Department of Chemistry
CH111: Principles of Chemistry
Writing Project
Fall 2005
(5Z,8Z,11Z,14Z)-N-(2-hydroxyethyl)
icosa-5,8,11,14-tetraenamide
(1S,cis)-4-[2-amino-6-(cyclopropylamino)9H-purin-9-yl]-2-cyclopentene-1-methanol
4-(acetylamino)phenol
(S)-N-methyl-1-phenyl-propan-2-amine
4-[4-(methylsulfonyl)phenyl]3-phenyl-2(5H)-furanone
www.gordon.edu
Table of Contents
Introduction.............................................................................................iv
1.
Chocolate, Marijuana, and Anandamide .................................................1
2.
AIDS Drugs: Life-saving and Feasible?................................................12
3.
The Shot Heard Round the World:
AIDS and its Treatment in the US and Around the World ...................15
4.
Dioxin Poisoning ...................................................................................21
5.
Vioxx: The Phantom Menace of the Pharmaceutical World.................27
6.
The Essentials of Anthrax......................................................................35
7.
Methamphetamine:
The Chemical Nature and Human Impact of the Drug .........................40
8.
Methamphetamine: Fun, Cheap, Deadly ...............................................46
9.
Over the Counter Killers........................................................................51
10. Encephalitis: a Chemical Swelling of the Brain....................................56
11. The Mortality of the Immortal:
The true cause of death of the great emperor Napoleon Bonaparte ......61
12. Was Napoleon Poisoned? ......................................................................68
13. The Secret Behind Anastasia Romanov ................................................75
14. The Bright Side of Fireflies: Bioluminescence .....................................82
15. Bioluminescence in the Firefly..............................................................91
16. The Venus Flytrap .................................................................................93
17. Presidential Award for Green Chemistry:
Optimyze and Its New Paper Recycling Technology .........................100
18. The Crisis at Bhopal ............................................................................105
iii
CH111: Principles of Chemistry
Writing Project
Fall 2005
This booklet is a compilation of student writing projects in the Principles of
Chemistry course at Gordon College in the fall of 2005. This was a group
assignment in which each group chose a subject to write about from a list
provided. Each group, designated by a specific element of the periodic
table, was asked to compose a list of questions to be answered. These
questions were both chemistry and non chemistry based topics. Each group
was also asked to propose at least one question that was open-ended and
needed an opinion to be answered. Each group, working collaboratively, is
responsible for the content of its paper. In general, limited editing was done
in completing this compilation.
It provides me great satisfaction be able to create this compilation for the
class.
Dr. Dwight Tshudy
Department of Chemistry
December 2005
iv
Chocolate, Marijuana, and Anandamide
Group: Strontium
Timothy Ciampa, Alyssa Fisher, Benjamin Sunny and Joyce Wu
1
Since its discovery, mankind has been fascinated with chocolate.
It was first found among the ancient Mayans and Aztecs who used the
cacao beans as currency. European explorers then brought this product
back to their homelands where it became a popular drink in the royal
courts. It was also believed to be able to cure any illness. It was not until
the 1800’s when chocolate began to appear in foods, cakes, and pastries.
From the mid-1800’s came the first candy bar and from there on, the rest
is history (Spadaccini, accessed 10/23/05). It is now estimated that each
year the chocolate industry sells five billion dollars of chocolate in the
U.S. alone (Kuwana, accessed 10/23/05).
19th century engraving
of a cacao bean
For decades, scientists have been hypothesizing as to what causes
chocolate to have such a euphoric feeling after consumption. It was
discovered that there are over 300 different chemicals in chocolate (Spadaccini, accessed
10/23/05). Some have suggested that the “feel good” feeling of eating chocolate is a result of the
stimulants in chocolate such as theobromine, phenylethylamine, and methylxanthines. Other
research has shown that chocolate triggers the production of opioids, which could then lead to
the production the “feel good” feelings (Kuwana, accessed 10/23/05). However, another
intriguing possibility is a fairly unknown chemical called anandamide.
“Nerve cells communicate by releasing ‘key’ molecules that are intercepted by other
nerve cells. There are many different types of molecular keys, and each has its own distinctive
shape. The surfaces of the target nerve cells are studded with receptors, which are like locks to
fit the keys. When the key fits into the receptor, the surface of the nerve cell changes in some
way” (Anandamide, 2005). The brain has receptors for tetrahydrocannabinol (THC). The active
compound will lock itself to the protein on the membrane cell, and that triggers a reaction inside
the cell. It is this chemical reaction that makes a person feel ‘high’ (Spadacinni, 2005). “In the
body THC undergoes rapid oxidation to produce initially hydroxylated products, one of which is
as active as THC itself. Hence Cannabis activity is apparently due both to THC and to some of
its metabolites” (Mechoulam, 2000).
An artist’s rendition of how nerve cells communicate via neurotransmitters.
2
Anandamide first appeared on the scene in 1996 when di Tomaso, Beltrano, and Piomelli
first published their paper Brain cannabinoids in chocolate. What is so fascinating about
anandamide is that it is an endogenous cannabinoid, (a chemical that helps control mental and
physical processes when produced naturally by the body, but can produce intoxication and side
effects when absorbed from marijuana) that binds to the tetrahydrocannabinol (THC) receptor.
Upon the discover of anandamide and its similarity to THC, researchers were flooded with phone
calls concerning whether or not a Surgeon General warning would have to be placed on
chocolate products. Rest assured that chocolate is not a drug and that the quantities of
anandamide in chocolate are rather small. It is estimated that in order to get a marijuana-like
high, a 130-pound person would have to eat 25 pounds of chocolate in one sitting (Kuwana,
accessed 10/23/05). That is approximately 250 Hershey’s bars.
