Introduction
In the information age and knowledge-driven economy, powered by the information communications technology (ICT), increasing population uses internet-enabled gadgets. These gizmos include near-end-of-life facilities that soon outlive their usefulness and become outright electronic wastes (e-wastes). Annually, 50 million tons of e-wastes are generated worldwide, increasing at 3–5%, faster than any other category of waste generation, indicating that the global volume of e-wastes produced annually will soon double [1]. Reasons for the increasing e-wastes generation include derivable gains from ICT and e-waste businesses, rapid technology change, planned obsolescence and low initial cost. The industrialized countries generate a majority of e-waste which contains hazardous chemicals, but transfer much of it to poor countries with technological backwardness, poor environmental management infrastructure, and weak waste treatment and regulatory capacity. The discarded e-waste is poorly disposed and released into the air, water and soil, thereby worsening environmental pollution and degradation conditions with attendant public health challenges in poor countries. Toxic out-of-use electrical and electronic equipment retained in homes and offices pollute the indoor air by emission of toxic gases inhaled by humans. They are improperly disposed and finally end in water and soil resources to adversely affect lives through the food chain [2,3].
Eneh [4] categorized the 45 chemical components of e-waste items by quantity and toxicity (Table 1). Notably, lead and beryllium oxide are 2 hazardous components that occur in significant quantities in e-waste items.
A toxic chemical contained in significant quantity causes more health risk and challenges than a toxic chemical contained in small quantity which in turn causes more health risk and challenges than a toxic chemical contained in a trace amount. Mercury, polychlorinated biphenyls (PCBs), cadmium, lead and beryllium oxide are five hazardous chemicals contained in significant quantities in e-waste items. They are transported through the air, water, soil and food chain and constitute threats to ecological integrity. They are taken in through inhalation, ingestion and/or dermal contact and can adversely affect various human organs and systems and constitute threats to ecological integrity [5,6]. This also negates the Sustainable Development Goals (SDGs) Targets 12.4 and 3.9 which seek to reduce the number of deaths and illnesses from hazardous chemicals, achieve environmentally friendly management of chemical and waste products, and significantly reduce their release to air, water and soil. The SDGs aim to end poverty, protect the planet and ensure prosperity for everyone by 2030. Specifically Goal 12 Target 4 aims to reduce illnesses and death from hazardous chemicals and pollution. By 2030, the number of deaths and illnesses from hazardous chemicals and air, water and soil pollution and contamination needs to be substantially reduced. Goal 3 Target 9 is aimed at responsible management of chemicals and waste. By 2020, environmentally sound management of chemicals and all wastes throughout their life cycle need to be achieved through significantly reducing the release of toxic chemicals to air, water and soil in order to minimize their adverse impacts on human health and the environment. Goals 3 and 12 are parts of the 17 life-changing SDGs which almost all the countries of the world have set as promises in 2015 to improve the lives of its citizens on the planet by 2030. The countries have committed to working together to ensure that none of the countries is left behind in the targets of ending extreme poverty, giving people better healthcare, and achieving equality for women [7].
The study aimed to identify hazardous chemicals contained in significant quantities in e-waste items, describe their public health challenges and mitigation measures to enable stakeholders prepare basic information to serve as appropriate environmental health education technology policy (AEHETP) to guide the design of prophylactic, therapeutic and decontamination plans for awareness creation and raising to mitigate the toxic effects of e-waste items on users in a poor country setting.
Appropriate Environmental Health Education Technology (AEHET)
Policy is a documented principle to guide decisions towards achieving goals. It is a statement of intent, to be implemented as a procedure or protocol. It is a set of ideas or plans adopted by a governing body within an organization for use as a basis for taking actions, especially in politics, socio-economic and business endeavours [8].
Technology is the tool/machine/method for undertaking activities, including educating. Appropriate education technology (AET) is an education tool that uses the rich environment for education materials. It harps on activity-based learning through learner exploration and experimentation [9].
