ELECTRONIC WASTE COMPONENTS: HARMLESS SUBSTANCES OR POTENTIAL CARCINOGEN A SEMINAR PRESENTED BY

AKINSEYE, VICTOR OLUWATOYIN MATRIC NO : 154687

SUBMMITED TO CANCER RESEARCH AND MOLECULAR BIOLOGY UNIT, FACULTY OF BASIC MEDICAL SCIENCE, UNIVERSITY OF IBADAN.
IN PARTIAL FULFILMENT FOR THE AWARD OF DEGREE OF MASTER OF SCIENCE IN BIOCHEMISTRY.

FEBRUARY, 2011

DEDICATION

This seminar write up is dedicated to Almighty God, the giver of wisdom, knowledge, and understanding, and to my dearest parent Mr and Mrs F.K Akinseye.

ACKNOWLEDGEMENT

My special gratitude goes to Almighty God, the supreme being who has being with me all this while. I want to appreciate Him for His mercy, kindness and favour, may His name be praised forever. I want to appreciate in a special way the effort of my parents Mr. and Mrs. F.K. Akinseye, who God have been using as the brain behind my progress so far, may God continue to grant good health of mind, body, and soul, Amen. You are too much! Kudos to my supervisor and the head of cancer research and molecular biology unit, Dr O.A. Odunola, Dr. Owumi and Dr. Gbadegesin of cancer research and molecular biology unit for their untiring effort and understanding at time, may the Lord continue to grant success to the work of your hand. To all my colleagues especially cancer research and molecular biology unit, may you always experience Gods goodness, Amen. In a special way, I wish to express my sincere gratitude to the HOD Department of Agronomy, Faculty of Agriculture, University of Ibadan for his assistance and word of encouragement during the course of this research work. Finally, I wish to acknowledge my following friends and colleagues for their assistance in the course of this work Tolu, Aboki, Ayo, Tobi, Fatoki, Efe you guys are too much.

TABLE OF CONTENT

1. INTRODUCTION

2. WHAT IS E-WASTE?

3. COMPONENTS OF E-WASTE. 3.1. Hazardous components 3.2. Generally non-hazardous components

4. E-waste and its effect on health and the environment 4.1. Effect of the hazardous e-waste component. 4.2. Biological importance of generally non hazardous component

5. MECHANISM OF TOXICITY OF SOME SELECTED METALS 5.1. Lead 5.2 Cadmium 5.3 Mercury 5.4 Chromium

INTRODUCTION The production of electrical and electronic equipment (EEE) is one of the fastest

growing global manufacturing activities. Rapid economic growth, coupled with urbanization and a growing demand for consumer goods, has increased both the consumption and the production of EEE[Ramech et al ,2007]. The Indian information technology (IT) industry has been one of the major drivers of change in the economy in the last decade and has contributed significantly to the digital revolution being experienced by the world. New electronic gadgets and appliances have infiltrated every aspect of our daily lives, providing our society with more comfort, health and security and with easy information acquisition and exchange[Sincha et al, 2007]. The knowledge society however is creating its own toxic footprints. The same hypertechnology that is hailed as a crucial vector for future modern societal development has a not-so-modern downside to it: electronic waste (e-waste)[Swerts T et al, 2006]. E-waste broadly covers waste from all electronic and electrical appliances and comprises of items such as computers, mobile phones, digital music recorders/players, refrigerators, washing machines, televisions (TVs) and many other household consumer items.[Sincha S et al, 2007] The increasing market penetration in the developing countries, replacement market in the developed countries and high obsolescence rate make e-waste one of the fastest waste streams. This new kind of waste is posing a serious challenge in disposal and recycling to both developed and developing countries. While having some of the world's most advanced high-tech software and hardware developing facilities, India's recycling sector can be called medieval.[Swerts T et al, 2006] The dumping of e-waste, particularly computer waste, into underdeveloped and developing countries from developed countries[Wankhede K et al, 2005] (green passport according to Gutierrez), because the latter find it convenient and economical to export waste, has further complicated the problems with waste management.

A lot of the reasoning behind the need to control e-waste is for its health and environmental effects. The chemicals and metals usually put into the manufacturing and production of electronics contain properties harmful to our bodies, sometimes their

effects are not noticeable right away and often not harmful until the electronics' end of life. Much of the substances in computers are not biodegradable. The toxic metals contained in them are contaminating the water, air, and soil. When these elements are safely encased in our refrigerators and laptops, e-waste dangers aren't much of an issue. Problems can occur when devices break -- intentionally or accidentally. Then they can leak and contaminate their immediate environment, whether that's in a landfill or on the streets within a region full of struggling laborers. Over time, the toxic chemicals of a landfill's e-waste can seep into the ground (possibly entering the water supply) or escape into the atmosphere, affecting the health of nearby communities.

How? When this materials are disposed, their components i.e. heavy metals and other harmful components leaches into the underground water and surrounding water bodies, they contaminates these water sources, thus posing a health risk. Also when some of them are burnt, these heavy metals are released into the atmosphere, thus polluting the air. Properly recycling of electronics waste would not only be a benefit to our environment but for our health.

Unfortunately, if these hazardous components within computers are not disposed off carefully they can cause permanent health issues. Some of the common harmful heavy metals are lead, mercury, chromium, and beryllium. In nature these metals are sometimes harmless but when used to manufacture electronics, often result in compounds that are hazardous. For example, chromium becomes chromium VI as it is used in floppy disks and to protect metal parts from corrosion; exposure can cause permanent eye injury, DNA damage, and cancer.

The fifth most widely used metal is lead. Lead is used in solder, batteries, cable sheathing and in the glass of cathode ray tubes for computer monitors. Short-term high exposure to lead can cause appetite loss, fatigue, vomiting, diarrhea, convulsions, coma or even death. Long-term exposure, as in an industrial setting, can cause damage to the nervous, blood and reproductive systems in adults. Children and pregnant women that are exposed to lead can suffer from damage to their nervous connections and cause brain disorders.

One of the most toxic metals used in the production of electronics is mercury. It can be

found in flat screen displays, switches, housing, thermostats, and florescent lamps. Mercury is a metal that accumulates in living organisms causing brain and liver damage if ingested or inhaled. Lastly, there is beryllium, which has recently been classified as a human carcinogen because exposure to it can cause lung cancer. Workers exposed to beryllium, even in small amounts, can develop what is known as Chronic Beryllium Disease (beryllicosis). Studies have shown that people can still develop beryllium diseases years from the last exposure. Granted, the metals stated above are only a few of the many hazardous materials contained in our electronics. To better understand the scale we are talking about, take the example of a cellphone that contains 500 to 1000 components.

