Report on Vinyl Chloride
Report on Vinyl Chloride
The case involves a man who went into a polymerization tanks measuring 8 feet in high and 5 feet wide. The man went into the tank alone at night, and there was no light in the pit. After 20 minutes, the man did not return, and somebody went to check him. The man was found lying in the pit. The person who was looking for the man climbed in order to get the man out, but the person was overwhelmed by the gas. The person immediately shut the open valve feeling dizzy. The person dragged himself on his knees and hands for a distance of 15 yards after which he called for help. He recovered quickly and was able to assist in removing the body of the victim. The body was removed through the help of another man wearing a gas mask. Artificial respiration was tempted with no success, and the man was confirmed dead. Eight hours after death confirmation, an autopsy was done which gave negative toxicological results (Danziger, 1960).
The man was 39 years old, 167cm in height and weighed about 70-75 kg. The finger nails of the man were deeply cyanotic, and there were cuts of the skin on the man’s face. Both bulbar conjunctivas had a wedge-shaped brown discoloration that corresponded to the palpebral slits. The heart of the victim was not remarkable and weighed 390 g. The blood had a dark red color and did not clot for the four hours of observation. The lungs had an increase in the amount of fluid content with the right lung weighing 525 grams and the left lung weighed 470 grams. There was a slight swelling in the trachea and the larger bronchi and reddening of the mucosa was also observed. The kidney was normal in terms of size and weight. There was intense submucosa hyperemia that was seen in the bronchi and trachea. The spleen and the liver were less hyperemic (Danziger, 1960).
The analysis of these results indicated that the man died as a result of inhaling a highly concentrated vinyl chloride. This was contributed by the fact that vinyl chloride is heavier than air, and the valve was opened. This caused the man to inhale the gas in a form that was highly concentrated (Danziger, 1960).
Vinyl chloride, also known as vinyl chloride monomer or chloroethene, refers to an organochloride molecule that has a molecular formula of H2C=CHCl. The compound is colorless and plays a significant role in industrial chemistry where it is used in the production of polymer polyvinyl chloride (PVC) (Dreher, Torkelson, & Beutel, 2011). Annually, more than 13 billion kilograms of vinyl chloride are produced making it one of the twenty most produced petrochemicals in the world. United States is the leading producer of vinyl chloride. This is enhanced by the low production cost that it enjoys due to the availability of raw materials such as chlorine and ethylene. The other country that produces vinyl chloride is China, which is also a huge consumer of vinyl chloride. Some of the major properties of vinyl chloride include having a sweet odor, highly flammable, toxic and carcinogenic.
Where is Vinyl Chloride Found? (PRODUCTION and use of Vinyl Chloride)
The first production of vinyl chloride took place in 1835 by Justus von Liebig and Henri Regnault (Wilkes, Summers, Daniels, & Berard, 2005). The first production was done by treating 1, 2-dichloroethane with potassium hydroxide solution in ethanol. There are several methods through which vinyl chloride is produced. The first method is using ethylene as the raw material in a process that integrates sets of reactions that use ethylene, chlorine and air as the starting materials. The other method is through direct chlorination where ethylene is reacted with chlorine using iron (III) chloride as a catalyst. The third method through which vinyl chloride is produced is through oxychlorination process. In this process, recycled HCl is used in a reaction together with ethylene and oxygen to produce vinyl chloride using copper (II) chloride as the catalyst. Thermal cracking is the other method through which vinyl chloride is produced. This occurs when ethylene dichloride is heated to 500OC and at a pressure of between 15–30 atm. These conditions cause the ethylene dichloride to decompose producing vinyl chloride and anhydrous hydrogen chloride. The reaction involving thermal cracking is highly endothermic and thus requires fired heater.
Other ways through which vinyl chloride is produced is in the process of treating waste waters and from acetylene and ethane. In the production of vinyl chloride using acetylene, acetylene is usually reacted with anhydrous hydrogen chloride gas using mercuric chloride as the catalyst. This produces vinyl chloride in an exothermic reaction. This process is mainly used by China since they have a large coal reserve which is used to produce acetylene. Where ethane is readily available, ethylene is produced by cracking ethane to produce ethylene, which is then used to produce vinyl chloride.
What Are Routes of Exposure for Vinyl Chloride?
