The Effect of Environmental Lead on Human Physiology

Introduction

Lead (Pb) is a nonessential, highly toxic metal that has been identified in at least 1,272 of
1,684 waste sites that have been proposed for the inclusion on the EPA National Priorities
List (NPL) (ATSDR, 2007).

Lead and lead alloys are commonly found in pipes, storage batteries, weights, ammunition,
and cable covers. They are used to shield us from radiation (ATSDR, 2007). The largest use
of lead is in storage batteries in automobiles and other vehicles. It is primarily released into
the environment as a result of anthropogenic activities such as mining, the smelting of ore,
the manufacture of lead-containing products, combustion of coal and oil, and waste
incineration. Anthropogenic emissions have resulted in lead levels in soil and water up to
several orders of magnitude higher than naturally occurring concentrations. In the air, lead is
in the form of particles and is removed by rain or gravitational settling (Patte and Pain, 2002).
Lead compounds may be transformed in the environment to other lead compounds; however,
lead is an element and it cannot be destroyed (ATSDR, 2007). Lead is introduced to the air in
the form of particles. In other words, lead isnt going anywhere. Hence, we must develop
strategies to reduce the emissions of lead in the environment.

Human exposure to lead above the baseline levels is common. Both the chemical and
physical forms of lead influence its distribution and behaviour within the environment and its
potential for absorption by and toxicity to living organisms (Patte and Pain, 2002). Solubility
and particle size are particularly important, as they affect the intercompartmental and
geographical distributions of lead, its adsorption into sediments, and its absorption by living
organisms. Baseline refers to the naturally-occurring level of lead in soil or dust that is not
due to the influence of humans (ATSDR, 2007). If one is exposed to lead, the dose, duration
and medium of contact will determine the extent of the harm. One may also consider other
chemicals they are exposed to as well as ones age, sex, diet, family traits, lifestyle and state
of health (ATSDR, 2007).

The goal of this research paper is to develop the argument that environmentally available lead
can have several detrimental effects on biological systems, particularly the human nervous
systems.

Sources of Lead Emissions

Lead poisoning has occurred for the last 2,500 years. There are several emission sources of
lead such as smelters, the renovation of homes containing lead-based paint, lead pipes used in
plumbing, pica (an abnormal eating habit in children), occupational exposure, dyes, and caulk
(Patte and Pain, 2002). However, the two primary sources of lead in the environment are
atmospheric emissions and water exposure.

1. ATMOSPHERIC EMISSIONS

a) Emission of Antiknock Agents due to incomplete fuel combustion -

 Tetraalkyl lead is used as an antiknock agent. These agents allow for high engine
compression ratios without spontaneous air/gasoline ignition in the cylinder (Patte
and Pain, 2002). During fuel combustion in the cylinder lead alkyls are converted to
oxides, which foul spark plugs. At the end, they remain in the cylinder. To prevent
this, ethylene dichloride and ethylene dibromide are added to scavenge the lead. The
lead chlorides and bromides consequently formed are relatively volatile and allow for
approximately 70 to 75% of gasoline lead to be emitted into the atmosphere in the
form of exhaust fumes. These inorganic lead salts are emitted as very small particles
of approximately 0.015 m aerodynamic diameter, that are considered to increase in
size rapidly in the atmosphere by combination with other particles. A small amount of
lead may also be emitted as larger particles (5 to 50 m) that are re-suspended from
the exhaust system. The atmospheric lifetime of emitted lead depends on particle size,
topography, and weather conditions. Their relatively longer atmospheric residence
time results in smaller particles can be carried by winds and deposited over very large
areas. Although most organic leads in gasoline are converted to inorganic forms
during combustion, evaporation and incomplete combustion can release organic leads
into the atmosphere in the vapour phase. These fine particles tend to persist in the
atmosphere and can be transported long distances; their small diameter further allows
for their absorption into the bloodstream. Several studies have shown that the
principal source of airborne lead in urban environments is the lead-containing aerosol
emitted with exhaust fumes from motor vehicles running on petrol containing lead
alkyl antiknock agents.

