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Exposure to lead remains a major environmental matter around the world as measures to deal efficiently with this problem in both developed and developing countries have been heightened. Each year, the cost of the health effects of lead exposure in the United States alone was estimated at US$43.5 billion in 1997, which was far much higher than any other environmental toxin. Doubts that lead exposure has weighty health significances at levels below those considered medically acceptable decades ago are held by a few while the debate over what levels of lead exposure in the contemporary world, if present, can be considered as of nominal harm is still evident.

The exposure to and the uptake of this element has consequently increased. However, in most of the developed nations, the introduction of lead into the human environment has reduced over the years, mainly due its commercial usage, particularly in petrol and also due to public health campaigns. Even though severe lead poisoning has become infrequent in such countries, chronic exposure to lower levels of the element still remains a public health issue. This is particularly among some socioeconomically disadvantaged groups and other minorities. In developing nations, sentience of the impact of exposure to lead to public health is rising but very few of these nations have formulated policies that would combat this problem.

Lead is a highly toxic substance, exposure to which can produce a wide range of adverse health effects. Both adults and children can suffer from the effects of lead poisoning, but childhood lead poisoning is much more frequent, Pocock SJ, Smith M, Baghurst PA.(1994). Over the past years through which we have learnt of the hazards of lead, millions of children have undergone its health effects. Presently also, 2010, an estimated 310,000 children who are under the age of six have too much lead in their blood, Centers for Disease Control and Prevention (2006).

There are many recognized ways through which human beings may be exposed to lead. This could be through: waning paint, bare soil, house dust, air, food, drinking water, porcelains, hair dyes and other cosmetics. Children with elevated blood lead levels, more often, are exposed to lead in their own home.


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Lead, an ever-present and nifty metal, has been on the use ever since prehistoric days. It has become extensively spread and accumulated in the environment. Human exposure to and uptake of this non-essential element has consequently increased. Damage to almost all organs of the human body is evident at higher levels of exposure. Some of the organs affected are exemplified by: the kidneys and blood, the central nervous system, which can further lead to death in excessive levels.

Most researches that have been carried out in the past 30 years have shown adverse health effects of abstemiously increased blood lead levels, i.e. below 25 mg/dl. The allowable exposure levels in the ambient (air, water, soil, etc.) atmosphere, as well as in the working environment, has consequently been gradually lowered. Furthermore, exposures through occupation or the environment has remained a serious problem in many developing and industrializing countries, Centers for Disease Control and Prevention (2006).

This review focuses on lead poisoning in children because of the high prevalence of lead in the environment, and because the impact of lead exposure on children's neurocognitive development, in particular, is substantial.  Emerging data suggest a health impact on neurocognitive function at much lower blood concentrations of lead than thought earlier.2-5 children are particularly sensitive and susceptible to lead toxicity and as such are a subpopulation at which prevention strategies need to be targeted. Childhood lead remains a major public health problem for certain groups of children, specifically African-American children in the USA, children living in areas of low socioeconomic status, children living in rural mining communities, and children in developing countries such as India and the Philippines, Zietz B, de Vergara JD, Kevekordes S, Dunkelberg H. (2001). This paper also presents a case study of the assessment of children exposed to lead in different areas of the world such as Esperance, Western Australia, America among others to illustrate the principles of managing such events from a public health perspective, as well as the scientific rationale for this approach.

History and Epidemiology of Lead Exposure and Poisoning

Exposure was first reported in 370 BC. It was most common among industrial workers in the 19th and early 20th centuries. This was due to their exposure through plumbing, painting, smelting, printing and a host of other industrial activities, Pocock et al (1994). Franklin, in 1767, received a list of patients in La Charite´ Hospital, Paris, who had been admitted due to some symptoms, although not recognized then, were clearly those resulting from lead poisoning.

Tanqueral des Planches, in 1839, defined the symptoms of acute lead poisoning. His study was so detailed that little has been added to the clinical signs and symptoms of acute lead poisoning in adults. At around mid-19th century in the United Kingdom, lead poisoning through occupation was a common condition. However, in 1882, after the deaths of several employees working in the lead industry, a legislative enquiry was instigated to look into the working conditions in lead factories. This resulted in the 1883 Factory and Workshop Act (Prevention of Lead Poisoning), which required lead factories to conform to certain minimum standards, e.g. the provision of ventilation and protective clothing, Zietz Bet al (2001).