By extension, appropriate environmental health education technology (AEHET) is an education method that uses the environment for teaching materials through activity-based learning. Education syllabus has to be adapted to suit AEHET. This calls for AEHET policy to guide the design of prophylactic, therapeutic and decontamination plans for awareness creation and raising so as to mitigate the toxic effects of e-waste items on the population in poor countries.
E-waste toxic effects and poverty/death nexus in poor countries
Through inhalation, ingestion and dermal contact, people are exposed to hazardous chemicals occurring in small and significant quantities in e-waste items. The risk and threats are increasing as the population using electronic and internet-enabled gadgets, with enormous generation of e-waste items in poor countries. This exacerbates poverty in poor countries through illness. Figure 1 illustrates the cycle of e-waste toxicity on the population.
There is the need to address this vicious cycle of e-waste toxic effects. One way to do this is through education and awareness creation/raising that derive from an appropriate environmental health education technology (AEHET) policy that guides the design of education, prophylactic, therapeutic and decontamination plans.
Materials and Methods
Critical research method was adopted to identify and discuss available secondary data and information on health/illness/death implications of each of the hazardous chemicals occurring in small and significant quantities in e-waste items. Desktop survey of the literature reveals the potential health risks and challenges of the hazardous chemicals in e-waste materials to point to the need and prescription of the appropriate environmental health education technology (AEHET) towards the achievement of SDGs 3.9 and 12.4.
Results and Discussion
The five environmentally significant chemical components of e-waste items are mercury, polychlorinated biphenyls (PCBs), cadmium, lead and beryllium oxides. All other chemical components of e-waste items are not of environmental health concern because each of them is either non-hazardous or occurs in trace amount in e-waste items. Americium is hazardous, but occurs in trace amount. Sulphur is hazardous, but the literature does not specify its quantitative content in e-waste items. Americium and sulphur were, therefore, excluded from the list of hazardous chemicals occurring in small and significant quantities in e-waste items.
Mercury (Hg)
Occurrence and sources of Hg
Hg occurs naturally in air, water, soil and rocks as elemental or metallic Hg, inorganic and organic Hg compounds. Hg is a liquid at room temperature that readily vaporizes into the air to contaminate and pollute rain water, soil, and water bodies, thereby posing a risk to plants, animals, and humans. Burning coal releases Hg in the environment, just as improper treatment and disposal of Hg-containing wastes does [10].
Exposure to Hg and vulnerability
Inhaling Hg-polluted air is the most common way to be exposed to elemental Hg, and is the most harmful to health [10]. Pregnant women are particularly sensitive to harmful effects of Hg which can pass from a pregnant woman to the developing foetus. Hg can also pass through breast milk to nursing infants. Children who play on floors where Hg may have been spilled, are more likely to breathe more vapours, as they breathe faster and have smaller lungs than adults [11].
Tests and health effects of Hg poisoning
Hair, urine or blood test can detect too much exposure to Hg. A urine test is preferred for measuring elemental Hg. A blood test can be used to measure exposure to high levels of Hg within three days of being exposed [10].
Exposure to high levels of Hg can harm the lungs, brain, kidneys, heart, and immune system. Short-term exposure to Hg vapour leads to chest pain, shortness of breath, sore throat, cough, nausea, vomiting, diarrhoea, a metallic taste in the mouth, headache, increase in blood pressure or heart rate, and eye irritation and defective vision. Long-term exposure to Hg vapour leads to anorexia, anxiety, sleeping problems, excessive shyness, irritability, loss of appetite, fatigue, tremors, forgetfulness, and changes in vision and hearing. Symptoms of acute elemental (metallic) Hg poisoning include insomnia, tremors, muscle atrophy, emotional changes, twitching, weakness, disturbances in sensations, headache, performance deficits on tests of cognitive function, and changes in nerve responses. Higher exposures may result in respiratory failure, kidney defects and death [10].