b) Industrial Emissions
Elevated levels of lead are emitted from several primary and secondary smelters.
Industries like the pigment and dye industry, car battery manufacturing and waste
incinerators also use, recycle, manufacture and/or dispose off lead products, which
also results in toxic emissions. The battery industry is the main consumer of lead and
is responsible for an estimated 80% of annual mined lead and secondary recycled lead
production. Approximately half of global lead production is derived from recycling
lead batteries. The expected increase in automobile, solar, telecommunications, and
computer sales in the developing world will increase the production and recycling of
lead batteries. It is estimated that between 60,000 and 70,000 people are employed
globally in lead battery manufacturing, in addition to a similar number working in
mining, smelting, and refining (Gottesfeld and Pokhrel, 2011). Therefore, these
industrial emissions will continue to increase over the years.

2. WATER CONTAMINATION

a) Sewage Effluent, Leaching and Seepage

Sewage treatment plants may receive, in addition to domestic wastewater, certain
industrial discharges and highway runoff, particularly following storms (Patte and
Pain, 2002). Sewage treatment plants do not treat for lead in their filtration process.
Lead may also reach waterways by leaching from fly ash and from soils that have
been subject to additions of lead (e.g., sewage sludge) and by leaching and seepage
from waste dumps, mine tailings, and tailing pond decant. Lead is relatively immobile
in soils; therefore, leaching is only likely to contribute a small amount of lead to
water. A certain amount of lead may be leached from the fly ash resulting from fossil
 fuel combustion. Fly ash is a waste material predominantly generated in the
production of electricity. As a gigascale material, it represents a potential major
environmental liability (Barry E. and Earle, 1998). A large proportion (80 to 100%) of
lead present in the effluent is incorporated into sewage sludge during treatment, and
the remaining effluent is discharged into waterways. An increase in lead
concentration can hence affect the marine life. Coral-reef ecosystems are extremely
sensitive to environmental perturbations, as they have narrow physiological tolerance
ranges for environmental conditions (Pastorok and Bilyard, 1985). Any variation of
physical-chemical conditions outside these narrow tolerance ranges has the potential
to be detrimental to coral growth and survival. Hence, scientists speculate the
potential harm lead contamination could have on the structure of the coral reefs.

b) Plumbing Systems
An investigation was undertaken into the clinical and metabolic effects of lead
acquired by soft domestic water from lead plumbing systems in 23 Glasgow
households. The lead content of water from cold taps was up to 18 times the upper
acceptable limit. This statistic is proportional to the amount of lead in the plumbing
system. The blood lead of 71 inhabitants of these houses showed a significant positive
correlation with water lead content. Deltaaminolaevulic acid dehydrase activity is an
extremely sensitive indicator of lead exposure. It showed a significant negative
correlation with water-lead content. Atmospheric lead was within acceptable limits in
all but one house and no significant correlation could be found with biochemical
measurements (Beattie et al, 1972). The results of the study underline the possible
health hazard of lead plumbing systems in soft-water regions. Lead contamination of
drinking water may increase due to lead-containing water infrastructures, changes in
water sources, and changes in water treatment, including disinfectant (Hanna-Attisha
et al, 2016). A soluble metal, lead leaches into drinking water via lead-based
plumbing or lead particles that detach from degrading plumbing components. The use
of lead in plumbing material has been prohibited since 1986, but older homes and
neighbourhoods may still contain lead service lines, lead connections, lead solder, or
other lead-based plumbing materials.

