Open access peer-reviewed chapter
Abstract
In view of the growing threat of trace metals to human health, this work set itself the objective of documenting the toxicity of the trace metals most in contact with humans on human health through food. Thus, this study revealed that organic matter, pH and CEC are the main soil parameters that influence the passage of trace metals from soil to plants. The study also revealed that agriculture, industry and road traffic contribute greatly to the input of trace metals into the environment. Regarding the mechanisms of toxicity, the study showed that chromium VI and copper manifested their toxicity by the formation of free radicals after reduction, those of zinc, nickel, manganese and nickel resulting from the disfunctioning of homeostasis. The study showed that lead caused toxic effects by replacing certain cations such as Ca2+, Mg2+, Fe2+, Na+ which have important functions in the cell. Cadmium expresses its toxicity by binding to albumin, thus altering the homeostasis of metals such as calcium. All these mechanisms have revealed both acute and chronic toxic effects.
Keywords
- trace metal element
- toxicological profile
- toxicity
1. Introduction
The term metallic trace elements or heavy metals denote the elements of the periodic table having densities greater than 5.0 g.cm−3. They contain metals and metalloids [1]. They are naturally present in the environment, but the various industrial revolutions and the exponential progress of heavy industries have led to an increasingly massive release of these pollutants into the environment.
The environment is made up of several compartments, which are the final recipients of these heavy metal discharges. One of these compartments is the soil. Soils are the precursors of food for the majority of the world’s inhabitants; their pollution by these metals therefore presents a threat to human health. Indeed, metallic trace elements can, under certain conditions, pass from soils to crops grown on them.
Among the metallic trace elements most in contact with human food, we can cite lead, cadmium, manganese, chromium, copper, nickel and zinc. Manganese, copper, zinc and nickel are considered as trace elements. However, depending on their concentrations, studies have shown that these trace elements can have different toxicities on human health. Lead, chromium and cadmium are considered strict pollutants because of the harmful effects they can have on human health. Faced with this increasingly growing threat, several questions may arise: What are the soil parameters that influence the penetration of metals into the plants we or animals eat? Once contaminated food is consumed, what health problems are we exposed to?
To provide some answers to these concerns, the main objective of this work is to document the toxicity of the metallic trace elements mentioned above on human health through food. Specifically, it will be a question of recalling the main sources of contamination of these metallic trace elements, showing their behaviour in soils and drawing up their toxicological profiles.
2. Sources of metallic trace elements
2.1 Natural sources
Soil naturally contains metallic trace elements. They are generally in the natural pedogeochemical background (FPGN) resulting solely from the geological and pedological evolution of the soil. This natural pedogeochemical background varies greatly depending on the nature of the rock and the type of soil that has developed there [2, 3]. Other natural phenomena such as wind erosion and volcanic activities can transport metallic trace elements from one soil to another [4]. Indeed, according to Ilyinskaya and al [5], in 2018, emissions from a volcano in Hawaii had concentrations of cadmium, lead, and zinc respectively of 4.10−3 μg.m−3, 2.10−3 μg .m−3, 0.04 μg.m−3. In addition, Ma and al in 2019 [6] showed in volcanic ash, the presence of chromium, copper, lead, zinc and manganese respectively at concentrations of 0.824 mg.kg−1, 0.95 mg. kg−1, 16.16 mg.kg−1, 367 mg.kg−1, 518.6 mg.kg−1.
2.2 Anthropogenic origins of trace metals in soils
The main anthropogenic sources of increased fluxes of heavy metals in soils are urban and industrial discharges as well as agricultural activities [7, 8].
With regard to pollution linked to agricultural activities, inputs of trace metals come mainly from the spreading of NPK and phosphate fertilizers [9]. These types of fertilizers generally provide agricultural soils with cadmium, arsenic, chromium and lead. In addition, the application of certain pesticides, and the use of sewage sludge, untreated industrial wastewater, and landfill compost to amend agricultural plots can be an important source of chromium, molybdenum, lead, zinc, manganese, arsenic, copper, mercury, uranium, and vanadium, copper, nickel, and lead to the soil [1, 10, 11].
Industrial activities such as mineral processing, refining, galvanisation, manufacturing of electric batteries, pigments and plastics are releasing large amounts of trace metals into the environment [13].
In road traffic, the wear of car tyres and exhaust gases are also sources of nickel and zinc emissions, and lead [12, 13, 14].
