Physiological Responses To Cadmium Poisoning In Plants Biology Essay

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Cadmium is a by-product of the smelting of other metals and occur naturally occur in up to five isotopes that have found applications in radiology. Cadmium is a soft, malleable, ductile, bluish-white transition metal (group 2b) with excellent electrical conductivity. These properties endear the metal to industrial application with inadvertent and subsequent concomitant hazardous occupational exposure. Humans are additionally exposed to cadmium through cigarette smoking and consumption of contaminated food and water. These exposures are exacerbated by the absence of definite taste or odor in the metal, which enhances incidental consumption of the metal from environment. The environmental levels of the metals are magnified by incorporation of atmospheric cadmium salts into acid rain. The rain injects the cadmium into plants and ultimately into the food chain, where it is not essential for life. The metal hexagonal closed packed atomic structure is relatively larger than those in the same category. This characteristic hampers efficient physiological excretion of the metal by kidney, often leading to renal dysfunction. The dysfunction is mediated by the metal in its +2 oxidation state, as a product of conjugation with metallothionein in the kidney. Renal dysfunction due cadmium challenge is irreversible, even after withdrawal exposure to the metal and is unique to cadmium. Environmental pollution by cadmium adversely affects plant by deregulating stomata opening, transpiration, and photosynthesis, affecting physiology performance of the plant. Earth worms and other essential soil organisms are also sensitive to cadmium poisoning and therefore provide biological indications of environmental cadmium pollution. Terrestrial invertebrates are however relatively insensitive to deleterious effects of cadmium, putatively due to effective sequestration mechanisms of the metal in their systems. Interestingly, cadmium has disparate impact on salty and fresh water aquatic ecosystems where organisms in the salty water are counteract the toxicity better than their counterparts in fresh water. The phenomenon can be attributed to molecular competition for metal binding sites between cadmium and metals in the salts in the salty water whereas such competition is minimal in the organisms in the fresh water ecosystems. Despite various advantageous applications of cadmium in industry due to its unique properties, its deleterious effect on environmental health outweighs these benefits. Efforts to further minimize these applications and exposure to cadmium should be explored.

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Cadmium is produced mainly as a by-product from smelting, mining, and refining sulphide ores of primarily zinc, and to a lesser extent, lead and copper. This is because, cadmium minerals do not occur in concentrations and quantities sufficient to justify mining them in their own right (Nordic Council of Ministers, 2003). Cadmium occurring naturally has 8 isotopes. Isotopes 113Cd which has a beta decay and half-life of 7.7 - 1015 years and 116Cd which has two-neutrino double beta decay and half-life of 2.9 - 1019 years, are naturally radioactive. Some of these isotopes that are expected to decay include 114Cd with double beta decay and 106Cd and 108Cd where both have double electron capture; however this has not been confirmed experimentally. The other three isotopes: 110Cd, 111Cd, and 112Cd, are considered to be stable. Cadmium isotopes that do not occur naturally have 109Cd and 115Cd which are the longest lived with a half-life of 462.6 days and 53.46 hours respectively, with the remaining radioactive isotopes having half-lives that are less than 2.5 hours (Audi et al 2003). These stable cadmium isotopes are used for many different purposes and application in radiology: 110Cd is used for the production of the radioisotope In-110; 112 Cd is used in the production of the widely used diagnostic radioisotope In-111; 108Cd is used in the production of: 109Cd which is a calibration source for 88 keV gamma radiation and also in production of even numbered cadmium isotopes: 110Cd, 112Cd and 114Cd which are used to improve the power output and coherence length of Helium-cadmium (HeCd) lasers (www.tracesciences.com).

Cadmium is a soft, malleable, ductile, bluish-white transition metal (group 2b) with excellent electrical conductivity. These properties endear the metal to industrial application where it is used in making of; jewellery, stained glass window, nickel-cadmium rechargeable batteries, some cadmium containing paints, plastics, ceramic ware and even some metal containers. Cadmium is also used in textile work and for metal plating, welding/soldering, smelting and mining. (www.idph.state.il.us; www. Better health). Moreover, municipal solid waste recovery also enhances subsequent concomitant hazardous occupational exposure. However, the three primary sources of human's exposure to cadmium is through cigarette smoking, because cigarettes contain cadmium which is inhaled during smoking (ATSDR, 1997) and consumption of contaminated food such as potatoes, leafy vegetables and cereal grains which are grown in contaminated soils (www.idph.state.il.us) and/or water (ATSDR, 1997). The exposure ability of cadmium is explained by the various sequences of events that it undergoes once it reaches the environment. In air, Cadmium is in form of oxide, chloride, and sulfate, which appear as particles or vapors from areas of high temperature processes. It can be transported long distances in the atmosphere, where it will be deposited either wet or dry onto soils and water surfaces. In soil, Cadmium and its compounds may travel through, but its mobility depends on several factors such as pH and amount of organic matter, which will vary depending on the local environment. Generally, cadmium binds strongly to organic matter where it will be immobile in soil and taken up by plant life, eventually, entering the food supply thus resulting in incidental contamination of food substances. In water, Cadmium exists as the hydrated ion or as ionic complexes with other inorganic or organic substances. Soluble forms migrate in water enhancing contamination of the water with the cadmium heavy metal, where as insoluble forms of cadmium are immobile and will deposit and absorb to sediments and thus enhancing exposure of the cadmium heavy metal to plant and animal life (ATSDR, 1997). These accidental exposures are exacerbated by the absence of definite taste or odor in the metal, which enhances incidental consumption of the metal from environment.