3. DOMESTIC SOURCES

A study was conducted in which the estimated number of housing units in the United
States with lead-based paint and lead-based paint hazards were estimated.
Measurements of lead in intact and deteriorated paint, interior dust, and bare soil were
included. A nationally representative survey was conducted in which a random
sample of 831 housing units was evaluated in a survey between 1998 and 2000; the
units and their occupants did not differ significantly from nationwide characteristics.
Results indicate that 38 million housing units consisted of lead-based paint, which is
lower than the 1990 estimate of 64 million. Twenty-four million had significant lead-
based paint hazards. Of those with hazards, 1.2 million units housed low-income
families (< $30,000/year) (Jacobs et al, 2002) with children under 6 years of age. 17%
of government-supported, low-income housing had hazards, that were 35% of all low-
income housing had hazards. For households with incomes $30,000/year, 19% had
lead contamination hazards. 14% of all houses had significantly deteriorated lead-
based paint, and 16% and 7%, respectively, had dust lead and soil lead levels above
current standards of the U.S. Department of Housing and Urban Development and the
 U.S. Environmental Protection Agency. The prevalence of lead-based paint and
hazards increases with age of housing. However, most painted surfaces, even in older
buildings (Jacobs et al, 2002), do not contain lead-based paint. Between 2% and 25%
of painted building components were coated with lead-based paint. The highest risk
occurs in older units with lead-based paint hazards that will be, or are currently
occupied by families with children under 6 years of age and are low-income and are
undergoing renovation or maintenance that disturbs lead-based paint (Jacobs et al,
2002). Another study was done to prove the strong relationship between interior dust
lead loading and childrens blood lead levels. This study showed that the major source
for lead exposure in children was lead-contaminated house dust (Lanphear, 1998)

Mechanisms of Lead Toxicity Human Nervous System

1) THE BLOOD BRAIN BARRIER

Lead disrupts the blood-brain barrier. The blood-brain barrier has a very important
function in regulating the access of chemicals in the bloodstream to the brain. While
most organs are supplied by capillary beds that allow many molecules to pass from
the capillary to the interstitial fluid, the blood-brain barrier is very selective in that it
restricts access to only the essential water-soluble molecules, such as essential amino
acids, glucose, calcium, sodium, and potassium, and other specific molecules for
which there are transport carriers in the plasma membrane that enable transcellular
transport through endothelial cells. When exposed to high levels of lead, the blood
brain barrier is damaged and plasma moves into the interstitial spaces of the brain,
resulting in edema. High blood lead toxicity of the central nervous system causes
encephalopathy and edema (which leads to extreme pressure increases in the brain),
which can lead to irreversible brain damage (Brochin et al, 2008) that affects all the
regions of the brain, including particularly the cerebellum. This type of brain damage
results in decreased attention, affects visual-motor reasoning skills and social
behaviour and can damage mathematic skills and reading abilities as well.

2) SYNAPTIC TRANSMISSIONS

Neurotransmission plasticity is at the root of learning and memory in animals

including humans (ref). LTP (long-term potentiation) and LTD (long-term
depression) are thought to be cellular mechanisms of memory formation and learning
whereby synapses are strengthened (LTP) or weakened (LTD) subsequent to synaptic
activity (Hsiang and Daz, 2011). Leads effects on synaptic transmission have been
shown experimentally in long term potentiation and long term depression, in both
excitatory and inhibitory neurons. Zaiser and colleagues, as reported by Hsiang and
Daz (2011) exposed rats pre and postnatally to lead, and examined hippocampal
CA3-CA1 LTP. Rats treated with 1000 parts per million lead in their drinking water
did not exhibit LTP while those treated with 500 ppm were able to exhibit LTP.
However, they were unable to maintain the potentiated effects. The overall neuronal
excitability is altered by lead. Yan and colleagues, as reported by Hsiang and Daz
(2011) showed low level lead exposure on rat hippocampal slices increased evoked
action potential firing rate of CA1 neurons, and showed that the presence of calcium
and calcium channels are necessary for lead to affect the action potential firing rate.
The alterations in signal transduction caused by lead could explain the association
 with cognitive and behavioural deficits observed in epidemiological studies. In
addition to affecting neurons, lead also appears to target glial cells (Hsiang and Daz,
2011) in the CNS. Because glial cells are important components of the CNS,
providing critical support for neuronal function, abnormalities in glial cells may lead
to various complications or diseases. For example, oligodendroglia cells are important
for myelin sheath generation, and lack of myelin insulation leads to diseases such as
multiple sclerosis.

