Research Paper on Exposure Routes and Health Effects of Heavy Metals on Children

Abstract

Heavy metals are naturally existing elements that have relatively high atomic weight and a minimum density 5 times the density of water. They have extensive applications in industries, homes, agriculture, medicine, and technology, which cause their high distribution in the environment. Consequently, this increases human health concerns. Most Heavy metalss are highly toxic. As a result, they adversely impact on human health once they get into the body. More important, heavy metals implications on children health offers even a greater challenge. These elements harmful consequences on children health include mental retardation, neurocognitive disorders such as impaired memory and IQ, behavioral disorders, respiratory problems, cancer, and cardiovascular diseases. Because of their high toxicity potential, mercury (Hg), lead (Pb), chromium (Cr), cadmium (Cd), and barium (Ba) are of an urgent significance to public health. This review, therefore, examines their potential routes of exposure, negative health effects on children, and mechanism of toxicity.

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Introduction

Heavy metalss refer to metals with relatively high densities, atomic numbers or atomic weights. Heavy metalss include mercury (Hg), lead (Pb), chromium (Cr), cadmium (Cd), barium (Ba), aluminum (Al), and copper (Cu). There has been increase in environmental and public health concerns because of ecological contamination by Heavy metalss in recent times. Human exposure to these metals is also on the rise due to their growing applications in manufacturing, farming, homes, and technology (Tchounwou et al., 2012). Though Heavy metalss exist naturally, human activities such as mining smelting, farming, and manufacturing significantly contribute to their release into the environment (Tchounwou et al., 2012). Contamination may also occur because of their corrosion, atmospheric deposition, erosion of their ions, leaching, sediment re-surfacing, and the evaporation of the metals from contaminated water source into the soil and ground water (Tchounwou et al., 2012). Natural events such as volcanic explosions and weathering also contributes significant to environmental contamination (Tchounwou et al., 2012).

Studies indicates elements such as chromium and copper are essential components of diverse biochemical and physical purposes and their insufficient supply cause deficiency diseases or syndromes (Tchounwou et al., 2012). As such, Heavy metalss are either essential or non-essential. Essential metals employ biochemical and physical functions in plants and animals. For instance, copper is essential for hemoglobin formation and carbohydrates metabolism. In excess, however, it causes cellular damage (Tchounwou et al., 2012). Non-essential metals include barium, lead, cadmium, aluminum, and mercury.

Heavy metalss are known to inhibit cellular organelles and mechanisms including cell membrane, mitochondrial, lysosome, endoplasmic reticulum, nuclei, and some enzymes used in metabolism, body purification, and damage reparation (Tchounwou et al., 2012). They also interact with DNA and protein damaging the DNA and causing conformational alterations which may lead to cycle modulation, carcinogenesis, or apoptosis (Tchounwou et al., 2012).

For their high toxicity levels, mercury, lead, chromium, cadmium, and barium pose an urgent challenge to public health. In their part, mercury, lead, chromium, and cadmium are systemic toxicants. These metals are known to cause organ damage even at lower exposure degrees. They are also either classified as "confirmed" or "probable" human carcinogens. Heavy metals poisoning involves diverse mechanics. Each metal has unique characteristics and chemical properties that define its toxicity activities. For some of these elements, there is a lack of an adequate explanation of their taxological mechanisms and actions. Thus, this review examines mercury, lead, chromium, cadmium, and barium potential routes of exposure, negative health effects on children, and mechanism of toxicity.

Exposure and Health Effect of Heavy Metals on Children Health

Mercury Exposure Routes

Mercury exists in three forms: elemental mercury, organic, and inorganic mercury compounds (CDC, 2007). These forms of mercury have different properties, usage, and degree of toxicity. The distribution of mercury into the environment occurs from the natural degassing of the earth's crust (Gerstenberger, Pratt-Shelley, Dinis & Fiuza, 2011). Mercury pollution can also arise because of human activities. Estimates indicates that human activities accounts for thousands of tons of mercury released into the environment (Streets et al., 2017). It exists as mercury vapor in the atmosphere, which is the primary passageway of global transport of the pollutant. While in the atmosphere, it remains unaltered for about one year. After that it changes into a water-soluble form and is returned to the surface of the earth. It is then converted back to mercury vapor or mono-methyl mercury compounds by micro-organisms, mainly bacteria. Mono-methyl mercury enters the aquatic food chain through aquatic organisms (planktons then fish). When human beings eat fish contaminated with mercury, they are too exposed to mercury (Diez et al., 2009; Sagiv, Thurston, Bellinger, Amarasiriwardena, & Korrick, 2012). Therefore, exposure in human beings is primarily dietary (Habiba et al., 2017). Also, mercury entry routes may include eye and skin contact, skin absorption, and inhalation (NIOSH (n.d.).

Mercury Health Effects on Children

The impact of mercury exposure in children can be examined in two dimensions. First, fetal exposure of mercury through mothers' intake of contaminated shellfish and fish has been associated with adverse developmental outcomes such as impaired neurological development in children (Kampa & Castanas, 2008; Rice, Walker, Wu, Gillette, & Blough, 2014). Impaired nervous and cognitive development is linked to the neurotoxicity of mercury (Myers et al., 2009). Children exposed to mercury via their mothers have also been found to have low verbal Intelligence Quotient (IQ) scores and suboptimal scores in social development, fine motor skills, and prosocial behavior (Oken & Bellinger, 2008).