Moreover, foods such as shellfish, mussels, cocoa powder, dried seaweed and animal organs such as kidneys and livers are known to contain higher levels of cadmium than other foods (www.lenntech.coma). Thus consumption of this food leads to deliberate ingestion of the poisonous cadmium metal (www. Better health). The exposure of cadmium is facilitated by its release to the atmosphere through either natural activities such as land and deep sea volcanic activity, river transport, weathering and erosion (WHO, 2000) or by anthropogenic airborne emissions which include fossil fuel combustion, production of iron, steel and non-ferrous metal, waste incineration and cement production (UNEP, 2011). Cadmium taken in which does not enter the body is usually released. That taken in through the lungs or from food and water is breathed out or excreted in feces and urine respectively. Uptake of food that does not contain enough iron or other nutrients may lead to increased uptake of cadmium from food than usual. Cadmium does not enter the body through the skin, without exposure to very high concentrations for long times or exposure to skin that was not damaged (ATSDR, 2008). Inhalation of cadmium either through smoking or working and consumption of cadmium either during eating of contaminated food or drinking of contaminated water has negative human health implications. Breathing air with very high levels of cadmium can severely damage the lungs causing impairment of lung function and may cause death, whereas breathing air with lower levels of cadmium over long periods of time results in a build-up of cadmium in the kidney, and if sufficiently high, may result in kidney disease (ATSDR, 1997), because most of the cadmium that enters your body goes to the kidney and liver and can remain there for many years (ATSDR, 2008). Ingestion of food or water with very high cadmium levels severely irritates the stomach, leading to vomiting and diarrhea, and sometimes results in death, whereas eating lower levels of cadmium over a long period of time can lead to a build-up of cadmium in the kidneys (ATSDR, 1997; Bernard, 2008). This accumulation of cadmium in the vital organs is usually irreversible.

The metal hexagonal closed packed atomic structure is relatively larger than those in the same category, thus hampering efficient physiological excretion of the metal by kidney, often leading to renal dysfunction. Once cadmium is in the body, it is first transported to the liver through the blood. There, it is bond to proteins to form complexes that are transported to the kidneys. The kidney is the critical organ of intoxication after long-term exposure to cadmium where it accumulates damaging filtering mechanisms (www.lenntech.coma). The kidney is the main storage organ of cadmium and also the critical target which is the first organ to display signs of toxicity (Bernard, 2008). Renal dysfunction is mediated by the metal in its +2 oxidation state, since in the kidney, most renal cadmium is bound to a special metal known as metallothionein, forming the Cd+2 ion. This highly toxic ion is the form of poisonous cadmium responsible for renal damage since it avidly reacts with cellular components (Bernard, 2008). The renal dysfunction is manifested in terms of proteinuria, where the amount of proteins excreted by the urine is highly increased and this is caused by an impaired re absorption function of the proximal tubules (Hutchinson, 1987). Proteinuria is considered to be the first sign of tubular dysfunction and is said to occur when renal cortical levels of cadmium reach about 200 parts per million of wet weight compared to normal levels of about 50 parts per million in adults (Fassett, 1975). The most validated protein for routine screening of tubular proteinuria include: β2-microglobulin, retinol-binding protein and alpha1-microglobulin. An increase in the urinary excretion of these proteins found at the early stage of cadmium nephropathy might even be reversible after removal from cadmium. However cadmium toxicity may lead to irreversible tubular dysfunction that may be associated with a lower glomerular filtration rate exposure. In addition, other solutes excreted in greater amounts in the urine as an indication of cadmium nephropathy include; total protein, albumin, amino acids, tubular antigens, glucose, calcium, phosphate and enzymes for example N-acetyl-β-D glucosaminidase. Normally, these proteins are almost completely reabsorbed by the proximal tubular cells, thus a decrease of fractional tubular reabsorption results in increase in urinary excretion (Bernard, 2008).