There are a couple important differences between anandamide and THC that make
anandamide much less threatening than marijuana. For one, anandamide is produced naturally in
the brain.
“Anandamide, also known as
arachidonoylethanolamine or AEA, is a naturally
occurring endogenous cannibinoid neurotransmitter
found in the brain, as well as other organs” (Travis,
1999). The endogenous nature of anandamide has
pharmacological implications that will be discussed
later. Secondly, anandamide affects a localized area
of the brain.
THC activates several receptors
throughout the brain, which increases its potency and
produces a much stronger “high” (Kuwana, accessed
Left: An example of a marijuana plant.
10/23/05). The third major difference between THC
Right: A baby rhesus monkey.
and anandamide is that anandamide degrades rapidly.
“Unlike THC, anandamide is fragile. It breaks down very quickly in the body” (Senese, 2005).
The system naturally limits anandamide's lifespan, and, thereby, the duration of this
cannabinoid's effects (Piomelli, 1996).
Another intriguing aspect of chocolate is that it also contains two other chemical
compounds related to anandamide: N-oleoylethanolamine and N-linoleoylethanolamine
(Chianese, 1997). As previously stated, anandamide in the brain is quickly broken down.
Hence, the “high” produced from anandamide dissolves rapidly. However, the presence of Noleoylethanolamine and N-linoleoylethanolamine slow the break down of anandamide, allowing
anandamide to have a prolonged effect. The presences of N-oleoylethanolamine and Nlinoleoylethanolamine may have a larger contribution to the euphoric feeling from chocolate than
anandamide itself.
There are many cannabinoids involved with marijuana, but the active constituent is
known as THC (tetrahydrocannabinol). In 1964 the isolation of THC was reported. “The isolated
THC was then assessed for psychotropic activity on rhesus monkeys, and only THC showed
potent activity. The monkeys become sedated and sleepy after a small intravenous dose of the
ingredient. None of the other constituents of marijuana showed any activity. Furthermore, when
all the major constituents were administered, all the activity could be attributed to THC alone”
(Mechoulam, 2000). So what is it that causes THC to have this effect?
3
The neurotransmitter anandamide has twenty-two carbon atoms, thirty-seven hydrogen
atoms, a nitrogen atom, and two oxygen atoms; is one of the many neurotransmitter molecules
that nerve cells use to communicate. It binds with G protein-coupled receptors as well as THC
receptors. Anandamide molecules have a shape that is very similar to that of THC molecules.
Their molecular structures are shown below:
This allows anandamide to react with the THC receptors in the nerve cells of the human brain.
Studies have shown that AEA may also affect memory, pain, and fertility because of the way that
it interacts with nerve cells.
The discovery of the anandamide receptor of the brain has led many medical studies to
hope to use the information research provides to further medical advances, and “is a potential
target for the development of novel therapeutic drugs in the treatment of various conditions, such
as pain, feeding disorders and vascular disease among others“ (Mendizabal and AdlerGraschinsky, 2003). As previously discussed, the anandamide receptor produces such effects as
hunger, pain relief, impaired mental capacity and a cause in hypotension, or low blood pressure.
Each of these symptoms, researchers hope, can be isolated and studied to produce medicine to
treat diseases such as “pain, feeding disorders and vascular disease” (Mendizabal and AdlerGraschinsky, 2003).
French pharmaceutical company Sanofi-Aventis developed an appetite-curbing drug
called Rinmonabant, which uses “the premise that if cannabinoids stimulate appetite, blocking
cannabinoid receptors in the brain might reduce appetite” (Acomplia (Rinmonabant) –
Investigational Agent for the Management of Obesity, accessed 11/4/05). The idea stemmed
from studying the exaggerated effects that the cannabis plant causes on the anandamide receptor
that causes a user to be hungry. After discovering these affects and the possibility of developing
a prescription drug to treat over-eating, “compounds with potential inhibitory activity against this
receptor were then screened for inhibitory activity. Rinmonabant emerged from this screening
process as a potent CB1 receptor antagonist,” and Sanofi-Aventis started to develop
Rinmonabant into a pharmaceutical (Acomplia (Rinmonabant) – Investigational Agent for the
Management of Obesity, accessed 11/4/05).
Laboratory tests on animals as well as humans have been performed using Rinmonabant,
and positive effects have been observed: “Preclinical animal studies subsequently showed that it
could reduce consumption of fats and sugars, which contribute to weight gain…The promising
preclinical findings with Acomplia (Rinmonabant) have been confirmed in studies in man [as
well]. Results from a 16-week phase II trial showed that treatment with Rinmonabant produced
significant weight loss in obese patients and was well tolerated” (Acomplia (Rinmonabant) –
4
Investigational Agent for the Management of Obesity, accessed 11/4/05). However, short-term
results have been historically easy to achieve, especially when it comes to weight-loss medicine.
Tests are now being performed both in Europe and the United States on a variety of patients,
including “patients with concomitant type 2 diabetes and dyslipidaemia” (Acomplia
(Rinmonabant) – Investigational Agent for the Management of Obesity, accessed 11/4/05).
Concerns about Rinmonabant not only include long-term results but the fact that some
bodies may build up a resistance to the drug over time, as well as
rebound weight gain, therefore the FDA must have two years
worth of research on the drug before approval for prescription to
patients.
Preliminary findings based on information found on
anandamide have been positive and give more hope to medical
researchers. It is possible that anandamide will lead to the
production of many new drugs to aid common diseases plaguing
our population. There is even talk of anandamide becoming the
new miracle drug. However, a word of caution should be
emphasized in respect to miracle drugs. All drugs have side effects and this should not be taken
lightly. Thorough research ought to be given to all drugs before being placed on the market.
