Lead Poisoning, Its Toxicology and Health Impact

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Table of Contents

Summary
Suspected Toxic Substance
ADME
Toxicology of Lead
Other Information
Possible Impact of Lead on the Health of Populations
Communication Strategy
References

Summary

The case study looks at a case of three children who display the neurological symptoms of lead poisoning. Medical reports show that the levels of lead in the children’s blood are higher than the maximum allowable levels thus indicating that lead poisoning was to blame for their current status. The children’s lawyer claims that there is a need for scientific evidence to confirm that the children’s health was due to lead poisoning. On the other hand, the proprietor of Mount Isa Mines Ltd, which is a mining industry in the area, argues that the mine is not to blame for lead poisoning since lead is a naturally occurring substance.

Suspected Toxic Substance

Lead falls under the category of heavy metals. It has a blue to greyish color and has a low melting point of 327.46 °C. Lead is denoted by the chemical symbol Pb, which is derived from its Latin name plumbum (Goyer 2013). Its atomic number and mass are 82 and 207.2 respectively. Being a heavy metal, lead has a density of 11.34 g/cm³. Lead can be molded into various shapes with ease. It can also blend very well with other metals hence is used in the manufacture of metal alloys.

Therefore, it is commonly used in a wide range of products such as metal pipes, storage batteries, paints, glasses, weights, ammunition, cable covers, and in the manufacture of shields against radioactive radiations. Lead exists in various forms including elemental lead, naturally occurring ores, inorganic lead, and organic lead. Lead ores such as lead sulfides, sulfates, carbonates, chloroarsenates, and chlorophosphates (also known as galena, anglesite, cerussite, mimemite, and pyromorphite respectively) make up approximately 0.002% of the earth’s crust.

The form of lead that is present in paint, soil, dust, and some consumer items is inorganic lead, which may be found as lead carbonates, chromates or tetraoxides. On the other hand, the organic form of lead is tetraethyl lead, which is commonly found in leaded fossil fuels. Organic lead exhibits higher toxicity levels than inorganic lead due to its ability to be readily absorbed via the skin.

ADME

Possible Routes of Uptake of Lead

Lead gains access into the body through several routes such as ingestion, inhalation and absorption through the skin. Among children, the common route of exposure is ingestion. Ingested lead is commonly found in food cans with lead solders, drinking water that passes through lead pipes, makeup, playthings, herbal and traditional medicines, and paints containing lead (when eaten by children). It is also possible for lead to enter the food chain through polluted soil.

Food items grown in such soils are eaten together with traces of lead. Inhalation of lead may occur when waste products containing lead are incinerated. The burning of leaded gasoline, which leads to the emission of gaseous lead into the atmosphere also contributes to the inhalation of lead. Contact with lead may arise from occupational hazards particularly for painters and mine workers who make regular contact with the lead that is present in paints, soil and lead ores. Industrial sites that liberate emissions containing lead may also contaminate the air and predispose the inhabitants of the surrounding areas to lead inhalation.

Routes of Excretion

Approximately 5 to15 percent of ingested inorganic lead is taken into the body through the gastrointestinal tract while the remaining is excreted in the form of feces. However, during fasting conditions, the amount of absorbed lead increases to about 45%. Additionally, the absorption rates are higher in neonates and young children (53%) than in adults. A reduction in the concentration of minerals such as calcium and zinc and an increase in iron concentration promote the absorption of lead (Flora, Gupta, & Tiwari 2012).

Overall, the rate of elimination of lead is slow. The renal elimination of untransformed lead occurs through glomerular filtration. However, when excessive amounts of lead are present in the body, active tubular transport may also facilitate the elimination of lead. Urinary elimination constitutes 76% of daily clearance while gastrointestinal products contribute to the riddance of 16% of lead. On the other hand, dead cells such as hair and nails, perspiration and other routes only remove 8% of the total lead from the body.