3. Behaviour of trace metals in soils
In soils, trace metals, depending on their speciation, can have several types of behaviour. Since this study aims to provide information on the toxicology of these metals, we will focus on the behaviour of metals in agricultural soils, which we consider to be the most important source of food for humans.
3.1 Cadmium
Cadmium is a relatively rare element in the earth’s crust, with content of between 0.1 and 1 mg.kg−1 [15]. In soils, the mobility of cadmium is strongly dependent on the pH and organic matter content of the soil. Thus, an acid pH favours cadmium phytoavailability [16], while a high soil organic matter content significantly reduces phytoavailability [17]. Indeed, soil organic matter easily forms complexes with cadmium and thus makes it less available to plants [17, 18]. According to European Union (EU) directives, the limit value for cadmium in soils should be between 1 and 3 mg.kg−1 [19].
3.2 Chromium
Chromium is naturally present in soils. Its content depends on the content of the parent rock in which it is found. Generally speaking, the average content in the earth’s continental crust is 35 mg.kg−1. In soil, the migration and speciation of chromium are influenced by many factors such as the valence state of chromium ions, soil pH, redox potential, soil organic matter and the concentration of manganese dioxide in the soil [20, 21, 22]. The maximum allowable chromium content in agricultural soils is 100 mg.kg−1 [22, 23].
3.3 Copper
Copper is a relatively abundant metal in the earth’s crust. Its presence in the soil is therefore natural but can be enhanced by anthropogenic activities. The concentration of copper in the earth’s crust is between 10 and 100 mg.kg−1 [24]. In soil, the availability of copper to plants depends mainly on pH, cation exchange capacity (CEC), organic matter content, the presence of iron, manganese and aluminium oxides and redox potential [1]. Thus, in neutral or basic soil with a high CEC, copper will be adsorbed to the solid phase of the soil and therefore less available to the plant.
3.4 Manganese
The origin of manganese in soils and plants is mainly from rock decomposition and to a lesser extent from anthropogenic activities. Natural levels of manganese in soils are between 400 and 1500 ppm. In the soil, manganese is moderately mobile, compared to highly fixed elements such as cesium or lead. Its mobility depends on soil characteristics such as pH, cation exchange capacity, organic matter, and especially clay content.
3.5 Nickel
Nickel is naturally present in the soil from the weathering of rocks, which may contain about 0.009%, and from volcanic eruptions [25]. The maximum permissible nickel limit in agricultural soils is 75 mg.kg−1 [19]. Nickel uptake by plant roots is highly dependent on the pH, CEC, soil texture, water content, redox potential, organic matter content, as well as on the concentrations of competing ions such as Ca2+, Cu2+, Mg2+ and Zn2+ [25, 26].
3.6 Plomb
Natural lead levels in the soil range from 5 to 20 mg.kg−1. The maximum lead content in agricultural soils set by the European Union is 300 mg.kg−1. Once in the soil, the behaviour of lead depends on its speciation and also on the characteristics of the soil [27, 28, 29]. As lead is generally very bound to soil colloids, it is one of the least mobile metallic micropollutants in the soil. However, it can accumulate in the roots with little diffusion to other plant organs [30]. Lead can also be delivered directly to plants through the discharge of lead-containing fuel from automobiles. This type of discharge usually occurs when plants (lettuce, cabbage) are grown on the roadside in many African countries.
3.7 Zinc
Zinc is a ubiquitous metal in the earth’s crust. According to Taylor et al. 1964 in Ondo, 2011 [31], the average zinc content of the West African land crust is between 40 and 100 mg.kg−1. In soil, the important factors controlling zinc mobility are clay and organic matter contents and pH. liming, the addition of high clay content soil, iron or phosphorus reduces the transfer of zinc to plants. Thus, clays and organic matter retain zinc, while an acid pH favours its release into the soil solution [24, 32].
4. Toxicological profile of metallic trace elements through dietary intake
4.1 Cadmium
Food is one of the main sources of cadmium exposure [29]. After absorption from the gastrointestinal tract, cadmium is transported into the blood plasma, initially bound to albumin [33, 34]. Albumin-bound cadmium is preferentially absorbed by the liver.