Works Cited
Acomplia (Rinmonabant) – Investigational Agent for the Management of Obesity.
http://www.drugdevelopment-technology.com/projects/rimonabant/ (accessed 11/06/05).
Anandamide – Wikepedia, the free encyclopedia. http://en.wikipedia.org/wiki/Anandamide
(accessed 11/12/05), part of Wikepedia, the free encyclopedia.
http://en.wikipedia.org/wiki/Main_Page (accessed 11/12/05).
Chianese, C. Briefer Madness: Brain candy of a milder variety. The Sciences [Online] 1997, 37,
47. Available from Academic Search Premier EBSCOhost. http://search.epnet.com/ (accessed
10/23/05).
di Tomaso, E.; Beltrano, M.; Piomelli, D. Brain cannabinoids in chocolate. Nature [Online]
1996, 382, 677-678. Available from Academic Search Premier EBSCOhost.
http://search.epnet.com/ (accessed 10/23/05).
Dubuc, B. The Brain from Top to Bottom: How Drugs Affect Neurotransmitters.
http://www.thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_heroine.html
(accessed 11/11/05), part of The Brain from Top to Bottom.
http://www.thebrain.mcgill.ca/flash/index_i.html (accessed 11/11/05)
5
Kuwana, E. Discovering the Sweet Mysteries of Chocolate.
http://faculty.washington.edu/chudler/choco.html (accessed 10/23/05), part of Neuroscience for
Kids – Chocolate (accessed 10/23/05).
Mechoulam, R. Science Spectra [Online] 2000, 44, 8. Available from Academic Search Premier
EBSCOhost. http://search.epnet.com/ (accessed 11/03/05).
Mendizabal, V. E.; Adler-Graschinsky, E. Cannabinoid System as a Potential Target for Drug
Development in the Treatment of Cardiovascular Disease. Curr. Vasc. Pharmacol. [Online]
2003, 1, 301-313. Available from Academic Search Premier EBSCOhost.
http://search.epnet.com/ (accessed 11/06/05).
Neurotransmitter – Wikepedia, the free encyclopedia.
http://en.wikipedia.org/wiki/Neurotransmitter (accessed 11/12/05), part of Wikepedia, the free
encyclopedia. http://en.wikipedia.org/wiki/Main_Page (accessed 12/11/05).
Raloff, J. Prescription-strength Chocolate.
http://www.sciencenews.org/pages/sn_arch/10_12_96/food.htm (accessed 11/05/05), part of
Science News Online. http://www.sciencenews.org/ (accessed 11/05/05).
Senese, F. General Chemistry Online: The Bliss Molecule.
http://antoine.frostburg.edu/chem/senese/101/features/anandamide.shtml (accessed 11/10/05),
part of General Chemistry Online. http://antoine.frostburg.edu/chem/senese/101/index.shtml
(accessed 11/10/05).
Spadaccini, J. Exploratorium Magazine: Chocolate.
http://www.exploratorium.edu/exploring/exploring_chocolate/index.html (accessed 10/23/05).
Travis, J. Science News [Online] 1999, 155, 215. Available from Academic Search Premier
EBSCOhost. http://search.epnet.com/ (accessed 11/05/05).
6
AIDS Drugs: Life-saving and Feasible?
Group: Zirconium
Autumn Brown, Benjamin Moulton, Sarah Swift and Apurva Thanju
7
General introduction
AIDS (Acquired Immuno-Deficiency Syndrome) is caused by the HIV (Human
Immunodeficiency Virus). HIV itself does not harm humans directly but attacks the immune
system, weakening it and thus reducing the tolerance of the body to infections. The HIV virus
belongs to a group of viruses called retroviruses that are unique from other living things because
they contain RNA (Ribo Nucleic Acid) instead of DNA (Deoxyribose Nucleic Acid). RNA and
DNA are similar and the only difference is the different building block from which they are
made. However, it is DNA that is passed from one generation to another not RNA (Campbell,
2005).
There are two major forms of HIV virus: HIV-1 and HIV-2. There are not many
differences between the two types; clinically they both induce identical AIDS. However, HIV-1
is by far more prominent as the HIV-2 virus seems to be less easily transmitted. In addition, the
time delay between initial infection and the first symptoms appears to be longer in HIV-2 than in
HIV-1. HIV-2 is locally contained within West Africa, while HIV-1 is found worldwide. Since
HIV-1 is more common, the term HIV usually refers to this strand in general (AIDS info, 2005).
Viruses are not self-sufficient and need a host to survive. Retroviruses like both types of
HIV can produce DNA from their RNA but they need another organism to reproduce (replicate)
their DNA. The general method in which the retrovirus does this is that it binds with its host,
inserts its newly made DNA (called retrovirus) into the host’s DNA and then uses the host’s
metabolic resources to replicate more retroviruses and molecules of a certain RNA which makes
proteins. Once the process is complete, the protein and provirus come together to form HIV
virus, thus completing its reproduction process.
In the case of the retrovirus HIV, it attaches itself to human CD4 cells, which are cells in
the human immune system. Their main function is to alert T-killer cells of harmful foreign
substance, called antigens. Once informed, the T-killer cells then destroy the antigen thus
defending the body. If an HIV binds to a CD4 cell, the cell dies. If the number of CD4 cells
decreases substantially in this way, then not enough T-cells can react to satisfactorily defend the
body, and the body is susceptible to sickness.