Exposure to vinyl chloride to the general population occurs through inhalation of the ambient air, as well as in ingesting food or other items, which may be contaminated with low levels of vinyl chloride. Vinyl chloride has a high mobility especially in plastics and may thus able to leach into beverages, food, or water contents.
Who Is at Risk of Overexposure to Vinyl Chloride?
Most people are at a greater risk of exposure if they are smokers or work where vinyl chloride is produced. Vinyl chloride is not usually found in areas such as urban areas, suburban and rural areas since these areas are far from vinyl chloride production areas. However, high quantities of vinyl chloride are found in areas that are close to the processing and manufacturing plants, landfalls, and hazardous waste sites. The quantity of vinyl chloride in the environment near these sites ranges from very minute quantities to more than 1 ppm. Levels of vinyl chloride that are as high as 44 ppm have been recorded in the air surrounding some landfills. Exposure to vinyl chloride may also occur after drinking water from wells that have been contaminated (ATSDR, 2006).
What Are Standards and Regulations for Vinyl Chloride Exposure?
International Agency for Research on Cancer or IARC has named vinyl chloride as one of the chemicals that have carcinogenic properties. In the United States, there are set standards for vinyl chloride in drinking. The Congress has identified vinyl chloride as an air pollutant that is hazardous to human health under the Clean Air Act. Vinyl chloride exposure has been a subject even in safety standards set in working places especially in case of airborne concentrations.
The Environmental Protection Agency (EPA) has derived a reference dose of 0.003 mg/kg/day, and this is based on the NOAEL recorded in liver cell polymorphism obtained from rats that were administered with vinyl chloride in their food for a lifetime. The FDA takes the responsibility of regulating the amount of vinyl chloride that is used as an indirect additive in the food industry. In the cases of the components in papers, coatings, and paperboards, the FDA has indicated that copolymerizing vinyl chloride with other substances makes it a safe-food contact surface. The quantity of vinyl chloride added to the polymers varies, and this depends on the nature of the polymer being made, as well as on the use of the polymer (ATSDR, 2006).
According to the Occupational Safety & Health Administration (OSHA), those employees who are engaged in operations that are hazardous such as entering the vessels to clean residues of polyvinyl chloride from the walls should be provided with protective garments. The employees are also required to wear respiratory protection. These employees should also wear garments that protect them from having skin contact with the liquid vinyl chloride or residues of polyvinyl chloride that are on the walls of the vessel. The OSHA regulations also indicate that no employees should be exposed to vinyl chloride that is at a concentration of more than 1 part per million for a period of 8 hours or 5 part per million for a period not greater than 15 minutes. OHSA regulations also indicate that no employee may be subjected to vinyl chloride directly without using protection (OSHA, 2013).
Metabolic Pathways for Vinyl Chloride (How Does Vinyl Chloride Induce Pathogenic Change?)
The vinyl chloride metabolism involves both non-microsomal and microsomal enzymatic pathways and leads to the vinyl chloride conversion to 2-chloroethylene oxide, a polar metabolite, as well as subsequent oxidation to monochloroacetic acid and 2-chloroacetaldehyde. This saturable pathway seems to function at low exposures resulting in the polar metabolites production, which are largely egested in the urine. This metabolism takes place basically through microsomal enzymes in the liver. The proof strongly shows that the vinyl chloride toxicity is ascribable to its enzymatic oxidation as well as transformation into reactive polar metabolites. Vinyl chloride metabolism in animals is a saturable process that is dose dependent (Guengerich & Watanabe, 1979). For instance, low concentrations inhalation exposure in the rat is broken down with 86 minutes, a comparatively short half-life, in comparison with 261 minutes, a longer half-life, from a high dose (Withey, 1976).
The initial vinyl chloride metabolism step involves microsomal oxidation resulting in oxidation across the double bond (Andrews & Snyder, 1991). Vinyl chloride is converted into chloroethene oxide through this microsomal enzyme pathway that can spontaneously reorganize to make 2-chloroethylene oxide and, later, monochloroacetic acid. The latter monochloroacetic acid can then go through conjugation with glutathione. Further breakdown of the ensuing conjugates of glutathione can generate several compounds, among them S-(carboxymethyl) cysteine, monochloroacetic acid, N-acetyl-S-(2-hydroxymethyl) cysteine, N-acetyl-vinylcysteine and thiodiglycolic acidin the rats’ urine exposed to vinyl chloride through both the oral and inhalation routes (Green & Hathaway, 1977). Chloroacetic acid chloride and thiodiglycolic acid have been discovered in the urine of laborers with exposure to atmospheric vinyl chloride (Muller, Norpoth, Kusters, Herweg, & Versin, 1978).
