Negative Effects Produced By Pollution Biology Essay

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Although pollution had been known to exist for a very long time (at least since people started using fire thousands of years ago), it had been seen the growth of the truly global proportions only since the onset of the industrial revolution during 19th century.environmental pollution england 19th century

The industrial revolution brought with it the technological progress such as the discovery of oil and its virtually universal use throughout different industries.

Technological progress facilitated by super efficiency of capitalist business practices (division of labour - cheaper production costs - overproduction - overconsumption - over pollution) had probably become one of the main causes of serious deterioration of the natural resources.

At the same time, of course, the development of natural sciences led to the better understanding of negative effects produced by pollution on the environment.

Environmental pollution is a problem both in the developed and developing countries. Factors such as population growth and urbanization invariably have greater demands on the planet and stretch the use of the natural resources to the maximum.

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It has been argued that the carrying capacity of Earth is significantly smaller than the demands placed on it by large numbers of the human population. And overuse of natural resources often results in the nature's degradation.

Environmental pollution is any discharge of materials or energy into water, soil, or air that causes or may cause acute (short-term) or chronic (long-term) detriment to the Earth's ecological balance or that lowers life quality. Pollutants may cause primary damage, with direct identifiable impact on the environment, or secondary damage in the form of a minor perturbations in the delicate balance of the biological food webs that are detectable only over the long periods of time.

Sources of Environmental Pollution

Fossil Fuel Sources of Environmental Pollution  

In the modern industrialized societies, fossil fuels which are the oil, gas, coal transcended virtually all imaginable barriers and firmly established themselves in our everyday lives.

Not only do we use fossil fuels for our obvious everyday needs (such as filling a car), as well as in the power-generating industry, they, specifically the oil are also present in such products as all sorts of plastics, solvents, detergents, lubricating oils, asphalt, a wide range of chemicals for the industrial use, etc.

Combustion of fossil fuels produces extremely high levels of air pollution and is widely recognized as one of the most important "target" areas for the reduction and control of environmental pollution.

Fossil fuels also contribute to 2 results which are the soil contamination and water pollution. For example, when oil is transported from the point of its production to further destinations by the pipelines, an oil leak from the pipeline may occur and results in polluting soil and subsequently groundwater. When oil is transported by tankers by ocean, an oil spill may occur and results in the pollution of ocean water.

Of course, there are other natural resources whose exploitation is a cause of serious pollution; for example, the use of uranium in nuclear power generation produces very dangerous waste that would take thousands of years to neutralize.

But there is no doubt that fossil fuels are among the most serious sources of environmental pollution.

Power-generating plants and transport are probably the biggest sources of fossil fuel pollution.

The Common sources of fossil fuel pollution are:

Industry:

Power-generating plants

Petroleum refineries

Petrochemical plants

Production and distribution of fossil fuels

Other manufacturing facilities

Transport:

Road transport (motor vehicles)

Shipping industry

Aircraft

Fossil fuel combustion is also a major source of carbon dioxide (CO2) emissions and perhaps the most important cause of the global warming.

Other (Non-Fossil Fuel) Sources of Environmental Pollution

Among other pollution sources, agriculture (livestock farming) is worth mentioning it as the largest generator of ammonia emissions resulting in air pollution. Chemicals such as the pesticides and fertilizers are also widely used in agriculture, which may lead to water pollution and soil contamination as well.

1: Air Pollution

Description:

The body's primary defense against the air pollutants is the respiratory system. When deposited on the lung epithelium, particulate pollutants are cleared from the lungs by either coughing or ciliary action, or ingested by the alveolar macrophages. Because of their small molecular size, most gaseous pollutants bypass the pulmonary immune defenses and are absorbed directly into blood stream.

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The damage produced depends on the nature of the pollutant. In the case of a particulate pollutant, such as tobacco smoke or asbestos, the alveolar macrophages, which ingest the particles, eventually serve as the localized sites of inflammation or cancer of the lung. Because gaseous pollutants usually enter the blood circulation, damage occurs throughout the body. It has been difficult to establish a relationship between the specific air pollutants and cancers. It is hard to identify the level and frequency of exposure to environmental toxins. Environmental chemicals are never encountered singly, but in combinations which may negate, or even promote, the cancer-causing potential of the individual pollutants.

People vary in their sensitivity and susceptibility to cancer. A person's nutritional status may have a protective effect against cancer, such as has been hypothesized for cadmium, zinc and prostate cancer. The presence of other risk factors, i.e.  Tobacco smoking, or occupational exposure to high-levels of carcinogens, also influences the outcome.

The formation of smog:

Air pollution is formed as a result of many natural (pollen grains, fungal spores, forest fires and volcanic eruptions) and manmade (vehicles exhaust, incinerators, mining, tobacco smoking and smelting) sources.