Due to poor regulations on e-waste recycling in developing countries a lot of the methods used to retrieve certain metals from electronics are polluting the environment. A report done in 2007 by the Chinese Academy of Science found that Guiyu, China has the world's highest levels of environmental pollutants that threaten human health. Pollutants are released into the air through the burning of plastics and circuit boards coated with flame retardants to extract gold, platinum, copper and other metals. About 1.7 million tonnes of e-waste is processed each year in Guiyu. Shantou health researchers found in a study from 2008 that 81 percent of blood samples from Guiyu infants has significantly higher levels of blood lead and high levels of cadmium in 20.1 percent of infants. The research indicates that these levels are leading to stillbirths, low birth weights, premature deliveries and impacts on child growth rates and nervous developments. Developed countries and places that are not home to e-waste landfills are not completely excluded from the effect of e-waste.

Pollutants in the air are able to travel across the Pacific and into our air. As a result of the waste not properly monitored, it can seep into the ground and water. Mercury is a commonly known metal found in fish populations which seems to have a tie to e-waste harming bodies of water.

WHAT IS E-WASTE Electronic waste, e-waste, e-scrap, or Waste Electrical and Electronic Equipment (WEEE) describes loosely discarded, surplus, obsolete, or broken electrical or electronic devices. Electronic waste may be defined as all secondary computers, entertainment device electronics, mobile phones, and other items such as television sets and refrigerators, whether sold, donated, or discarded by their original owners. This definition includes used electronics which are destined for reuse, resale, salvage, recycling, or disposal. Others define the re-usables (working and repairable electronics) and secondary scrap (copper, steel, plastic, etc.) to be commodities, and reserve the term waste for residue or material which was represented as working or repairable but which is dumped or disposed or discarded by the buyer rather than recycled, including residue from reuse and recycling operations. Because loads of surplus electronics are frequently commingled (good, recyclable, and non-recyclable), several public policy advocates apply the term e-waste broadly to all surplus electronics. Electronic-waste (or e-waste) is a collective name for trashed electronic items like obsolete PCs, laptops, fax machines, cell phones, batteries, consumer electronics etc.Ewaste is a term used to cover almost all types of electrical and electronic equipment that has or could enter the waste stream. Although e-waste is a general term, it can be often considered to cover TVs, computers, mobile phones, white goods (fridges, washing machines, dryers etc.), home entertainment and stereo systems, toys, toasters, kettles almost any household or business item with circuitry or electrical components with power or battery supply. This definition includes used electronics which are destined for reuse, resale, salvage, recycling, or disposal. Others define the re-usables (working and repairable electronics) and secondary scrap (copper, steel, plastic, etc.) to be "commodities", and reserve the term "waste" for residue or material which was represented as working or repairable but which is dumped or disposed or discarded by the buyer rather than recycled, including residue from reuse and recycling operations. Because loads of surplus electronics are frequently commingled (good, recyclable, and non-recyclable), several public policy advocates apply the term "e-waste" broadly to all surplus electronics.

E-waste is any refuse created by discarded electronic devices and components as well as substances involved in their manufacture or use. The disposal of electronics is a growing problem because electronic equipment frequently contains hazardous substances. In a personal computer, for example, there may be lead in the cathode ray tube (CRT) and soldering compound, mercury in switches and housing, and cobalt in steel components, among other equally toxic substances. According to the Environmental Protection Agency (EPA), more than four million tons of e-waste go to U.S. landfills each year. Electronic waste or e-waste is the term used to describe old, end-of-life electronic appliances such as computers, laptops, TVs, DVD players, mobile phones, mp3 players, etc., which have been disposed by their original users. E-waste has been categorized into three main categories, i.e., Large Household Appliances, IT and Telecom and Consumer Equipment. Refrigerator and washing machine represent large household appliances; PC, monitor and laptop represent IT and Telecom, while TV represents Consumer Equipment. Each of these e-waste items has been classified with respect to 26 common components found in them. These components form the building blocks of each item and therefore they are readily identifiable and removable. These components are metal, motor/ compressor, cooling, plastic, insulation, glass, LCD, rubber, wiring/electrical, concrete, transformer, magnetron, textile, circuit board, fluorescent lamp, incandescent lamp, heating element, thermostat, brominated flamed retardant (BFR)-containing plastic, batteries, CFC/HCFC/HFC/HC, external electric cables, refractory ceramic fibers, radioactive substances and electrolyte capacitors (over L/D 25 mm). The composition of WEEE/e-waste is very diverse and differs in products across different categories. It contains more than 1000 different substances, which fall under hazardous and non-hazardous categories. Broadly, it consists of ferrous and non-ferrous metals, plastics, glass, wood and plywood, printed circuit boards, concrete and ceramics, rubber and other items. Iron and steel constitutes about 50% of the WEEE followed by plastics (21%), non-ferrous metals (13%) and other constituents. Non-ferrous metals consist of metals like copper, aluminium and precious metals, e.g. silver, gold, platinum, palladium, etc. The presence of elements like lead, mercury, arsenic, cadmium, selenium and hexavalent chromium and flame retardants beyond threshold quantities in WEEE/e-waste classifies them as hazardous waste.

COMPONENTS OF ELECTRONIC WASTE Some computer components can be reused in assembling new computer products, while others are reduced to metals that can be reused in applications as varied as construction, flatware, and jewelry[Haffenreffer D. et al, 2003] Substances found in large quantities include epoxy resins, fiberglass, PCBs, PVC (polyvinyl chlorides), thermosetting plastics, lead, tin, copper, silicon, beryllium, carbon, iron and aluminium. Elements found in small amounts include cadmium, mercury, and thallium[ Becker et al,
2005].

Elements found in trace amounts include americium, antimony, arsenic, barium, bismuth, boron, cobalt, europium, gallium, germanium, gold, indium, lithium, manganese, nickel, niobium, palladium, platinum, rhodium, ruthenium, selenium, silver, tantalum, terbium, thorium, titanium, vanadium, and yttrium. Almost all electronics contain lead and tin (as solder) and copper (as wire and printed circuit board tracks), though the use of lead-free solder is now spreading rapidly The components of electronic waste can be arbitrarily divided into two based on their effects : Hazardous components and Generally non hazardous component

Hazardous components

Americium: Smoke Alarms (radioactive source). Mercury: Fluorescent Tubes (numerous applications), tilt switches (pinball games,

mechanical doorbells, thermostats). There are no liquid mercury switches in ordinary computers, and the elimination of mercury batteries in many new-model computers is taking place.[28]

Sulphur: Lead-Acid Batteries. PBBs: Predecessor of PCBs. Also used as flame retardant. Banned from 1973-1977 on. PCBs: Prior to ban, almost all 1930s1970s equipment, including capacitors,

transformers, wiring insulation, paints, inks, and flexible sealants. Banned during the 1980s.

Cadmium: Light-sensitive resistors, corrosion-resistant alloys for marine and aviation

environments, nickel-cadmium batteries.