The interaction between CD4 cells and HIV is complex. First, the protein on the outer
surface of HIV binds to a CD4 cell. Then the virus’ outer surface fuses with the cell’s membrane
and a process called absorption begins. This process refers to the incorporation of genetic
material of HIV into the CD4 cell. Once the RNA is inside the cell, HIV converts it into DNA
using an enzyme called reverse transcriptase. The DNA- now a provirus- is then inserted into the
DNA of the CD4 cell. The HIV then primes the cell to make copies of the retrovirus in forms of
special kind of RNA called mRNA (messenger RNA). This type of RNA can then make long
chains of proteins that can be used together with the provirus to make a new generation of HIV
viruses.
Within the nine HIV genes, the ones that are of the most concern to HIV drugs are the set of
genes called gag and pol (AIDS Map Treatment and Care, 2005). The reason for this is that the
coding for the three main enzymes, reverse transcriptase, protease, and integrase, all reside
within these three genes. Most of the effective drugs focus on inhibiting the actions of these
enzymes. HIV drugs can be categorized into three groups:
8
•
•
•
reverse transcriptase inhibitors
protease inhibitors (PIs)
fusion inhibitors
Reverse transcriptase inhibitors
All of these inhibitors target one type of enzyme: the reverse transcriptase enzyme. As
mentioned in the introduction, reverse transcriptase transforms the RNA of the HIV into the
DNA so it can be replicated. If the activity of the reverse transcriptase is blocked, then no
replication takes place and the HIV virus is contained. So far, three groups of drugs have been
developed to do this:
•
•
•
nucleoside reverse transcriptase inhibitors (NRTIs)
nucleotide reverse transcriptase inhibitors (NtRTIs)
non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Nucleoside Reverse Transcriptase Inhibitors (NRTI’s)
DNA is made from single units called nucleotides. When HIV creates its DNA from
RNA, it takes individual nucleotide blocks and combines them together in a specific sequence.
NRTI’s- commonly referred to as nukes- are biochemical mimics which become activated by
the addition of three phosphate groups (PO43-) (Campbell Biology, 2005). When there is a high
concentration of NRTI’s in the body, HIV takes up a NRTI molecule instead of a normal
nucleotide. The difference between a normal nucleotide and a NRTI is that the defective NRTI
lacks a hydroxyl (OH-) group. This means that the DNA chain can no longer be continued and
viral replication stops so HIV is contained. Notice however, that NRTI’s do not actually kill the
HIV but only stop the replication process.
The harmful aspect of NRTI’s is that humans also use DNA replication. If our own cells
use the NRTI’s then, like the HIV virus, our DNA replication will stop and no new cells can be
formed. Scientists have long argued over this matter. Some say that the direct danger outweighs
the benefits especially since there are other effective drugs on the market. However, research
has shown that the while the HIV enzyme reverse transcriptase has high affinity for this group
of drugs, the human equivalent enzyme called DNA polymerase shows very low affinity. This
means that reverse transcriptase is much more likely to use NRTI’s than is DNA polymerase. In
addition, HIV viruses do not proofread or correct any mistakes made during replication, while
human cells do. This means that if mistakes like this are made, then the human cells will
automatically correct the malfunction but the virus’ will not, further downplaying the dangers
of NRTI’s (AIDS Map and Treatment, 2005).
One type of organelle however, that seems to have high affinity for NRTI’s is the
mitochondrium (pl. mitochondria), the powerhouse of the cell. Mitochondria, unlike other cell
organelles, replicate their own DNA. The enzyme in this case is called polymerase gamma,
which, very much like the reverse transcriptase of HIV, has high affinity for NRTI’s. Research
9
has shown that the mitochondria cannot properly divide in high concentrations of NRTI’s, and
thus the cell dies as a result of lack of energy.
In addition to these dangers, there are also side effects that are common to nukes. Many
effects depend on the type of drug used, but the most common ones include side effects such as
headache, nausea, fatigue and diarrhea, while rarer effects include pancreatitis and rare blood
disorders. However, despite these concerns NRTI’s are still widely used.
Nucleotide Reverse Transcriptase Inhibitors (NtRTI’s)
This form of anti-HIV drug works in the exact same way that the NRTI’s do: they prompt the
reverse transcriptase to substitute a defective nucleotide for a normal one, stopping HIV
replication. The only difference between the Nucleoside and Nucleotide Reverse Transcriptase
Inhibitor is that the latter is activated much faster and lasts longer in the cell, often requiring
only a single dosage a day. This is due to the fact that NRTI’s, as mentioned above, require
three phosphorylation steps while NtRTI’s require only one step. Both the types of drugs share
similar side effects, like diarrhea, headache etcetera, but NtRTI’s also cause lower blood
phosphate levels (AIDS info, 2005).
Non-nucleoside Reverse Transcriptase Inhibitors
While the general way in which this class of drugs inhibits is known with almost full
certainty, according to Thomson, director of one of UK’s leading AIDS organization NAM, “the
precise way by which they inhibit reverse transcriptase remains unknown”. (AIDS Map and
Treatment, 2005). Like all enzymes, reverse transcriptase has a specific site on its surface where
it can bind to its target molecule or substrate. Since RNA is the molecule on which reverse
transcriptase acts, the substrate for this enzyme is RNA. The site where RNA binds to the
enzyme so it can catalyze the reaction is called the active site. These active sites have a certain
shape into which only RNA can fit; any other molecule cannot enter it. If the shape of the active
site is changed, then reverse transcriptase cannot bind with RNA and no replication occurs. This
is precisely what NNRTI’s or non-nukes achieve. By attaching to a different site on the enzyme
called the allosteric site, NNRTI’s change the shape of reverse transcriptase and thus disable it.
However, NNRTI’s work only for the HIV-1 type virus. Side effects for this class of drugs
include headache, nausea, dizziness, and liver toxicity; severe cases may include psychosis and
depression.