In the liver, cadmium induces the synthesis of metallothionein and a few days after exposure, cadmium bound to metallothionein appears in the blood plasma. Due to the low molecular weight of metallothionein, this protein transports cadmium to the tubules via the glomerulus of the kidney. Cadmium then accumulates in the human kidney throughout life [35, 36, 37]. The accumulation of cadmium in the kidneys leads to the most serious chronic effect of oral cadmium exposure, which is renal toxicity. This critical effect is characterised by tubular proteinuria resulting from renal tubular dysfunction [38]. In addition, the fixation of cadmium to albumin can lead to the disruption of calcium, zinc and iron homeostasis [39]. This lack of stability of calcium, zinc and iron concentration is capable of causing liver damage.
In addition, the disruption of calcium homeostasis due to the decrease in serum parathyroid hormone (PTH) concentration induces the release of calcium from bone tissue [40, 41]. This leads to loss of strength and bone fracture. Also, having the same oxidation states as zinc, cadmium can replace the zinc present in metallothionein (MT), thus preventing this protein from acting as a free radical scavenger in the cell [42].
According to Andujar, et al., 2010 [43], cadmium also has cardiovascular, hematological and hepatic effects. Inaba et al., 2005 [44], showed that cadmium was responsible for Itaï-Itaï disease, which occurred after long exposure to a concentration of up to 1 ppm. All these health effects have led to a very low tolerable daily intake of 0.36 μg.kg−1 is proposed by the National Agency for Food, Environmental and Health Safety [45]. Note that acute cadmium toxicity is very rare and requires very high concentrations.
4.2 Chromium
Depending on its degree of oxidation, chromium can be a trace element or a toxic element. According to Cotte and Duret, 2011 [46], trivalent chromium (III) is implicated in the action of insulin. Although, the human body is highly exposed to chromium through ingestion, a small percentage of ingested chromium enters the body through the digestive tract [47]. In fact, chromium (VI) is more absorbed in the small intestine than chromium (III) because of the structural similarity between chromium VI and sulphates. In humans, the adsorption of chromium III does not exceed 1%, whereas that of chromium VI can be around 10% [48, 49]. Moreover, once absorbed, chromium VI represents the real danger for the human body. It can enter many cells and be reduced by hydrogen peroxide (H2O2), glutathione (GSH) reductase and ascorbic acid to produce reactive intermediates including chromium (V), chromium (IV), thiyl radicals, hydroxyl radicals, which can disrupt cellular functions by attacking DNA, membrane proteins and lipids [50, 51]. This ability to produce oxidants makes chromium VI responsible, according to the French National Institute for Occupational Safety and Health, for gastric corrosion and renal failure [52, 53]. Also, according to the Agency for Toxic Substances and Disease Registry, chromium (VI) is responsible for ulcer and anaemia. These different actions of chromium VI on the body make chromium one of the eight metals present in the top 50 toxic substances in the world [47]. The World Health Organization (WHO) has classified chromium as carcinogenic to humans [54].
4.3 Copper
Copper is an essential element for good health and the proper functioning of certain biological processes [55]. Copper in food can be in monovalent Cu (I) or divalent (Cu (II)) form [56]. The predominantly active copper uptake involves the copper transporter 1 (Ctr1) which is specific for the transport of monovalent copper (CuI) into cells (including gastrointestinal cells). Copper absorption occurs mainly in the small intestine and is likely to be inhibited by transition metals such as iron or zinc [57, 58, 59]. Copper absorbed by the small intestine is transported in the blood by binding mainly to albumin, but also transcuprein [60]. Copper is transported to the liver and can be stored in hepatocytes. Copper present in hepatocytes is mainly linked to metallothionein or transcuprein [61].
Once absorbed into the body, plays a particularly important role in seed production, disease resistance and water regulation in plants [62, 63]. As a result, it participates in various metabolic processes and maintains the functions of organisms. However, the transition of copper from its oxidised to its reduced form can lead to the production of superoxide and hydroxyl radicals which cause damage to the body [60]. Indeed, Myers and al, 1993; Sokol and al 1933 [64, 65] have shown in studies on rats that at high concentrations of copper, these radicals can attack the cell’s membrane lipids. As a result, copper disrupts the total antioxidant capacity of the body [63, 66]. Free radicals from copper reduction also tend to be responsible for amyotrophic lateral sclerosis, which results in progressive muscle paralysis [67].
According to Ellingsen and al, 2015 [68], nausea is the most frequently observed symptom of acute copper toxicity. These authors showed that the minimum concentration that can cause nausea is 4 mg.L−1. In addition, Araya and al, 2007 [69], have shown that acute effects from a single, short-term exposure to copper result in gastrointestinal manifestations.