Half-Life of Lead

Even though blood only holds a small portion of the entire lead in the body, it receives the absorbed lead before disseminating it to other parts of the body. The half-life of lead in the blood of a grownup human is approximated to range from 28 days to 36 days. The half-life of lead in the blood has been reported to stabilize at six months following exposure. Almost all the absorbed lead interacts with erythrocytes while the remaining small portion (1%) is found in plasma. Blood lead levels are vital because they enable the estimation of lead exposure. The half-life of lead in soft tissues such as the renal, hepatic and nervous tissues is estimated to be 40 days. Conversely, the half-life of lead in the bones ranges from 20 to 30 years.

Toxic Metabolites in the Body

Lead does not undergo metabolism to form primary and secondary metabolites in the body. It interacts with enzymes in its inherent state to exert toxic effects.

Accumulation of Lead in the Body

Once the absorbed lead reaches the bloodstream, it is disseminated among three key body compartments namely blood, mineralizing tissue, and palpable tissues. Most of the absorbed lead is absorbed by the bones and tends to accumulate in these tissues for years. Therefore, lead bio-accumulates in the bone tissues. Human bones and teeth hold more than 90% of the entire body lead burden. As a result, the health indications of lead exposure may manifest even in the absence of substantial current exposure.

When the body undergoes demanding situations such as during gestation and lactation, it responds by mobilizing lead reserves hence leading to an increase in blood lead concentrations. Therefore, the accumulation of lead is inversely proportional to its elimination. Previous and present high-lead exposures increase a patient’s susceptibility to the adverse health effects of the metal. The dispersal of lead in the mineralizing tissues is not homogenous and is likely to pile up in sections of the bone undergoing dynamic calcification when exposure occurs. Based on the documented rates of bone calcification during various stages of growth, it is predicted that lead buildup takes place mainly in the trabecular bone during the early years and in the cortical as well as trabecular bone later in life.

Toxicology of Lead

The Toxic Effects of Lead

Lead toxicity rarely occurs following one exposure or ingestion of lead. The indications or continued exposure include abdominal discomfort and cramping, belligerent behavior, constipation, trouble sleeping, headaches, tetchiness, poor appetite, poor developmental skills in children, lethargy, elevated blood pressure, tingling of limbs, poor memory, anemia, and kidney problems (Goyer 2013). Mental impairment may occur in children and may manifest as problem behaviors, diminished IQ, developmental delays, difficulties hearing as well as short-term and long-term learning snags.

Elevated doses of lead bring about severe indicative poisoning that is marked by colic (in children), emesis, difficulties walking, anemia, and impairment of the central nervous system leading to coma, seizures and mortality. The effects of brain damage due to lead exposure in the early stages of life bring about the loss of intelligence, a decline in attention span, and disruptive behavior. The human brain has limited repair capabilities and cannot undo the damage caused by lead. As a result, the effect of lead on the brain are terminal and permanent. Affected individuals continue to have diminished brain function as and low achievements throughout their lives.

Target Organs

Lead toxicity affects various organs including the heme biosynthetic pathway, which results in hematological consequences such as anemia. The nervous system (central and peripheral) and renal systems are also affected by lead. Other organs targeted by lead toxicity include the gastrointestinal system and reproductive systems.

Toxicity Mechanism

Lead neurotoxicity is brought about by the ability of lead to take the place of other polyvalent cations especially divalent ions, for example, calcium and zinc in biological processes and reactions (Baranowska-Bosiacka et al. 2012). The physical and chemical properties of lead enhance its attachment to protein binding sites, which leads to the interference with significant biological processes such as the transport of metals, metabolic reactions, programmed cell death, conduction of ions, cellular interactions, cellular binding, and enzymatic reactions.

The interactions may also impair crucial biological functions such as conveyance of signals between and within cells, maturation of proteins and control of genetic processes. Interference with membrane ionic channels and molecules that convey biological signals are the most important features that bring about the neurotoxicity of lead (Baranowska-Bosiacka et al. 2012). Other toxicities occur when lead attaches to the sulfhydryl functional groups of proteins and gets in the way of certain biochemical processes. Some of the affected enzymes are those that take part in the function of heme, myoglobin, cytochromes, and catalases (Khan, Liu, & Shah 2014).

