**2. Occurrence, exposure to cadmium, arsenic, lead, and mercury (CALM)**

## **2.1 Heavy metals**

Heavy metals, such as CALM, have received attention as both environmental contaminants and potential toxicological hazards due to their ubiquitous distribution in the environment. Although they are normally present in the environment at ultralow concentrations (e.g., ng/L–μg/L), they have the tendency to bio-accumulate in the different environmental compartments (e.g., soil, water, air), including body tissues and organs [18]. For instance, these toxicants affect the chemical synaptic transmission in the brain and the peripheral and central nervous system [19, 20]. CALM cations are known to disrupt the brain functioning system and may interfere with the cellular calcium (Ca) levels, leading to severe impairment of many body functions and metabolic pathways. Similarly, the interference with Ca levels in the brain often leads to the impairment of cognitive development and, in extreme cases, degenerative central nervous system (CNS) diseases [19, 20]. Toxic metals have also been found to affect cellular transfer and levels of other important minerals and nutrients that have significant neurological and health effects such as magnesium (Mg), lithium (Li), zinc (Zn), iron (Fe), and vitamins B-6 & B1-12 [19, 21]. Against this background, heavy metals, particularly the CALM species, must be monitored in dietary constituents, especially in drinking water.

### **2.2 Cadmium**

Cadmium (Cd) occurs naturally in ores together with zinc (Zn), lead (Pb), and copper (Cu). Cd-containing products and waste are rarely recycled, but frequently dumped together with other household waste, contaminating the environment caused by leaching residual Cd, especially if the waste is incinerated [22]. Natural and anthropogenic sources of Cd, which may include industrial and landfill emissions, application of Cd-bearing fertilizers and Cd-containing sewage sludge and/or biosolids to farmland, may lead to contamination of soils and groundwater and, in severe instances, promote Cd uptake by farm crops intended for human consumption [23]. Food is, so far, the most identified route of exposure to humanity [24]. It is present in most foodstuffs, but concentrations vary considerably, and individual intake also varies considerably due to the differences in dietary habits [25]. For instance, women have lower daily Cd intakes because of comparatively lower energy consumption and/or requirements than men.

Gastrointestinal absorption of Cd may be influenced by nutritional factors, such as iron (Fe) levels in the body [26]. Therefore, exposure to Cd may cause kidney damage [25]. In contrast, long-term exposure may cause skeletal damage, as first reported in Japan, where the itai-itai (ouch-ouch) disease (i.e., a combination of osteomalacia and osteoporosis) was discovered in the 1950s [27]. In recent years, new data have emerged suggesting that even low Cd exposure may also result in skeletal damage as well. Such conditions are evidenced and characterized by low bone mineral density (osteoporosis) and vulnerability to fractures [28]. Until recently, the International Agency for Research on Cancer (IARC) classified and included Cd in a list of human carcinogens (group I) [10–12].

Although sources of Cd pollution in drinking water are widespread, several other pollution routes are emerging such as from corrosion of old-generation galvanized pipes, erosion of natural deposits, discharge from metal refineries, and from waste batteries and paints.

#### **2.3 Arsenic**

Arsenic (As) is a widely distributed metalloid occurring in rocks, soils, water, and air [29, 30]. It occurs naturally in three forms: organic, inorganic, and arsine gas. The inorganic form is highly soluble in water (i.e., hydrophilic), and this explains its presence and persistence in several water bodies, predominantly in groundwater as previously discovered in As-impacted terrains such as in Bangladesh, Canada, China, and Japan [31]. The main toxic As forms found in water are the tri- and pentavalent inorganic forms: arsenite (As3+) and arsenate (As5+), with As5+ being comparatively toxic. The implication is that overreliance on groundwater abstraction for potable water, as is the case in developing countries such as Botswana, may constitute a health risk unless otherwise cleared of As contamination.

Regarding organic As (i.e., organoarsenic species), several As-bearing organic compounds have been identified, such as trimethylarsine, arsenobetaine, arsenocholine, etc. and are of varying toxicity. For example, arsenobetaine and arsenocholine are found in most seafood and fish. They are of no known toxicologic relevance because they are not fully metabolized in the body but excreted as intact species [32]. Arsenic toxicity is related to its within-body metabolism and bioaccumulation in the blood and tissues [31]. This explains why the primary route of exposure is ingesting contaminated potable water and food [33]. Beside ingestion, other potential routes of exposure include inhalation of contaminated air (i.e., atmospheric pollution from gaseous As emissions), smelting of nonferrous metals, and producing energy from fossil fuel. So far, smelting activities are the largest single anthropogenic source of atmospheric pollution [34], as has been a health concern in Selibe Phikwe, Botswana, regarding the recently decommissioned Cu-Ni smelter.

