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The Effects of Endocrine
Disrupting Chemicals on
Obesity
Sarah Ly
Niles North High School
















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Table of Content
Acknowledgements

3
Purpose

4
Hypothesis

4
Review of Literature

5
Variables

16
Materials

16
Procedures

16
Results: Data Tables

18
Data/Data Analysis

21
Statistical Analysis

30
Conclusion

42
Reference List

45







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Acknowledgements
I would like to thank the Niles Norths STEM teachers, Christine Camel, Richard Thielsen, and
Susan Posnock for their guidance and assistance throughout this project. I would also like to
thank Katherine France for helping me preform statistical analysis. Lastly, I would like to thank
my friends and family for their love and support.












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Purpose: The purpose of this experiment is to determine if there is a correlation between the
concentrations of endocrine disrupting chemicals (EDC) found in common foods and the obesity
rate.
Hypothesis: If there is an increase in the concentration of the studied endocrine disrupting
chemical in various foods, then there will be a direct relationship to obesity.
Rationale: Human exposure to endocrine disrupting chemicals (EDC) mainly occurs through
contaminated food or water. If there are higher concentrations of these chemicals in food, then
there is a higher chance for disruptions to occur in the endocrine system. EDCs mainly interfere
with the endocrine system by binding to certain receptors such as the androgen and estrogen
receptor. When bound to receptors, EDCs may act as an agonist by activating hormones and
mimicking their actions leading to overproduction. EDCs may also bind to receptors and act as a
block by inhibiting the actions of the receptors leading to underproduction. By interfering with
important weight maintaining hormones such as leptin, EDCs can potentially lead to obesity
and obesity related diseases.