Gaseous pollutants include substances which are gaseous at normal temperatures and pressures, as well as vapors of substances that are liquid or solid at normal temperatures and pressures. Gaseous pollutants include, hydrocarbons, carbon monoxide, ozone, nitrogen oxides, hydrogen sulfides and sulfur oxides. Particulate pollutants include dust, fumes (such as zinc or lead oxides), mists, sprays or smoke.

Primary pollutants are those that are emitted into the air. While, Secondary pollutants are those formed in the atmosphere, such as photochemical smog and ozone. Nitrous oxides and hydrocarbons from the combustion of the fuel react with the ultraviolet waves in sunlight in the atmosphere for production of ozone.

Production of the ozone and smog is light-dependent. Levels are at their lowest at night, increase through the morning, peak at mid-day, decrease at the afternoon, only to mildly increase during the evening rush when there are many cars on the road. Pollution levels then drop to the minimum at overnight.

Smog can build to unhealthful levels when a meteorological condition called an "inversion layer" occurs. This layer of warm air prevents the pollutants from escaping vertically, and is usually accompanied by low surface winds which will prevent horizontal dilution of the irritants. The smog thus accumulates over an area until a change in weather condition happens.

Monitoring air pollution and smog levels:

Environmental monitoring of the air pollution and toxic chemical exposure can be measured by biological indicators. Blood and urine specimens can be used in measuring the exposure to at least 100 different chemicals. Hair analysis is also reliable indicator for the exposure to arsenic, mercury, cadmium, manganese, antimony, nickel and cobalt. Environmental pollution studies should sample a groups of a 10-year olds, because they are generally non-smokers, who have had no occupational exposure to the toxic chemicals.

Types Of Environmental Pollution

Smog and vehicles:

Vehicles are the major sources of the toxic and carcinogenic air pollutants. Gaseous pollutants, such as nitrogen oxide, carbon monoxide and hydrocarbons, and particulate matter, such as lead and smoke, are released in exhaust from the automotive engines. Diesel engines from trucks, buses, and some cars, use to emit carcinogenic carbon compounds, odors and visible smoke.

The switch to the catalytic converters and fuel injection systems has resulted in a decrease of the carbon monoxide and nitrous oxide emissions. The unleaded gasoline required by newer cars has resulted in less atmospheric lead. However, catalytic converters, and the fuel additives in unleaded gasoline results in the release of manganese, a trace metal which accumulates in tissues, displaces zinc and can be toxic at high concentrations.

Causes:

Cadmium

Characteristic:

It is one of the rarer elements in nature. It competes with zinc for the binding sites in body.

Sources:

90% of emissions into the atmosphere are from the smelting ores, and the processing and manufacture of metallic alloys. The rest is from automobile tire wear, incineration, tobacco smoke, burning of car motor oils and other industrial processes. The exposure in urban areas with no cadmium emitting industries is low. Cadmium levels in the kidneys and liver of smokers are twice than that of non-smokers. Non-smoking individuals, who are not employed in the cadmium-related industries, take in most of their cadmium through the food.

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Lab diagnosis:

Tests that should be done if cadmium inhalation is detected.

Chest X-ray - looking for chemical pneumonitis and pulmonary edema.

Measurement of oxygen saturation.

Renal and hepatic functions - to check for the signs of liver or kidney damage.

Cadmium blood levels. Blood cadmium indicates a recent exposure and urine cadmium indicates a body burden.

Tests that should be done in case of acute cadmium ingestion.

Hepatic and renal functions.

Electrolytes.

Effects:

Ingestion of low-levels of cadmium has been shown to cause emphysema and reduced lung function in male rats. Cadmium which is absorbed through the lungs is first stored in the liver, and then they are slowly released to the kidneys and the endocrine glands. Chronic occupational exposure to cadmium can result in the production of glomerular and tubular kidney dysfunction. Chronic occupational exposure to cadmium may also promote the development of cancer of the prostate, by disruption of zinc-hormonal balance in the organ.

Treatment:

Currently, there are no treatments for cadmium poisoning. Only symptoms can be treated. There are several steps that can be taken inorder to help aid the body in processing excess or toxic levels of cadmium. With minor exposure the symptoms and effects of cadmium exposure usually subside within few days. Higher levels of exposure will lead to a serious problem.

To aid in the removal of cadmium, chelating agent can be used. The agent will help to bond the excess metals present in the bloodstream which will speed up the removal of the excess cadmium. Hemodialysis can also be used to remove the toxins from the bloodstream.

Note: The above treatments are only effective for cases of oral poisoning. They have no effect in the cases of cadmium fume inhalation.

Lead

Characteristics:

A dense, grayish, soft and extremely toxic metal; one of the most common particulate pollutants.

Sources:

Combustion of tetraethyl lead in leaded gasoline. Lead smelters and paint. Contaminated dust, soil and foods which is grown in urban environments.

