. Epinephrine and norepinephrine are an important part of the fight or flight response while dopamine has been associated with sleep.
Disturbance of Lipid metabolism.

2.3.1 Chronic effects
It has been predicted that the toxicity of CS2 could be due to its reaction with endogenous macro molecules16 these reactions can lead to the formation of thiocarbamates, isocyanates, thiourea and urea.17

2.3.1.1 Effects on the Nervous System
The effect of CS2 on the central Nervous system (CNS) and the peripheral nervous system (PNS) has been well documented.17 CS2 binds neuro-filaments resulting in the formation of disulphide cross-links and thus leading to subsequent swelling of the axons.18 The chemical change and covalent binding of CS2 to the micro filaments results in increased viscosity and reduced velocity of impulse transfer. Myelin alterations are also common
(secondary), Ataxia and paresis are other conditions observed as manifestations of neuropathy of the peripheral nervous system.19 Changes in morphology also results from the spinal cord and PNS(peripheral Nervous system) due to the swelling of axons by an increase neuro-filament binding with CS2. Occupational studies have also revealed neurobehavioral changes.20-21

2.3.1.2 Effects on the Heart
Changes in morphology and function of the heart including death (necrosis) of the myocardial tissues have been observed when relatively high dosages and exposure concentrations of CS2 are encountered, this has been speculated to be due to the effect of CS2 in the heart, leading to increase in the deposition of cholesterol and lipoproteins a process important in the development of arteriosclerosis.19

2.3.1.3 Effects of Reproductive System
Reproductive effects have been observed and reported in both male and female workers. Reports of reduced sperm count and changes in the morphology of the sperm cells have been reported at 8h TWA exposures of around 30mg/m3 (10ppm19) this report is yet to be confirmed in other studies,22-23 even though reduction in the potency and libido of studied workers have been observed when CS2 exposures reached 10ppm and above.23

Future research
The acute effects of CS2 should be studied to ascertain the exposure-time relationship of the compound. Current geographical based exposures to the substance should also be ascertained to determine ways protecting life and avoiding the danger that it poses.



References
Biological effects of Exposure (Accessed: Sepetember 2, 2015) Center For Disease Control and Prevention http://www.cdc.gov/niosh/pdfs/77-156c.pdf

World Health Organization, International Programme on Chemical Safety (IPCS). Carbon Disulphide. Concise International Chemical Assessment Document 46. 2002, 6 –8
U.S. Environmental Protection Agency. Chemical summary for carbon disulfide. 1994 Available at: http://www.epa.gov/chemfact/s_carbds.txt. Accessed July 19, 2010.

Rolecki R, Tarkowski S (2000) Draft document for carbon disulfide. Lodz, The Nofer Institute of Occupational Medicine.
ATSDR (1996) Toxicological profile for carbon disulfide (update). Atlanta, GA, US Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, 219 pp.
Crookes MJ, Diment J, Dobson S (1993) Environmental hazard assessment: carbon disulfide. Garston, Watford, United Kingdom Department of the Environment, Building Research Establishment (TSD/14).
Environment Canada (1997b) Results of the CEPA Section 16 Notice respecting the second Priority Substances List and di(2-ethylhexyl) phthalate. Hull, Quebec, Environment Canada, Commercial Chemicals Evaluation Branch, Use Patterns Section.
Camford Information Services (1995) CPI product profiles: Carbon disulfide. Don Mills, Ontario, Camford Information Services Inc.
Vigliani EC (1954) Carbon disulfide poisoning in viscose rayon factories. Br J Ind Med 11, 235–44.
Seppäläinen AM, Haltia M (1980) Carbon disulfide. In: Experimental and clinical neurotoxicology. eds. By Spencer PS, Schaumburg HH, 356–73, Williams & Wilkins, Baltimore.
Beauchamp RO, Bus JS, Popp JA, Boreiko CJ, Goldberg L (1983) A critical review of the literature on carbon disulfide toxicity. CRC Crit Rev Toxicol 11, 169–278.
Demus, H. (1967) The mechanism of absorption, metabolism and excretion of carbon disulphide in the human body. In H. Brieger and J. Teisinger, eds. Toxicology of Carbon disulphide. Amsterdam: Excerpta Medica Foundation. P. 42-49.
DeMatteis, F., and Seawrigh, A. A. (1973) Oxidative Metabolism of carbon disulphide by the rat. Effect of treatments which modify the liver toxicity of carbon disulphide. Chem. – Biol. Interact. 7: 375-388.
Dalvi, R. R. and Nall, R.A. (1978) Metabolism in vivo of Carbon disulphide to Carbonyl sulphide and carbon dioxide in rat. Biochem. Pharmacol. 27: 1608 -1609.
World Health Organisaton(1979) Environmental Health Criteria 10: Carbon disulphide. Geneva: World Health Organisation.
DeCaprio, A.P., Spink, D.C., Chen, X., Fowke, J.H., Zhu, M., Bank, S. (1992).Characterisation of isocyanates, thioureas and other lysine adduction products in carbon disulphide-treated peptides and proteins. Chem. Res. Toxicol. 5, 496-504.
Recommendation from the Scientific Committee on Occupational Exposure Limits for Carbon Disulphide (2008) http://www.gezondheidsraad.nl/sites/default/files/Carbon_disulphide2011.pdf pp. 27-29 (Accessed October 10 2015)
Graham, D.G., Armarnath, V., Valentine, W.M., Pyle, S.J. and Anthony, D.C. (1995)Pathogenic studies of hexane and carbon disulphide neurotoxicity. Crit. Rev.Toxicol. 25, 91-112.
BUA (GDCh-Advisory Committee on Existing Chemicals) (1993). Carbon disulphide: BUA Report 83 (August 1991). S Hirzel, Wissenschaftliche Verlagsgesellschaft, Stuttgart.
Cassitto, M.G., Camerino, D., Imbriani, M., Contardi, T., Masera, L., Gilioli, R. (1993). Carbon disulphide and the central nervous system: a 15-year neurobehavioural surveillance of an exposed population. Environ. Res. 63, 252-263.
Herborn, H. (1992). Gesundheitsgefährdung durch Schwefelkohlenstoff (CS2) – Ergebnisse einer epidemiologischen Studie. In: Schäcke, G., Ruppe, K., Vogel-Sührig, C. (eds). Verhandlungen der Deutschen Gesellschaft für Arbeitsmedizin eV, 31st annual meeting in Berlin from March 11th-14th, 1991. Vol.31. Gentner Verlag Stuttgart,263-265.
Vanhoorne, M., Vermoeulen, A., De Bacquer, D. (1993). Epidemiological study of endocrinological effects of carbon disulphide. Arch. Environ. Health. 48, 370-375.
Vanhoorne, M., Comhare, F., De Bacquer, D. (1994). Epidemiological study of the effects of carbon disulphide on male sexuality and reproduction. Arch. Envron. Health. 49, 273-278.


PHILIP EPHRAIM ALABI " Msc. Chemistry, SIUE.

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