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In Australia, lead poisoning in children was first reported in 1892, although it was not until 12 years later that the source, peeling lead-based paint, was identified in a series of ten children with lead colic. In 1943 a follow-up study of 20 schoolchildren in the USA who had experienced acute lead poisoning in infancy or early childhood found that exposure to environmental lead at levels insufficient to produce clinical encephalopathy was associated with long-term deficits in neuropsychological development, Centers for Disease Control and Prevention (2006). Studies of Case-control on hyperactivity and mental retardation in relation to environmental lead exposure revealed that children who lived through acute intoxication of lead were every so often left with severe insufficiencies in neurobehavioral function.

Sources of Lead Exposure and Poisoning

The exposure of environmental lead to human populations was comparatively low before the industrial revolution but has however heightened with large-scale mining and industrialization. Globally, the extensive processing of lead ores is estimated to have released about 300 million tones of lead into the environment over the past five millennia, mostly within the past 500 years. Following the introduction of automobiles at the beginning of the 20th century, environmental lead has substantially been on the increase due to the use of leaded fuel. This in turn increased the community's exposure to environmental lead, Counter SA, Buchanan LH, Ortega F. Lead (2006).

Lead emitted by vehicles continues even today and presents a health risk to the population. Much of emitted lead remains in soil where it was dumped over the years, mainly in frequented roads and highways. Pets can as well come into contact with lead-contaminated soil hence lead to human exposure when in contact with the pet. In each such case, an elevated blood lead level can easily result, Zietz Bet al (2001).

More recently identified sources of lead exposure for children include industrial environmental sources, such as the shipping of lead in the case of Esperance. Newly identified sources of lead poisoning over the last 10 years also include fishing weights, otherwise known as sinkers, snooker chalk, and lead paint found on products including children's toys and barbeques. Increasing globalization has a marked impact on risk as, for example, in the case of lead paint on toys made in China appearing in shops in the USA and Australia. As a result, there is an increasing need for public health authorities to be vigilant for both domestic and imported lead hazards and to put surveillance systems in place for early identification of such hazards, Pocock et al (1994). The most recent US death associated with lead toxicity was in a child who swallowed metal jewelry, Centers for Disease Control and Prevention (2006). This 'imported risk' may affect certain ethic groups more than others. For example, significant amounts of lead are found as a contaminant or an intentional adulterant in some herbs and ethnic remedies including ayurvedic herbal products, imported spices, or Hispanic folk remedies such as 'litargirio'. However, toys made with lead paint are distributed more widely than these remedies.

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Diagnostic modalities for assessing lead poisoning in children

The best way to assess the degree of lead poisoning in children is by taking venous blood for lead estimation. Heel or finger prick testing is susceptible to significant errors due to environmental skin contamination. However, with prior thorough cleaning of the skin, it has been used by many to collect bio-monitoring samples. Recently, in undertaking health surveillance after the lead-dust exposure scenario in Esperance, venous blood testing was performed on children under five years of age without the anticipated difficulties of difficult venous access. Retesting was carried out at three monthly intervals in children with lead concentrations 45 mg/dl, and showed significant expected falls (with the estimated elimination half-life of lead from blood being 30 days), Zietz Bet al (2001). This showed that bioaccumulation from ongoing environmental exposure was not occurring, since a rapid fall in concentration indicates long-term exposure. Roberts et al. found that the average time for blood lead to decline was linearly related to the peak concentration of blood lead, but the time for 50% of the blood lead to decline to 10 mg/dl was not linear and varied with peak lead levels. Venous blood lead estimation is a short-term measure of lead exposure (half-life of 30 days) that reflects exposure from current exogenous sources and the release of lead from bone, Centers for Disease Control and Prevention (2006).

Effects of Lead Poisoning

Young children, who are especially under the age of six, are susceptible to lead's harmful health effects, since their brains and central nervous system are still undergoing development. For the children, even lower levels of exposure can result in learning disabilities, reduced IQ, impaired hearing, attention deficit disorders, stunted growth, behavioral problems, as well as kidney damage. Higher levels of exposure can result in the child's mental retardation, comas or even result in death. Within the last ten years, children have died from lead poisoning in New Hampshire and in Alabama, Centers for Disease Control and Prevention (2006).