Lead: Solder, CRT monitor glass, lead-acid batteries, some formulations of PVC.[29] A

typical 15-inch cathode ray tube may contain 1.5 pounds of lead,[1] but other CRTs have been estimated as having up to 8 pounds of lead.[11]

Beryllium oxide: Filler in some thermal interface materials such as thermal grease used

on heatsinks for CPUs and power transistors,[30] magnetrons, X-ray-transparent ceramic windows, heat transfer fins in vacuum tubes, and gas lasers.

Polyvinyl chloride: Third most widely produced plastic, contains additional chemicals

to change the chemical consistency of the product. Some of these additional chemicals called additives can leach out of vinyl products. Plasticizers that must be added to make PVC flexible have been additives of particular concern. Burning PVC in connection with humidity in the air creates Hydrogen Chloride (HCl), an acid.

Generally non-hazardous components

Tin: Solder, coatings on component leads. Copper: Copper wire, printed circuit board tracks, component leads. Aluminium: Nearly all electronic goods using more than a few watts of power

(heatsinks), electrolytic capacitors.

Iron: Steel chassis, cases, and fixings. Germanium: 1950s1960s transistorized electronics (bipolar junction transistors). Silicon: Glass, transistors, ICs, printed circuit boards. Nickel: nickel-cadmium batteries. Lithium: lithium-ion batteries. Zinc: plating for steel parts. Gold: connector plating, primarily in computer equipment.

The graphs of large household appliance

E-WASTE AND ITS EFFECT ON HEALTH AND THE ENVIRONMENT

E-waste cannot be considered or treated like any kind of waste, because it contains hazardous and toxic substances such as lead, mercury, cadmium or others such as dioxins and furans, bromined flame retardants (produced when e-waste is incinerated). For instance, lead represents 6% of the total weight of a computer monitor. Another example: nearly 36 chemical elements are incorporated in electronic equipment.

EEEs are made of a multitude of components, some containing toxic substances that have an adverse impact on human health and the environment if not handled properly. Often, these hazards arise due to the improper recycling and disposal processes used. It can have serious repercussions for those in proximity to places where e-waste is recycled or burnt. Waste from the white and brown goods is less toxic as compared with grey goods. A computer contains highly toxic chemicals like lead, cadmium, mercury, beryllium, BFR, polyvinyl chloride and phosphor compounds.

For instance, lead represents 6% of the total weight of a computer monitor. Another example: nearly 36 chemical elements are incorporated in electronic equipment. Even though in the last years recycling has become a regular practice almost everywhere in the world, some e-waste components present difficulties when they are recycled mainly because of their complexity and the lack of methods. Such is the case of plastics used in electronic equipment which contain flame retardants that impede the recycling process.

Table 1 : Environment and health hazards

Computer/ewaste component Process Cathode ray tubes Cathode ray tubes dumping and

Potential occupational hazard

Potential environmenta l hazard

Silicosis, Cuts from CRT glass, Inhalation contact phosphor containing cadmium other metals or or with Lead, and heavy leaching ground barium other metals into water

and release of toxic phosphor

Printer circuit boards

Desoldering and removing computer chips

Tin

and

lead

Air emission of the same

inhalation, Possible brominated dioxin,

substances

beryllium, cadmium mercury inhalation Dismantled printed circuit board processing Open burning of Toxicity workers of and Tin and lead contamination of immediate and

waste boards

nearby residents rom tin, lead, brominated dioxin, beryllium, cadmium mercury inhalation and

environment, including surface and

ground waters, brominated dioxins, beryllium, cadmium mercury inhalation and

Chips other plated

and gold-

Chemical stripping using and hydrochloric acid along nitric

Acid

contact

Hydrocarbons, heavy metals, brominated substances etc. discharged directly into and

with eyes, skin may result in permanent injury Inhalation if

compounds

riverbanks

river banks. Acidifies river

mists and fumes of chlorine sulfur acids, and dioxide

the

gases can cause respiratory irritation severe to effects,

destroying fish and flora

including pulmonary

edema, circulatory failure death Plastics from the computer and peripherals Shredding and lowProbable hydrocarbon, brominated dioxin and PAH exposure workers to living Emission brominated dioxins heavy and hydrocarbons and metals of and

temperature melting

in the burning works area Secondary steel copper precious metal smelting Wires Open burning recover copper to Brominated and chlorinated dioxin and PAH exposure workers to living Hydrocarbon and including PAHs discharged into air, water and soil ashes, or and Furnace recovers steel or Exposure dioxins to and Emission dioxins of and

heavy metals

heavy metals

copper from waste

in the burning works area

EFFECTS OF THE HAZARDOUS E-WASTE COMPONENETS

Lead Lead is found in many electronic equipment components. For example, in a PC, the largest amount of this metal is found in the CRT of the monitor: 0 to 3% in the panel, 70% in the frit, 24% in the funnel and 30% in the neck. Lead is also present in weldings (40%), motherboards, circuits and wiring plastic. Humans are exposed to this metal by particle inhalation and through contaminated foods. The first effects and symptoms of lead exposure are anorexia, muscle pain, malaise and headache but an extended exposure can cause a decrease in nervous system performance, weakness, brain damage and even death. Lead exerts toxic effects on various systems in the body such as the central (organic affective syndrome) and peripheral nervous systems (motor neuropathy), the hemopoietic system (anemia), the genitourinary system (capable of causing damage to all parts of nephron) and the reproductive systems (male and female). Likewise, it can affect the reproductive system both in men and women and is considered carcinogen. The chemical structure of this metal is directly affected by its pH but most lead compounds are insoluble in water and remain in that state. They are difficultly accumulated in plants or transferred to food. Lead doesnt bio-accumulate in fish but it does in other seafood. If broken or incinerated to the environment, particles will be transmitted by air and soil.

Lithium Lithium is present in computer batteries and modern electronic equipment. Typically batteries contain an anode of lithium or lithium oxide, a magnesium dioxide (magnesium oxide and carbon) cathode and lithium salt dissolved in anorganic solvent. This type of batteries replaces alkaline and NiCd batteries. It is environmentally more sustainable than its predecessors. Lithium is present in computer batteries and modern electronic equipment. Typically batteries contain an anode of lithium or lithium oxide, a magnesium dioxide (magnesium oxide and carbon) cathode and lithium salt dissolved in an organic solvent. This type of batteries replaces alkaline and NiCd batteries. It is environmentally more sustainable than its predecessors.