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Review of Literature
One-third of the United States is currently classified as obese. Since the 1980s the
obesity rate as not only doubled but continues to drastically increase (Center for Disease
Control and Protection, 2013). As obesity increases, the rates of diseases that correlate with it
increase as well. Obesity can lead to many chronic diseases such as diabetes, cardiovascular
disease, high blood pressure, and even some types of cancer (Obesity, 2013). The cause for
obesity is often linked to overeating and underactivity, but some studies suggest that these
arguments may not be as valid as they once were. According to the Department for
Environment, Food, and Rural affair, daily caloric consumption has decreased throughout the
20th century, while no hard evidence has proven that inactivity is linked to the increasing
obesity rate (Baille-Hamilton et al, 2002). If overeating and underactivity are not the cause of
the increase in the obesity rate, then what is? One factor to consider is environmental
conditions. With the rise of industrialization, more and more toxic chemicals are being released
into the environment. Amongst these toxins are endocrine disrupting chemicals (EDC).
Endocrine System
Endocrine disrupting chemicals, EDC for short, are chemicals that interfere with the
chemical processes that take place in the endocrine system. The endocrine system is similar to
the nervous system, but instead of using neurotransmitters to control the body, it uses
hormones (Carter, 2004). Often times the endocrine system and the nervous system play hand
and hand in regulation of the body. The nervous system will allow for rapid transmission
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throughout different regions, while the endocrine system is more suited for long term
situations (Hiller-Sturmhfel and Bartke, n.d).
The main function of the endocrine system is to regulate growth and development,
metabolism, electrolyte composition of body fluids, and reproduction through the use of
hormones (Hiller-Sturmhfel and Bartke, n.d). Hormones are molecules that are secreted by
endocrine glands such as the pituitary gland, thyroid gland etc. When stimulated, the glands
release a product (called hormones) into the bloodstream which are then carried to their target
cells (Carter, 2004). Hormones can differ in the number of target cells but all target cells are
determined by the presence of a receptor. The relationship between a hormone and its
receptor is similar to a lock and key, meaning that biochemical reactions can only occur if the
hormone fits the right receptor (Hiller-Sturmhfel and Bartke, n.d).
In order to maintain homeostasis, hormone production and secretion must be tightly
controlled in order to allow hormones to quickly adapt to the changing environment.
Deregulation of hormones that are responsible for weight control, fat distribution, and
metabolism could potentially cause an increase rate of obesity (Baille-Hamilton et al, 2002).
Weight-Controlling Hormones
Leptin is a hormone that maintains homeostasis of the adipose mass. Typically, leptin is
produced by adipose tissues before it is dispersed into the bloodstream to travel to the brain to
regulate food intake and stimulate metabolism. By binding to its receptor located in the
hypothalamus, leptin can regulate most, if not all, other physiological systems; although,
leptins main focus is to maintain stability in the adipose tissue mass. Because leptin is
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produced in the adipose tissues, when the mass of the adipose tissues declines so does the
concentration of leptin. As the concentration falls, appetite is stimulated and energy
expenditure is suppressed until the lost mass is restored; this process is known as set point.
Similarly, when adipose tissues gain mass, the concentration of leptin increases as well. The
extra leptin will suppress appetite until the additional weight is lost. By adjusting to the amount
of fat lost and gained, leptin allows for organisms to maintain the optimal about of fat needed
to cope with environmental changes (Friedman, 2010).
Because leptin plays such a crucial role in food intake and metabolism, when its signals
are interrupted, it can lead to overeating and a slow metabolism which eventually plays into
obesity. Individuals who are obese actually produce higher levels of leptin due to the fact that
there is an increase in the adipose mass. Typically, higher levels of leptin indicate a reduction in
appetite and an increase in metabolic rate, but for obese individuals, this is not the case. Obese
individuals are more insensitive to the effects of leptin, a condition known as leptin resistance
Those who experience leptin resistance will experience an increase in appetite and decrease in
metabolism due to lack of the leptin signals (Obesity and Hormones, 2013).
In 1996, Considine et al performed a cross-sectional study on the effects of leptin on
obesity. Having gathered approximately 140 obese men and women, Considine et al 1996
measured the concentration of serum leptin in obese individuals which was later compared to
the serum leptin concentration of normal individuals. After losing weight, seven of the obese
subjects were later tested to determine if the serum leptin concentration had changed. The
experiment concluded that the serum leptin concentrations are correlated with the
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percentage of body fat, suggesting that most obese persons are insensitive to endogenous
leptin production (Considine et al, 1996).
Another important weight-controlling hormone is insulin. Insulin is a hormone produced
by the pancreas used to regulate carbohydrates and metabolize fats. Insulin is secreted in
response to high glucose levels in the bloodstream, although low levels of insulin are always
secreted by the pancreas. Once secreted, insulin stimulates glucose uptake in tissues such as