In other studies (Bolt, Filser, & Laib, 1981), the cytochrome P-450 system gets involved in metabolism of vinyl chloride. The authors showed that 50 ppm of vinyl chloride intake in a closed system was totally blocked by cytochrome P-450 inhibitors like 6-nitro-1, 2, 3-benzothiodazole or 3-bromophenyl-4(5)-imidazole. Pretreatment with the DDT, which is a cytochrome P-450inducer, was effectual in increasing intake as well as absorption, though, another P-450 inducer, Phenobarbital, has demonstrated no effect on metabolism of vinyl chloride (Guengerich & Watanabe, 1979). These results propose that the cytochrome P-450 system can have a crucial function in metabolism of vinyl chloride at low doses. Other studies by Bolt et al (1981) and Hefner et al (Hefner, Watanabe, & Gehring, 1975) proposed that the enzyme systems that are responsible for metabolism of vinyl chloride in rats get saturated at over 250 ppm atmospheric concentrations and higher concentrations give comparatively little extra reactive metabolite.
Health effects of Vinyl Chloride Exposure and the primary routes of Vinyl Chloride entry into the body
Acute (Immediate) Health Effects
There have been studies on the effects of exposure to vinyl chloride in animals and human beings, with the same results being demonstrated in all species. Exposure to vinyl chloride in humans has a high likelihood to take place through oral or inhalation exposure routes.
- Dermal Health Effects
The dermal exposures effects are unlikely since the absorption of vinyl chloride across the skin is poor. However, dermal exposure effects of vinyl chloride include thickening of skin, reduced elasticity, edema, local frost bites, irritation and blistering. The total loss of elasticity of skin conveys itself in Raynaud’s Disease. Chronic exposure results in respiratory failure as well as the focused Hepatotoxicity. Continuous exposure may lead to depression of the CNS including disorientation and euphoria (Hathaway & Proctor, 2004).
- Inhalation Health Effect
Chronic-duration, occupational exposures to high vinyl chloride levels have led to a particular suite of effects in human beings, which include Raynaud’s phenomenon, narcotic effects, scleroderma-like skin modifications, hepatocellular alterations, acroosteolysis as well as the hepatic angiosarcoma development. Exposure of laboratory animal to vinyl chloride has led to liver, cancer, and neurological effects as well as reproductive, lymphoreticular, respiratory, and developmental effects. Although acute exposure through the inhalation route, of mice, to vinyl chloride led to a developmental effect, liver, as well as neurological effects were consistently detected in vinyl chloride laborers, and a number of species of animal throughout durations of exposure, proposing that these are the key effects of exposure to vinyl chloride (ATSDR, 2006).
Vinyl chloride has been reported to have slight irritation to the respiratory tract and the eyes. Acute exposure to extremely high vinyl chloride levels has led to loss of consciousness, kidney and lung irritation, and blood clotting suppression in human beings as well as cardiac arrhythmias in animals. Tests that involve acute exposure of mice have demonstrated that vinyl chloride have high acute toxicity once a person been exposed through the inhalation route. A number of case reports propose that sexual performance of males may be impacted by vinyl chloride (ATSDR, 2006).
Some epidemiological studies have described a link between exposure to vinyl chloride in pregnant women and raised incidences of congenital defect (ATSDR, 2006). There have also been suggestions by some epidemiological studies that there is a link between men who have been exposed to vinyl chloride and miscarriages in pregnancies of their wives. There have also been reports on testicular impairment as well as reduced fertility of males in rats exposed to low vinyl chloride levels for one year. Other reports on animal studies indicate reduced weight of the fetus and congenital defect at levels, which are also toxic to maternal animals in the young ones of rats with inhalational exposure to vinyl chloride.