Lab diagnosis:

The list of the diagnostic tests mentioned in various sources as used in the diagnosis of Lead poisoning includes:

Lead blood test

Lead urine test

Effects:

Lead interferes with the development and maturation of red blood cells. Chronic exposure damages the reproductive organs, kidneys and the central nervous system. Symptoms include: stippled red blood cells, apathy, fatigue, drowsiness, insomnia, irritability, behavior disorders, constipation and vomiting.

Treatment:

Chelation therapy. In this treatment, medications that is taken binds with the lead so that it's excreted in urine.

EDTA therapy. Doctors treat lead levels which is greater than 45 mcg/dL of blood with a chemical named ethylenediaminetetraacetic acid (EDTA). Depending on lead level, it will decide if it is required to have more than one treatment. In such severe cases, however, it may not be possible to reverse the damage that has already occurred.

Manganese-fuel additives

Characteristics:

A soft, silvery or reddish-gray metal. It is used in the alloy steel industry for deoxidation, for strengthening and hardening steel.

Sources:

The combustion of fossil fuels containing thylcyclopentadienyltricarbonyl manganese anti-knock additives, and the catalyst in automotive catalytic converters.

Effects:

Manganic pneumonia may result from a low-level environmental air pollution. Manganese accumulates in the body organs that are rich in mitochondria, especially the liver. Excessive exposure results in disorders of the lung, and liver, in addition, the central nervous, gastrointestinal and genitourinary systems. Occupationally-related manganese poisoning is characterized by headaches, dermatitis, insomnia, itching and decreased libido. Manganese accumulates in the brain; the chronic toxicity produces Parkinson-like symptoms: spastic muscle movements, tremors, and slow, slurred speech.

Chlorinated hydrocarbons

Characteristics: Vary.

Sources:

Gasoline incompletely burned in auto engines or evaporates from the tanks or fuel lines. Industries which use solvents. Paints and dry-cleaning fluids.

Lab diagnosis :

By measuring the amount of the chemical in the breath is one of the ways for testing of either trichloroethylene or tetrachloroethylene exposure. The breath test, if it is performed soon after exposure, it can detect if the individual has been exposed to a small amount of trichloroethylene. Because it is stored in the body's fat and slowly released into bloodstream, tetrachloroethylene can be detected in the breath for weeks following a heavy exposure. Both trichloroethylene and tetrachloroethylene and trichloroacetic acid (TCA), the breakdown product of both chemicals, can be detected in the blood.

These procedures are useful only in case if the exposure is recent (within weeks or less), because both solvents are rapidly eliminated from the body. In addition, samples of blood and urine tests can be used in identifying the chemicals and their breakdown products in individuals suspected of being exposed to both the trichloroethylene and tetrachloroethylene.

A chest x-ray or ECG monitoring may also be necessary.

Effects: Form photochemical smog in a reaction with ozone. Photochemical smog causes reduced visibility and eye irritation.

Treatment:

Treatment is non-specific and includes the removal from exposure, decontamination and supportive care (oxygen). Benzodiazepines are administered for seizures.

Sulphur dioxide

Characteristics:

It is a colourless gas with a pungent odor. It is corrosive to metal.

Source:

It is a by-product of combustion of coal and oils for heat and power; acid and paper manufacturing; petroleum refineries.

Effects:

In the respiratory tract, it combines with water in order to form the irritant, sulfuric acid. It causes constriction of the bronchi, and slowing down the beating and clearing action of the respiratory tract's cilia. Symptoms include decreased lung function, throat and lung irritation, increased susceptibility to respiratory infection, and exacerbation of cardiac and pulmonary diseases.

Carbon monoxide

Characteristics:

An odourless, colourless, and tasteless gas.

Source:

By incomplete combustion of carbon-containing fuel. Motor vehicles.

Lab diagnosis:

Because the signs and symptoms of carbon monoxide poisoning are not specific, a blood test to look for it is considered to be the best way to perform the diagnosis.

Effects:

This gas achieves its damage by combining preferentially with hemoglobin, to the exclusion of oxygen. Symptoms include: throbbing headaches, giddiness, weakness, nausea, dizziness, vomiting, irritability, proceeding to collapse, coma, convulsions and even death. Carbon monoxide can cause ion of coronary heart disease and even precipitate attacks of angina pectoris.

Treatment:

The treatment of carbon monoxide poisoning is high-dose oxygen, usually by using a facemask attached to an oxygen reserve bag.

Carbon monoxide levels in the blood may be periodically checked until they are low enough to be for the patients to be back home.

In severe poisoning, if available, a hyperbaric pressure chamber can be used to give even a higher doses of oxygen.

Nitrogen oxides

Characteristics:

A yellow-brown gas with a disagreeable pungent odour.

