studying the toxicity of chromium

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Chromium is a naturally occurring element that is found in animals, plants, rocks and soil. It can exist in several different forms, depending on the form it takes; it can be a liquid, solid, or a gas. It is a blue-white metal. Chromium is hard, brittle and resistant to corrosion. The most common forms of chromium are chromium (0), chromium (III), and chromium (VI).

Chromium was discovered in 1797 by Louis-Nicholas Vauquelin as he was experimenting with a substance known as Siberian red lead (mineral crocoite- (PbCrO4)). The production of chromium oxide (CrO3) on mixing crocoite with hydrochloric acid was the first step to discovery. Heating the chromium oxide in a charcoal oven was the second and final step to discovering metallic chromium. He was responsible for naming chromium after the Greek word 'khroma', which means color. In the present world, chromium is primarily synthesized by heating the mineral chromite (FeCr2O4) in the presence of aluminum or silicon.

Chromium products are tasteless and odorless. There are various uses for chromium products. The use of Chromium (VI) and chromium (III) for chrome plating (responsible for shiny surfaces) is on a large scale. Chromium is also used in pigments and dyes, tanning of leather, and in preservation of wood. Chromium is also added to steel to form stainless steel (an alloy) which is used in a number of incidents such as making armor plates, ball bearings and cutting tools. Chromium compounds are used in the anodization of aluminum, which is a process that involves coating aluminum with a thick, protective layer of oxide. Because of it high melting point, Chromium's primary ore (Chromite) is used to make molds for the firing of bricks.

The toxicity of chromium is mainly attributed to Chromium hexavalent (VI) compound. Major studies pin point Cr (VI) as a human lung carcinogen. These are the studies which have been performed on workers involved in chromate production, chromate pigment production and chromium plating. Chromium plantings and related industries present a risk of exposure that is two orders of magnitude higher than in the regular population. The general routes of exposure to populations include air, food, and drinking water containing chromium. Exposure through skin to chromium can occur from contact with certain consumer products that contain chromium. The primary route is food ingestion. Processing and preparation of food are the main reasons for the raised content of chromium in food. According to statistics given by the Agency for Toxic Substances and Disease Registry (ATSDR), "OSHA set a legal limit for chromium (VI) of 0.005 mg/m3, for chromium (III) of 0.5 mg/m3, and for chromium (0) of 1.0 mg/m3 chromium in air averaged over an 8-hour work day". The ATSDR also states that "most fresh foods in general contain chromium levels ranging from <10 to 1,300 μg/kg" and that "rural air contains less chromium than urban air (<10 ng/m3 in rural areas vs. 0-30 ng/m3 in urban areas)"

For any given chromium compound, its toxicokinetics depends on the valence state of its atom and the nature of its ligands. In the case of inhaled chromium compounds, regardless of the valence state, the amount and location of deposition of chromium will be determined by various factors that influence convection, diffusion, sedimentation, and interception of particles in the airways. Water-soluble chromium compounds have longer retention time in the lungs than other forms. Many studies regarding the gastrointestinal absorption of chromium in humans has suggested that the absorption rate of soluble chromium is higher than insoluble forms. Among the various chromium compounds, the absorption fraction is higher for soluble chromium (VI) compounds than chromium (III). When chromium enters the stomach, Chromium (VI) is reduced to chromium (III) and lowers the absorbed dose. The texture, depth and the condition of the human skin also determine the extent of penetration of Chromium (III) and Chromium (VI). If the skin is damaged, the extent of penetration can be higher. Once chromium is absorbed into the skin, it is distributes itself to all the tissues majorly in the kidney and liver. The human bone is also another major depository for chromium and may lead to a long term deposition of chromium. In the human body, when Chromium (VI) enters the body, it is first reduced to Chromium (III) via the intermediate forms of Chromium (V), Chromium (IV). During the reduction process of Chromium (VI) to Chromium (III), along with reactive intermediates, chromium adducts with proteins, deoxyribonucleic acid (DNA), and secondary free radicals are also formed. In blood, when Chromium (VI) is moved into red blood cells, it undergoes reduction and forms stable complexes with hemoglobin and other intracellular proteins. Some of the other areas which are affected by absorbed chromium include fetuses which can transfer to infants via breast milk. Absorbed chromium is excreted predominantly in urine and can also be eliminated by transfer to hair and nails.

The mechanisms of Chromium toxicity are very complex. The toxicity of the chromium compound is determined by the oxidation state of the chromium atom, where Chromium (VI) is more potent than Chromium (III). The reactive intermediates and oxidation reactions formed during the reduction of Chromium (VI) to Chromium (III) help in mediating the mechanisms for chromium to spread its toxicity. The mechanisms are also partly mediated by Chromium (III), which is finally produced during the reduction of Chromium (VI) and they form harmful complexes with critical target macromolecules. Chromium (III) may also form these toxic complexes with peptides, proteins, and DNA, which result in DNA-protein crosslinks, DNA strand breaks, and alterations in cellular signaling pathways. All these factors contribute to the toxicity and carcinogenicity of chromium compounds. The higher redox potential of Chromium (VI) and the greater ability to enter cells are the two main factors for the high toxic strength of Chromium (VI). Chromium (VI) when compared to Chromium (III) has a different molecular structure which answers the reason why Chromium (VI) has greater cellular uptake. The Chromium (VI) chromate anion has a structure similar to the form of other natural anions such as phosphate and sulfate that are permeable across non-selective membrane channels whereas, Chromium (III), however, forms octahedral complexes which are not permeable through these channels. Hence, the lower toxicity of Chromium (III) can be explained due to the lack penetration through these channels.