Chronic (long-term) health effects
- Inhalation Health Effects
The liver seems to be the most sensitive target organ by toxicity of vinyl chloride. The effects on the liver act as the ground for the intermediate-duration inhalation minimal risk levels as well as the chronic-duration oral minimal risk levels. Alterations in the liver have been detected in workers who were exposed to unknown vinyl chloride levels through inhalation. The typical change pattern discovered through peritoneoscopy and affirmed in a number of studies include hyperplasia and hypertrophy of sinusoidal and hepatocytes cells. Other change patterns detected are sinusoidal dilation linked to destruction of the cells lining the sinusoids, and sinusoidal occlusion, degeneration of focal areas of hepatocellular as well as fibrosis of septa, portal tracts, and intralobular perisinusoidal and periportal areas. As a matter of fact, the degree of hepatic fibrosis seem to stand for the basic difference between effects seen in animals and human beings as deposition of collagen and reticulin in tissue of human liver was more than the one seen in animals. Species differences in fibrosis can also have been affected by ethanol co-exposure through consumption of alcohol (ATSDR, 2006).
There have been demonstrations of cancer development in human beings resulting from exposure to vinyl chloride in several studies involving people working in the production industry of vinyl chloride. The most strong prove is from the bunch of reports of more than anticipated occurrences of liver angiosarcoma. Although there were no available data on exposure for these workers, a convincing association exists between exposure to vinyl chloride as well as the liver angiosarcoma development as this kind of liver cancer is regarded as very rare in human beings (Hathaway & Proctor, 2004). The latency phase for the hepatic angiosarcoma development seems to be prolonged as angiosarcoma keeps occurring in people employed before 1960. Other cancer types that have demonstrated a significant rise in occurrence among workers in environments with vinyl chloride include cholangiocellular carcinoma and hepatocellular carcinoma, cancer of the respiratory tract and lung, the hematopoietic/lymphatic system, as well as the central nervous system and brain. Nevertheless, there is an existing uncertainty in the connection of exposure to vinyl chloride to a number of tumors of soft tissue. A met analysis of data for more than 22,000 people proposed no excess risk of cancer for soft tissue sarcoma, lymphoid, brain, and cancers of the hematopoietic system (ATSDR, 2006).
Reference Lists
Andrews, L., & Snyder, R. (1991). Toxic effects of solvents and vapors (4th ed.). (L. Casarett, J. Doull, & C. Claassen, Eds.) New York: Pergamon.
ATSDR. (2006). Toxicological Profile for Vinyl Chloride. Retrieved November 13, 2013, from Agency for Toxic Substances and Disease Registry: http://www.atsdr.cdc.gov/ToxProfiles/tp20.pdf
Bolt, H. M., Filser, J., & Laib, R. (1981). Covalent binding of haloethylenes. Adv Exp Med Biol, 136(Pt A), 667-683.
Danziger, H. (1960). Accidental Poisoning by Vinyl Chloride: Report of Two cases. Canadian Medical Association Journal, 82(16), 828-830.
Dreher, E. L., Torkelson, T. R., & Beutel, K. (2011). Chlorethanes and Chloroethylenes. Weinheim: Wiley-VCH.
Green, T., & Hathaway, D. E. (1977). The chemistry and biogenesis of the S-containing metabolites of vinyl chloride in rats. Chem-Biol Interact, 17, 137-150.
Guengerich, F. P., & Watanabe, P. G. (1979). Metabolism of [ 14 C]-and [ 36 C]-labeled vinyl chloride in vivoand in vitro. Biochem Pharmacol, 28(5), 589-96.
Hathaway, G., & Proctor, N. (2004). Chemical Hazards of the Workplace (5th ed.). New Jersey: John Wiley & Sons.
Hefner, R., Watanabe, P., & Gehring, P. (1975). Experimental Studies. Preliminary studies of the fate of inhaled vinyl chloride monomer in rats. Ann NY Acad Sci, 246, 135-148.
Muller, G., Norpoth, K., Kusters, E., Herweg, K., & Versin, E. (1978). Determination of thiodiglycolic acid in urine specimens of vinyl chloride exposed workers. Arch Occup Env Health, 41, 199-205.
OSHA. (2013). Vinyl Chloride 1910.1017. Retrieved November 15, 2013, from Occupational Safety & Health Administration: https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=10021
Wilkes, C. E., Summers, J. W., Daniels, C. A., & Berard, M. T. (2005). PVC handbook. München: Hanser Verlag.
Withey, J. (1976). Pharmacodynamics and uptake of vinyl chloride monomer administered by various routes to rats. J Toxicol Environ Health, 1(3), 381-94.