3) THE DIVALENT NATURE OF LEAD

a) Calcium
Lead is a divalent cation and is able to bind to both calcium and zinc sites on
proteins, and this higher affinity has been hypothesized as the mechanism of lead
toxicity. Intracellular concentrations of Ca2+ generally increase in one of two
following ways: the opening of calcium channels in the cell membrane or the
release of stored calcium in the endoplasmic reticulum (Brochin et al, 2008). Both
of these are results of the stimulation of a G-protein. In the case of the former,
once a first messenger binds to a binding site, a G-protein, attached to the cell
membrane (Brochin et al, 2008), facing the inside of the cell, is activated. This G-
protein then stimulates the opening of the calcium channel. Extracellular calcium
then enters the cell and combines with calmodulin, a calcium-binding protein,
which affects and stimulates many intracellular functions (Brochin et al, 2008).
These include inflammation, metabolism, apoptosis, muscle contraction,
intracellular movement, nerve growth and immune response. Lead can interfere
with both pathways, as it has a higher affinity for CaM binding sites than does
calcium.

b) Iron
Iron and lead occupy similar niches within the human body and so compete for
likely binding sites particularly during absorption. While the primary toxicity of
lead in the body is due to its ability to mimic calcium it also interferes with the
iron metabolism (LEAD, 2009). The displacement of iron by zinc (due to their
divalent nature) in the haemoglobin, producing zinc protoporphyrin, is one of the
primary consequences of lead toxicity. It can also result in iron deficiency. This
kind of lead toxicity can result in hypochromic anaemia and reduced oxygen
supply, as iron is the element responsible for most of haemoglobins oxygen
carrying capacity (LEAD, 2009). Lead also reduces the production of red blood
cells (erythropoiesis), as well as their size and their longevity. It prevents the
normal increase of erythropoiesis in response to anaemia. These are far from the
only effects, however. Leads effect on the iron metabolism impacts on functions
as diverse as cardiovascular response, neurotransmitter behaviour, nerve
transmissions, liver detoxification and bone development. Individuals with sickle
cell disease may be particularly vulnerable (LEAD, 2009).

4) VITAMIN D

Lead interferes in the formation of active vitamin D, which has an important role due
to its influence on calcium metabolism (Lowry, 2010). Calcium is under tight
homeostatic control in all cells. The active form of Vitamin D is produced, primarily,
 from activation of Vitamin D by sunlight on the skin (Shatha Hussein kadhim et al,
2016). Vitamin D is a hormone that binds receptors in the nucleus of cells in the
gastrointestinal tract, kidney and bone. This binding activates a series of events which
increase calcium absorption. Because of its similar biochemical nature, lead can be
absorbed by this mechanism especially in children who have decreased calcium intake
(Lowry, 2010).

Consequences

The route of entry depends on the age of exposure. When in the life span of the person was
he/she exposed? This question is essential to answer the mode through which lead entered the
human body and is also an important piece of information for gauging the ideal method of
treatment.