The most salient toxicological property of cadmium heavy metal is its exceptionally long half-life in the human body (Bernard, 2008). If the levels reach a high enough level, the cadmium in the kidney will cause kidney damage (ATSDR, 1997). Exposure to lower levels of cadmium for a long time can also cause bones to become fragile and break easily (Bernard, 2008). Bone demineralization could be either through direct bone damage or indirectly as a result of renal dysfunction (Bernard, 2008). The latter can be explained by the disturbances of calcium and phosphate metabolism accompanying cadmium nephropathy which may lead to bone demineralization, formation of kidney stones and bone fractures (Bernard, 2008). A good example of bone complication caused by exposure to cadmium is the Itai-Itai disease which was reported in the English literature about by Tsuchiya (1969). It was experienced in Japan in 1960s and was characterized by osteomalacia, roteinuria, and glycosuria. Patients complained of severe bony pain in the back and in the extremities, difficulties in walking and pain on bone pressure (Fassett, 1975; Bernard, 2008). Hence the name Itai-Itai which means Ouch-Ouch in Japanese (Bernard, 2008). It was observed in women who had lived for many years in an area contaminated by mine drainage. The disease had been caused by a greatly increased intake of cadmium and possibly other metals in water and rice, plus a low calcium and Vitamin D intake, stresses of pregnancy and lactation among other factors (Fassett, 1975). For a long time, bone lesions have been regarded as late manifestations of intoxication, occurring only after relatively high exposures in the industry or environment. Effects on the bone, especially at high exposure, are mainly the consequence of cadmium nephropathy, resulting in an altered vitamin D metabolism and a urinary waste of calcium and phosphate (Bernard, 2008).

Other health factors resulting from cadmium toxicity include: reproductive failure/infertility, psychological disorders, damage of the DNA, immune system and central nervous system (Bernard, 2008).However no study has reported signs of hepatic damage either in cadmium workers or among inhabitants of polluted areas. Similarly, there is no report documented of severe effects on the nervous system or the reproductive system caused by occupational or environmental exposure to cadmium (Järup, 1998). Epidemiologic studies assessing the cadmium exposure effects on blood pressure have provided largely inconsistent results (Bernard, 2008) thus, making it difficult to draw any conclusion in regards to cadmium and its influence on blood pressure. Animals exposed to high enough levels of cadmium during pregnancy have shown to result in harmful effects in the young, where the nervous system appears to be the most sensitive target in these newly born, thus the young ones have shown negative effects on behavior and learning. In addition, it could lead to reduced body weights and also affects the skeleton in the developing young. However, it is not known whether cadmium causes birth defects in people. Moreover, infants can also be exposed to cadmium by their mothers through breastfeeding, since cadmium is found in breast milk and the amount of cadmium that can pass to the infant depends on how much exposure the mother may have had (ATSDR, 1997).

Cadmium is a known carcinogen. Lung cancer has been found in some studies of workers exposed to cadmium in the air and studies of rats that breathed in cadmium (ATSDR, 1997). Moreover, there is sufficient evidence to classify cadmium as a human carcinogen. The most convincing evidence comes from the finding of increased risks of lung cancer in workers exposed to cadmium by inhalation as well as from animal. It has been shown that cadmium administered by various routes can produce cancer at multiple sites, including in the lung. In the industry cadmium exposure has also been linked to prostate and renal cancer but this linkage is much weaker than that for lung cancer. However, the mechanism of cadmium carcinogenesis remains largely unknown. Since the metal is not strongly genotoxic and does not cause direct genetic damage, therefore epigenetic mechanisms and/or indirect genotoxic mechanisms that includes blockage of apoptosis, alterations in cell signaling or inhibition of DNA repair might be involved in the cadmium metal carcinogenesis mechanism (Bernard, 2008).

The metal is soluble in acids and thus is most often present in nature as complex oxides, sulphides, and carbonates (UNEP, 2011). The environmental levels of the metals are magnified by incorporation of atmospheric cadmium salts into acid rain. The rain injects the cadmium into plants and ultimately into the food chain, where it is not essential for life. Soils that are acidified facilitate the cadmium uptake by plants and this is a potential danger to herbivores, since cadmium can accumulate in their bodies, especially when they eat multiple plants. For example, cows may end up with large amounts of cadmium in their kidneys (www.lenntech.coma). In addition, agricultural application of fertilizers, for example artificial phosphate fertilizers and cadmium waste water streams from industries and domestic use, usually result in cadmium ending up in the soil and even in surface water. Cadmium can be transported over great distances when it is absorbed by sludge, leading to pollution of surface water as well as soil. Hence cadmium affects several ecosystems. Cadmium strongly adsorbs to organic matter in soils (www.lenntech.comb). Experimental procedures indicate that, environmental pollution by cadmium adversely affects plant by deregulating stomata opening, transpiration, and photosynthesis, affecting physiology performance of the plant. The metal is taken up into plants more readily from nutrient solutions than from soil. However, no field effect of the same has been reported (Nordic Council of Ministers, 2003). Moreover, cadmium has been identified as the most potent causative agent for reduction of leaf litter decomposition.

