Biomonitoring Of The Toxicity Of Some Heavy Metals In Occupationally Exposed Workers In Uyo Nigeria

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Biomonitoring Of The Toxicity Of Some Heavy Metals In Occupationally Exposed Workers In Uyo Nigeria

INTRODUCTION

Background of study.

Heavy metals pose serious health challenges especially among occupationally exposed workers. Work has it’s positive health promoting effects, as the financial benefits provides the worker with the basic necessities of life. There is however a reciprocal and interactive relationship between the workers and the work environment.

Occupational hazard is the risk, harm or danger that an individual is exposed to at the workplace, whereas occupational diseases result from such exposures to the individual (WHO, 1986). Although these occupational diseases appear less frequently, there is evidence that they affect a considerable number of people particularly in rapidly industrializing countries.

Thousands of toxic chemicals pose serious health hazard, potentially causing cancer, respiratory and skin disease as well as adverse effects on the reproductive function and around 350 chemical substances have been identified as occupational carcinogens (WHO, 2000).

Heavy metals are natural components of the earth’s crust. These elements are the oldest toxins known to humans, having been used for thousands of years. They are group of environmental chemicals which are ubiquitous and non-biodegradable. Many different definitions of heavy metals have been proposed. One of such definitions entails that heavy metals are defined as metallic elements that have a relatively high density compared to water (Fergusson, 1990). Due to increase in automobiles and urbanization in towns and cities in the world, there is an exponential increase in exposure to toxicants which include heavy metals, solvents and vehicles exhaust, gasoline, paints, dust and silica exposure from sundry, sand blasting etc. Heavy metals are significant environmental pollutants and their toxicity is a problem of increasing significance for ecological, evolutionally, nutritional and environmental reasons (Jaishankar, Mathew, Shah, & Gowda, 2014; Nagajyoti , Lee, & Sreekanth, 2010).

These metals are essential to maintain various biochemical and physiological functions in living organism, when in very low concentrations; however they become noxious when they exceed certain threshold concentrations. Although these metals have crucial biological functions in plants and animals, sometimes their chemical coordination and oxidation-reduction properties have given them an additional benefit so that they can escape control mechanisms such as homeostasis, transport, compartmentalization and binding to required cell constituents. They displace original metals from their binding sites causing malfunctioning of cells and ultimately toxicity. Previous research has found that oxidative deterioration of biological macromolecules is primarily due to binding of heavy metals to the DNA and nuclear proteins (Flora, Mittal & Mehta, 2008).

Among workers occupationally exposed to heavy metals include: automobile technicians otherwise known as mechanics. They are made up of spray painters, welders, panel beaters and brake and clutch liners etc. Those in the automobile repairs industry constitute a significant number of those practicing vocational trade in Nigeria (Anyadike, Emeh, & Ukah, 2012). One of the many hazardous habits automobile technicians engage in include sucking of fuel (Oluwagbemi,

2007; Anetor, Babalola, Adeniyi, & Akingbola, 2002; Landrigan, 1989); washing of hands and vehicle parts with gasoline (Oluwagbeni, 2007; Udonwa, Uko, Ikpeme, Ibanga & Okon, 2009) and applying diesel to bruised body parts (Omokhodion, 1999).

TOXICITY MECHANISMS OF HEAVY METALS AND IT’S INDUCED DISEASE PATHOPHYSIOLOGY.

Although several heavy metals, including copper (Cu) and zinc (Zn), serve as enzymes that are essential for intracellular processes and have DNA-binding domains, almost all heavy metals induce various cancers and diseases (Fergusson, 1990; Stern, 2010; Hambidge & Kreb, 2007). Oxidative stress caused by reactive oxygen species (ROS) is a well-known mechanism of heavy metal-induced damages (Bánfalvi, 2011). Despite such serious toxicity, heavy metals are utilized in various industrial products. They are found in batteries, paints, and vehicle emissions. Furthermore, heavy metals are used in pigments that are then used in consumer products like children’s jewelry and toys (Finch, Hillyer, & Leopold, 2015). Electronic waste from heavy metal-containing batteries is an important source of heavy metal contamination in the environment through erosion by rain and groundwater flow to soil, rivers and the sea (Worsztynowicz & Miller,1995). Dissolved forms of toxic heavy metals can be magnified via circulation in the bio-system, including the food chain, and finally end up in very high concentrations in humans ( Bánfalvi, 2011; Tchounwou, Yedjou, Patlolla, & Sutton, 2012).