Lead concentrations in blood lower the lifecycle of red blood cells. The influence of lead on the nervous system is brought about by interfering with the working of the mitochondria. Renal function is hampered when lead causes lacerations in the proximal tubules and the loop of Henle (Flora, Gupta, & Tiwari 2012).

Among adults, the dosage needed to trigger adverse effects is undocumented. However, fatal poisoning occurs when the intake carbonates and acetates of lead exceed 30 grams. A daily intake of 0.5mg per day leads to accumulation and toxicity. Devastating effects are noted if the absorbed amounts reach 500 mg. The minimum dosage required to elicit adverse effects is 3.2 µg/m³ via inhalation and 20 µg/kg/day of daily intake for three weeks. Among children, blood lead levels of 1250 µg/L and above have resulted in deaths.

The minimum dosage required to elicit adverse effects in children is 10 µg/L in blood, which is linked to a reduction in IQ scores. Current research shows that lead causes neurobehavioural destruction at blood concentrations of 5 µg/dl and below. Consequently, it appears that lead damages the developing human brain irrespective of its concentration. Other body systems such as the reproductive and cardiovascular systems are also harmed by lead concentrations of 10 µg/dL and below.

The Time Course of the Effects

The adverse effects of lead may be acute or long-term. Acute effects may manifest in a few hours to several days following exposure while long-term effects may manifest several years after exposure. Long-term include neurological disorders such as Alzheimer’s disease, which may occur in old age. Exposure to low levels of lead in utero may impair a child’s growth by affecting the brain and nervous system.

Other Information

How Environmental Lead Exposure Can Occur

Lead contact occurs through an exposure pathway, which must possess five constituents. The typical features of an exposure pathway include the origin of contamination, an ecological medium and conveyance machinery, a point of contact, a route of exposure and an exposed population. In lead exposure, origins of contamination include depreciating lead-containing paint on walls, doors, and windows among other surfaces, old car batteries, the incineration of waste material containing lead, and industrial processes with lead emissions.

The environmental medium and conveyance machinery include lead smoke from open combustion, combustion of leaded fuel, or a dusty floor within a home. The point of contact may include limbs, the floor, or toys, whereas a route of exposure may be eating of dust that is common in children’s hand to mouth behavior. An exposed population, conversely, may include expectant women in contaminated surroundings, children in a typical home setting or mine workers.

Possible Impact of Lead on the Health of Populations

The toxic features of lead have been recognized since 2000 BC and have been reported to cause adverse health effects such as lead poisoning. In the olden days, lead poisoning occurred from the use of lead pipes and traditional processes of sweetening wine using a syrup called sapa, which contained lead. Lead has also led to occupational hazards where certain occupations predispose individuals to poisoning.

One common impact of lead on the health of populations is its toxicity among children. Lead poisoning among children was first identified approximately 100 years ago when 10 children were reported dead. An investigation of the case revealed that a common occurrence in all the ten instances was peeling of lead-based paint in the dead children’s homes. That occurrence led to the realization that children were more sensitive to lead poisoning than adults.

The high susceptibility of children to lead can be attributed to three vulnerable periods in early life, which are embryonic development, fetal growth and neonatal stages (Grandjean & Landrigan 2014). A mother’s exposure to lead during gestation affects the unborn baby. During the early stages of life, children eat and drink more than adults. Also, the amount of air inhaled per unit of body weight is higher than in adults, which increases their chances of inhaling contaminated air. In the initial stages of development, children have high levels of curiosity and tend to touch anything they can see. Additionally, the inherent hand-to-mouth behavior increases their ingestion of lead (Barbieri et al. 2014).

In some instances, children have nutritional inadequacies of minerals such as calcium and zinc, whose deficiency promotes the absorption of lead. Children have more time to grow and exhibit the delayed effects of lead exposure. Another effect of lead on the populations is an increase in the global burden of disease, which increases health expenditures related to the adverse effects of lead. Due to the adverse effects of lead among children, parents need to take precautions to safeguard their children.