muscles or fats, which then lowers the glucose concentration in the bloodstream (Obesity and
Hormones, 2013).
There are two different ways that insulin irregularities are linked to obesity. The first,
being the most well-known, is that individuals who are obese exhibit lower sensitivity to insulin,
and thus cannot regulate their blood sugar level, which can lead to insulin resistance or
diabetes type II. On average, 80 to 90% of individuals with diabetes type II are also diagnose
with obesity. The second way that an insulin irregularity affects obesity occurs when insulin is
overproduced. Overproduction of insulin can lead to weight. The reason being is that an
increase in the amount of insulin corresponds to an increase in the amount of glucose being
taken in. With more insulin, more glucose is uptaken rather than eliminated causing an increase
in weight (A Codependent Relationship: Diabetes and Obesity, n.d).
In one experiment, a researcher, James Johnson, fed two groups of mice high-fat diets.
The control group consisted of only normal mice, while the experimental group consisted of
mice bred with half the regular concentration of insulin. The results concluded that the mice
with lower levels of insulin did not gain weight because their fat cells burned more energy while
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storing less; the normal mice, however, did in fact gain weight. This suggested that too much
insulin can be detrimental and that humans overproduce the necessary amount of insulin
(Glynn, 2012).
The last type of hormones commonly associated with obesity are growth hormones. As
its name suggests, growth hormones are responsible for development in terms of both height
and muscle build of an individual. In addition, growth also affects metabolism. Individuals who
are obese have lower levels of growth hormone than their healthier counterparts (Obesity and
Hormones, 2013). Except for the fact that obese individuals have a lower concentration of
growth hormones than normal, no other connection to obesity has been established. The
application of this knowledge is still being tested but one possible idea that stems from this is
growth hormone treatment. In an experiment performed in 2012, Shadid and Jensen tested the
effects of the administration of growth hormones on obesity. The test was done in a clinical
trial where those who participated received the hormones through high-caloric diets. It was
concluded that the effects of growth hormones administration did little to preserve lean tissue
or enhance fat loss (Shadid and Jensen, 2012).
Endocrine Disrupting Chemicals (EDC)
By altering the hormonal processes of leptin, insulin, sex hormones, and growth
hormones, EDCs can act as an obesogens. EDCs mainly interfere with the endocrine system by
binding to estrogen and androgen receptors. But in addition, EDC can be an agonist by binding
and activating hormones and then mimicking their actions. EDCs may also just bind to the
receptor and act as a block by inhibiting the receptors actions. Finally, EDCs may also interfere
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with the synthesis, transport, metabolism and elimination of hormones, thereby decreasing the
concentration of natural hormones (Mnif et al, 2011).
Persistent Organic Pollutants (POPs)
One example of an EDC is persistent organic pollutants or POPS. POPS are synthetic
carbon based chemicals that are derived from industrial production and the use of pesticides
that can also sometimes act as an EDC. Using natural processes that involve water, soil, and air,
POPs can spread rapidly on a global scale. Once introduced to the atmosphere, they remain
there for long periods of time due their ability to resist photolytic, chemical and biological
degradation as a result of their carbon-chlorine bonds (Stockholm Convention, 2008).
POPs are often halogenated, but are more likely to be chlorinated due to the fact
carbon-chlorine bonds are stable when dealing with hydrolysis (decomposition of a compound
using water). The larger the number of chlorine substitutes, the more resistant the chemical is
to different types of degradation. In addition, chlorines attraction to aromatic or benzene
rings, creates POPs with a ring and chain structure or a branching framework (Ritter et al, n.d).
As a result of their halogenation or chlorination, POPs have high lipophilicity, the ability to
dissolve in lipids, thus POPs have the ability to readily pass through phospholipid structures and
bioaccumulate in the adipose tissues of various living organisms including humans (IOMC,
1999). The concentration of bioaccumulation of POPs is correlated to the level the organism
resides in the food chain, meaning higher concentrations are found at higher trophic levels
(Stockholm Convention, 2008).
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Two POPs commonly known for its endocrine disrupting properties are dibenzofurans
(sometimes known as furans) and dioxins. Dioxins and furans are unintentional byproducts
produced during manufacturing of pesticides or other chlorinated substances. They also often
found being emitted off of hazardous waste and automobile emissions, as well as peat and coal,
and are therefore easily exposed to humans. The most common form of exposure for humans is
through the contaminated food and water (Stockholm Convention, 2008). Like other POPs,
dioxin and furans are lipophilic and tend to accumulate in adipose tissue of different organisms
meaning that foods such as beef, pork, fish, and even some dairy products can have high
concentrations of either one or both chemicals (ATSDR, n.d).
Once exposed, dibenzofurans and dioxins can have numerous adverse health effects on
humans. Both chemicals have been classified as possible carcinogens, meaning that furans and
dioxins can potentially lead to cancer. There have also been reports of hormonal changes in
both humans and animals. These changes include developmental issues of fetuses,
reproductive issues, and weakened immune systems (ASTDR, n.d).