In adults, lead can cause fertility problems, increase blood pressure, cause nerve disorders, irritability, muscle and joint pain, and memory or concentration problems. Most lead poisoning in adults occurs at their work places. When a pregnant woman has an elevated blood lead level, that lead can easily be transferred to the fetus, as lead crosses the placenta, Counter SA et al (2006).Evidence has shown that pregnancy in itself can cause lead to be freed from the bone, where it is stored when it first gets into the blood. Moreover, if a woman had been earlier exposed to lead in her childhood, pregnancy can also trigger the release of lead hence exposure of the fetus too to the element. In such instances, the baby is often born with a high blood lead level.

New research which has been published in the New England Journal of Medicine offers new proof that very harmful effects could as well occur. This could be as low as 5 micrograms of lead per deciliter of blood. According to scientific research, no level of exposure to lead is considered safe.

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Lead is neurotoxic. It interferes with signal transmission at the synapse and interferes with cellular adhesion molecules, causing disruption in cellular migration during critical times of nervous system development. Disruption of subunit expression of the N-methyl-D-aspartate receptor (NMDAR) and NMDAR-mediated calcium signaling in glutamatergic synapses is considered the main mechanism of lead-induced deficits in synaptic plasticity, and in learning and memory deficits documented with animal models of lead toxicity, Pocock et al (1994). At fairly substantial levels of exposure, lead inhibits the enzymes ferrochelatase and delta amino levulinic acid dehydratase, resulting in microcytic hypochromic anemia.

Deficits have been reported in verbal IQ, performance IQ, academic skills such as reading and mathematics, visuo-spatial skills, problem solving, fine and motor skills, memory and language skills. As methods of measuring both lead exposure and cognitive development become more sensitive, subtle adverse impacts of very low blood lead levels become more quantifiable, Counter SA et al (2006). One of the greatest challenges facing clinicians dealing with lead issues today is determining what this means for individual patients and populations, and mitigating these risks.  

Prevention and Treatment

Check the water to ensure your drinking water does not contain a hazardous level of lead. One is advised to test his/her water at the faucets. Eat right. The amount of lead the human body retains can be reduced if you make sure that the diet includes plenty of foods that contain iron, calcium and zinc. Foods rich in iron include eggs, raisins, greens, beans, peas, and other legumes Lean red meat and oysters are examples of foods that contain zinc, Zietz Bet al (2001). Avoid fried or fatty foods-although remember that a certain amount of dietary fat is vital for children under two years of age. And make sure that hands are washed before any meal is taken. One is also advised not to store alcohol in crystal containers. This is due to the fact that most of the crystal decanters and glasses are often made out of lead. When an acidic element or alcohol is stored in such containers for long, lead could leach into the liquid hence pose as a health risk.

Bare soil areas where children play need to be covered. You should ensure your children avoid playing in bare soil areas unless those areas are known to be lead free. Every so often, bare soil would contain some lead which may have been deposited there either through from deteriorated exterior paint, or vehicle emissions from leaded gasoline days. This is most often in vacant lots, where old buildings previously existed, or in regions with extensive renovation. For people with bare soil problems, they would be advised to cover the soil with mulch such as pebbles, grass or even shrubbery.

Lead poisoning from retained lead foreign bodies has been commonly reported within the medical literature. The pathophysiology of lead absorption from retained bullets has not been clearly delineated. Bullet disintegration increases the surface area for the absorption of lead and has been observed to increase blood lead levels by at least 25.6%, Centers for Disease Control and Prevention (2006). The location of the lead foreign body also determines the amount of lead that will be absorbed. Bullets in contact with bony fractures and within synovial fluid, pleural fluid, and cerebrospinal fluid have all been associated with elevated absorption rates and lead toxicity.

In symptomatic patients with retained bullet fragments, definitive treatment involves the removal of the lead fragments. Parenteral administration of calcium disodium ethylenediaminetetraacetate (EDTA) has been associated with the redistribution of lead from soft tissue to brain, increasing the risk of encephalopathy in patients with continued lead absorption and high body burdens of lead. Dimercaprol (BAL, British Anti-Lewisite) is an excellent chelator, but is only available as an intramuscularly injection and is associated with marked patient discomfort and a number of potential adverse drug events. Succimer (2, 3-dimercaptosuccinic acid, DMSA) can be given orally, does not appear to cause redistribution from tissues to the brain, and has a much lower adverse-effect profile when compared with dimercaprol. Past reports have shown significant success in chelation with oral succimer before the surgical removal of bullet fragments, Counter SA et al (2006).

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