Protease Inhibitors
While Reverse Transcriptase Inhibitors stop the action of the enzyme reverse
transcriptase, another class of drugs, called protease inhibitors disable the enzyme
Protease. The other type of enzyme that HIV heavily relies on for its replication is the HIV
version of protease. HIV uses the host’s protein synthesis capabilities to create an outer protein
covering for the newly replicated viruses. CD4 cells, however, make a polyprotein, a molecule
composed of many proteins. The HIV then uses protease to cleave this large molecule into
smaller more useful proteins. Very much like the NNRTI’s, Protease Inhibitors occupy an
10
allosteric site and change the conformation of the active site, disabling the protease from
cleaving the proteins. No replication takes place and no new HIV viruses can be formed.
Fusion Inhibitors
The last class of drugs that help in the fight against HIV are called Fusion Inhibitors.
Unlike reverse transcriptase or protease inhibitors, this class aims to stop HIV even before it is
inserted into the CD4 cells by stopping the HIV virus from sending its viral material into CD4
cells. HIV cells use proteins called glycoprotein 120 and glycoprotein 41 for inserting its genetic
material into the cells. The glycoproteins create the path for the HIV virus to infect its genetic
material into the CD4 cell. Fusion inhibitors disable the glycoproteins and thus stop the insertion.
Fusion inhibitors, unlike enzyme inhibitors, prevent HIV from ever entering your cell. The
downside however is that fusion inhibitors cannot be taken orally, and must be injected since the
enzymes in our digestive tract can digest them (AIDS Map and Treatment, 2005).
The main difference between the NRTI’s and NNRTI’s and the protease inhibitors
therefore, is that the first two types of drugs prevent healthy immune cells from being infected
with HIV, whereas protease inhibitors prevent cells that have already been infected from
producing more HIV. Much research has shown that the drugs effectiveness is extremely limited
when taken by themselves and must be taken in combination with each other (Manos, 1998).
When taken alone (called monotherapy), these drugs are too weak to halt HIV replication
completely. As a result HIV alters its own structure to resist antiviral activity of the offending
drug, a process called resistance.
Drug resistance can take anywhere from a few weeks, such as with NNRTI’s, to several
months, as is the case with NRTI’s, to set in. Resistance can be delayed by taking these drugs in
combination. Many studies have shown that by taking one protease inhibitor with two NRTI’s—
a combination of therapies called highly active antiretroviral therapy, or HAART—it may be
possible to reduce the rate of HIV replication in the body to significantly low levels for a long
period of time (Manos, 1998). As a result, HIV has a difficult time trying to mutate itself into a
resistance strain. More importantly, researchers have found that by significantly decreasing the
amount of viral replication for a long period of time—a feat only possible with HAART—
disease progression can be slowed dramatically.
The downside is that HAART is also associated with many problems. First, each of these
drugs comes with a number of side effects that can cause a significant amount of discomfort for
people who take them and, quite possibly, can prevent them from taking the drugs at all. (For
example, the nausea associated with these drugs). Another drawback: many of the HIV drugs
cannot be taken with other types of drugs often used by people with HIV/AIDS because of
harmful drug interaction. In order for the drugs to be effective, they must be taken under fairly
strict circumstances. The protease inhibitors, for example, generally need to be taken three times
a day, some with food and some on an empty stomach (Manos, 1998). When people miss doses,
which determine the drug levels in the blood stream, the drug levels constantly fluctuate and can
lead to drug resistance.
In addition, drug phenomenon called cross resistance has been observed in which
resistance to one class of drugs can often lead to resistance to others. This means that a patients
11
chances of using all the types of drugs to combat AIDS is severely lessened and the patient must
be extremely careful to choose which drug or drug combination to take.
AIDS Treatments - targeting the cause of the disease, the symptoms, or the disease itself?
Conventional medicine treats both the cause of AIDS and its symptoms. As of yet, there
is no cure for AIDS. Slowing down the effects that HIV has on the immune system is the
objective of HIV drug treatments. Successful treatments can keep AIDS and related diseases at
bay almost indefinitely. Every case is different, however, and not all treatments are as effective
as is hoped.
When the body’s CD4 cell count finally reaches less than 14% and/or the viral load (the
amount of HIV in a blood sample) becomes too high, the diagnosis is AIDS
(http://aidsinfo.nih.gov, 2005). At this point in the deterioration of the immune system,
opportunistic infections, infections that would otherwise be non-life-threatening, attack the body
and are deadly if not treated promptly. The most common infections are PCP (Pneumocystis
pneumonia), a lung infection, KS (Kaposi’s sarcoma), a skin cancer, CMV (Cytomegalovirus),
an infection that usually affects the eyes, and Candida, a fungal infection that can cause thrush (a
white film in the mouth) or infections in the throat or vagina (www.thebody.com, 2005).
Fortunately, these infections are treatable.
Advances in the medical field have produced treatments that are dramatic improvements over
traditional treatments for the HIV virus and subsequent diseases, treatments created as recently
as even two years ago. These stronger drugs are making treatments more effective and less
demanding for patients. Still, HIV and AIDS are wreaking havoc on undeveloped and developed
nations alike despite improved treatments. There is yet no cure for AIDS. Therefore, the first
and most important step for eradicating the affliction, awareness, is mankind’s best hope.
Drug Patents
The efficacy of AIDS and HIV drugs does not make a difference unless these drugs can
be obtained by those who are sick. Unfortunately, due to economic situations, the areas of the
world most affected by AIDS can often not acquire the medicines they need. The problem is that
HIV is a disease that only relatively recently came to public attention and the HIV drugs are
therefore only recently invented. Because of this, they are still under patent. A patent is a
protection given by a country for an invention so that the inventors can make a profit for the
work they did. The company is allowed to be the sole agent that can sell the product or the right
to the product for a certain amount of time. This means that the prices are much higher than if a
generic company was allowed to make the product. This is, of course, the problem many
countries that are most affected by AIDS have with acquiring AIDS drugs. Some
pharmaceutical patents last longer than twenty years in some countries and can even be extended
beyond that. For example, one antiretroviral drug, called delavirdine, is patented by the
pharmaceutical company Upjohn. This drug was first patented on December 28th of 1989. Its
patent is not due to expire in Europe until 2010 and in the United States until 2013 (Boulet,
2000).