Communication Strategy

This communication is intended to educate parents regarding the possible effects of lead toxicity on children. Parents include men and women from different occupations and varying levels of formal and informal knowledge. These parents are concerned about the safety of their children based on the findings of recent reports that lead exposure during childhood damages a child’s neurological system and lowers the child’s learning capacity and IQ levels.

The main interest of the parents is how best they can protect their children from this deadly pollutant. However, they have limited knowledge regarding lead poisoning, and the little information they have is what is reported in the case study on three children with cognitive problems. Therefore, this strategy aims at providing them with a summary of lead poisoning including the properties of lead, its sources, methods of lead exposure, other health effects of lead, and ways of preventing lead exposure. The preferred mode of communication is the use of flyers.

I intend to implement the strategy by creating attractive flyers and distributing them to members of the community in common places such as bus stops and the marketplace where I am likely to meet a large number of people. The flyers will be written in a simplified language and include as many details as possible on the topic. Most importantly, the flyer will lay emphasis on ways of preventing lead exposure in children such as maintaining proper household hygiene and the cleaning of children’s toys.

Flyers are preferred to newspapers because they are relatively inexpensive. It is also possible to hand a flyer to each parent. Newspapers may not be ideal in the situation because they contain a lot of information, which increases the possibility of failing to see the information.

However, before the actual distribution of the flyers, it will be necessary to have a brief meeting with the stakeholders to brief them about the problem at hand and communicate the need to safeguard their children’s health. It will be necessary to have this communication to emphasize the gravity of lead poisoning and why strict measures must be taken to protect children. The communication would also entail informing parents to have the blood lead levels of their children tested at regular intervals to ensure that the children are not poisoned.

Previous studies and reports show that there are no safe blood lead levels among children and that even the smallest concentrations are likely to result in long-term health and cognitive complications. Therefore, it would be necessary to ensure that the communication strategy yields the desired outcome, which is reducing the levels of lead exposure among children. To monitor the progress of the strategy, the number of children brought to health facilities to be tested for lead poisoning will be evaluated.

Additionally, comparisons of the children’s blood lead levels will be made at the start of the study and after the tests have been done. An increase in the number of children being tested for blood lead levels will be a sign that more parents have realized the need to track their children’s health. On the other hand, a decrease in blood lead levels of the children over time will be an indication of the success of the communication strategy. If negative progress is realized, the shortcomings of the communication strategy will be looked into followed by the devising and implementation of better stratagems.

References

Baranowska-Bosiacka, I., Gutowska, I., Rybicka, M., Nowacki, P. & Chlubek, D 2012, “Neurotoxicity of lead: hypothetical molecular mechanisms of synaptic function disorders,” Neurologia Neurochirurgia Polska, vol. 46, no.6, pp. 569-578.

Barbieri, E., Fontúrbel, F. E., Herbas, C., Barbieri, F. L. & Gardon, J 2014, “Indoor metallic pollution and children exposure in a mining city,” Science of the Total Environment, vol. 487, no. 2014, pp. 13-19.

Flora, G., Gupta, D. & Tiwari, A 2012, “Toxicity of lead: a review with recent updates,” Interdisciplinary Toxicology, vol. 5, no. 2, pp. 47-58.

Goyer, R. A 2013, Metal toxicology: approaches and methods, Elsevier, New York.

Grandjean, P. & Landrigan, P. J 2014, “Neurobehavioural effects of developmental toxicity,” The Lancet Neurology, vol. 13, no. 3, pp. 330-338.

Khan, S. A., Liu, X. & Shah, B. R 2014, “Impact of acute toxicity of lead acetate on the level of essential trace metals and histopathological changes in Crucian carp (Carassius auratus gibelio),” Journal of Animal and Plant Science, vol. 24, no. 5, pp. 1405-1414.

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