Source:

It is a product of high temperature combustion. It is a product or by-product of fertilizer, metal-cleaning, explosive or nitric acid manufacturing industries.

Mechanism:

There are several mechanisms by which nitrogen oxides have been demonstrated to affect the biology of living cells. These include the oxidation of iron-containing proteins such as ribonucleotide reductase and aconitase, activation of the soluble guanylate cyclase, ADP ribosylation of proteins, protein sulfhydryl group nitrosylation, and iron regulatory factor activation. NO has been shown to activate the NF-κB in the peripheral blood mononuclear cells, an important transcription factor in iNOS gene expression in the response to inflammation. It was found that NO acts through stimulation of the soluble guanylate cyclase, which is a heterodimeric enzyme with subsequent formation of the cyclic GMP. Cyclic GMP cause the activation of the protein kinase G, which causes phosphorylation of myosin light chain phosphatase, and therefore, inactivation of myosin light-chain kinase, which leads ultimately to the dephosphorylation of the myosin light chain, causing a smooth muscle relaxation

Effects:

Results in the production of the orange to reddish brown haze that clouds the view in certain cities. It is primary component in the formation of photochemical smog. In the respiratory tract, it combines with moisture in order to produce the irritant, nitric acid. Symptoms of exposure include: pulmonary edema and shortness of breath. Nitric oxide poisoning is detected by chest pain, bloody sputum, fever, chills, coughing, nausea and vomiting.

2: Water Pollution

Water pollution is any type of contaminant which is released into the water supply. The classical image of this is the pipe outside a factory dumping waste into a river or lake, but water pollution can also happen through the illegal trash dumping near a water source, or simply by pesticides seeping through the soil and into the groundwater, where they will gradually pass into the sea and the rivers.http://www.braceforimpact.thomasalewis.com/Images/water%20pollution_china.jpg

Sources :

The important sources of water pollution are the industrial effluents, domestic wastes and agricultural wastes. Other sources include oil spills, marine dumping, atmospheric deposition radioactive waste, global warming and eutrophication. Among these, domestic waste and industrial waste are the most important sources leading to water pollution. 

Domestic Waste: Domestic waste is waste water generated from the household activities. It contains organic and inorganic materials such as the phosphates and nitrates. Organic materials are food and vegetable waste, whereas, the inorganic materials come from soaps and detergents. Usually people dump the household wastes in the nearby water source, which will result in water pollution. The amount of the organic wastes that can be degraded by the water bodies is measured in terms of Biological Oxygen Demand (BOD). BOD is the amount of oxygen which is required by microorganisms to decompose the organic waste present in the sewage. The higher the amount of BOD, the more the water is polluted with organic waste. Many of the people are not aware of the fact that soaps and detergents causes the enrichment of the water bodies with phosphates. These phosphates often contribute to algal bloom and eutrophication, which is the most common in stagnant water bodies such as ponds and lakes. Algal bloom and eutrophication lead to the suffocation of fish and other organism in the water.

Industrial Waste: Waste water from the manufacturing and processing industries contributes to water pollution. The industrial wastes contain organic pollutants and other toxic chemicals. Some of the pollutants from industrial source include mercury, lead, asbestos, nitrates, phosphates, oils…etc. Wastewater resulting from food and chemical processing industries contribute more to the water pollution than other industries such as distilleries, thermal power plants and leather processing industries. Also dye industries generate waste water which affects the water quality especially water color. Since the water color is changed, there will be alteration in the light penetration and hence it will disturb the aquatic plants and animals. Large numbers of the big industries have come up with waste water treatment plants. However, it is not the case with small-scale industries. It is very difficult to treat the waste water from industries.

Agricultural Waste: Agricultural waste includes slurries, manure and runoffs. Most of the agricultural farms use the pesticides and chemical fertilizers .The runoffs from these agricultural fields cause water pollution to the nearby water sources such as the streams, rivers and lakes. The seepage of fertilizers and pesticides causes the ground water pollution, which is commonly known as leaching. Although, quantity of agricultural waste is low, the effects are highly significant. It causes nutrient and organic pollution to both the water and soil. Nutrient pollution causes an increase in the level of nitrates and phosphates in the water bodies, which leads to eutrophication.

Depending upon the origin, the sources of water pollution are classified as point source and non-point source and ground-water pollution. Point source pollution discharges the harmful waste materials directly into water bodies, for example, disposal through wastewater treatment plants. On the other hand, non-point source pollution delivers materials indirectly through other ways, for example, water pollution from acid rain.

Causes

Mercury Toxicity:

The consumption of fish is the most significant source of the ingestion-related mercury exposure in humans and animals, although plants and livestock also contain mercury due to the bioaccumulation of mercury from soil, water and atmosphere, and also due to biomagnification by the ingestion of other mercury-containing organisms

Signs and symptoms:

The common symptoms of mercury poisoning includes peripheral neuropathy (displayed as  itching, burning or pain), skin discoloration (fingertips, pink cheeks and toes), swelling, and desquamation (shedding of skin).

