Although the mechanisms of cadmium toxicity are poorly understood, it has been speculated that cadmium causes damage to cells primarily through the generation of ROS [ ], which causes single-strand DNA damage and disrupts the synthesis of nucleic acids and proteins [ ]. Studies using two-dimensional gel electrophoresis have shown that several stress response systems are expressed in response to cadmium exposure, including those for heat shock, oxidative stress, stringent response, cold shock, and SOS [ — ]. In vitro studies indicate that cadmium induces cytotoxic effects at the concentrations 0.
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However, cadmium is a weak mutagen when compared with other carcinogenic metals [ ]. Previous reports have indicated that cadmium affects signal transduction pathways; inducing inositol polyphosphate formation, increasing cytosolic free calcium levels in various cell types [ ], and blocking calcium channels [ , ]. Cadmium compounds are classified as human carcinogens by several regulatory agencies. National Toxicology Program have concluded that there is adequate evidence that cadmium is a human carcinogen.
This designation as a human carcinogen is based primarily on repeated findings of an association between occupational cadmium exposure and lung cancer, as well as on very strong rodent data showing the pulmonary system as a target site [ 91 ]. Thus, the lung is the most definitively established site of human carcinogenesis from cadmium exposure. Other target tissues of cadmium carcinogenesis in animals include injection sites, adrenals, testes, and the hemopoietic system [ 91 , , ].
In some studies, occupational or environmental cadmium exposure has also been associated with development of cancers of the prostate, kidney, liver, hematopoietic system and stomach [ , ].
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Carcinogenic metals including arsenic, cadmium, chromium, and nickel have all been associated with DNA damage through base pair mutation, deletion, or oxygen radical attack on DNA [ ]. Animal studies have demonstrated reproductive and teratogenic effects. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood, maternal blood or maternal urine and birth weight and length at birth [ , ].
Chromium compounds are stable in the trivalent [Cr III ] form and occur in nature in this state in ores, such as ferrochromite. The hexavalent [Cr VI ] form is the second-most stable state [ 28 ]. Elemental chromium [Cr 0 ] does not occur naturally.
Chromium enters into various environmental matrices air, water, and soil from a wide variety of natural and anthropogenic sources with the largest release coming from industrial establishments. Industries with the largest contribution to chromium release include metal processing, tannery facilities, chromate production, stainless steel welding, and ferrochrome and chrome pigment production. The increase in the environmental concentrations of chromium has been linked to air and wastewater release of chromium, mainly from metallurgical, refractory, and chemical industries. Chromium released into the environment from anthropogenic activity occurs mainly in the hexavalent form [Cr VI ] [ ].
Hexavalent chromium [Cr VI ] is a toxic industrial pollutant that is classified as human carcinogen by several regulatory and non-regulatory agencies [ — ].
The health hazard associated with exposure to chromium depends on its oxidation state, ranging from the low toxicity of the metal form to the high toxicity of the hexavalent form. All Cr VI -containing compounds were once thought to be man-made, with only Cr III naturally ubiquitous in air, water, soil and biological materials.
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Chromium is widely used in numerous industrial processes and as a result, is a contaminant of many environmental systems [ ]. Commercially chromium compounds are used in industrial welding, chrome plating, dyes and pigments, leather tanning and wood preservation. Chromium is also used as anticorrosive in cooking systems and boilers [ , ]. It is estimated that more than , workers are exposed annually to chromium and chromium-containing compounds in the workplace. In humans and animals, [Cr III ] is an essential nutrient that plays a role in glucose, fat and protein metabolism by potentiating the action of insulin [ 5 ].
However, occupational exposure has been a major concern because of the high risk of Cr-induced diseases in industrial workers occupationally exposed to Cr VI [ ]. Also, the general human population and some wildlife may also be at risk. It is estimated that 33 tons of total Cr are released annually into the environment [ ]. The U. Non-occupational exposure occurs via ingestion of chromium containing food and water whereas occupational exposure occurs via inhalation [ ].
Chromium content in foods varies greatly and depends on the processing and preparation. Present day workers in chromium-related industries can be exposed to chromium concentrations two orders of magnitude higher than the general population [ ]. Even though the principal route of human exposure to chromium is through inhalation, and the lung is the primary target organ, significant human exposure to chromium has also been reported to take place through the skin [ , ].
For example, the widespread incidence of dermatitis noticed among construction workers is attributed to their exposure to chromium present in cement [ ]. Occupational and environmental exposure to Cr VI -containing compounds is known to cause multiorgan toxicity such as renal damage, allergy and asthma, and cancer of the respiratory tract in humans [ 5 , ]. Breathing high levels of chromium VI can cause irritation to the lining of the nose, and nose ulcers.
The main health problems seen in animals following ingestion of chromium VI compounds are irritation and ulcers in the stomach and small intestine, anemia, sperm damage and male reproductive system damage. Chromium III compounds are much less toxic and do not appear to cause these problems. Some individuals are extremely sensitive to chromium VI or chromium III , allergic reactions consisting of severe redness and swelling of the skin have been noted.
An increase in stomach tumors was observed in humans and animals exposed to chromium VI in drinking water.
Accidental or intentional ingestion of extremely high doses of chromium VI compounds by humans has resulted in severe respiratory, cardiovascular, gastrointestinal, hematological, hepatic, renal, and neurological effects as part of the sequelae leading to death or in patients who survived because of medical treatment [ ]. Although the evidence of carcinogenicity of chromium in humans and terrestrial mammals seems strong, the mechanism by which it causes cancer is not completely understood [ ].