1. TIMING OF EXPOSURE

Lead exposure from ingestion is different from lead exposure from other sources.
Exposure via ingestion is disproportionately affects developmentally vulnerable
children and pregnant mothers. Children can absorb 40% to 50% of an oral dose of
water-soluble lead compared with 3% to 10% for adults (Hanna-Attisha et al, 2016).
Young children are particularly vulnerable to lead poisoning because they absorb 4 to
5 times as much ingested lead as adults from a given source. Moreover, childrens
mouthing and swallowing of lead-containing or lead-coated objects, such as
contaminated soil or dust (or flakes) from decaying lead-containing paint is due to
their innate curiosity and their age-appropriate hand-to-mouth behaviour. This route
of exposure is magnified in children with pica (persistent and compulsive cravings to
eat non-food items), who may eat leaded paint from walls, door frames and furniture
(WHO, 2016). Lead accumulates in our bodies where it is stored in our bones along
with calcium. During pregnancy, lead is released from bones as maternal calcium
(EPA, 2017) and is in bone formation of the developing fetus. This stands true if a
woman does not have enough dietary calcium. Lead can also cross the placental
barrier. This results in dangerous exposure of the fetus to lead. This can result in
serious effects (EPA, 2017) on the mother and her developing fetus, including
reduced growth of fetus or premature birth. Even though children and pregnant
women are the main victims of lead exposure, lead can cause cardiovascular effects,
increased blood pressure and incidence of hypertension, decreased kidney function
and reproductive problems in both men and women (EPA, 2017).

Lead exposure that occurs in utero or postnatally will have different effects than
exposure that occurs in adulthood. Earlier reports suggested associations between
child lead levels and symptoms of hyperactivity, including inattention and
disruptiveness (Wasserman, 1998). Early in life, blood lead represents recent
exposure from the external environment. Because lead tends to redistributes into bone
and soft tissues, it persists in the body over long periods of time. Lead ingestion
declines with age, and blood lead increasingly reflects both external exposure and
body lead burden, as lead from bone re-enters the blood. Lead can cross the placenta,
and hence the blood lead concentration of the infant is similar to that of the mother
(Committee on Environmental Health, 2005). The source of lead in an infants blood
seems to be a mixture of approximately two-thirds dietary and one-third skeletal lead,
 as shown by studies that explored the differences in lead isotopes stored in the bones
of women migrating from Europe to Australia. Although lead appears in human breast
milk, the concentration is closer to plasma lead and much lower than blood lead, so
little is transferred. Because infant formula and other foods for infants also contain
lead, women with commonly encountered blood lead concentrations who breastfeed
their infants expose them to slightly less lead than if they do not breastfeed
(Committee on Environmental Health, 2005). Thus, infant exposure to lead in breast
milk or in infant formula are of continued concern.

The Institute for Health Metrics and Evaluation (IHME) has estimates that in 2013,
lead exposure accounted for 853,000 deaths worldwide due to long-term effects on
health, with low and middle income countries bearing the highest burden. IHME also
estimated that lead exposure accounted for 9.3% of the global burden of idiopathic
intellectual disability, 4% of the global burden of ischaemic heart disease and 6.6% of
the global burden of stroke (BlackDoctor, accessed 25th October 2017) (WHO, 2016).
However, its most detrimental effects occur in the human nervous system; these
effects were mentioned in the Mechanisms of Lead Toxicity Human Nervous
System section.

2. DURATION OF EXPOSURE

The duration of exposure to toxic chemicals is divided into two categories: acute and chronic.
Either may cause health effects may surface immediately or health effects may occur days or
years later. Acute exposure is a short contact with a chemical that may last few seconds or
even few hours. It may last a few seconds or a few hours. For example, it might take a few
minutes to clean windows with ammonia, use nail polish remover or spray a can of paint. The
fumes (NY Department of Health, accessed 2nd July 2017) inhaled during these activities are
examples of acute exposures. Chronic exposure is continuous or repeated contact with a toxic
substance over a long period of time, which can last months or years. If a chemical is used
every day on the job, the exposure would be chronic due to extreme exposure. Over time,
some chemicals, such as PCBs and lead, can build up in the body and cause long-term health
effects. Chronic exposures can also occur at home. Some chemicals in household furniture,
carpeting or cleaners can be sources of chronic exposure (NY Department of Health,
accessed 2nd July 2017). Lead poisoning is usually a chronic disease. The clinical signs and
symptoms of lead poisoning are nonspecific. In the majority of cases, children with lead
poisoning are asymptomatic resulting in a delay in the appropriate diagnosis. However,
during this time effects on a cellular level are occurring resulting in changes in the child.
These include impairment of IQ and other cognitive effects, decreased heme synthesis, and
interference in vitamin D metabolism. In children, clinical symptoms of cumulative lead
poisoning usually begin with loss of appetite and abdominal pain. They are, however, easily
confused with other diseases that can cause the same symptoms. If the disease is not
recognized at this stage, the clinical presentation in children may proceed to signs of
increased intracranial pressure such as projectile vomiting, altered state of consciousness and
seizures. Hence, different durations of exposure can affect the human body differently
(Lowry, 2010).