Because mercury blocks degradation pathway of the catecholamines, epinephrine excess causes profuse sweating, tachycardia , increased salivation, and hypertension. Mercury is thought to inactivate S-adenosyl-methionine, which is necessary for the catecholamine catabolism by catechol-o-methyl transferase.

Affected children may display red cheeks, nose and lips, teeth, loss of hair, and nails, transient rashes, hypotonia (muscle weakness), and increased sensitivity to light. Other symptoms may include kidney dysfunction (e.g. Fanconi syndrome) or neuropsychiatric symptoms such as the emotional lability, memory impairment, or insomnia.

Thus, the clinical presentation may display pheochromocytoma or Kawasaki disease.

Mechanism:

Mercury is such a highly reactive toxic agent that it is very difficult to identify its specific mechanism of damage .It causes damage to the central nervous system, endocrine system, kidneys, and other organs, and adversely affects the mouth, gums, and teeth. Exposure over long period of time or heavy exposure to mercury vapor can result in a brain damage and ultimately death. Mercury and its compounds are very toxic to fetuses and infants. Women who have been exposed to mercury in the pregnancy have sometimes given birth to children with a serious birth defects

Young Children exposed to mercury can have severe neurological consequences, preventing nerve sheaths from developing properly. Mercury inhibits the formation of myelin.

There is some evidence that the mercury poisoning may predispose to Young's syndrome (men with bronchiectasis and low sperm count).

Mercury poisoning's effects partially depend on whether it has been caused by the exposure to elemental mercury, inorganic mercury compounds, or organomercury compounds.

Lab diagnosis :

Mercury testing is done in order to detect the presence of an excessive amount of mercury. It may be ordered by the doctor to indicate whether it is acute or chronic exposure to increased levels of mercury. It may also be ordered to monitor those who are exposed to mercury in workplace.

More than one type of sample may be collected and tested.

Blood is primarily tested in order for the detection of the presence of methyl mercury. Other forms of the mercury can also be detected in the blood, but according to the Agency for Toxic Substances and Disease Registry (ATSDR), the amount present will decrease by half about every 3 days as the mercury moves into other organs.

Urine is used for test of metallic mercury and inorganic forms of mercury, but it cannot be used to determine the exposure to methyl mercury.

Hair testing may also be useful in the detection of methyl mercury exposures that occurred several months previously, but because hair testing is relatively complex, it is not used frequently.

However, not routinely ordered tests, mercury has been shown to be present in nails, stool, breast milk, and breath.

Treatment:

Treatment steps of mercury toxicity consists of removal from the source of exposure, supportive care, and chelation therapy. However, laboratory studies are important, acute treatment in critical situations should be based on the history and clinical presentation without waiting for the laboratory confirmation.

Chelating agents containning thiol groups, which bind to the mercury. For acute, inorganic toxicity, dimercaprol has been recommended traditionally, but oral agents are gaining prominence. Chelation with 2,3-dimercaptosuccinic acid (DMSA or succimer) has been shown to result in increased mercury excretion compared to the N -acetyl-D,L-penicillamine in adults with acute mercury vapor exposure. DMSA is well tolerated and has recently shown efficacy in children exposed to mercury.

Exchange transfusion has also been used as a treatment.

Despite the increased excretion of mercury with the chelating agents, chelation removes only a small portion of the body mercury stores. Moreover, the efficacy of chelating agents in curing neurological complications has not been established; however, among the patients with amalgam fillings, placebo responses to chelation treatment have been reported.

Chlorine Toxicity:

Excess chlorine usage in water will affect the fish and will cause bioaccumulation resulting in toxicity, and as a result affecting animals and humans.

Signs and symptoms:

Eye irritation

Bladder cancer

Nose irritation

Asthma

Lung irritation

Anemia

Copper toxicity

Pharynyx irritation

Lead toxicity

Weakended immune system

Stomach discomfort

Lab diagnosis:

History: Symptoms may occur immediately or shortly after the exposure. The individual may suffer from irritation of the eyes, nose, and throat; lacrimation, coughing; bloody nose; chest pain; or burning of the skin. Pertinent history includes the nature and duration of exposure as well as any previous lung problems. Patients may complain from tender abdomen, weak muscles, headache, nausea, and emesis.

Physical exam: Signs of respiratory distress, such as rapid breathing, bluish skin due to the lack of oxygen, difficulty breathing, flaring of the nose, retractions of the chest muscles, wheezing, rales (a sign that fluid is in the lungs), crepitus (heard when there is air in the thoracic cavity), and diminished breath sounds) may be present. Symptoms of pulmonary edema can be delayed up to 2 days after the exposure. A rash may be presented on the skin. Shock or coma may also occur. Patients may also have an elevated heart rate, increased hoarseness, and tears.