Furans and dioxins can also act as obesogens by disrupting the creation of cytokines
such as leptin and adipokines (Shurk et al, 2007). When furnas or dioxins are introduced to the
body, the adipose tissues will absorb its toxins to reduce amount of exposure to other organs.
By absorbing the toxins, the tissues begin to increase in size (hypertrophy) due to inflammation
(Barret, n.d). Once this occurs, the production of adipokines becomes irregular leading to an
increase in food intake, decrease in the rate of metabolism, and a decrease in insulin sensitivity
(Shurk et al, 2007).
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Arsenic
Not all EDCs are organic pollutants, some EDCs are natural elements like arsenic. Arsenic
is a naturally occurring element that is typically found in soil and minerals. In nature, arsenic
will bind with oxygen, chlorine, or sulfur to form inorganic compounds that can be used as a
preservative for wood, as a pesticide, and in some industries. Arsenic can also form organic
compounds by binding with carbon and hydrogen. Organic arsenic is used as a pesticide for
crops such as cotton (ASTDR, 2011).
Arsenic is widely distributed throughout the air, water, and land. Similar to the POPs,
the most common form of arsenic exposure is through contaminated food or water (ASTDR,
2011). High levels of inorganic arsenic, its most toxic form, can be found in groundwater of
many countries such as China, Mexico, and United States. Crops that are irrigated with the
contaminated water will become a contaminated as well and act as a source of exposure. Foods
such as fish, meat, and dairy products can become dietary sources of exposure as well (WHO,
2012).
Long term exposure to arsenic can lead to arsenic poisoning which if left untreated can
potentially lead to death. The first signs of overexposure to arsenic usually occur through
discoloration of the skin or skin lesions will begin to form. This can eventually progress to skin
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cancer. Arsenic has been linked to other forms of cancer as well such as bladder and lung
cancer. In addition, arsenic has also been linked adverse health effects such as insulin resistance
and cardiovascular diseases, conditions typically linked with obesity (WHO, 2012).
By acting as a block, arsenic can decrease the production of insulin which can lead to
diseases like diabetes type II, but if arsenic acts as a agonist instead, overproduction of insulin
can occur. Too much insulin can potentially lead to obesity because instead of eliminating
excess glucose, it is uptaken by the excess insulin. When excess glucose is uptaken in can lead
to an increase in weight (Tseng, 2004).
Mercury
Similar to arsenic, mercury is a naturally occurring element that can act as an EDC. It is
found in air, land, and water in many different forms: elemental/metallic mercury, inorganic
compounds, or organic compounds. With its multiform, mercury has been used in many
products such as light bulbs or thermometers. Although mercury can be utilized in many ways,
using mercury can be dangerous due to its toxicity (Sloane, n.d). Mercury exposure typically
occurs through contaminated water or seafood. This is because mercury that is released in the
air eventually settles into the water or land where it will be washed into the water. Once
deposited in water water, microorganisms will convert mercury into methylmercury.
Methylmercury is a highly toxic form of mercury that builds up in seafood and animals that eat
other contaminated organisms. If exposed to mercury, there can be harm to the brain, heart,
kidneys, lungs, and immune system. In addition, mercury has been known to cause
developmental effects both mentally and physically in unborn babies (EPA, 2013).
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Like POPs, mercury is also lipophilic and dissolves in adipose tissues of various organisms
making it difficult to remove. It is possible that mercury disrupts the endocrine system by
increasing the size of the adipose tissue and therefore, disrupting the creation of leptin. It is
also possible that mercury disrupts other hormones located in the pituitary glands or thyroid
glands. How mercury acts as an endocrine disrupting chemical is still relatively unknown. There
are many theories available but a lack of data to prove any one true (Endocrine Disruptor,
n.d.).
Lead
Like mercury and arsenic, lead is another naturally occurring element that has been
classified as an endocrine disrupting chemical. Lead has been used since ancient times due to
its malleability and continues to be used today in the form of an alloy (CDC, 2013). Exposure to
lead commonly occurs when lead dust and fumes are inhaled or through contaminated food
and water. Due to lack of symptoms, lead poisoning often goes unnoticed until it increases in
severity. Lead exposure can infect practically every part of the body causing neurological
effects, gastrointestinal effects, and reproductive effects (Lead Exposure in Adults - A Guide for
Health Care Providers, 2009).
Like the other chemicals, lead can play a role in obesity by acting as an endocrine
disruptor. Lead can affect majority of the endocrine organs and glands, but has been mainly
associated with the hypothalamic and pituitary axis. By interrupting synthesis of growth
hormones produced in the pituitary glands, obesity can be resulted. By decreasing the
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concentration of growth hormones, lead can potentially lead to obesity. (Doumouchistist et al,
2009).
If EDCs factor into obesity then it is important to monitor the main source of exposure.
In the case of humans, exposure typically occurs through contaminated food and water. If a
correlation between the concentrations of EDCs in food is established, then foods high in these
chemicals can be more readily monitored. This can potentially help tame the obesity epidemic
leading to a better and healthier future.