Mercury Mercury is found in three specific places in a computer. The largest amount is found in LCD screen fluorescent light, computer or monitor switches, which enable them to shut down while idle, and finally in batteries. Mercury is very volatile and easily liberated by

incineration or breaking, which could liberate up to 90% of the mercury contained in the monitor screen, for example. All forms of mercury represent a risk to human health, but mercury in metal form that is not combined with other components and organic methyl mercury are the ones that possess the greater risk, especially to the nervous system. Short-term exposures to this compound cause lung damage, nausea, vomiting, diarrhea, high pressure, and, skin and eye irritation. Long or permanent exposure might cause permanent damages to the brain, kidneys and fetus development, besides neurological changes, irritability, tremors, short-sightedness, deafness, memory problems, delirium, hallucinations and suicidal tendencies. Mercury causes damage to the genitourinary system (tubular dysfunction), the central and peripheral nervous systems as well as the fetus. When inorganic mercury spreads out in the water, it is transformed into methylated mercury, which bio-accumulates in living organisms and concentrates through the food chain, particularly by fish.

Nickel(Ni) Nickel is present in the batteries of some electronic equipment (NiCd), which are being gradually replaced with lithium batteries. Likewise, nickel is used in CRT of computer monitors. Nickel causes skin damages and asthma symptoms in about 10 to 20% of the population that has direct contact. Workers that are exposed to dust containing nickel suffer bronchitis and lung damages. There is evidence that many nickel compounds such as nickel hydroxide are carcinogen. Nickel generally enters the environment through air. These particles are then placed in water and soil, especially if they contain magnesium and steel. Nevertheless, this compound does not bio-accumulate in living organisms.

Arsenic (As) Arsenic is present in small amounts in electronic equipment in forms such as Gallium Arsenide GaAs, which has semiconductor properties and can be found in electronic equipment diodes. GaAs is carcinogen and causes skin and lung cancers. The most common means of exposure is direct contact with dust containing this compound especially by workers of semiconductor manufacturers. Gallium Arsenide is an inorganic compound with low water solubility. It is transformed into an organic compound when bioaccumulated in fish and crustaceans.

Cadmium (Cd) Cadmium is a heavy metal included in many electronic components, such as contact plates, switches, or used to prevent corrosion. Cadmium is particularly found in chip resistors, infrared detectors, and semiconductors. Old monitors contain around 5 to 10 grams of Cadmium and some batteries are made of Nickel Cadmium. It is added as a plastic stabilizer and pigment to wiring, motherboards, pcs, monitors and printed circuit boards.

Cadmium exposure commonly occurs through inhalation and ingestion of food or contaminated water. Inhaling large amounts of Cadmium can cause lung damage and

death. Exposure to small amounts over a long period of time can cause high pressure and kidney damage. This metal is a carcinogen. Cadmium enters the environment through water and soil that is absorbed by plants. Low concentrations can cause alterations in the ecology and balance of soil nutrients.This metal can bio-accumulate in mushrooms, oysters, shrimps, mussels and fish. Cadmium is a potentially long-term cumulative poison. Toxic cadmium compounds accumulate in the human body, especially in the kidneys. There is evidence of the role of cadmium and beryllium in carcinogenicity.

Chromium IV(Cr +6) Chromium VI, i.e. chromium ions with a charge of +6, is chromiums only toxic form. Its presence is small in electronic equipment where it is used as a plastic hardener and protection layer for some metal components. When electronic components are burned, 99% of Chromium VI stays in residuals and ashes, contaminating soil in a toxic way, which could reach water currents with significant higher risk. Chromium VI, i.e. chromium ions with a charge of +6, is chromiums only toxic form. Its presence is small in electronic equipment where it is used as a plastic hardener and protection layer for some metal components. When electronic components are burned, 99% of Chromium VI stays in residuals and ashes, contaminating soil in a toxic way, which could reach water currents with significant higher risk.

Polycyclic aromatic hydrocarbons (PAH) Affects lung, skin and bladder. Epidemiological studies in the past on occupational exposure to PAH provide sufficient evidence of the role of PAH in the induction of skin and lung cancers.

Polychlorinated Biphenyl (PCB) Humans are exposed through contaminated food consumption or direct contact at their workplace, (e.g inadequate disassembly of electronic equipment). Exposure to this compound can cause anemia, damages to the skin, liver, stomach and thyroid. Contamination of pregnant women is very risky and research results show that it can be carcinogenic. This chemical compound could drip through subsurface layers reaching water and contaminating it if buried in landfills. Because it is poorly soluble, it is very dangerous when it enters water currents as it could contaminate the chain of production of some foods.

Tetra Bromo Bisphenol-A (TBBPA) It has not been proved that it can cause mutations or carcinogen effects on human beings. Nevertheless, it has been proved that TBBA may interfere in the transport and metabolism of some hormones. A technical study has demonstrated that there is a direct correlation between TBBA in the blood flow and in the air. TBBA is toxic to aquatic organisms. Unlike other flame-retardants, TBBA when used as a reactive, bounds chemically to plastic or polymers for protection. This impedes its liberation into the environment. It is biodegradable but one of the products of this biodegradation is bisphenol which can cause damages to the endocrine system. The fact that TBBA dissolves poorly in water and tends to adhere to soil, where it can reach food, has created great concern because TBBA levels magnify while passing through the food chain from 20 to 3200 times.

Polybrominated Biphenyls (PBB) Exposure to this substance can damage kidneys, liver and thyroids. Fetuses that were exposed to PBB had endocrinal problems. Likewise it is suspected that PBB is a carcinogen it dissolves poorly in water but can adhere strongly to soil, through which it could reach food. It keeps magnifying while passing along the food chain.

BIOLOGICAL COMPONENTS

IMPORTANCE

OF

NON

HAZARDOUS

E-WASTE

Some components of electronic waste are relatively non-toxic to the living system, however their reaction with other compound can pose a health threat. Metals like tin, copper, iron , germanium, silicon, nickel, lithium, zinc, gold e.t.c. perform one or two biological importance in the maintenance of the normal body functions. Some of these uses include:

1. Zinc In the periodic table of the elements, zinc can be found in group IIb, together with the two toxic metals cadmium and mercury. Nevertheless, zinc is considered to be relatively non-toxic to humans [Fosmire GJ et al,1990.]. This is reflected by a comparison of the LD50 of the sulfate salts in rats. According to the Toxnet database of the U.S. National Library of Medicine, the oral LD50 for zinc is close to 3 g/kg body weight, more than 10fold higher than cadmium and 50-fold higher than mercury [U.S Nat.Lib. fo Med.,2010.]. An important factor seems to be zinc homeostasis, allowing the efficient handling of an excess of orally ingested zinc, because after intraperitoneal injection into mice, the LD50 for zinc was only approximately four-fold higher than for cadmium and mercury [Jones MM et al,1993.]. In contrast to the other two metals, for which no role in human physiology is known, zinc is an essential trace element not only for humans, but for all organisms. It is a component of more than 300 enzymes and an even greater number of other proteins, which emphasizes its indispensable role for human health. Optimal nucleic acid and protein metabolism, as well as cell growth, division, and function, require sufficient availability of zinc [Vallen BL et al,1993]. The human body contains 23 g zinc, and nearly 90% is found in muscle and bone [Wastney ME et al,1986.]. Other organs containing estimable concentrations of zinc include prostate, liver, the gastrointestinal tract, kidney, skin, lung, brain, heart, and

pancreas [Bentley BJ, et al,1991, He LS et al,1991, Liobet JM et al,1988.]. Oral uptake of zinc leads to absorption throughout the small intestine and distribution subsequently occurs via the serum, where it predominately exists bound to several proteins such as albumin, -microglobulin, and transferrin [Scott BJ et al,1983.]. On the cellular level, 3040% of zinc is localized in the nucleus, 50% in the cytosol and the remaining part is associated with membranes [Vallen BL et al,1993]. Cellular zinc underlies an efficient homeostatic control that avoids accumulation of zinc in excess . The cellular homeostasis of zinc is mediated by two protein families; the zinc-importer (Zip; Zrt-, Irt-like proteins) family, containing 14 proteins that transport zinc into the cytosol, and the zinc transporter (ZnT) family, comprising 10 proteins transporting zinc out of the cytosol [Licthen et al,2009.]. The same transporter families also regulate the intracellular distribution of zinc into the endoplasmic reticulum, mitochondria, and Golgi. In addition, many mammalian cell types also contain membrane-bound vesicular structures, so-called zincosomes. These vesicles sequester high amounts of zinc and release it upon stimulation, e.g., with growth factors [Haase H et al, 2003]. Finally, metallothioneins (MTs) play a significant role in zinc homeostasis by complexing up to 20% of intracellular zinc [Taylor KM et al,2008.]. MTs are ubiquitous proteins, characterized by a low-molecular weight of 67 kDa, high cysteine content, and their ability to complex metal ions. One MT molecule can bind up to seven zinc ions. Through different affinities of the metal ion binding sites, it can act as a cellular zinc buffer over several orders of magnitude [Krezel A et al,2007]. Dynamic regulation of cellular zinc by MT results from the synthesis of the apo-form thionein (T) in response to elevated intracellular zinc levels by triggering the metal response element-binding transcription factor (MTF)-1 [Laity JH et al,2007.]. In addition, oxidation of cysteine residues can alter the number of metal binding thiols, connecting redox and zinc metabolism. An in-depth discussion of this complex subject can be found in a recent review [Maret W et al, 2006]. Zinc Supplementation and Cancer Whereas several other metals are well-known carcinogens, zinc is not generally considered to be a causative agent for cancer development. In contrast, displacement of zinc from zinc-binding structures, e.g., finger structures in DNA repair enzymes, may

even be a major mechanism for carcinogenicity of other metals such as cadmium, cobalt, nickel, and arsenic [Tapiero H et aaal,2007.].

Immunological Effects Sufficient availability of zinc is of particular importance to the immune system. Thereby, it plays a key role in multisided cellular and molecular mechanisms . For instance, zinc influences the lymphocyte response to mitogens and cytokines, serves as a co-factor for the thymic hormone thymulin, and is involved in leukocyte signal transduction. An influence of zinc excess on T cell function was observed in several in vitro studies. In cell culture, very high zinc concentrations (above 100 M) in a serum-free culture medium stimulate monocytes to secrete pro-inflammatory cytokines, but actually inhibit T cell functions. In general, T cells have a lower intracellular zinc concentration and are more susceptible to increasing zinc levels than monocytes. Also, in vitro alloreactivity was inhibited in the mixed lymphocyte reaction (MLC) after treatment with more than 50 M zinc. A similar inhibition was observed when the MLC was done ex vivo with cells from individuals that had been supplemented with 80 mg zinc per day for one week, indicating that zinc supplementation has the potential to suppress the allogeneic immune response at relatively low doses.

COPPER Copper is an essential trace element that is vital to the health of all living things (humans, plants, animals, and microorganisms). The human body normally contains copper at a level of about 1.4 to 2.1 mg for each kg of body weight. Copper is distributed widely in the body and occurs in liver, muscle and bone. Copper is transported in the bloodstream on a plasma protein called ceruloplasmin. When copper is first absorbed in the gut it is transported to the liver bound to albumin. Copper metabolism and excretion is controlled delivery of copper to the liver by ceruloplasmin, where it is excreted in bile. Daily dietary standards for copper have been set by various health agencies around the world. Researchers specializing in the fields of microbiology, toxicology, nutrition, and health risk assessments are working together to define precise copper levels required for essentiality while avoiding deficient or excess copper intakes.

Copper excess and deficiency It is believed that zinc and copper compete for absorption in the digestive tract so that a diet that is excessive in one of these minerals may result in a deficiency in the other. The RDA for copper in normal healthy adults is 0.9 mg/day. On the other hand, professional research on the subject recommends 3.0 mg/day. Because of its role in facilitating iron uptake, copper deficiency can often produce anemia-like symptoms. Conversely, an accumulation of copper in body tissues are believed to cause the symptoms of Wilson's disease in humans. Copper deficiency is also associated with neutropenia, bone abnormalities, hypopigmentation, impaired growth, increased incidence of infections, and abnormalities in glucose and cholesterol metabolism. Severe deficiency can be found by testing for low plasma or serum copper levels, low caeruloplasmin, and low red blood cell superoxide dismutase (SOD) levels. However, these tests are not sensitive to marginal but not severe copper status. The "cytochrome c oxidase activity of leucocytes and platelets" is another sign of deficiency, but the results have not been confirmed by replication.

IRON Iron is a necessary trace element found in nearly all living organisms. Iron-containing enzymes and proteins, often containing heme prosthetic groups, participate in many biological oxidations and in transport. Examples of proteins found in higher organisms include hemoglobin, cytochrome, and catalase. Uptake and storage In cells, iron storage is carefully regulated; "free" iron ions do not exist as such. A major component of this regulation is the protein transferrin, which binds iron ions absorbed from the duodenum and carries it in the blood to cells. In animals, plants, and fungi, iron is often the metal ion incorporated into the heme complex. Heme is an essential component of cytochrome proteins, which mediate redox reactions, and of oxygen carrier proteins such as hemoglobin, myoglobin, and leghemoglobin. Inorganic iron also contributes to redox reactions in the iron-sulfur clusters of many enzymes, such as nitrogenase (involved in the synthesis of ammonia from nitrogen and hydrogen) and

hydrogenase. Non-heme iron proteins include the enzymes methane monooxygenase (oxidizes methane to methanol), ribonucleotide reductase (reduces ribose to deoxyribose; DNA biosynthesis), hemerythrins (oxygen transport and fixation in Marine invertebrates) and purple acid phosphatase (hydrolysis of phosphate esters). Iron distribution is heavily regulated in mammals, partly because iron ions have a high potential for biological toxicity. Iron acquisition poses a problem for aerobic organisms because ferric iron is poorly soluble near neutral pH. Thus, bacteria have evolved high-affinity sequestering agents called siderophores.