Tests:, chest x-rays, Pulmonary function tests, ECG, ventilation perfusion scan (VQ scan), and arterial blood gases may be done. Patients may benefit from the serum electrolytes, pulse oximetry, and peak flow meters. The patient may also need either bronchoscopy or laryngoscopy to help establish the extent of harm done to the airway and lungs.

Treatment:

The individual should be removed from the exposure. The symptoms and effects are treated as they occur. The pH of the eye and skin is normally 7.4; the skin may need to be rinsed with saline in order to achieve the proper pH level. The eye needs to be examined with a slit lamp with fluorescent staining, after which an antibiotic ointment can be administered. Oxygen should also be provided, and the fluids should be reduced if the individual has acute respiratory distress syndrome. Individuals may also benefit from beta agonists if they have difficulty in breathing. Those with laryngeal spasm need to be intubated and placed on a mechanical ventilation.

Lead Toxicity:

The routes of exposure to lead include contaminated air, water, soil. Occupational exposure is a common cause of lead poisoning occurring in adults.

Signs and Symptoms:

Lead poisoning can cause a wide variety of symptoms and signs which vary depending on the individual and duration of the lead exposure. Symptoms are non specific and may be subtle, and someone with elevated lead levels may have no symptoms. Symptoms usually develop over weeks to months as lead builds up in the body during the chronic exposure, but acute symptoms can happens from brief, intense exposures. Symptoms from exposure to organic lead, which is probably more toxic than inorganic lead due to its lipid solubility, occur more rapidly. Poisoning caused by organic lead compounds has symptoms predominantly in the central nervous system, such as insomnia, cognitive deficits, delirium, tremor, hallucinations, and convulsions.

Symptoms may differs in adults and children; the main symptoms in adults are headache,  memory loss, abdominal pain, kidney failure, male reproductive problems, and weakness, pain, or tingling in the extremities. The signs and symptoms in the children are loss of appetite, vomiting, abdominal pain, weight loss, constipation, anemia, kidney failure, irritability, lethargy, learning disabilities, and behavior problems. Children may also show hearing loss, delayed growth, clumsiness, drowsiness, or loss of new abilities, especially speech skills. Symptoms may appear in children at a lower blood lead levels than in the adults.

The early symptoms of lead poisoning in adults are commonly non specific and include depression, diarrhea, loss of appetite, intermittent abdominal pain, nausea, muscle pain and constipation. Other early signs in the adults include malaise, fatigue, decreased libido, and insomnia.

Lab diagnosis:

The list of diagnostic tests used in the diagnosis of Lead poisoning includes:

Lead blood test

Lead urine test

Action Mechanism:

The lead's toxicity is largely due to its capacity to mimic calcium and substitute it in many of the fundamental cellular processes that depend on the calcium.

Lead can pass the cell membrane in various ways, which are not yet understood. Lead transport through the erythrocyte membrane is mediated by the anion exchanger in one direction and by the Ca-ATPase pump in the other direction. In other tissues, lead permeates the cell membrane through the voltage-dependent or other types of calcium channels.

Once it has penetrated the cytoplasm, lead continues its destructive action by occupying the calcium binding sites on numerous calcium-dependent proteins. Lead binds to calmodulin, is a protein, which in the synaptic terminal acts as a sensor of free calcium concentration and as a mediator of the neurotransmitter release. Moreover, it alters the functioning of the enzyme protein kinase C, is a virtually ubiquitous protein which is of crucial importance in many physiological functions. Kinase C is normally activated by modulators outside the cell (hormones, neurotransmitters, etc.) through an enzyme chain and in a calcium-dependent manner. Besides many other functions, the activated kinase directly affects the expression of the Immediate Early Response Genes (IERG). The lead has a high affinity for the sites which are typical calcium-binding sites in this protein; picomolar doses can take over the place of micromolar calcium doses. In model cell systems, it has been presented that lead can stimulate gene expression through a mechanism which is mediated by protein kinase C and it is postulated that this effect may be correlated with the alterations in synaptic functioning.

Treatment:

Chelation therapy. In this treatment, Medication taken binds with the lead so that it's excreted in urine.

EDTA therapy. Doctors treat lead levels greater than 45 mcg/dL of blood with a chemical called ethylenediaminetetraacetic acid (EDTA). Depending on your lead level, more than one treatment may be needed. In such severe cases, however, it may not be possible to reverse damage that has occurred already.

3: Soil Contaminationhttp://www.body-detox-info.com/image-files/soil-pollution.jpg

Soil contamination is any type of waste or poison which slowly leaches into the soil, rendering it unable to support life or growth. Many agricultural chemicals are linked to this type of the environmental pollution, especially veterinary medicines, and non-organic fertilizers, pesticides.