Remediation and prevention of mercury poisoning
Removal of the source of Hg exposure should be followed by treatment, supportive care, and chelation therapy to help remove the metal from the body. Recycling of Hg-containing waste items is one of the best ways to help prevent Hg releases to the environment [10].
Polychlorinated biphenyls (PCBs)
Sources and exposure to PCBs
PCBs are a group of 209 different chemicals sharing a common structure but varying in the number of attached chlorine atoms. They are released to the air, water, and soil during their manufacture, use, and disposal. They are also released from accidental spills, leaks during their transport, and leaks from or burning PCBs-containing wastes. Again, they are released from sites of hazardous waste (e.g. e-waste), improper disposal of industrial wastes and consumer products, leaks from old electrical transformers containing PCBs, and from wastes incinerators. They travel long distances in air. A small amount may remain dissolved and much of it sticks to organic particles and bottom sediments in water. PCBs also bind strongly to soil and accumulate in the ecosystem. They are absorbed into fat tissue, are not excreted, but accumulate over years, taking many years to degrade into nontoxic forms in the body. Workers in plants that extensively manufacture and use PCBs and PCB-containing equipment are more susceptible to relatively high levels of PCBs exposures. Aquatic animals accumulate PCBs thousands of times higher than in water and transfer them along the food chain. PCBs pass from women on to their infants through breast milk [12].
Health effects of PCBs
PCBs are probable human carcinogens and are potential occupational carcinogens. Acne and rashes are the most commonly observed health effects in people exposed to large amounts of PCBs. Changes in blood and urine may indicate liver damage in workers. Acute exposure manifests in skin irritations, severe acne and rashes, irritation of the nose and lungs, and eye problems. PCBs exposure before or during pregnancy results in birth of children with low intelligence quotience (IQ), under-weight, small head-size, poor memory performance, psychomotor and behavioural defects [12].
PCBs with a few chlorine atoms affect natural hormones, shorten menstrual cycles, play a role in premature puberty and reduced sperm counts, alter sex organs, and change sex ratios of children. Highly-chlorinated PCBs affect growth, intellectual and behavioural development. PCBs disturb the amounts of some immune system elements. In children, they increase prevalence of ear infections and chickenpox, lower immune system function, and increase susceptibility to disease [12].
Mechanism of PCBs toxicity
Enzyme metabolizes PCBs to phenols (via arene oxide intermediates) which can be conjugated or further hydroxylated to form catechol. Electrophilic arene oxide intermediates covalently bind to nucleophilic cellular macromolecules to induce DNA strand breaks and DNA repair, contributing to toxicity. Also, arene oxide intermediates can be conjugated with glutathione and further metabolized to contribute to toxicity of PCBs [12].
Cadmium (Cd)
Occurrence and exposure to Cd
Cd is a very poisonous element that forms a variety of complex organic amines, sulphur complex, chloro-complexes, and chelates. Its ions form soluble carbonate, arsenate, phosphate, and ferrocyanide salts. In their many forms, Cd products serve as alloys for electroplating in auto industries, in production of pigments, as stabilizers for polyvinyl plastics, and in rechargeable Nickel-Cd batteries. Other human activities, such as the use of fossil fuels, metal ore and waste combustion, also release Cd to the environment. Cd compounds contained in sewage sludge leak into soil and water and are adsorbed by plants and sea organisms. By consuming vegetables and sea foods, man accumulates Cd in various human organs. Smokers have 4–5 times Cd levels higher than non-smokers [13,14].
Health effects of Cd exposure
Human exposure to Cd compounds causes damage to the lungs, bone and kidney of workers and affects male reproductive system. In female, it inhibits the function of ovary and increases the rate of spontaneous abortion and time of pregnancy, and decreases the rate of live births. Exposure to Cd causes skeletal demineralization that manifests in pain, decreased bone density, increased risk for bone fractures, physical impairment, and decreased quality of life [15–18].