Strategies to Minimise Lead Poisoning

 1. ORAL CHELATION THERAPY

Once lead has entered the body, especially bone, it is very difficult to remove,
especially if it has been incorporated into bone. Accordingly, prevention is the
mainstay of treatment (Lowry, 2010). However, chelation therapy may be used to
decrease the blood lead concentrations acutely. Chelating agents bind metals at two or
more sites. Ideally, the chelated metal would be excreted; however, the lead:chelate
complex may exist in tissues where the binding has occurred or it will be redistributed
to other tissues. An optimal chelating drug should increase lead excretion, be
administered easily, and be affordable and safe. Lead removal should halt further
toxicity and reverse previous effects (Lowry, 2010).

Examples of Chelating agents Succimer is a water-soluble, oral chelating agent that

is appropriate for use with BLLs higher than 45 g/dL (Lead Toxicity Treatment &
Management, 2nd June 2017). D-penicillamine is a second-line oral chelating agent,
although it is not approved by the US Food and Drug Administration for use in lead
poisoning. Edetate (EDTA) calcium disodium (CaNa2 EDTA) is a parenteral
chelating agent. Dimercaprol (also referred to as British antilewisite [BAL]) is
another parenteral chelating agent recommended as an agent of first choice for
patients with lead encephalopathy (Lead Toxicity Treatment & Management, 2nd June
2017).

2. OTHER SAFETY METHODS

If the blood lead concentration is greater than 45 g/dL and the exposure has been controlled,
treatment with succimer should begin. The succimer label provides dosages calculated both
by body surface area and by weight. For the younger children typically given the drug, body
surface area calculations give higher doses, which are recommended. Children with
symptoms of lead poisoning, with blood lead concentrations higher than 70 g/dL, or who
are allergic or react to succimer (Committee on Environmental Lead, 2005) require parenteral
therapy with EDTA and hospitalization.

3. PREVENTION

Lead poisoning in children is an important, preventable environmental disease affecting

millions of children around the world. The effects of lead are popular and range from delayed
and adversely affected neurodevelopment to severe health outcomes including seizures,
coma, and death (Meyer et al, 2003). The best way to reduce the harmful effects of lead
poisoning is to prevent it altogether.

Environmental dust, soil and paint Identify and abate

Restrict play in area, plant ground cover,
wash hands frequently
Occupational Exposure Remove work clothing at work; wash work
clothes separately
Home Renovation Proper containment, ventilation
Hand-to-mouth activities (pica) Frequent hand washing; minimize food on
floor
 Inadequate Nutrition Adequate intake of calcium, iron, vitamins
Developmental Disabilities Enrichment programs

Table #: Sources of lead exposure and prevention strategies (from Committee on

Environmental Health, 2005).

Conclusion:

In this research paper, we aim to understand the toxic effects lead can have on the human
body, mainly the nervous system. The main populations affected by lead are pregnant women
and children. Hence, the governments must minimize the further entry of lead into the
environment. Regulations concerning airborne lead should be enforced, use of lead in
consumer products should be minimized, and consideration should always be given to
whether a child might come into contact with such a product (Committee on Environmental
Health, 2005). Once lead has entered the human body, it is very difficult to reverse its effects
completely. Therefore, people must be educated about the fatal effects of lead and prevention
strategies must be adopted before it causes irreversible damage and/or neurodevelopmental
disorders.

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