Sources:

Acid Rain

The oxides of the sulphur and nitrogen, chlorides, fluorides, ammonium etc….. emitted into the atmosphere in the combustion from various industries come down as dry or wet deposition (acid rain) onto the soil and result in lowering the soil pH. Increased acidity of soil will results in following effects.

The activity of soil microbes, particularly of the decomposers, is reduced. The decomposition of organic matter and consequently nutrient cycling in the soil is also reduced. This will adversely affects the growth of plants.

The soil bases are leached down as a result of soil acidity. As the exchangeable bases become deficient in the soil, plant growth is reduced due to the nutrient deficiency.

The roots, particularly the root hairs, are damaged due to the reduction in nutrient uptake by plants.

Increased acidity will mobilizes heavy metals like Al, Cd, Zn, Hg, Mn, Fe etc….. These spread rapidly in the soil along with soil water and reach to concentrations which are toxic to plants. Consequently, plants show species specific metal toxicity symptoms. Aluminuim-toxicity generally damages the root hairs and reduces nutrient uptake while iron-toxicity has a general adverse effect on plant growth.

In some soils, acidification increases the weathering of silicate minerals damaging the mineral structure of the soil. This will lead to poor growth of vegetation in general.

In some marginal soils and grasslands,the acidification increases the supply of plant nutrients such as sulphur and nitrogen. The vegetation is thus, benefited by soil acidification and plants may show better growth.

Chemical fertilizers

Chemical fertilizers are generally used far in excess of the requirements of the crop. The unutilized fertilizers leads to soil pollution.

The toxic concentration of nitrogen fertilizers causes characteristic symptoms of nitrate or nitrite toxicity in plants, particularly in the leaves. Nitrogenous fertilizers generally cause

potassium defficiency, increased carbohydrate storage and reduced proteins, alteration in the amino acid balance and consequently change in the quality of proteins.

Ammonium fertilizers result in the production of ammonia around the roots that may escape the soil and cause ammonia injury to the plants. Ammonium and nitrate produce acids in the soil and increase the soil acidity. Nitrate and nitrite bacteria are reduced while ammonifying bacteria are increased in the soil causing a disturbing to the nitrogen cycle. Excess potash in the soil decreases the amount of ascorbic acid and carotene in the plants. A super phosphate causes deficiency of Cu and Zn in the plants by interfering with their uptake. Excess lime prevents the release of Co, Ni, Mn and Zn from soil and their uptake by plants is reduced resulting in their deficiency symptoms. Excess deposition of various substances released from the chemical fertilizers into the soil will generally cause their over absorption by plants. These over absorbed substances will become accumulated in plant parts e.g. nitrogen and sulphur are deposited in the leaves.

Effects of industrial effluents:

Various inorganic and organic chemicals are present in the industrial effluents. These chemicalsmostly remain tied up in the soil and are not readily available to the plants. However, they affect several soil characteristics.

The Effluents affect mineral structure, soil pH, exchangeable base status etc….. of the soil and thus indirectly affect the plants.

The soil pH is disturbed results in making soil either acidic or alkaline.

Various inorganic and organic chemicals are accumulated in the soil up to levels which are toxic to the plants.

In highly polluted soils, plants absorb and accumulate the toxic substances. These substances may or may not produce direct injury symptoms in plants but are passed on to a higher trophic levels.

Herbicides & Pesticides

Herbicides and pesticides to kill the insects seeps into soil. This affects the soil at a biological level, killing organisms that live in the soil as well as insects and pests. Natural bacteria present in the soil carry nutrients to the roots of plants.The Topical applications of herbicides and pesticides will upset this balance. In addition, rain can also cause runoff that transports both herbicides and pesticides to local streams and rivers. This will pollutes the water source and the soil near the water source.

Sewage and ash pollution

Sewage matter is commonly used as a fertilizer or is deposited as waste on the soil. The effects of such pollution are mostly common to all plants.

The organic substances in sewage decomposes and produces nitrogenous substances that become in excess amount in the soil and harm the vegetation.

Decomposition of sewage may also release various toxic heavy metals that will cause the characteristic heavy metal toxicity symptoms in plants.

Detergent substances may also be released from the sewage resulting in characteristic injury to plants. Ash produced mainly from the combustion of coal in thermal and industrial plants is used for landfilling or deposited on the soil makes the soil unfit for vegetation. It may also release many toxic substances in the soil leading to characteristic plant injuries.

Causes:

Lead Toxicity:

The routes of exposure to lead include contaminated air, water, soil. Occupational exposure is a common cause of lead poisoning occurring in adults.