GERMANIUM Germanium has gained popularity in recent years for its reputed ability to improve immune system function in cancer patients. It is available in the U.S. as a nonprescription dietary supplement in oral capsules or tablets, and has also been encountered as an injectable solution. Earlier inorganic forms, notably the citrate-lactate salt, led to a number of cases of renal dysfunction, hepatic steatosis and peripheral neuropathy in individuals using it on a chronic basis. Plasma and urine germanium concentrations in these individuals, several of whom died, were several orders of magnitude greater than endogenous levels. The more recent organic form, beta-carboxyethylgermanium sesquioxide (propagermanium), has not exhibited the same spectrum of toxic effects

SILICON Silicon is contained in plants and also present in animals including humans.. The quantity in humans is 7 grams being more than all other trace elements together. Nevertheless Si is not (or hardly) considered as beneficial: there is a lot of scepticism in regular Medicine because silicon has been considered to be inert in humans. In 1973 the Joint FAO/WHO Expert Committee on Food Additives says: data on orally administered silica and silicates appear to substantiate the biological inertness of these compounds. This negative attitude is surprising because for several hundreds of years extracts of Si accumulating plants like Equisetum arvense (horsetail) have been used therapeutically for aging disorders, Alzheimer's disease, atherosclerosis, brittle hair, fractures, fragile nails, back pain, osteoporosis, skin disorders, tendinitis, improved wound healing and wrinkles.

On the other hand there is a lack on sufficient data on the metabolism of silicon in animals and humans. The absorption and bioavailability of silicon of the different silicon sources (silicates, metasilicates, etc.) is hardly known. There are neither standardised methods nor assays for assessing the silicon status in humans and animals. 1 . Effects of silicon on tissues, organs and diseases Bone and cartilage In 1972, Carlisle showed that a Si deficient diet in chickens induces skeletal deformities and joint abnormalities. Also in 1972, Schwartz published the same results in rats: deformities of the skull and peripheral bones, characterized by poorly formed joints, defective endochondral bone growth and reduced contents of articular cartilage, hexosamine, collagen and water. The concentrations of minerals like calcium, magnesium, zinc and manganese were also to low in the femur and vertebrae due to the diet only Si deficient. Both studies mark the beginning of the recognition of the importance of silicon as an beneficial even essential trace element that plays an important biological role in the processes by which connective tissue, bone, cartilage and skin are formed. A growing number of publications appear on the effects of Si on bone and cartilage as well in men as in animals: Schiano a.o. (1979) studied the activity of a soluble salt (drinkable and injectable) of Si on the evolution of the trabecular bone volume (TBV) in men. They note a significant increase in the TBV compared to controls. Eisinger e.a. (1993) showed in a prospective study that Si induced a significant (P < 0.05) increase in femoral bone mineral density in osteoporotic women compared to controls. Rico et al. showed in 2000 the effects of Si supplement on preventing bone mass loss induced by ovariectomy in rats. They proved that Si has an inhibitory effect on bone mass loss as well as the stimulatory effect on bone formation, so Si may have a potential therapeutic application in the treatment of involutive osteoporosis. Calomme et al. showed the positive effects of orthosilicic acid on bone density in chicks (2002) and on the bone density in ovariectomized rats (2004).. Skin, hair and nails The effects of Si on hair, skin and nails appear in regular literature: Lassus performed an open study in 1993 with oral Si (colloidal silicic acid) during 3 months. He found a

(statistically significant) improvement in the thickness and turgor of the skin, wrinkles and condition of the hair and nails. Barel et al. investigated the Si supplementation on skin, nails and hair in a double-blind, placebo controlled study. The (extra) Si had a significant positive effect on skin surface and mechanical properties, and on brittleness of hair and nails. The application of topical silicone gel is shown to be efficacious, both in the prevention and in the treatment of hypertrophic scar. Cardiovascular system / Atherosclerosis Animal studies f.e. in rabbits (Loeper 1979) indicate that Si can reduce the formation of atheromatous plaques. There is a low incidence of atherosclerosis in less developed countries where foods are not heavily processed before consumption and the diet has a higher Si content. In western diets the Si content is much lower and atherosclerosis is much higher. Moreover Si intakes decrease significantly with age (Jugdaohsingh, et al., 2002) suggesting that high Si intake is a factor in (partial) preventing atherosclerosis (Schwartz, 1977). Other observations supporting the concept that sufficient silicon intake is important for healthy blood vessels is that of an inverse relationship between the concentration of silicic acid in drinking water and the prevalence of cardiovascular disease in Finland (Schwartz 1977). Underlying mechanism: Silicon is essential for the strength and integrity of the tunica intima, the inner membrane of arteries.

Alzheimer's disease Some evidence suggests that aluminum may increase the risk of developing Alzheimer's disease. Si has been found to significantly reduce the absorption of aluminum by the body, and researchers hypothesize that dietary Si may therefore reduce the risk of developing aluminum induced Alzheimer's disease. The protective role of silicon against aluminum was also confirmed in a French population study of elderly subjects: high levels of aluminum in drinking water had a deleterious effect upon cognitive function when the silicon concentration was low, but when the concentration of silicon was high, exposure to aluminum appeared less likely to impair cognitive function.

MECHANISM OF TOXICITY OF SOME SELECTED METALS

LEAD Lead ranks second among the prioritized hazardous substances issued by the U.S. ATSDR[Agency for Toxic Substances and Disease Registry] in 1999. The noxious effects of this metal have long been well known, especially as regards acute forms of poisoning . However, as for many other contaminants, the threshold level of safety has been drastically lowered recently. Until approximately 30years ago, chronic lead poisoning was defined by blood lead levels above 80(gr/dl),while today a lead level of 30(gr/dl) in the blood is considered excessive and level at above 10(gr/dl) (0.1ppm) are considered potentially harmful, particularly in children. Once absorbed by the body, mainly through breathing and feeding, lead is not metabolized, but mostly expelled. The remaining portion (about 20%) settles into the tissues and notably:

In the blood, where it is carried almost exclusively by the erythrocytes In mineral tissues (bone and teeth), where it deposits In soft tissues (kidney, bone marrow, liver and brain)