Cd intoxication inhibits nitric oxide enzyme, suppresses acetylcholine-induced vascular relaxation, causes hypertension, risk of systolic and diastolic high blood pressures and increased cardiovascular mortality, myocardial infarction, loss of cell structure, and cell death. Long-term exposure to Cd increases peripheral arterial disease [19]. Cd poisoning induces damage in brain, increases production of free radicals in the central nervous system (CNS), decreases cellular defense against oxidation, causes olfactory dysfunction, attention defects, psychomotor activity disorder, and memory and behavioural defects [20].
Mechanism and diagnostic evaluation of Cd toxicity
At low concentration, Cd binds to the mitochondria to inhibit both cellular respiration and oxidative phosphorylation, and to inhibit the activity of antioxidant enzymes. The cells containing a zinc-concentrated protein that contains 33% cysteine, which scavenges hydroxyl and superoxide radicals, are generally resistant to Cd toxicity, while other cells are sensitive to Cd intoxication [25,26]. Paraclinic laboratory tests involve Cd levels in blood, urine, hair, nails and saliva. Trace elements level is measured in hair and nails. Saliva analysis is an excellent method for long term detection of heavy metal contamination [27–32]. Nanotechnology diagnoses and eliminates Cd to manage intoxication and increase environment safety [33].
Treatment and remediation of Cd poisoning
Treatment and remediation of Cd poisoning involve airways, breathing and circulation evaluation, followed by inducement of emesis. Supportive therapy helps to evaluate damage to liver, gastrointestinal, urinary and respiratory tracts [34]. Medicinal plants are used for natural decontamination of water. They include the seeds of Moringa oleifera, Arachis hypogaea (peanuts), Vigna unguiculata (cowpeas), Vigna mungo (urad) and Zea mays (corn) which purify the water by absorbing the negative charged impurities and metals [35]. Removal of heavy metals from contaminated soil could be achieved by (1) washing, leaching, flushing with chemical agents [36], (2) add some non-toxic materials to reduce solubility of heavy metals [37], (3) electromigration [38], (4) cover the original pollutants with clean materials [39], (5) mixing polluted materials with clean materials in surface and subsurface to reduce the concentration of heavy metals [40], and (6) phytoremediation [41]. Treatment can be achieved by using appropriate chelating agents and antidotes (Unithiol, DMPS), and new DMSA analogues [42–46]. The absorption yield depends on different factors such as pH of environment, ionic power, and metal concentration in solution or biomass. Chelating agents are ethylenediaminetetraacetic acid (EDTA), penicillamine, dimercaprol, dithiocarbamate, meso-2,3-dimercaptosuccinic acid (Succimer, DMSA), 2,3-dimercapto-1-propane sulfonic acid (Unithiol, DMPS), and new DMSA analogues [42–46].
Lead (Pb)
Source and contact with Pb
Pb occurs naturally as a toxic metallic mineral in earth crust. Mining, smelting, manufacturing, recycling, and leaded paint, petroleum motor spirit, gasoline and aviation fuel are sources of Pb contamination and pollution. Pb is used in the manufacture of lead-acid batteries, pigments, paints, solder, stained glass, Pb crystal glassware, ammunition, ceramic glazes, jewels, toys, cosmetics, traditional medicines and Pb pipes [47].
Pb absorption, poisoning and diagnostic tests
Skin-absorption, ingestion and inhalation of lead particles are routes of taking in Pb from Pb-glazed or Pb-soldered containers, leaded drinking water pipes or pipes joined with Pb solder and Pb-contaminated dust. The body absorbs higher levels of Pb through inhalation than through the skin and ingestion. In human body, Pb is distributed to brain, kidney, liver and bone/teeth, and stores blood, and tissues for continual internal exposure [48]. Pb absorbed in the body is measured as the blood Pb level or concentration (μg/dL) [47].