12
The vast majority, 95 percent, of those living with AIDS live in lower and middle income
countries. There are 25.4 million AIDS infected people living in sub-Saharan Africa alone. As
of July 2005, only one million of the six million of those living with HIV/AIDS in developing
countries were receiving the antiretroviral drugs they needed (Hirschler, 2004). There is some
good news, the cost of AIDS drugs in developing countries has plunged by 90 percent as
pharmaceutical companies have begun to listen to their critics and sell the life-saving drugs at
cost. Unfortunately, this is still very expensive. The drug companies refuse to give the drugs to
the governments for free in fear that they would be resold and undercut the market (Townsend,
2005).
Morals?
It isn’t hard to understand where the drug companies are coming from – they invested
millions of dollars in the research and development of their AIDS drugs. They need to make
back their losses and even make a profit so that their companies can stay afloat and continue to
make new drug discoveries. It isn’t hard to understand, that is, until one considers the disturbing
facts concerning HIV/AIDS. AIDS has become a pandemic that infects 13,500 new people each
day. In 2004, 3.1 million people died of the disease. That is over eight thousand people every
day, roughly a person dying every six seconds. Millions of people are dying because
pharmaceutical companies are concerned about making a profit. Moreover, these companies are
far from hurting financially. GlaxoSmithKline, the huge conglomerate that has the greatest share
of the HIV drug market, is worth $147 billion. Charles Medawar, the director of the United
Kingdom’s Social Audit, a part of the Public Interest Research Centre and a critic of the
pharmaceutical industry, expresses the arrogance of these companies beautifully, "The industry
is, frankly, running riot. It's like the 19th-century chemical industry in externalised costs: shove
the pollution up the chimney and not give a damn about who lives downwind" (Townsend,
2005).
Conclusion
AIDS and HIV have reached pandemic levels across the globe. There have been many
advances in the field of pharmaceuticals that have alleviated the suffering of those infected by
HIV who can afford them. These drugs can dramatically improve the person’s lifespan. As of
yet, however, there is no drug that cures the disease. The only cure is prevention. The saddest
part of the HIV/AIDS situation is that HIV is a wholly preventable disease. For the spread of
AIDS to stop, there needs to be more than just medicine; there needs to be a shift in the way
people live, think, and act.
Sources Cited:
AIDS Map Treatment and Care. Ways of Attacking HIV.
http://www.aidsmap.com/en/docs/9A46B119-E9CD-4C18-A064-B6C0024CC2FE.asp (accessed
10/23/2005)
13
Boulet, P., Perriens, J., Renaud-Théry, F. Patent situation of HIV/AIDS-related drugs in 80
countries. World Health Organisation. Geneva. January 2000.
Campbell, N; Reece, J. Biology, 7th edition. Pearson Education: San Francisco, 2005.
Hirschler, Ben. FACTBOX-How AIDS drugs save lives. Reuters, London, July 20, 2004.
HIV treatment. http://health.iafrica.com/doconline/hiv_and_aids/29132.htm (accessed
10/23/2005).
Manos, George; Negron, Leonard; Horn, Tim. Antiviral Drugs. In Encyclopedia of AIDS; 1st Ed.
Fitzroy Dearborn Publishing: Chicago, 1998; pp 70-72.
No Author. AIDSinfo. Offering Information on HIV/AIDS Treatment, Prevention, and Research.
http://aidsinfo.nih.gov/ (accessed 10/23/05)
No Author. The Body. How HIV Drugs Work. http://www.thebody.com/tpan/novdec_04/
how_drugs_work.html. (accessed 10/23/2005)
Staley, Peter et.al. Treatments for HIV/AIDS. http://www.aidsmeds.com/List.htm (accessed
10/23/2005).
Townsend, Abigail. In sickness and wealth: drugs firms on trial. The Independent [Online],
London, Oct 23rd, 2005
14
The Shot Heard Round the World
AIDS and its Treatment in the US
and Around the World
Group: Yttrium
Janet Loehwing, Jennifer Etesse and Prajjwal Bomzon-Tamang
15
The Acquired Immune Deficiency Syndrome (AIDS) is a fatal disease which is caused by
the Human Immunodeficiency Virus (HIV). HIV is a virus that attacks the immune system, the
body’s defense against foreign and harmful agents that may attempt to shut down activity, by
spreading throughout the bloodstream. Specifically, HIV infects the T-Cells of the immune
system, cells that recognize harmful cells and relay information to the rest of the immune system
so that it knows how to respond. HIV is what causes T-Cells to slowly deteriorate. The normal
T-Cell count for a person who is not infected with HIV can be anywhere from 800 to 1200
(Exploring, 2005). An infected person’s T-Cell count, however, can be below 200 (Exploring,
2005). This drop in the T-Cell count makes them vulnerable to opportunistic infections,
described by the National Institutes of Health as “an illness caused by an organism that usually
does not cause disease in a person with a normal immune system. People with advanced HIV
suffer opportunistic infections of the lungs, brain, eyes, and other organs” (Exploring, 2005). In
other words, opportunistic infections only affect people with dangerously low T-Cell counts. The
most prevalent of these infections are flu and pneumonia, which can be prevented by injecting
immunization shots (Exploring, 2005). The symptoms of an initial infection usually include
fever, headache, sore throat, swollen lymph glands and rash (Exploring, 2005). HIV is also a
retrovirus meaning that it can only survive by duplicating itself (Exploring, 2005). Reverse
transcriptase is the enzyme used to make a copy of the HIV’s RNA, further spreading the disease
in the body (Exploring, 2005). HIV is contracted through the sharing of infected needles, having
sexual contact with someone who is infected and any other way that bodily fluids can be
transferred. HIV may also be contracted to an unborn fetus by the mother if she is infected. Even
so, HIV is a slow virus, meaning it may take years for the symptoms to show up after being
infected.