4.4 Manganese
After ingestion manganese is absorbed in the gastrointestinal (GI) tract by passive diffusion or by active transport by divalent metal transporter 1 (DMT1), which transports other metals such as iron, copper, zinc and calcium [70]. Manganese is then distributed through the bloodstream to the liver, pancreas, bones, kidneys, brain, colon, urinary system and erythrocytes [71]. The amount of manganese absorbed from the gastrointestinal tract in humans is variable, but generally averages around 3–5% [72].
As an essential nutrient, absorbed manganese plays many physiological roles. Manganese is required for the formation of cartilage and healthy bones and for the urea cycle, and also plays a key role in wound healing [73, 74].
However, once absorbed at high concentrations, manganese can exhibit various toxic effects, of which neurotoxicity is a prominent one. Mn neurotoxicity may be associated with the interaction with other essential trace elements, including iron [75, 76, 77]. Indeed, according to the work of Olanow [78], when neurons are exposed to a high concentration of manganese, the cellular regulation of iron by the divalent metal transporter 1 (DMT1) decreases, in favour of that of manganese. This leads to an accumulation of iron in neurons and can consequently produce cellular oxidative stress that leads to neuronal damage [77, 79]. In addition, in studies on rats, Mohammad [80] found a delay in the development of the skeleton and fetal organs in pups born to pregnant rats exposed to manganese by gavage at a dose of 33 mg.kg−1.d−1. Also, Bouabid et al. in 2016 [81], showed that during ingestion of high concentrations of manganese, a decrease in neurological activity was observed in rats.
4.5 Nickel
Once absorbed into the bloodstream, nickel is bound to albumin. It can therefore go to all organs, such as the thyroid and adrenal glands, brain, kidneys, heart, liver, spleen and pancreas [82, 83]. This mobility confers beneficial effects on the body. In humans, nickel is involved in the metabolism of methionine, an amino acid involved in protein synthesis [84].
Although, easily eliminated from the body in faeces and urine, nickel can also have adverse health effects. Indeed, at high concentrations, much of the toxicity of nickel may be associated with its interference with the physiological processes of zinc, calcium and magnesium [85]. Nickel can thus replace magnesium in certain stages of complement activation. For example, replacing nickel with magnesium can increase the formation of the C3b enzyme by 40-fold, which amplifies the activation of the complement pathway [86]. Therefore, various disease states such as myocardial infarction and stroke are associated with altered transport and serum concentrations of nickel [86].
Aleksandra and Urszula in 2011 [87], reported that an accidental ingestion of 570 mg of nickel had caused cardiovascular effects and the death of a child who had 2 years old. It should be noted that the acute toxicity of nickel after oral exposure depends on the chemical form of nickel. For example, a death due to nickel-induced adult respiratory distress syndrome was reported in a worker spraying nickel using a thermal arc process [88]. The death occurred 13 days after a 90-minute exposure to an estimated nickel concentration of 382.1 mg/m3; the total nickel intake was estimated to be nearly one gram. Furthermore, Das et al. in 2002 [89], in a study on rats, demonstrated a decrease in body weight in rats after daily intakes of 8.6 mg.kg−1.d−1 for 91 days. According to some authors [85, 89], gastrointestinal disorders consisting of nausea, abdominal cramps, diarrhoea, and vomiting have been reported in workers who consumed water contaminated with nickel sulphate. To our knowledge, no study has demonstrated a carcinogenic effect of nickel, nor chronic toxicity of nickel on human health.
4.6 Lead
In contrast to manganese or nickel, lead is not a trace element and is well known to be toxic [90]. In general, absorption by ingestion is the predominant route of exposure to lead. After ingestion, lead absorbed from the gastrointestinal tract enters the bloodstream by attaching to red blood cells, which transport it to various tissues or organs in the body [91]. This distribution of Pb in the body is independent of the route of absorption. As it cannot be destroyed in the body, lead accumulates in the bones. In fact, in adults, more than 90% of the lead present in the body is stored in the adult bones, compared with 70% in children. However, certain phenomena such as pregnancy, breastfeeding, menopause and osteoporosis increase the passage of lead from the bones to the blood [92, 93].