Major factors governing the toxicity of chromium compounds are oxidation state and solubility. Cr VI compounds, which are powerful oxidizing agents and thus tend to be irritating and corrosive, appear to be much more toxic systemically than Cr III compounds, given similar amount and solubility [ , ].
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Although the mechanisms of biological interaction are uncertain, the variation in toxicity may be related to the ease with which Cr VI can pass through cell membranes and its subsequent intracellular reduction to reactive intermediates. It can be absorbed by the lung and gastrointestinal tract, and even to a certain extent by intact skin. The reduction of Cr VI is considered as being a detoxification process when it occurs at a distance from the target site for toxic or genotoxic effect while reduction of Cr VI may serve to activate chromium toxicity if it takes place in or near the cell nucleus of target organs [ ].
If Cr VI is reduced to Cr III extracellularly, this form of the metal is not readily transported into cells and so toxicity is not observed. The balance that exists between extracellular Cr VI and intracellular Cr III is what ultimately dictates the amount and rate at which Cr VI can enter cells and impart its toxic effects [ ]. Any of these species could attack DNA, proteins, and membrane lipids, thereby disrupting cellular integrity and functions [ , ]. Studies with animal models have also reported many harmful effects of Cr VI on mammals.
Subcutaneous administration of Cr VI to rats caused severe progressive proteinuria, urea nitrogen and creatinine, as well as elevation in serum alanine aminotransferase activity and hepatic lipid peroxide formation [ ]. Similar studies reported by Gumbleton and Nicholls [ ] found that Cr VI induced renal damage in rats when administered by single sub-cutaneous injections.
Bagchi et al. Adverse health effects induced by Cr VI have also been reported in humans. Epidemiological investigations have reported respiratory cancers in workers occupationally exposed to Cr VI -containing compounds [ , ]. DNA strand breaks in peripheral lymphocytes and lipid peroxidation products in urine observed in chromium-exposed workers also support the evidence of Cr VI -induced toxicity to humans [ , ].
Oxidative damage is considered to be the underlying cause of these genotoxic effects including chromosomal abnormalities [ , ], and DNA strand breaks [ ]. Nevertheless, recent studies indicate a biological relevance of non-oxidative mechanisms in Cr VI carcinogenesis [ ]. The toxicology of Cr VI does not reside with the elemental form.
It varies greatly among a wide variety of very different Cr VI compounds [ ]. Epidemiological evidence strongly points to Cr VI as the agent in carcinogenesis. Solubility and other characteristics of chromium, such as size, crystal modification, surface charge, and the ability to be phagocytized might be important in determining cancer risk [ ]. Studies in our laboratory have indicated that chromium VI is cytotoxic and able to induce DNA damaging effects such as chromosomal abnormalities [ ], DNA strand breaks, DNA fragmentation and oxidative stress in Sprague-Dawley rats and human liver carcinoma cells [ 27 , 28 ].
Recently, our laboratory has also demonstrated that chromium VI induces biochemical, genotoxic and histopathologic effects in liver and kidney of goldfish, carassius auratus [ ]. Various hypotheses have been proposed to explain the carcinogenicity of chromium and its salts, however some inherent difficulties exist when discussing metal carcinogenesis. A metal cannot be classified as carcinogenic per se since its different compounds may have different potencies.
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Because of the multiple chemical exposure in industrial establishments, it is difficult from an epidemiological standpoint to relate the carcinogenic effect to a single compound. Thus, the carcinogenic risk must often be related to a process or to a group of metal compounds rather than to a single substance.
Differences in carcinogenic potential are related not only to different chemical forms of the same metal but also to the particle size of the inhaled aerosol and to physical characteristics of the particle such as surface charge and crystal modification [ ]. Although lead occurs naturally in the environment, anthropogenic activities such as fossil fuels burning, mining, and manufacturing contribute to the release of high concentrations.
Lead has many different industrial, agricultural and domestic applications. It is currently used in the production of lead-acid batteries, ammunitions, metal products solder and pipes , and devices to shield X-rays. An estimated 1. Of that amount, lead-acid batteries production accounted for 83 percent, and the remaining usage covered a range of products such as ammunitions 3.
In recent years, the industrial use of lead has been significantly reduced from paints and ceramic products, caulking, and pipe solder [ ]. Despite this progress, it has been reported that among Lead in dust and soil often re-contaminates cleaned houses [ ] and contributes to elevating blood lead concentrations in children who play on bare, contaminated soil [ ]. Today, the largest source of lead poisoning in children comes from dust and chips from deteriorating lead paint on interior surfaces [ ]. Exposure to lead occurs mainly via inhalation of lead-contaminated dust particles or aerosols, and ingestion of lead-contaminated food, water, and paints [ , ].
Lead absorption is influenced by factors such as age and physiological status. In the human body, the greatest percentage of lead is taken into the kidney, followed by the liver and the other soft tissues such as heart and brain, however, the lead in the skeleton represents the major body fraction [ ].
The nervous system is the most vulnerable target of lead poisoning. Headache, poor attention spam, irritability, loss of memory and dullness are the early symptoms of the effects of lead exposure on the central nervous system [ , ]. Several federal programs implemented by state and local health governments have not only focused on banning lead in gasoline, paint and soldered cans, but have also supported screening programs for lead poisoning in children and lead abatement in housing [ ]. Despite the progress in these programs, human exposure to lead remains a serious health problem [ , ].
Lead is the most systemic toxicant that affects several organs in the body including the kidneys, liver, central nervous system, hematopoetic system, endocrine system, and reproductive system [ ]. Lead exposure usually results from lead in deteriorating household paints, lead in the work place, lead in crystals and ceramic containers that leaches into water and food, lead use in hobbies, and lead use in some traditional medicines and cosmetics [ , ].
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