Signs and Symptoms:

Lead poisoning can cause a wide variety of symptoms and signs which vary depending on the individual and duration of the lead exposure. Symptoms are non specific and may be subtle, and someone with elevated lead levels may have no symptoms. Symptoms usually develop over weeks to months as lead builds up in the body during the chronic exposure, but acute symptoms can happens from brief, intense exposures. Symptoms from exposure to organic lead, which is probably more toxic than inorganic lead due to its lipid solubility, occur more rapidly. Poisoning caused by organic lead compounds has symptoms predominantly in the central nervous system, such as insomnia, cognitive deficits, delirium, tremor, hallucinations, and convulsions.

Symptoms may differs in adults and children; the main symptoms in adults are headache,  memory loss, abdominal pain, kidney failure, male reproductive problems, and weakness, pain, or tingling in the extremities. The signs and symptoms in the children are loss of appetite, vomiting, abdominal pain, weight loss, constipation, anemia, kidney failure, irritability, lethargy, learning disabilities, and behavior problems. Children may also show hearing loss, delayed growth, clumsiness, drowsiness, or loss of new abilities, especially speech skills. Symptoms may appear in children at a lower blood lead levels than in the adults.

The early symptoms of lead poisoning in adults are commonly non specific and include depression, diarrhea, loss of appetite, intermittent abdominal pain, nausea, muscle pain and constipation. Other early signs in the adults include malaise, fatigue, decreased libido, and insomnia.

Lab diagnosis:

The list of diagnostic tests used in the diagnosis of Lead poisoning includes:

Lead blood test

Lead urine test

Mechanism:

The lead's toxicity is largely due to its capacity to mimic calcium and substitute it in many of the fundamental cellular processes that depend on the calcium.

Lead can pass the cell membrane in various ways, which are not yet understood. Lead transport through the erythrocyte membrane is mediated by the anion exchanger in one direction and by the Ca-ATPase pump in the other direction. In other tissues, lead permeates the cell membrane through the voltage-dependent or other types of calcium channels.

Once it has penetrated the cytoplasm, lead continues its destructive action by occupying the calcium binding sites on numerous calcium-dependent proteins. Lead binds to calmodulin, is a protein, which in the synaptic terminal acts as a sensor of free calcium concentration and as a mediator of the neurotransmitter release. Moreover, it alters the functioning of the enzyme protein kinase C, is a virtually ubiquitous protein which is of crucial importance in many physiological functions. Kinase C is normally activated by modulators outside the cell (hormones, neurotransmitters, etc.) through an enzyme chain and in a calcium-dependent manner. Besides many other functions, the activated kinase directly affects the expression of the Immediate Early Response Genes (IERG). The lead has a high affinity for the sites which are typical calcium-binding sites in this protein; picomolar doses can take over the place of micromolar calcium doses. In model cell systems, it has been presented that lead can stimulate gene expression through a mechanism which is mediated by protein kinase C and it is postulated that this effect may be correlated with the alterations in synaptic functioning.

Treatment:

Chelation therapy. In this treatment, Medication taken binds with the lead so that it's excreted in urine.

EDTA therapy. Doctors treat lead levels greater than 45 mcg/dL of blood with a chemical called ethylenediaminetetraacetic acid (EDTA). Depending on your lead level, more than one treatment may be needed. In such severe cases, however, it may not be possible to reverse damage that has occurred already.

Zinc Toxicity:

Sources:

Increased acidity will mobilize heavy metals like Zn .These spread rapidly in the soil along with soil water and reach concentrations which are toxic to the plants. Consequently, plants show species specific metal toxicity symptoms.

Signs and symptoms:

Vomiting, diarrhea, red urine, icterus (yellow mucous membranes), liver failure, kidney failure, anemia

Lab Diagnosis:

By measuring the levels of Zinc and Copper in the blood and urine is a good way in order to determine Zinc poisoning. Since it is a well-documented fact that Zinc poisoning leads to Hypocupremia or depletion of Copper, a test of Serum Ceruloplasmin in the blood is done in order to determine the level of Copper in the blood. Serum is that part of the blood stream which is free of cells. 90% of Serum Copper is found in the Serum Ceruloplasmin. Since, Hypocupremia is a direct result of Zinc poisoning, this test is fairly accurate and helps in the diagnosis.

Red Blood Corpuscles are blood cells which carries the oxygen to the various tissues in the body. Testing of Zinc RBC and Copper RBC levels in the blood, will also helps in the diagnosis of Zinc poisoning. Results of spot urine tests for Zinc and Copper are evaluated along with serum zinc and serum Copper concentration to form a conclusive diagnosis on Zinc poisoning.

Treatment:

Fluid therapy is very important to keep circulation to the kidneys adequate and help in preventing failure. Transfusion may be necessary to treat anaemia and anti-nauseal therapy is warranted. Zinc is very corrosive to the stomach so a medication is required to protect the stomach and antacids are helpful in order to reduce the absorption of zinc (which is enhanced by stomach acid).