The mechanism of lead toxicity is manifested by the ability of this metal to replace cations such as Ca2+, Mg2+, Fe2+ Na + that have important functions in the cell [94, 95]. This disrupts the metabolism of the cell and leads to significant changes in various biological processes such as cell adhesion, intra- and intercellular signalling, protein folding, ion transport, enzyme regulation and neurotransmitter release. Furthermore, this substitution may also affect protein kinase C, which regulates neuronal excitation and memory storage [96]. These phenomena will therefore lead to adverse effects on human health regardless of the age group, even if infants and young children are more at risk [96, 97]. Organic forms are more toxic to humans than inorganic forms of lead. These reach humans through the food chain [93]. The pathologies resulting from lead poisoning are numerous and can be separated into two categories: physiological disorders and neurological disorders [53]. About physiological disorders [98], demonstrated that an average concentration of 29 μg.L−1 caused arterial hypertension in men. Studies have also shown that blood lead concentrations below 100 μg.L−1 are associated with kidney failure [98]. Moreover, according to Robert and et al., in 2004 [99] prolonged exposure to lead can cause sterility or serious problems for the fetus in the case of a pregnant woman. There are numerous studies demonstrating the existence of neurotoxic effects of lead in adults and children. According to Oscar and al, 2017 and Sanders and al, 2009 [53, 101], lead is believed to cause a decrease in intelligence quotient in children. Also, in their studies, Hsiang and Díaz in 2011, [102] showed that this metal was the basis of neurological dysfunctions and neurodegenerative effects. According to the same authors, these disorders generally follow chronic exposure to lead. In addition, other studies have shown disturbances in cognitive and behavioural functions, resulting from changes in the brain caused by lead poisoning [100]. According to these authors, children were more affected by these disorders than adults. Also, lead poisoning leads to lead poisoning, which manifests itself by anaemia, digestive disorders and damage to the nervous system with memory loss and disturbances in cognitive and behavioural functions [103].
4.7 Zinc
The absorption of zinc after ingestion takes place in the central part of the small intestine (jejunum). Zinc is transported by metallothionein from the enterocytes to the blood. In the blood, zinc is bound to albumin which distributes it throughout the body [104]. As an essential element for living beings, it plays a major role in cellular metabolism. It is involved in enzymatic systems either as an integral part of the active site of numerous enzymes or as a cofactor regulating the activity of so-called “zinc-dependent” enzymes [32]. Zinc is therefore an essential micronutrient for human health [105]. This metal is involved in major metabolic pathways through its role in enzyme systems. It is also essential in the structure and function of a large number of macromolecules. It is implicated in gene expression and stabilises the structure of proteins [106]. Zinc also plays a role in cell signalling, hormone release and nerve transmission.
However, at high concentrations of zinc in the body, the concentration of metallothionein increases to regulate zinc. This leads to a decrease in the concentration of certain metals such as copper, whose homeostasis is ensured by metallothionein. This leads to a malfunction in the metabolism of copper, which can have several adverse effects. It is true that the acute toxicity of Zn is found in rare abnormal food conditions (poisoning). According to studies, several cases of gastrointestinal disturbances and diarrhea have been caused by high zinc ingestion [107, 108]. In a study by Samman and Roberts in 1989, and reported by the US Environmental Protection Agency [109] symptoms such as abdominal cramps, vomiting and nausea appeared in 26 of 47 healthy volunteers after six-week ingestion of zinc sulphate tablets, containing 150 mg.kg−1 of elemental zinc, for six weeks.
In addition, Gary in 1990 [110], stated that an ingestion of 1–2 g of zinc sulphate would have resulted in a concentration of nausea and vomiting, epigastric pain, abdominal cramps and diarrhoea (often bloody), while a young boy who ingested 12 g of elemental zinc over two days suffered only lethargy, dizziness, a slight shift in gait and difficulty in writing. These studies also show that the acute effects of zinc also depend on the form of zinc ingested.
In addition, chronic toxicity can manifest itself in bone marrow effects and polyneuropathy due to concomitant copper deficiency. It may also manifest itself as anaemia resulting from the malfunction of copper metabolism. Also, excessive zinc intake over a prolonged period of time increases the risk of prostate cancer and prostate cancer-related mortality [111].
5. Conclusion
The study aimed to document the toxicity of trace metals on human health via the food chain. At the end of this work, we can retain that the trace metals retained in our study have various sources and can all be present in the soil. In the soil, some trace metals are more phytoavailable than others. Also, we can retain that the metals characterized by strict pollutants such as cadmium and lead cause serious damage to health at low concentrations due to their accumulation in the body. Elements and also easily removable, it takes high concentrations to cause more or less significant effects on health.
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