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Independent Variable: The endocrine disrupting chemical and the food studied





Dependent Variable: Concentration of the chemical and how that correlates to the obesity rate
Control: Because this is a comparison between the obesity rate and the concentration of the
endocrine disruptor, there is no control.
Materials:
Computer with internet access
GEMS/Food Contaminant Database
Interactive map of the United States obesity trend (http://fasinfat.org/adult-obesity/)
Microsoft Excel
Microsoft MS
Procedures:
1. Using the interactive map of the United States obtained from the following link
http://fasinfat.org/adult-obesity/,find graph the obesity rate by determining which state has the
median trend [California]
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2. Access the GEMS/Food Contaminant Database
3. Analyze the mean yearly concentration of the EDCs in various types of food
*Be aware of the units



4. Graph the concentration of each chemical and food
5. Compare to the obesity rate to determine the correlation

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Results: Data Tables

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Data/Data Analysis
Dibenzofuran
















Graph 1A
Graph 1B
Graph 1F Graph 1E
Graph 1C Graph 1D
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In order to determine if there is a correlation between the studied endocrine disrupting
chemical in a specific food and the obesity rate, overlapping graphs were created. Each graph
shows both the obesity rate and the mean concentration of the chemical in a specific food from
2003 to 2007. The bar graphs, usually blue although red in Graph 1H, represents the obesity
Graph 1G
Graph 1H
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rate. The line, on the other hand, shows how the mean concentration of the studied EDC has
changed over time.
In total seven of the ten foods studied showed traces of dibenzofuran. Graph 1A,
Dibenzofuran Concentration in Milk vs. Obesity Rate, seems to demonstrate a positive
relationship when comparing the line to the obesity rate visually. In 2004, both the obesity rate
and the concentration of dibenzofuran in milk simultaneously fall. Following 2004, the obesity
rate stabilizes before rising again in 2007. Similar to the obesity rate, the concentration of
dibenzofuran in milk plateaus before spiking 2007.
Graph 2B, the Dibenzofuran Concentration in Cattle Milk vs. Obesity Rate, demonstrates
a significant indirect relationship to obesity. It is graphed again in Graph 2H to show its
similarities to the dibenzofuran concentration in cattle meat (Graph 1F). Both, the dibenzofuran
concentration in cattle milk and cattle meat indirectly follow the obesity rate. In 2004, when
the obesity rate fell, the concentration of dibenzofuran in both cattle milk and meat spiked
before falling in 2005. The obesity rate continued to gradually increase in the years following
2004. Although at first the concentration of dibenzofuran in cattle milk and meat increased
with the obesity rate, in 2008, the concentration fell and then continued on a general
downward trend.
For the other foods, determining the correlation, if one was present, between
dibenzofuran and the obesity was much more difficult. In general, no visual correlation could be
determined but by calculating the R-values, the type of correlation and its significance can be
determined. According to the R-value, 0.111281, Graph 1C demonstrates the only positive
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relationship between the concentration of dibenzofuran and the obesity rate. The positive
correlation between the obesity rate and the concentration of dibenzofuran in milk and dairy
products NES is made most clear in the second half of the graph. In general, after 2007, the
concentration of dibenzofuran in milk and dairy products NES follow the upward trend of the
obesity rate.
Like Graphs 1A and 1B, Graph 1D demonstrates an indirect relationship according to the
R-value, -0.43341. Interesting enough, although the R-value is not high enough to consider it a
moderate indirect correlation (-0.5), it is relatively close. The indirect relationship between the
concentration of dibenzofuran in butter and the obesity rate can best be seen in 2006, where
the obesity rate changes very little but a large decrease in the concentration occurs. The
concentration of dibenzofuran continues to decrease until it is at zero while the obesity rate
continues to increase at a more rapid speed.
While the last graph for dibenzofuran, Graph 1E, demonstrates a negative correlation
according to its R-value of -0.33206, visually, the correlation between the line and bar graphs is
difficult to see. The concentration of dibenzofuran in egg and egg products follows this pattern
of spiking and falling around every other year. Because of this pattern, it becomes difficult to
visualize the negative correlation that it shares with obesity rate.