The presence of lead in the blood stream(inside the red blood cells and mostly linked to haemoglobin) provokes anaemia Through the blood, lead reaches all other tissues. Because of its capacity to mimic calcium. Lead is stored in the bones and becomes a stable bone component, particularly in the case insufficient calcium intake. This lead deposits may be mobilized and return into the blood stream under particular state of physiological stress (pregnancy, breast-feeding, diseases ), but also as a consequence of greater calcium intake in the diet. This stable presence of lead in bones make recovery from lead poisoning extremely slow, even when toxic agent has been completely elimated. Lead can damage practically all tissues, particularly the kidneys and the immune system. The most deceptive and dangerous form of lead poisoning is that affecting the nervous system. In adults, lead damage mainly causes peripheral neuropathy, which is characterized predominantly by demyelination of the nerve fibres. Intense exposure to

lead to high level (from100 to 200 gr/dl) causes encephalopathy, with the following symptoms: vertigo, insomnia, migraine, irritability and convulsion, seizure and coma. Lower level of the metal gives rise to lead induced neuropathy, which mainly affects the developing brain and provokes behavioural problem and cognitive impairment. Epidemiological studies have shown a strong correlation between lead levels in blood and bones and poor performance in attitude tests(IQ or psychometric tests). A similar correlation has also been found in behavioural studies carried out on animals that had been exposed lead immediately after birth. The learning process is based on the creation and remodeling of synapses and the toxic effect of lead on this process suggests that this metal specifically damages the synaptic function. Action Mechanism Lead toxicity is largely due to its capacity to mimic calcium and substitute it in many of the fundermental cellular processes that depend on calcium. Lead can cross the cell membrane in several ways which are not well understood. Lead transport through the erythrocyte membrane is mediated by an anion exchanger in one direction and by the CaATPase pump in the other direction. In other tissues, lead permeates the cell membrane through voltage-dependent or other types of calcium channels. Once it has penetrate the cytoplasm, lead continues its destructive mimicking action by occupying the calcium binding sites on numerous calcium-dependent proteins. Lead bind to calmodulin, a protein which in the synaptic terminal acts as a sensor of free calcium concentration and as mediator of neurotransmitter release. Furthermore, it alters the functioning of the enzyme protein kinase C, a virtually ubiquitous protein which is of crucial importance in numerous physiological functions. Kinase C is normally activated by modulator outside the cell (hormones, neurotransmitters, etc) through an enzyme chain and in a calcium-dependent manner. Beside many other functions, the activated kinase directly affect the expression of the immediate response gene(IERG). Lead has high affinity for the sites which are typical calcium-binding site in this protein; picomolar doses can take the place of micromolar calcium doses. In model cell system, it has been demonstrated that lead can stimulate gene expression through a mechanism mediated by protein kinase C and it is postulated that this effect may correlate with alteration in synaptic functioning.

Other toxic effects include: Inhibition of heme biosynthesis. Heme is the essential structural component of hemoglobin, myoglobin andcytochromes. Binds to sulfhydryl groups (-SH groups) of proteins.

Fig 3 : Mechanism of lead toxicity. Source : Theodore et al, 2002.

Cadmium
Cadmium is potent poison, which causes different types of damage , including cell death or increase in cell proliferation. Cadmium is a metal which is widely used in industry in alloys, in plating, in batteries and in the pigments used in inks, paints, plastic, rubber and enamel. It is an extremely toxic substance and the major hazard is from inhalation of cadmium metal or cadmium oxide. Although it is present in food, significant oral ingestion is rare and absorption from the gut is poor (58%). However, various dietary and other factors may enhance absorption from the gastrointestinal tract. In contrast, up to 40% of an inhaled dose may be absorbed and hence its presence in cigarettes is a significant source of exposure. Cadmium is bound to proteins and red blood cells in blood and transported in this form, but 5075% of the body burden is located in the liver and kidneys. The half-life of cadmium in the body is between 7 and 30 years and it is excreted through the kidneys, particularly after they become damaged.

Cadium has many toxic effects, primarily causing kidney damage, as a result of chronic exposure, and testicular damage after acute exposure, although the latter does not seem to be a common feature in humans after occupational exposure to the metal. It is also hepatotoxic and affects vascular tissue and bone. After acute inhalation exposure, lung irritation and damage may occur along with other symptoms such as diarrhea and malaise. Chronic inhalation exposure can result in progressive fibrosis of the lower airways leading to emphysema. This results from necrosis of alveolar macrophages and hence release of degradative enzymes which damage the basement membranes of the alveolus. These lung lesions may occur before kidney damage is observed. Cadmium can also cause disorders of calcium metabolism and the subsequent loss of calcium from the body leads to osteomalacia and brittle bones. In Japan this became known as Itai-Itai (Ouch-Ouch!) disease when it occurred in women eating rice contaminated with cadmium. The raised urinary levels of proline and hydroxyproline associated with chronic cadmium toxicity may be due to this damage to the bones.

Kidney damage is a delayed effect even after single doses, being due to the accumulation of cadmium in the kidney, as a complex with the protein metallothionein. Metallothionein is a low molecular weight protein (6500 Da) containing about 30% cysteine, which is involved with the transport of metals, such as zinc, within the body. Due to its chemical similarity to zinc, cadmium exposure induces the production of this protein and 8090% of cadmium is bound to it in vivo, probably through SH-groups on the protein. Thus, exposure to repeated small doses of cadmium will prevent the toxicity of large acute doses by increasing the amount of metallothionein available. The protein is thus serving a protective function. The cadmium-metallothionein complex is synthesized in the liver and transported to the kidney, filtered through the glomerulus and is reabsorbed by the proximal tubular cells, possibly by endocytosis. Within these cells the complex is taken up into lysosomes and degraded by proteases to release cadmium which may damage the cells or recombine with more metallothionein.

Mercury
Mercury can exist in three forms, elemental, inorganic and organic, and all are toxic. However, the toxicity of the three forms of mercury are different, mainly as a result of differences in distribution. Some of these toxic properties have been known for centuries. Elemental mercury (Hg) may be absorbed by biological systems as a vapour. Despite being a liquid metal, mercury readily vaporizes at room temperature and in this form constitutes a particular hazard to those who use scientific instruments containing it for example. Elemental mercury vapour is relatively lipid soluble and is readily absorbed from the lungs following inhalation and is oxidized in the red blood cells to Hg2+. Elemental mercury may also be transported in red blood cells to other tissues such as the CNS. Elemental mercury readily passes across the blood-brain barrier into the CNS and also into the foetus. The metallic compound is only poorly absorbed from the gastrointestinal tract, however. Inorganic mercury, existing as monovalent (mercurous) or divalent (mercuric) ions is relatively poorly absorbed from the gastrointestinal tract (7% in humans). After absorption inorganic mercury accumulates in the kidney. Organic mercury is the most readily absorbed (9095% from the gastrointestinal tract), and after absorption distributes especially to the brain, particularly the posterior cortex. All the forms of mercury will cross the placenta and gain access to the foetus, although elemental

mercury and organic mercury show greater uptake. The concentrations in certain foetal tissues, such as red blood cells, are greater than in maternal tissue. Mercury is eliminated from the body in the urine and faeces with the latter being the major route. Thus, with methyl mercury 90% is excreted into the faeces. Methyl mercury is secreted into the bile as a cysteine conjugate and undergoes extensive enterohepatic recirculation. The halflife of mercury is long but there are two phases, the first being around 2 days, then the terminal phase which is around 20 days. However the half-life will depend on the form of mercury. Thus methyl mercury has a half-life of about 70 days whereas for inorganic mercury this is about 40 days.