Earth worms and other essential soil organisms are extremely susceptive to cadmium poisoning and therefore provide biological indications of environmental cadmium pollution. They can die on exposure of very low concentrations and this has negative consequences for the soil structure. High cadmium concentrations in soils can influence soil processes of micro organisms and threat the whole soil ecosystem (www.lenntech.comb).Terrestrial invertebrates are however relatively insensitive to deleterious effects of cadmium, putatively due to effective sequestration mechanisms in specific organs. However, terrestrial snails are affected by sub lethal levels of cadmium and the main effect is on food consumption and dormancy, but only at very high dose levels (Nordic Council of Ministers, 2003). In aquatic ecosystems, cadmium can bio accumulates in mussels, oysters, shrimps, lobsters and fish. Interestingly cadmium susceptibility can vary greatly between aquatic organisms where, salt-water organisms are known to be more resistant to cadmium poisoning than freshwater organisms (www.lenntech.comb), because high calcium concentrations in the water protect fish from cadmium uptake by competing at uptake sites (Nordic Council of Ministers, 2003). However, zinc increases the toxicity of cadmium to aquatic invertebrates. The most susceptible life-stages are the embryo and early larva while eggs are the least susceptible. (Nordic Council of Ministers, 2003).

Despite various advantageous applications of cadmium in industry due to its unique properties, its deleterious effect on environmental health outweighs these benefits. Therefore, efforts to further minimize these applications and exposure to cadmium should be explored. There are various ways one can adopt to prevent exposure of this hazardous metal. Tobacco smokers are advised to stop smoking since cadmium accumulates in tobacco leaves resulting to the mean cadmium level to increase from the normal (0.47 μg/L) to 1.58 μg/L in adults. To avoid accidental consumption of cadmium one needs to; check and obey local fishing advisories before consuming fish or shellfish from local waterways, ensure a balanced diet that includes enough calcium, iron, protein, and zinc which will help reduce the amount of cadmium that may be absorbed into the body from food or drink, employ water filters that remove cadmium, as well as lead and other metals in case a water well is suspected to contain cadmium (ATSDR, 2008). Proper disposal of cadmium containing products for example, the nickel-cadmium battery, is important and should not be disposed as municipal waste. It has been observed that traditional waste disposal by burning rubbish in the garden in the Pacific region also hampers efforts to reduce exposure to toxic fumes from plastics and metals containing cadmium (UNEP, 2011). Actually it is preferred to recycle old batteries when possible. Workers can prevent occupational exposure through personal protective equipment, good industrial hygiene practices and reduction of cadmium emissions. In addition, good hygiene practices such as bathing and changing clothes before returning home may help reduce the cadmium transported from the job to the home (ATSDR, 1997). Moreover, many electronic products such as laptops and cell phones have moved away from Nickel Cadmium to Nickel metal hydride batteries or Lithium-ion batteries in recent years and over time a corresponding decline in the amount of cadmium in the waste stream may be seen (UNEP, 2011).

In case one suspects exposure to cadmium metal, it is important to confirm this so as to prevent further cadmium accumulation. This can be done by conduction of various tests: Chronic cadmium poisoning can be diagnosed basically by relying on the screening of proximal tubular dysfunction on patients and the assessment of the cumulative exposure to cadmium using environmental or biological indicators (Bernard, 2008). Urine test is primarily employed since earliest manifestation of cadmium nephropathy consists in an increased urinary excretion of micro proteins. These proteins: β2-microglobulin, retinol-binding protein and alpha1-microglobulin, are usually measured in untimed urine samples and the results are expressed per gram creatinine to adjust for variations in diuresis (Bernard, 2008). β2-microglobulin and retinol-binding protein are stable, specific and as sensitive, whereas alpha1-microglobulin is very stable in urine but because of its larger size it is less specific of tubular damage (Bernard, 2008). Blood test can also be conducted, where amount of cadmium in blood can be detected. Test for cadmium levels in nail and hair are not as useful as an indication of when or how much cadmium one may have taken in, partly because cadmium from outside the body may attach to the hair or nails giving a false high positive. However, there are tests available to measure the amount of cadmium inside the liver and kidneys (ATSDR, 1997).

CONCLUSION

Renal dysfunction due to cadmium challenge is irreversible, thus, even after cessation of exposure, renal dysfunction and pulmonary impairment may progress. This phenomenon is unique to cadmium toxicity only. Moreover, chronic cadmium poisoning has no efficient treatment. The only possible intervention measure is removal of cadmium from exposure. This implies that, in health surveillance programmes, the emphasis must be placed on primary prevention in order to maintain the levels of cadmium in the environment or in the food chain as low as possible (Bernard, 2004).

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