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Dioxin 1,2,3,4,6,7,8-HpCDD



Graph 2A
Graph 2B
Graph 2F Graph 2E
Graph 2D
Graph 2C Graph 2C
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Similar to dibenzofuran, in total, seven of the ten foods studied showed traces of dioxin
1,2,3,4,6,7,8-HpCDD. The most significant of the seven would be the concentration of dioxin
1,2,3,4,6,7,8-HpCDD in fish, Graph 2G, which demonstrates a negative relationship with
obesity. Like other foods that showed a negative relationship, in 2004, the concentration of
dioxin 1,2,3,4,6,7,8-HpCDD increased rather than decrease like the obesity rate. Following
2004, the obesity rate generally increases while the concentration of dioxin 1,2,3,4,6,7,8-
HpCDD in fish generally decreases.
In contrast to Graph 2G, Graph 2A demonstrates a direct relationship between dioxin
1,2,3,4,6,7,8-HpCDD and obesity. In Graph 2A, the concentration of dioxin 1,2,3,4,6,7,8-HpCDD
decreased slightly in 2004 which reflects the decrease in the obesity rate. Later, in 2005, the
obesity rate increases as does the concentration of dioxin 1,2,3,4,6,7,8-HpCDD. Although, the
Graph 2G
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concentration of dioxin 1,2,3,4,6,7,8-HpCDD drops in 2006 which differs from the obesity rate
trend, the years following show the same upward sloping trend as the obesity rate. In addition,
the calculated R-value was 0.485526 which is only extremely close to 0.5. This shows that there
was basically a moderate direct correlation between the concentration of dioxin 1,2,3,4,6,7,8-
HpCDD in milk and the obesity rate.
Both Graph 2B and Graph 2C express a positive correlation similar to Graph 2A. Visually
it can be difficult to see but according to the calculated R-value, 0.30619 (for Graph 2B) and
0.252166 (for Graph 2C), both show direct relationships. In Graph 2B, the concentration of
dioxin 1,2,3,4,6,7,8-HpCDD decreased in 2004 and continued to decrease through 2005 which is
slightly different from the obesity rate but in general, is still very similar. The obesity rate
continued to increase after 2005 while the concentration of dioxin 1,2,3,4,6,7,8-HpCDD
increased at first, but then stabilized and only expressed small changes. Graph 2C, on the other
hand, best shows the direct correlation to the obesity rate in the more recent years. In 2008
and the years following, both the obesity rate and the concentration of dioxin 1,2,3,4,6,7,8-
HpCDD increased.
In contrast to the last two graphs, Graph 2D demonstrates a negative correlation. At
first it may appear as if the concentration of dioxin 1,2,3,4,6,7,8-HpCDD in butter is mirroring
the obesity rate but the two trends diverge later. In 2006, rather than increasing like the
obesity rate, the concentration of dioxin 1,2,3,4,6,7,8-HpCDD in butter continued to decrease.
In the years following, although there are some spikes, generally the trend continued to
decrease which differed from the upward sloping trend of the obesity rate.
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Like many of the other graphs, Graphs 2E and 2F demonstrate a positive correlation.
Similar to the obesity rate, the concentration of dioxin 1,2,3,4,6,7,8-HpCDD in both egg and egg
products and cattle meat fell in 2004. After 2004, the obesity rate and the concentration of
dioxin 1,2,3,4,6,7,8-HpCDD in both foods expressed the same increasing trend. Graph 2F,
although expresses a positive relationship with the obesity rate, the significance of the trend is
basically zero. The calculated R-value was approximately 0.060838, which is almost zero. This
shows that there is not a well-established correlation which is why it is difficult to find similar
points in the concentration and obesity rate.
Arsenic
Graph 3A
Graph 3C
Graph 3B
Graph 3D
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Graph 3E
Graph 3I
Graph 3H
Graph 3G
Graph 3F
Graph 3J
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In contrast to the results for dibenzofuran and dioxin 1,2,3,4,6,7,8-HpCDD, arsenic was
found present in all ten foods studied. Although arsenic was the most widely found EDC, it also
had many foods that showed a low correlation to obesity. In total, six of the ten foods had a
calculated R-value that was essentially zero. One example of this is Graph 3A, Arsenic
Concentration in Milk vs. Obesity. According to the calculated R-value, 0.078405, there is a
direct correlation between the concentration of arsenic in milk and obesity. Because of this low
calculated R-value, finding corresponding points is difficult. In the case of Graph 3A, the areas
that best show the direct correlation between obesity and the concentration of arsenic is in
2004, where both the concentration and obesity rate decreased, and later in 2007 and
following years, where there is a general upward trend in both the concentration and obesity
rate.
Graph 3K
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Graph 3E, Arsenic Concentration in Egg and Egg Products, is very similar to Graph 3A in
terms of the R-value. The calculated R-value of Graph 3E is 0.064903. This means that there is
direct correlation but very low significance. The correlation between the concentration of
arsenic in Egg and Egg Products and the obesity rate is actually relatively easy to see in
comparison to the other graphs with low R-values. Although there were only small changes in
the concentration, from 2005 to 2008, both the obesity rate and the concentration of arsenic
increased gradually.
Similar to Graph 3E, Graphs 3B, 3G, 3I, and 3J also have low R-values but in contrast,
Graphs 3B, 3G, 3I, and 3J show negative correlations. Graph 3B, visually, is very difficult to see
the negative correlation. As stated earlier, the low R-value makes it difficult to find
corresponding points, and in the case of this graph, adequate corresponding points are not
present. In comparison to Graph 3B, Graph 3G also have inadequate corresponding points to
view the indirect relationship visually. Actually, Graph 3G, if the R-value was not accounted for,
would most likely have been considered a positive relationship. Although it does not fall in 2004
like many of the other positive relationships, it demonstrates the same upward trend as the
obesity rate. The same can be said for Graph 3I. Other than the fall in the concentration in
2004, Graph 3I mirrors the obesity rate trend and would have been considered positive if it was
not for its R-value. The last of these low R-value graphs is Graph 3J. Graph 3J is similar to Graph
1E. Both Graphs show this repeating pattern of spiking and falling approximately every other
year which does not show a clear correlation to the obesity rate.
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Unlike the earlier graphs, Graph 3F does not have a R-value that is essentially zero.
Graph 3F shows the positive correlation between arsenic in cattle meat and the obesity rate. As
many of the other direct correlation graphs show, in 2004, there is a decrease in the
concentration of arsenic similar to the decrease in the obesity rate. In 2005, there are increases
in both the obesity rate and the concentration of arsenic. Following 2005, the two trends
diverged a little but rejoin in 2008, where both the obesity rate and the concentration of
arsenic continued to increase. In contrast to Graph 3G, Graph 3H, Arsenic Concentration in
Apples vs. Obesity Rate, shows a negative correlation. In 2004, there is an increase in the
concentration of arsenic but a decrease in the obesity rate. Later in 2007, while the
concentration of arsenic is decreasing, the obesity rate is increasing.
In Graph 3K, the concentration of arsenic in milk and dairy products NES and butter is
graphed in comparison to the obesity rate. Both demonstrate a positive relationship. Similar to
other graphs that demonstrate direct correlations, in 2004, a decrease in both the obesity rate
and concentration of arsenic occurred. After 2004, there is a general increase in the obesity
rate. In the case of the concentration of arsenic in milk and dairy products NES (see Graph 3C
for individual graph) there was an increase in the concentration of arsenic in 2005 but then a
fall occurred in 2006. Although there are minor difference between the obesity rate and the
concentration of arsenic in milk and dairy products NES, there is still a positive correlation
because from 2007 to 2010, the concentration of arsenic mimicked the obesity trend by
steadily increasing and then decreasing in 2010. Similarly, there are slight differences between
the obesity rate and the concentration of arsenic in butter (see Graph 3D for individual graph).
For example, in 2007 and 2008, there was a decrease in the concentration of arsenic but an
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increase in the obesity rate. As stated before, because the general trend of the concentration of
arsenic in butter mimics the obesity rate, there is still a positive relationship despite the slight
differences.
Mercury