Once the Chromium (VI) compound is absorbed into the cells, it is reduced into Chromium (III) and produces Chromium (V) and Chromium (IV) compounds as intermediates. Due to this higher redox potential of Chromium (VI), it has a higher toxic potency than Chromium (III). Some of the compounds like ascorbate, glutathione, or amino acids are commonly involved among these reactions.

Chromium toxic exposure or carcinogenicity is considered to have adverse health effects on the human being. The formation of radicals during the reduction process of Chromium is believed to be responsible for the deleterious effects of chromium on cells, lipid peroxidation, alterations in cellular communication, signaling pathways and cytoskeleton. Oxygen radicals are considered to be a big reason for causing the toxicity of chromium. They support the hypothesis that cellular damage from exposure to chromium compounds can be blocked by radical scavengers.

To sum up the mechanism of chromium toxicity, firstly the byproducts of reduction of Chromium (VI) to Chromium (III) (free radicals, Chromium (V) and (IV)) are mainly responsible for the carcinogenicity in humans and animals. The interactions of these free radicles with the DNA results in structural damage of the DNA, functional damage, and other cellular effects. The results of these chromium induced structural damages include DNA strand breaks, DNA-protein crosslinks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, and chromosomal aberrations. Functional damage includes DNA polymerase arrest, RNA polymerase arrest, mutagenesis, and altered gene expression. However, DNA strand breaks may not be due to free radical formation all the time. They can also be due to the formation of chromium-DNA ternary adducts, which lead to repair errors and collapsed replication forks. In the recent times, studies show that this chromosome instability in the human lung cells due to chromium toxicity is an important mechanism in the development of lung cancers.

Chromium toxicity can be dealt with by reducing peak absorption following exposure, by reducing the body burden and by interfering with mechanisms of action for toxicity. Different methods exist to treat different levels of exposures for chromium. Following an acute inhaling exposure to chromium, the victim should be moved to a fresh air location, should be monitored for respiratory infection or diseases and should be supplied with humid oxygen with assisted ventilation if it is necessary. If more serious damage occurs to the respiratory system (bronchoconstriction, for example), then treatment with oxygen and bronchodilator drugs may be used. The rate of absorption and general absorption of inhaled compounds depend on different factors such as particle size, oxidation state, solubility etc. The absorption of Chromium (III) is poor in the GI tract and when Chromium (VI) is converted in Chromium (III) in the GI, the bioavailability of Chromium (VI) is limited. Hence, the oral toxicity of chromium metal is low. Chromium (VI) compounds are highly corrosive in the intestines which lead to renal, hepatic and neurological effects. At low pH and during increased gastric juice secretion (which happens on eating), the reduction of Chromium (VI) to Chromium (III) in the stomach is significantly improved (De Flora et al. 1987a). That is one reason that the intake of food might help reduce the gastrointestinal absorption of chromium. The better reduction of chromium (VI) at low pH implies that oral dispensation of bicarbonates and antacids should be shunned. Ways to reduce intestinal absorption of chromium include close administration of food, diluting food with water or saline. If the skin is dermally exposed to chromium, it should be thoroughly washed to prevent absorption. Use of the calcium disodium salt of ethylenediamine tetraacetic acid (EDTA), (a chelating agent), has also been recommended after washing with water and application of ascorbic acid (Nadig 1994), especially in cases where the skin has been damaged.

According to research done by the ATSDR, "the reduction of chromium (VI) to chromium (III) inside of cells may be an important mechanism for the toxicity of chromium, whereas reduction of chromium (VI) outside of cells may be a major mechanism of protection". Under physiological conditions, Chromium (VI) can be metabolically reduced by a variety of cellular components. Reduction caused by cysteine or glutathione may head towards creation of all valence states (particularly chromium (V)) and radicals. Changes in the intracellular metabolic pathways that consequence in the reduction of chromium (VI) will affect the nature of the reactive intermediates. An example of this situation can be chelating ligands (such as glutathione) that stabilize chromium (V) as an oxidation state, which causes an increase in its longevity in the cell and the capability to reach DNA in the nucleus

The above paragraphs summarized a brief history of chromium; it's industrial as well as general uses, its general toxicity causes, the specific modes of action or mechanisms and the practices used to curb the toxicity induced my chromium. In conclusion, chromium continues to be of considerable importance due to its toxic effects especially in the industrial setting. Also, exposure to chromium is taken seriously due to its enhanced effects on children through different routes of exposure such as air, water, soil, etc. The most recent update on Chromium (VI) is that it is currently regulated under the 50-micrograms per liter (µg/L) maximum contaminant level (MCL) for total chromium. There are a variety of things a person can do to reduce his/her risk of exposure which include (but not limited to) avoid smoking in general and also in enclosed spaces, testing for chromium levels in drinking water sources, using good hygiene and laundry practices especially for people working in industrial settings and avoiding older pressure treated lumbar. For example, the use of chromated copper arsenate was a big deal until 2003 after which it was banned for use in residential settings.

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