Toxic effects
Elemental mercury vapour Although there may be toxic effects to the respiratory system from the inhalation of mercury vapour, the major toxic effect is to the CNS. This is especially true after chronic exposure. There are a variety of symptoms such as muscle tremors, personality changes, delirium, hallucination and gingivitis.

Inorganic mercury Mercuric chloride and other mercuric salts will, when ingested orally, cause immediate acute damage to the gastrointestinal tract. This may be manifested as bloody diarrhoea, ulceration and necrosis of the tract. After 24 h renal failure occurs which results from necrosis of the pars recta region of the proximal tubular epithelial cells. The epithelial cells show damage to the plasma membrane, endoplasmic reticulum, mitochondria and effects on the nucleus. The result of this damage is excretion of glucose (glycosuria), amino acids (aminoaciduria), appearance of proteins in the urine (proteinuria), and changes in various metabolites excreted into urine.

Organic mercury Mercury in this form, such as methyl mercury, is extremely toxic, mainly affecting the CNS. However, some organomercury compounds such as phenyl and methoxyethyl mercury cause similar toxic effects to inorganic mercury. There have been a number of instances in which human exposure to methyl mercury has occurred, and consequently data is available on the toxic effects to man as well as experimental animals. Methyl

mercury was responsible for the poisoning which occurred in Japan, known as Minamata disease. This resulted from industrial effluent containing inorganic mercury contaminating the water of Minamata Bay in Japan. The microorganisms in the sediments at the bottom of the bay biotransformed the inorganic mercury ions into methyl and dimethyl mercury. As this form of mercury is lipid soluble it was able to enter the food chain and so become concentrated in fish as a result of their eating small organisms which had absorbed the methyl mercury. The local population who consumed the fish therefore became contaminated with methyl mercury. Another episode occurred in Iraq when seed grain treated with a methyl mercury fungicide was used to make bread. Over 6000 people were recorded as exposed and more than 500 died. The major features of methyl mercury poisoning are paresthesia, ataxia, dysarthria and deafness..

Mechanism Mercury is a reactive element and its toxicity is probably due to interaction with proteins. Mercury has a particular affinity for sulphydryl groups in proteins and consequently is an inhibitor of various enzymes such as membrane ATPase, which are sulphydryl dependent. It can also react with amino, phosphoryl and carboxyl groups. Brain pyruvate metabolism is known to be inhibited by mercury, as well as lactate dehydrogenase and fatty acid synthetase. The accumulation of mercury in lysosomes increases the activity of lysomal acid phosphatase which may be a cause of toxicity as lysosomal damage releases various hydrolytic enzymes into the cell, which can then cause cellular damage. Mercury accumulates in the kidney and is believed to cause uncoupling of oxidative phsophorylation in the mitochondria of the kidney cells. Thus, a number of mitochondrial enzymes are inhibited by Hg2+. These effects on the mitochondria will lead to a reduction of respiratory control in the renal cells and their functions such as solute reabsorption, will be compromised

Chromium
Chromium (IV) has long been recognized as a toxin in plant systems and as a carcinogen in human and mammalian systems. The actual mutagenic or toxic species of chromium is one or more of the reactive intermediate produced in the reduction of Cr(IV) to Cr(III). Glutathione is suspected to be a reductant here due to its ability to produce long-lived Cr(V/IV) intermediate during the reduction of chromium(IV). GSH-Cr interaction in

plant have been fairly well elucidated (Shanker et al, 2004). Dichromate reacts with glutathione at the sulfhydryl group forming an unstable glutathione-Cr03 complex. The halliwel Asada pathway is the key pathway whereby Cr toxicity or tolerance is mediated. The high content of dihydro-ascorbate (DHA) in combination with an absence of active scavenging of free radicals and blockage of normal cell cycle progression by DHA is one of the main mechanism of chromium induced toxicity in plant (Shanker et al, 2004). Cr(VI) can function as a hill reagent and can inhibit electron transport both in the photosynthetic and mitochondrial apparatus thus accounting for reduced NADPH pool. The critical balance between the available NADPH pool and ROS production by chromium would decide the redox status of a cell in both plants an animals. ChromiumDNA interaction is one of the well explained mechanism of action of Cr in apoptosis and carcinogenesis. Chromium associate with both DNA bases and the phosphodiester

backbone and the binding occur through both covalent binding and electrostatic interactions. The base specific binding of Chromium has revealed a genera, but not absolute , preference towards the formation of Cr(III) guanine DNA adducts and polyriboguanylic acid (poly(G)) in the case of RNA(Obrien et al,2003). Cr-DNA crosslinks (Cr-DPCs) have been reported to extensively developed respectively between DNA and non histone proteins and RNA and cytoplasmic protiens in many animal system. (Reem et al,2007). Cr(VI)-containing compounds are well known carcinogenic compounds. Evidence also have it that chromosomal

abnormalities(micronuclei) and genomic instability are possibly involved in the induction of cancer by Cr(VI) (Wise et al, 2008). DNA interstand crosslinks(ICLs) are caused by Cr interacting with reaction centers on the complementary strands of DNA. A notion that has received much attention is that intracellular Cr(VI) mediate a fenton-like reaction mediating ROS production which are responsible for nearly all the toxicity and genotoxicity caused by Cr(VI) (Shanker et al, 2005)

Conclusion
According to UNEPA(United Nation Environmental Programme Agency) about 5.3 million tones of electronic waste was generated worldwide in year 2009 and only 13% was recycled, and most of these recycling were done in the developed countries. Due to poor regulations on e-waste recycling in the developing countries, a lot of methods to retrieve certain metals from electronics and disposing e-waste are polluting the environment. These toxic materials in the e-waste when disposed indiscriminately or even used as landfills, can leach into the underground water and accumulates in sea foods and plants. This may cause health hazard ranging from tissues or organs damage to chromosomal abnormalities, DNA damage, cancer and eventually death.

Developed countries and places that are not home to e-waste landfills and pollution are not completely excluded from the effects of e-waste. Pollutants can seep into the oceans or travel in the air, thus making e-waste not to be limited by boundaries. There fore individuals, NGOs and the government together to put up a functioning regulations and well structured recycling programme that will help ,if not to stop

completely, but to reduce to minimal the challenges of e-waste.

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