Graph 4A
Graph 4F
Graph 4E
Graph 4D
Graph 4C
Graph 4B
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Of the seven foods that showed traces of mercury, the most significant correlation
between mercury and the obesity rate was found in milk and dairy products NES. Graph 4G
demonstrates the negative relationship between the mercury concentration and the obesity
rate. In Graph 4G, the concentration of mercury peaks in 2004 and then gradually falls
throughout the next four years. Unlike the trend for the concentration of mercury, the obesity
rate falls in 2004 and then continues to increase throughout the next four years.
Similar to arsenic, some of the calculated R-values for mercury are relatively close to
zero as well such as Graph 4A, Mercury Concentration in Milk vs. Obesity Rate. Graph 4A
demonstrates a slight negative correlation. In 2004, the concentration actually rises while the
obesity rate falls. The concentration of mercury continues to rise throughout 2005 until 2006
Graph 4G
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where it falls to zero and remains there for the next few years. Graph 4C shows a similar trend
to Graph 4A in that both increase in concentration in 2004. In addition, in Graph 4C, the
concentration of mercury opposes the obesity rate in 2008, where the concentration of
mercury falls and then remains at zero for the next few years while the obesity rate increases
gradually. Graph 4B, on the other hand, shows a slight positive correlation but due to the low R-
value, good corresponding points between the mercury concentration and obesity rate and
difficult to find.
Graph 4D demonstrates a negative correlation. The negative correlation is not quite
considered moderate but is relatively close with an R-value of -0.41475. As seen, the obesity
rate is gradually increasing for most of the graph while the concentration of mercury in egg and
egg products remains relatively constant. Besides the fall in the concentration from 2003 to
2005 and the spike that occurs in 2007, the concentration of mercury in egg and egg products
does not change. Similar to the concentration of mercury in egg and egg products, the
concentration of mercury in cattle meat (Graph 4E) remains constant for a decent amount of
the time. From 2003 to 2006, the concentration of mercury in cattle meat was zero. Although it
is difficult to see graphically, the correlation between the concentration of mercury in cattle
meat and the obesity rate is direct according to the calculated R-value which was 0.304904.
Graph 4F, Mercury Concentration in Fish vs. Obesity Rate, demonstrated a direct
relationship. As expected, the concentration of mercury was highest in the fish since mercury is
mainly found in contaminated sea food. Surprisingly though, although there was a positive
relationship, the R-value was low and did not show a significant correlation. A clear drop in
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mercury concentration occurred from 2003 to 2004 which is similar to the obesity rate. After
2004 though, no significant changes occur. As can been seen in the graph, the concentration of
mercury increases from 2005 to 2008 but only minimally. Never the less, this demonstrates a
positive relationship since the obesity rate follows the same increasing trend.
Lead




Graph 5A
Graph 5D
Graph 5C
Graph 5B
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Graph 5E
Graph 5I
Graph 5H
Graph 5G
Graph 5F
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All ten foods studied showed traces of lead. Of the ten, the most significant is the
concentration of lead in milk and dairy products NES (Graph 5J). The lead concentration in milk
and dairy products demonstrated a negative correlation. Like many of the other graphs that
were also negative correlations, in 2004, rather than falling like the obesity rate, the
concentration of lead increases. Later in 2008, the concentration of lead falls and continues to
falls in the years after while the obesity rate increases.
Graphs 5A, 5G, and 5I are also indirect relationships. In 2004, the concentration of lead
opposes the obesity rate by continuing to increase rather than fall. The concentration continues
to rise throughout 2005 in Graph 5A, and throughout 2006 in Graphs 5G and 5I. Beginning in
2007, the concentration of lead decreases in Graphs 5G and Graph 5I. Both show a decreasing
trend which opposes the increasing trend of the obesity rate.
Graph 5J
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Graph 5H can also be considered a negative relationship. The concentration of lead
differs from the obesity rate in 2004 and 200. In 2004 the concentration increases but the
obesity rate fall while in 2009, the obesity increases but the concentration of lead falls. In
addition, in 2005, the concentration of lead decreases which contrasts the increasing obesity
rate. Although the indirect relationship between the concentration of lead and the obesity rate
can be seen relatively easy on the graph, the actual significance of the correlation is very low.
The R-value calculated was -0.03729 which is essentially zero. Graph 5D is similar to Graph 5H
except it shows a low positive correlation. In Graph 5D, the concentration of lead decreases
throughout 2004 and 2005 before it begins to rise and mirror the obesity rate.
Graphs 5B, 5C, 5E, and 5F are all direct correlations. Of the four graphs, Graphs 5C, 5E,
and 5F are similar to one another while Graph 5B is more of an outlier. Graphs 5C, 5E, and 5F
begin by opposing the obesity rate. Rather than decreasing in 2004, all three graphs show an
increasing concentration of lead throughout 2004 and 2005. In Graph 5C, the concentration of
lead decreases in 2006 before it increases like the obesity rate. Similarly, Graph 5E shows a
decrease in the concentration and then an increase in the concentration. Graph 5F differs from
the two in that, rather than decreasing for a year and then increasing the next, Graph 5F shows
the concentration gradually decreasing before spiking much later on in 2008. In contrast to all
three graphs, Graphs 5C, 5E, and 5F, Graph 5B shows a constant concentration of lead. From
2003 to 2004 and 2005 to 2008, the concentration of lead in Cattle Milk remains constant.


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Statistical Analysis
The graphs below are linear regression models that show the correlation between the studied
endocrine disrupting chemical in a specific food and the obesity rate. These graphs were chosen
based off of the calculated R-value. If the R-value was 0.5 to 1 or -0.6 to -1, then it is graphed
below.

