Symptoms of Pb poisoning, age and menopause
Pb poisoning results from exposure to high levels of Pb over a short period of time and manifests in abdominal pain, constipation, tiredness, headache, irritability, loss of appetite, coma, convulsions, pain or tingling in the hands and/or feet, weakness, anaemia, kidney and brain damage, memory loss, reduced attention span and educational attainment, and death. Pb passes through the placenta of pregnant woman to damage the nervous system of the unborn child, affecting at low-level behaviour and intelligence and causing miscarriage, stillbirth, and infertility. Children show signs of severe lead toxicity at lower levels than adults because they absorb 4–5 times as much ingested lead as adults from a given source. Economically disadvantaged or undernourished children absorb more Pb because other nutrients, such as calcium and iron, are lacking. The bone demineralizes with age and during menopause to release Pb from its tissues, thereby increasing internal exposures. A safe blood lead concentration is unknown, since 5μg/dL concentration is associated with reduced intelligence in children, behavioural difficulties and learning problems. The range and severity of symptoms and effects increase as lead exposure increases. Prolonged exposure to lead over time may manifest in abdominal pain, constipation, depression, distraction, forgetfulness, irritability, nausea/sickness, risk of high blood pressure (hypertension), cancer, heart disease, kidney disease, and reduced fertility [47,48].
In 2017, lead exposure accounted for 1.06 million deaths and 24.4 million years of healthy life lost (disability-adjusted life years, DALYs) worldwide due to long-term effects on health. In 2016, lead exposure accounted for 63.2% of the global burden of developmental intellectual disability, 10.3% of the global burden of hypertension, 5.6% of the global burden of heart disease and 6.2% global burden of stroke [49–51].
Beryllium(II) oxide (BeO)
Physical properties, uses, contact and symptoms of BeO toxicity
BeO is a white, odorless powder used in the manufacture of ceramics, glass, electron tubes, electronics, nuclear fuels and nuclear moderators. It can be contacted by inhalation and skin absorption. Acute (short-term) health effects that may occur immediately or shortly after exposure to BeO are eye irritation, redness, itching and burning, swelling of the eyelids, skin irritation and burning, nose irritation, throat irritation and lungs irritation causing nasal discharge, tightness in the chest, and cough. Chronic (long-term) health effects can occur after exposure to BeO and can last for months or years as cancer and reproductive hazards. Other long-term (high exposure) effects include skin ulcers, bronchitis and/or pneumonia with fever, cough and shortness of breath. High or repeated exposure can cause permanent scars in the lungs with fatigue, weight loss, and shortness of breath. Lung damage and heart failure can occur years later [52].
BeO is on the list of Hazardous Substances Fact Sheet as a carcinogen, and there is no safe level of exposure to a carcinogen; all contacts should be reduced to the lowest possible level. Employers ought to label chemicals in the workplace and train and enlighten employees on chemical hazards and control. Exposure to BeO should be routinely evaluated through personal and area air samples [52]. To reduce and remediate BeO exposure, e-waste management and control measures ought to be improved. Use of protective clothing and washing thoroughly immediately after exposure to BeO and e-waste ought to be practiced in workplace. Hazard and warning information ought to be posted, and all information on the health and safety hazards of BeO and e-waste ought to be communicated.
Conclusions
Generation of e-waste items is rapid in poor countries because of increasing demand for end-of-life ICT facilities that soon outlive their usefulness and are discarded. The study identified mercury, PCBs, cadmium, lead and beryllium oxide as the five hazardous chemicals contained in small and significant quantities in e-waste items. Through inhalation, ingestion, dermal contact and food chain, the items poison humans, with harmful effects on various human organs and systems. Ignorance, poor waste management infrastructure and throw-away mentality lead to improper disposal of the e-waste items into air, water and soil. The population is exposed to these materials through inhalation, ingestion, and dermal contact. To mitigate the toxic effects of e-waste items in poor resource countries, the study recommends crafting appropriate environmental health education technology policy (AEHETP) to guide stakeholders in developing appropriate management and control measures and decontamination plans, and also to create awareness on the environmental health challenges of the toxic materials in e-waste products.
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