Arsenic (As), cadmium (Cd), chromium (Cr), and nickel (Ni) are category 1 heavy metals according to the International Agency for Research on Cancer (IARC, 2012). Various reports have found that exposure to these compounds leads to disruptions in tumor suppressor gene expression, damage repair processes, and enzymatic activities concerned in metabolism via oxidative damage (Ercal, Gurer-Orhan & Aykin-Burns, 2001; Bánfalvi G, 2011). Some studies have indicated that the risk of heavy metal exposure is interrelated with the contamination source (Harvey, Handley & Taylor, 2015; Gul, Shah, Khan, Khattak, & Muhammad, 2015). For example, recent studies found an increased risk of occupational disease and cancer in workers in heavy metal-using industrial areas (Grimsrud & Anderson, 2012; Grimsrud, Berge, Martinsen, & Anderson, 2003).

MERCURY

CADMIUM ALUMINUM

ARSENIC

APOPTOSIS

IRON NICKEL

CHROMIUM LEAD

The attack of heavy metals on a cell and the balance between

ROS production and the subsequent defense presented by antioxidants.

The attack of heavy metals on a cell and the balance between

ROS production and the subsequent defense presented by antioxidants.

Production of ROS
O2., OH, NO., RO.,

ONOO., H2O2

Resulting in

oxidative stress

SOD, GSH, GST,

CATALASE

Defense by anti oxidants

CADMIUM (Cd)

SOURCES AND ROUTE OF EXPOSURE.

Cadmium is rare in the natural environment. It generally comes from environmental pollution from industrial and agricultural waste. Cadmium poisoning is an occupational hazard associated with industrial processes such as metal plating, production of nickel-cadmium batteries, pigments, plastics, and other synthetics. In addition, it is a component of paint for car spraying, plastic products, acrylic colors, and watercolor pigments (Kawasaki, Kono, Dote, Usuda, Shimizu, and Dote, 2004).

In agriculture, some fertilizers which contain Cd cause an increase of Cd concentration in the soil, and farmland near industrial areas becomes contaminated. The main sources of exposure to cadmium are specific professional atmospheres, diet, drinking water, and tobacco. The primary route of exposure in industrial settings is inhalation of cadmium-containing fumes which can result initially in metal fume fever but may progress to clinical pneumonitis, pulmonary edema, and death. Cadmium possessing a long biological half-life (17–30 years) in humans accumulates primarily in liver and kidney (Shimada, Yasutake, & Hirashima, 2008). This long half-life of Cd is mainly due to its low ratio of excretion and its continued accumulation in the organism.

MECHANISM OF TOXICITY AND PATHOPHYSIOLOGY.

The main mechanism of toxicity of cadmium is by oxidative stress. Cd2+ being a non-redox-active metal cannot initiate by itself the Fenton reactions. However, it may generate non-radical hydrogen peroxide, which may become a source of free radical via the Fenton reaction. It therefore induces oxidative stress through indirect processes. Some of the mechanisms through which Cd induces the formation of ROS include the following:

(1) Decrease in the intracellular GSH content,

(2) Cd combines with thiol groups of enzymes involved in antioxidant mechanisms, such as SOD, glutathione peroxidase (GPx), and catalase, and inhibits their activities ,

(3) Cd forms cadmium-selenium complexes in the active centre of GPx and inhibits the enzyme activity, and

(4) Cd inhibits complex III of the mitochondrial electronic transport chain and increases production of ROS which may damage mitochondrial membrane and trigger onset of apoptosis.

These cadmium induced oxidative stress are possibly involved in causing DNA damage / mutations, oxidation of proteins and lipid peroxidation , which may cause alterations in lipid composition of cellular membranes and functions.