As is undoubtedly a systemic toxicant known to cause cardiovascular diseases, neurological disorders, diabetes, gastrointestinal, and renal disorders. Moreover, chronic As exposure has been associated with various cancers (bladder, kidney, skin, and liver) [10–12]. The adverse health effects are related to the speciation of As, where inorganic arsenic is more toxic than organic arsenic. Inorganic arsenic is acutely toxic, and intake of large quantities leads to gastrointestinal symptoms, severe cardiovascular and central nervous system disturbances, and eventually death. In survivors, bone marrow depression, hemolysis, hepatomegaly, melanosis, polyneuropathy, and encephalopathy are widespread [33]. Populations exposed to As impacted drinking water are at risk of lung, bladder, and kidney cancer mortality, with risk directly proportional to exposure [35]. Skin cancer and other skin lesions, such as hyperkeratosis and pigmentation changes, are also a health concern [36, 37]. More recently, evaluations of as exposure from drinking water have been linked to cancer of the lungs, kidney, bladder, and skin, and in all these cases, there were observable and identifiable precancerous lesions [33].

### **2.4 Lead**

Lead (Pb), occurring in various concentrations in rocks and soils, is one of the most pervasive and persistent heavy metals posing threats to the environment, soil quality, and human health [38, 39]. In the environment, Pb occurs naturally and from human activities such as mining, smelting, production, processing, recycling, waste disposal activities, and emissions from auto exhausts [40]. Six major environmental exposure sources of Pb include leaded paint, leaded petrol, stationary sources, dust/soil, food, and water [41]. In drinking water, the common contamination sources include corrosion of household plumbing systems and erosion of natural deposits [2, 42].

## *Occurrences of Cadmium, Arsenic, Lead, and Mercury in Potable Water in Greater Gaborone… DOI: http://dx.doi.org/10.5772/intechopen.113716*

There is consensus in scientific and medical literature that the primary route of exposure to Pb in children is oral ingestion of Pb-based paint and Pb-contaminated dust and soil. For adults, the primary route of exposure is inhalation of Pb-containing dust and fumes from occupational settings. Pb-contaminated soils are a recognized exposure source for humans. Pb can enter the human body through inhalation [43], geophagia [44], and through skin lesions [45]. Pb in water is another important pathway for exposure, particularly in developing countries, where regulations on Pb containing plumbing materials are limited or nonexistent. At the household level, the sources of Pb contamination are corrosion of household plumbing systems and erosion of natural deposits. As a result, Pb levels in drinking water can vary from one homestead to another due to the variations in plumbing infrastructure [46, 47]. Pb in drinking water is efficiently absorbed by the body compared to other sources. This was confirmed by a study by Heard and others (1983), who found that 40–50% of radioactive Pb is retained and absorbed by the dermal tissues and/or skin [48].

Some short-term effects of exposure to Pb, either through drinking water or any other route of exposure, include persistent fatigue, irritability, temporary loss of appetite, stomach discomfort and/or constipation, reduced attention span, and insomnia [49]. Pb is a neurotoxin; therefore, its main target is the CNS, as observed in adults and children [50] and evidenced by the symptomatic loss of motor coordination, especially in fingers, wrists, and ankles. Other known health effects are that it promotes the onset of anemia due to its strong affinity for the hemoglobin protein in which it readily replaces Fe in the binding sites of the hemoglobin protein inside the red blood cells [51]. The resulting phenomenon of Fe replacement is the elevated levels of blood lead levels [51] and the onset of anemic conditions [49]. Its effects on the excretory system are evidenced by severe damage of the nephron functional units, resulting in renal and/or kidney failure. It also impedes the normal functioning of the reproductive system, as shown by high miscarriage cases among pregnant women. Similarly, it impairs the normal function of sperm production in males [50].

#### **2.5 Mercury**

Mercury is a ubiquitous heavy metal that exists in organic, inorganic, and elemental forms, and the general population is exposed through ingestion and inhalation of Hg-contaminated food, air, and water [14, 52]. Drinking water sources are contaminated by mercury through erosion of natural deposits, discharge from refineries and factories, and runoff from landfills and croplands [52].

Exposure to organic mercury (MeHg) is associated with adverse effects, particularly in children exposed in utero [53]. Other effects include mental retardation and cerebral palsy [54–56]. Acute mercury exposure may give rise to lung damage [57]. Chronic Hg poisoning is characterized by neurological and psychological symptoms, such as tremors, changes in personality, restlessness, anxiety, sleep disturbance, and depression [58]. Metallic mercury may cause kidney damage [59]. Methyl mercury poisoning has a latency of 1 month or longer after acute exposure, and the main symptoms relate to nervous system damage [60, 61].