Model 1
Model 4
Model 3
Model 2
Model 4
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All five graphs shown above are very similar in that they have significant R-values.
Models 3 and 5 have a calculated R-value of approximately - 0.5 which shows a moderate
indirect relationship. The negative correlation can also be seen visually due to the downward
sloping trend line. Around the trend line are data points that show what the obesity rate is for
different concentrations of the chemical. In Model 3, it can be seen that the points lie around
the line and follow the trend but do not cluster as much as some of the other graphs. Model 5
shows a cluster of points around the trend line when the concentration was between 0 and
0.01 but towards the end of the line, there are some outliers.
Models 1, 2, and 4 have slightly higher R-values than Models 2 and 5. Models 1 and 4
have an R-value that is approximately - 0.6 while Model 2 has the highest R-value of - 0.7.
Similar to Models 3 and 5, Models 1,2, and 4 all shows a negative correlation as can be seen
from the R-value and the downward sloping trend. In Models 1 and 4, the data points again
follow the trend line but do not cluster as much as Model 2. Model 2 indicates a much stronger
correlation between the EDC and the obesity rate. All but one point cluster at the top of the
trend line. Because these R-values are significant it validates the correlation and can help
predict the obesity rate in the future with less error.
Model 5
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Conclusion
The purpose of this experiment was to determine if a correlation between the
concentration of EDCs and obesity could be found by analyzing the concentration of various
EDCs in different foods from 2000 to 2010. This experiment was conducted by using the
GEMS/Food Contaminant Database to analyze the mean concentration of each EDC in each
food for ten year. This was then graphed and compared to the obesity rate trend for the United
States.
In conclusion, this experiment produced both positive relationship and negative
relationships for each chemical, meaning that the hypothesis was both refuted and supported.
The hypothesis was supported when a direct correlation was established between the
concentration of an EDC in a food and the obesity rate. A positive relationships means that
EDCs are factors of obesity.
How each chemical factors into obesity slightly differs depending on the chemical. In the
case of dibenzofurans and dioxin 1,2,3,5,6,7,8-HpCDD, an increasing obesity rate was most
likely a result of the induced state of leptin resistance due to the increase concentration of the
chemicals. Being lipophilic, the chemicals were most likely absorbed into the adipose tissue
causing hypertrophy. The inflammation that occurred due to the toxins led to irregularities in
the synthesis of leptin leading to the increase in obesity.
For arsenic, a positive relationship with obesity can be a result of two things. The
hormone disrupted in the presence of arsenic is insulin. By acting as block, arsenic can decrease
the about of insulin in the bloodstream leading to uncontrolled glucose levels and diabetes type
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II. Majority of individuals with diabetes type II are also considered obese, thus an increase in
diabetes type II is directly related to the increasing obesity rate. The other thing that can occur
is arsenic can act as an agonist and overproduce the insulin hormone. Overproduction of insulin
hormone leads to obesity because more glucose is absorbed instead of eliminated.
Because mercury has been determined as an EDC but the hormonal system it disrupts is
yet to be determined, the reason a positive relationship between mercury and the obesity rate
occurred is more difficult to determine. The increase in obesity could have resulted from the
same cause as the increase in obesity for dibenzofuran and dioxin 1,2,3,5,6,7,8-HpCDD. Because
mercury is lipophilic as well, it is always a possibility that leptin resistance has occurred because
of the toxicity of mercury. Mercury is also a proven neurotoxin so it is also possible that it
affected hormones in the hypothalamus or pituitary glands located in the brain.
A direct relationship for lead and obesity is a result of the disruption of growth
hormones that occur in the pituitary gland. By acting as a block, the amount of growth
hormones produced is inhibited leading to obesity. In comparison to the other chemicals, the
best correlation between the concentration of lead and obesity was an indirect relationship.
Because there are negative relationships, the hypothesis was also refuted. Most of the valid
correlations determined by the R-value meant were indirect relationships. Rather than
suggesting that there was no relationships, negative relationships most likely occurred because
endocrine disrupting chemicals are not the sole perpetrator for obesity, other factors such as
eating consumption, amount of physical activity, and genes factor in as well. In addition,
negative relationships can result from the fact that most EDCs affect more than one type of
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hormone and not all hormones are related to obesity. It is possible that the EDC has more of an
affinity to a hormone that is not linked to obesity, therefore creating negative results.
Because there were both negative and positive relationships, the experiment is
considered inconclusive since it cannot be definitively determined whether endocrine
disrupting chemicals factored into obesity or not. To improve this experiment, it would be
beneficial to study eating trends and average daily physical activity trends to how they factor
into obesity. If there is a correlation, it could explain why the obesity rate continues to increase
while the concentration of endocrine disrupting chemicals do not.
None the less, whether a correlation was established for not, it is clear that these toxic
chemicals are present in common foods. Although for some foods, the amount is minimal and
may not affect the obesity rate, for other foods, the amount can be concerning. Through this
experiment, it can be determined which foods have high endocrine disrupting chemical
concentrations and must be better monitored. Hopefully, by monitoring the food, the obesity
rate will stabilize and eventually decrease..






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