Oxidative stress following Cd exposure accelerates transcriptional activity of the metallothionein (MT) coding gene (Andrews, 2000). MT is a ubiquitous protein in most organs. It can form a complex with metal elements such as Cd. When chronic Cd exposure occurs, a complex form of Cd and MT called Cd-MT is found, especially in the kidney. It accumulates in tubules via a reuptake process and causes conformational change of renal tubular cell as well as degradation of glomerular cell function. These functional problems disrupt calcium metabolism and augment the calcium load in the kidney, thereby resulting in an increase of kidney stones and cancer. Moreover, disruption of calcium metabolism causes bone damage (Nordberg, Goyer, & Nordberg, 1975).

Taking into account the effect of Cd on the central nervous system (CNS) and endocrine system, it is currently classified as an endocrine/neuroendocrine disruptor (Henson & Chedrese, 2004; Retto, deQueiroz, & Waissmann, 2006). It disrupts the ovarian steroidogenic pathway, production of progesterone and testosterone, and mimics endogenous estrogen, thus increasing the risk of ovarian cancer and breast cancer (Yang, Kim, Weon, & Seo, 2015)

Clinical Symptoms.

People chronically exposed to cadmium have headache, sleep disorders, and memory deficits. These diseases are related to alterations in neurotransmitters (GABA, serotonin) by altering GABAergic and serotoninergic systems. Other symptoms include increased salivation, choking, throat dryness, cough, chest pain, restlessness, irritability, nausea, vomiting, kidney dysfunction (glucosuria, proteinuria, and aminoaciduria), itai-itai disease, and renal and hepatic failures. Pulmonary involvement includes pneumonitis, edema, and bronchopneumonia. Permanent lung damage and cardiovascular collapse may occur. Lung and prostate are the primary targets for the Cd induced cancer.

Values of cadmium toxicity (Flora et al., 2008).

Cadmium toxicity
Decreases the concentration of copper in liver and plasma and also reduces the concentration of ceruloplasmin in plasma
Cadmium disturbs zinc metabolism, inhibits the enzymes containing Zn, competes for gastrointestinal absorption and replaces zinc present in metallothionein
Interacts with iron and decreases the hemoglobin and hematocrit concentration, leads to anemia
Cadmium interacts with calcium and leads to osteoporosis, cadmium deposition in bones, hypercalciuria
Cadmium causes a disruption of neuroendocrine hormones. This gives it a significant role in cancer development.
Oxidation of proteins and lipid preoxidation, leading to alteration in cell membrane composition and functions.

LEAD (Pb)

Lead (Pb) is another ubiquitous toxic metal detectable practically in all phases of the inert environment and biological systems (Qureshi N et al., 2012). Lead is frequently used in the production of batteries, metal products (solder and pipes), ammunition, and devices to shield X-rays leading to its exposure to the people working in these industries. Use of lead in gasoline, paints, ceramic products and pipe solder has been dramatically reduced in recent years because of health concerns. Ingestion of contaminated food and drinking water is the most common source of lead exposure in humans. Exposure can also occur via inadvertent ingestion of contaminated soil/dust or lead-based paint. Lead poisoning (also known as saturnism, plumbism, Devon colic, or painter’s colic) is a medical condition caused by increased

LEAD (pb)

SOURCES AND ROUTE OF EXPOSURE.

Lead (Pb) is another ubiquitous toxic metal detectable practically in all phases of the inert environment and biological systems (Qureshi & Sharma, 2012). Lead is frequently used in the production of batteries, metal products (solder and pipes), ammunition, and devices to shield X-rays leading to its exposure to the people working in these industries. Use of lead in gasoline, paints and ceramic products and pipe solder has been dramatically reduced in recent years because of health concerns. Ingestion of contaminated food and drinking water is the most common source of lead exposure in humans. Exposure can also occur via ingestion of contaminated soil/dust or lead-based paint. Lead poisoning (also known as saturnism, plumbism, Devon colic, or painter’s colic) is a medical condition caused by increased levels of lead in the blood (Heard, 2014). Young children are particularly vulnerable because they absorb 4-5 times as much ingested lead as adults from a given source ( Lanphear. Hornung, Khoury, Yolton, Baghurst, and Bellinger, 2005).

TOXICITY AND PATHOPHYSIOLOGY.