There are thousands of classes of different drugs, each with their own specific function,
used to treat HIV and AIDS. The effectiveness of medicine
is greater for early and middle stages of AIDS because
fewer amounts of the HIV virus have been copied and
spread in the body (Exploring, 2005). The chances of
resisting the drug effects, however, are high in AIDS
patients (Exploring, 2005). Different varieties of drugs are
used to suppress the effects of disease in the body
(Exploring, 2005). These multiple drugs are called highly
active antiretroviral therapy (HAART) (Exploring, 2005).
Although this type of treatment does not cure the disease it
has reduced the death rate and has improved the health of
AIDS patients (Exploring, 2005). It has also greatly Provided by: National Institute of Viral
Infections and Disease
lowered the amount of virus that is present in the blood
(Exploring, 2005). Although HAART has been one of the effective treatments for HIV and AIDS
it has several side effects (Exploring, 2005). HAART, which is a treatment that is done by using
multiple types of nucleoside RT inhibitors, decreases the red and white blood cells in the body
(Exploring, 2005). This causes an inflammation of the pancreas and nerve damage, which can
even lead to death (Exploring, 2005). Despite the side effects, health professionals highly
recommend the use of antiretroviral medications, or HAART, for HIV treatment (Exploring,
2005). The main goal of this treatment is to achieve maximum suppression virus for as long as it
16
is possible (Exploring, 2005). Although it reduces the amount of virus in the blood to very low
levels the virus is not completely gone (Exploring, 2005). Thus, the goal of the medicine used to
treat AIDS is to suppress the virus as much as possible by having a fewest side effects
(Exploring, 2005).
The overall functions of the drugs used to treat HIV and AIDS are to keep the virus from
duplicating itself, and preventing the virus from continuing to enter the body (RxList, 2004).
Fusion Inhibitors block the virus from entering cells (RxList, 2004). Non-nucleoside reverse
transcriptase inhibitors block transcriptase from entering the cell (RxList, 2004). This as
discussed earlier, is the enzyme it needs to duplicate itself (RxList, 2004).
An example of a non-nucleoside reverse transcriptase drug is Sustiva (RxList, 2004). The
capsules contain lactose monohydrate, magnesium stearate which is used to build strong bones
and muscles, sodium lauryl sulfate, and sodium starch glycolgate which hydrates the system, and
the starch which breaks down compounds into smaller, more
digestible units (RxList, 2004). The capsule shell contains gelatin,
sodium lauryl sulfate, titanium dioxide, and silicon dioxide
(RxList, 2004). The tablets contain croscarmellos sodium,
hydroxophyl cellulose, lactose monohydrate, magnesium stearate,
microcrystalline cellulose, and sodium lauryl sulfate (RxList,
2004). The empirical formula for Sustiva is C14H9ClF3NO2 (RxList,
2004).
Structural Formula of Sustiva
- Provided by RxList.com
Ziagen is a nucleoside
come in tablet form or oral
milligrams of the tablet usually contains colloidal silicon
dioxide which is a non-metal found in soil and is used to
preserve strong bones and teeth. Ziagen tablets contain
magnesium stearate, microcrystalline cellulose, and sodium
starch glycolate (RxList, 2004). The oral solution contains
abacavir sulfate, artificially flavored strawberry and
banana, citric acid, methylparaben, propylparaben, an
antifungal substance, propylene glycol sacchrine sodium,
sodium citrate, and crystalline alcohol in berries and fruits,
which serves as a sweetening agent also known as sorbital
solution (RxList, 2004). The molecular formula for Ziagen
is (C14H18N60) *H2SO4.
reverse transcriptase which can
solution (RxList, 2004). 300
Structural Formula of Ziagen - Provided
by RxList.com
The last example of medicine used to treat HIV in tabletform is called Lexiva (RxList, 2004). 700 milligrams of this drug
contains the same ingredients as three hundred milligrams of the
Ziagen tablets in addition to croscarmellose sodium and povodone
K30 which is a synthetic polymer used as a "dispending and
suspending drug manufacturing" (RxList, 2004). The molecular
Structural Formula of Lexiva
– Provided by RxList.com
17
formula for Lexiva is C25H34CaN309PS (RxList, 2004).
The last treatment for the HIV virus is Fuzeon which is a fusion inhibitor (RxList, 2004).
Fuzeon is an injection and it is a clear, sometimes white, lyophilized powder usually giving in
one milliliter doses, injected beneath the skin (RxList, 2004). This dosage contains 19 milligrams
of Fuzeon, twenty two milligrams of mannitol, 2.39 milligrams of sodium carbonate, sodium
hydroxide, and hydrochloric acid. The PH is nine (RxList,
2004). The empirical formula is C204H301N51O64 (RxList,
2004).
As of the end of 2004, there were 39.4 million
people affected with either HIV or the AIDS virus (Avert,
2005). World wide, the distribution of infected people is
fairly even except for the exceptions of Sub-Saharan Africa
and South and South-East Asia where numbers are
strikingly higher (Avert, 2005). See chart below for further
analysis.