Exposure to mercury in children has also been found to lead to mental retardation (Ip, Wong, Ho, Lee, & Wong, 2004; Huang, Law, Li, Yu, & Li, 2014; Mohamed et al., 2015; Mahmud, Huq, & Yahya, 2016; Ye, Leung, & Wong, 2017). According to Liu, McDermott, Lawson, and Aelion (2010), mercury toxicity may also be manifested through growth disorders, epilepsy, excessive salivation, deformity of limbs, chorea, and athetosis, dysarthria, damaged cerebellum, misalignment of the eyes, and primitive reflexes. Furthermore, according to the World Health Organization (2017), inhalation of mercury vapor has been found to lead to impairment of vital body organs such as the kidneys, the lungs, digestive and immune systems, and the nervous system. Mercury exposure has also been reported to cause eye and skin corrosion as well as to lead to neurocognitive disorders. Examples of neurocognitive disorders linked to mercury toxicity include impaired memory (Tang, Wang, & Jia, 2015; Aaseth, Ajsuvakova, Skalny, Skalnaya, & Tinkov, 2018; Kaur, Kaur, Singh, & Bhatti, 2018), insomnia (Zhou et al., 2014; Do et al., 2017; Sun, Hu, Yuan, Zhang, & Lu, 2017), and tremors (World Health Organization, 2017; Calabrese, Iavicoli, Calabrese, Cory-Slechta, & Giordano, 2018).

Mercury poisoning has also been linked to increased cases of type 2 diabetes (Schumacher & Abbott, 2017; Jeon, Ha, & Kim, 2015; Wallin et al., 2017; Jeppesen, Valera, Nielsen, Bjerregaard, & Jorgensen, 2015). According to Schumacher and Abbott (2017), consumption of foods contaminated with mercury cause type 2 diabetes. This is because methylmercury has been found to have detrimental impacts on pancreatic beta (v) cell development and function. Impaired pancreas functioning has been reported to lead to hyperglycemia and insulin resistance which eventually lead to diabetes. On the other hand, Jeon et al. (2015) reported that mercury poisoning leads to oxidative stress which results in the death of the pancreatic beta cells as well as their dysfunctioning. Mercury-stimulated oxidative stress has also been established to disrupt insulin signaling pathway (Jeon et al., 2015). Moreover, mercury poisoning has been reported to cause cardiorenal metabolic syndrome (Jia, Aroor, Martinez-Lemus, & Sowers, 2015). This is because mercury affects the structure and normal functioning of the mitochondria. Consequently, renal, metabolic, and cardiovascular abnormalities have been found in individuals exposed to mercury (Jia et al., 2015).

Mechanism of Mercury Toxicity

The entry of mercury ions into the body produces toxic impacts through generalized corrosion, inhibition of enzymes, and precipitation of proteins. Mercury ions bind proteins with different groups including amine, amide, carboxyl, and phosphoryl. Proteins made up of these groups have a high susceptibility to mercury reaction. After binding with mercury, these proteins become inactive. Mercury toxicity depends on its oxidative state and chemical form. For instance, elemental Hg is highly soluble in lipids. Hence, it readily crosses the plasma membranes. In its divalent oxidized state, Hg is more toxic than in the monovalent state. Additionally, organic forms of mercury have higher absorption rates (90%) than inorganic forms (10%). Because of this, organic compounds of mercury have greater corrosive impacts on the gastrointestinal mucosa (Broussard, Hammett-Stabler, Winecker, & Ropero-Miller, 2002).

Lead

Exposure Routes

According to the World Health Organization (2018), the primary routes of exposure of lead include ingestion of lead-contaminated substances and inhalation of lead particles given out by burning lead-containing materials. The target organs of mercury toxicity include bones, kidney, liver, and central nervous system (World Health Organization, 2018). Lead is primarily stored in the bones and teeth and undergoes accumulation over time.

Impacts on Health

The negative impact of lead on human health occurs when the concentration of lead in the blood exceeds 10 mg/dL (Lanphear et al., 2005). Lead exposure above this limit has been linked to lowered intelligence in children. For instance, in a study conducted by Rodrigues et al. (2016) to determine the relationship between environmental exposure to lead and neurodevelopmental impacts among Bangladeshi children, children exposed to high levels of lead were found to have lower cognitive scores on the the Bayley Scales of Infant and Toddler Development, Third Edition (BSID-III). Similarly, Hong et al. (2015) found out that exposure to low levels of lead negatively affects intelligence as well as increased impulsivity in school-age children. The adverse impact of lead exposure on children intelligence has been poor academic performance among children exposed to lead (Skerfving, Lofmark, Lundh, Mikoczy, & Stromberg, 2015). More specifically, Skerfving et al. (2015) found out that exposure to lead was negatively associated with school performance. The highest negative impact of lead on academic achievement was found in lead blood levels of 50 mg/L than for higher levels (Skerfving et al.,...