The Centers for Disease Control and Prevention (CDC) and others state that a blood lead level (BLL) of 10?g/dL or above is a cause for concern (Jones, Homa & Meyer, 2009; CDC, 2012). However, lead can impair development of animals even at BLLs below 10 ?g/dL (Lanphear, Dietrich, Auinger & Cox, 2000). After exceeding this safe concentration limit, lead can induce a broad range of physiological, biochemical, and behavioral dysfunctions in humans and laboratory animals including peripheral and CNS, haemopoietic , cardiovascular , kidney, liver, and reproductive systems of males and females. It has been shown to cause permanently reduced cognitive capacity (intelligence) in children (Lockith, 1993). This neurotoxicity was later found to be associated with lead-induced production of reactive oxygen specie.

Since lead has no known physiologically relevant role in the body, its toxicity comes from its ability to mimic other biologically important metals, most notably calcium, iron, and zinc which act as cofactors in many enzymatic reactions. Lead is able to bind to and interact with many of the same enzymes as these metals but, due to its differing chemistry, does not properly function as a cofactor, thus interfering with the enzyme’s ability to catalyze its normal reaction(s). The following are mechanisms of lead induced toxicity:

Production of reactive oxygen species. Due to the ability of lead to produce ROS, it causes oxidative stress via the following; damage to cell membrane and DNA, enzymatic damage (catalase, SOD, GPx, and glucose-6-phosphate dehydrogenase (G6PD) and damage to pool of nonenzymatic antioxidant molecules such as thiols including GSH of animals and human systems.
Lead-Induced Perturbations in Hematological Indices.
Lead has multiple hematological effects. In lead-induced anemia, the anemia results from two basic defects: Shortened erythrocyte life span: the shortened life span of the red blood cells is due to the increased mechanical fragility of the cell membrane.

Impairment of heme synthesis: In the heme biosynthesis pathway, the enzymes are a target of the toxic effect of metals. Among these, delta-aminolevulinic acid dehydrate (ALAD), which catalyses the conversion of two molecules of ?aminolevulinic acid (ALA) into one molecule of porphobilinogen (PBG) at the second step of heme biosynthesis pathway, represents one of the most sensitive sites of inhibition of heme biosynthesis by lead. The lead poisoning causes an increase in ALA in the circulation in the absence of an increase in porphobilinogen. The accumulation of ALA has been shown to be involved in lead-induced oxidative damage by causing formation of ROS.

Influence of Lead on Divalent Metals Working as Cofactors and Their Binding Sites. . Lead has ability to cross the blood-brain barrier (BBB) and to substitute for calcium ions. It interferes with the regulatory action of calcium on brain cells functions and disrupts many intracellular biological activities. Brain homeostatic mechanisms are disrupted by exposure to higher levels of lead. The final pathway appears to be a breakdown in BBB.
Neurotoxicity of Lead. Lead as a systemic toxicant is a neurotoxin that has been linked to visual deterioration, central and peripheral nervous system disorders, (Bressler, Kim, Chakraborit & Goldsten, 1999), renal dysfunction (Damek-Poprawa & Sawicha-Kapusta, 2004), and hypertensive cardiovascular disease (Khalil-Manesh, Gonick, Weiler, Prins, Weber and Purdy, 1993). Khalil-Manesh et al (1993) have presented the interplay of reactive oxygen species and nitric oxide in the pathogenesis of experimental lead-induced hypertension pointing out towards the role of oxidative stress (OS) as a major mediator in this disease. Lead affects virtually every organ system in general and the central nervous system (CNS) of developing brain in particular. Children therefore are more prone to the risk of lead toxicity.
Lead Adversely Influences Neurotransmission Systems. The effects of lead on the brain, including mental retardation and cognitive deficit, are mediated by its interference with three major neurotransmission systems: (1) the dopaminergic, (2) cholinergic, and (3) glutamatergic systems. The effects of lead on the first two systems are well established, but their mechanisms have not yet been described exhaustively. Lead is known to directly interfere with the action of glutamate, the brain’s essential excitatory neurotransmitter at more than half of the synapses in the brain, and is critical for learning.

 

 

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