Structural Formula of Fuzeon - Provided
by RxList.com
Regional Breakdown of HIV & AIDS Patients (Avert, 2005)
Region
Adults &
Children
living with
HIV & AIDS
Deaths of
Adults &
Children
Sub-Saharan Africa
25.4*
2.3*
Oceania
.035*
.0007*
North African & Middle East
.54*
.028*
North America
1.0
.016
Eastern Europe & Central Asia
1.4*
.060*
West & Central Europe
.61*
.0065*
East Asia
1.1*
.051*
Latin America
1.7*
.095*
South & South East Asia
7.1*
.049*
Caribbean
.44*
.036*
Global Total
39.1*
3.1*
*million
18
Living in a medicinally advanced culture, the average American might assume that the
drugs available to American AIDS and HIV patients are also available to the AIDS and HIV
patients world wide. That assumption, however, is erroneous. According to Avert, an
international AIDS charity, there are 6.5 million people in developing and transitional countries
that are affected by AIDS and who need AIDS drugs (2005). Fewer than 1 million of these
people are receiving them (Avert, 2005).
In response to such horrifying statistics, a common question may be, what is the United
States doing to help the AIDS and HIV patients that can not afford access to the drugs and help
they need? The Clinton Presidential Foundation gained some ground in this area, when they
began mediating deals between the low-income countries and pharmaceutical companies (Avert,
2005). The foundation was able to coerce the drug companies into reducing the prices of their
drugs or allowing generic versions to be made, to where the treatment would be as low as $140
per person per year (Avert, 2005). Unfortunately, even that low cost is too much for many of
the people in these AIDS infected, low-income countries.
Similarly, in Bush’s 2003 State of the Union Address, he announced plans for the
President’s Emergency Plan for AIDS Relief, abbreviated PEPFAR, which would increase the
United State’s spending for HIV and AIDS around the world (Avert, 2005). According to
Avert, “President Bush has increased funding for Global HIV/AIDS, Tuberculosis and Malaria
from $840 million in 2001 to a request (to Congress) of $2.8 billion in the financial year of
2005” (2005). The World Bank has also promised $1.7 billion dollars to increase availability of
treatments to those with currently unmet medicinal needs (Avert, 2005).
As a leading developed nation, are the United States efforts enough? Should we be doing
more? In situations like this one, pertaining to the AIDS pandemic, there will always be more
and more needs, thus when a solution is so out of sight, whatever is being done must suffice as
good enough. Of course everyone would love to see an end to this horrifying disease, but the
resources of the United States and other countries will always be limited. Rather than worrying
about whether a certain country is contributing enough to the cause, we must be content with the
notion that the efforts being made are the best they can be right now, and rather focus on the
positive results of these efforts. In reality, fewer people are contracting and dying of AIDS or
HIV each year. That is only due to the continued improvements and greater availability of
resources to the infected individuals – improvements and availability provided by the efforts of
caring nations doing as much as they can.
Literature Cited
Exploring. http://www.niaid.nih.gov/factsheets/howhiv.htm (accessed October 2005)
RxList : The Internet Drug Index – Sustiva. http://www.rxlist.com/cgi/generic/efaviren.htm.
(accessed November 2005)
19
RxList : The Internet Drug Index – Ziagen. www.rxlist.com/cgi/generic2/abavir/htm. (accessed
November 2005)
Rx List: The Internet Drug Index – Lexiva. http://www.rxlist.com/cgi/generic3/lexiva.htm.
(accessed November 2005)
Rx List: The Internet Drug Index – Fuzeon. http://www.rxlist.com/cgi/generic3/fuzeon.htm.
(accessed November 2005).
World HIV and AIDS Statistics. http://www.avert.org/worldstats.htm. (accessed October 2005)
Providing Drug Treatment for Millions. http://intranet.avert.org/drugtreatment.htm (accessed
October 2005)
20
DIOXIN POISONING
Group: Cesium
Daniel Ashley, Rebecca Havens and Mary Kate Jordan
21
Dioxin poisoning is the result of overexposure to the harmful chemical compound dioxin.
There are currently many different theories and positions relating to dioxin and dioxin poisoning.
Society and scientists are asking pertinent questions about dioxin, such as what is the chemical
makeup of a dioxin? Or, chemically, how does dioxin affect the body? How are dioxins
produced and how are we exposed to them? How is the release of dioxins through industry
currently being addressed? Is dioxin really that dangerous to humans? How have dioxins affected
the human race in the past, and how might dioxins affect our future? The following seeks to
address these questions in a broad overview of the various positions currently offered today
concerning dioxin poisoning.
Chemically, the term dioxin refers to a group of chlorinated organic compounds that
share the same basic biological characteristics and structure; it commonly covers polychlorinated
dibenzo-dioxins (abbreviated PCDDs) and polychlorinated dibenzo-furans (abbreviated PCDFs)
(EPA). Dioxins are hydrophobic, stable, and very poorly biodegradable (Zimpleman). There are
many of these compounds; in fact, they number in the hundreds. The structure of 2,3,7,8-TCDD,
one of the most toxic and seemingly well-known dioxins, serves as a good example of the
chemical structure of a dioxin. The figure below is the molecular structure of 2,3,7,8-TCDD.
The number and placement of chlorine atoms in its structure determine the toxicity of a
dioxin. There are eight spaces around the structure to which chlorine may bind. These spaces are
clearly shown in the figure above. The chlorine atoms are attached at the sites corresponding to
the numbers at the beginning of the dioxin’s name, in this case 2, 3, 7, and 8. Generally, only
dioxins with the same number of chlorine atoms as TCDD or more chlorine atoms than TCDD
are toxic (Greenfacts).
Interestingly, dioxins actually seem to play a deceptive role when it comes to their
interactions with human cells. When a dioxin molecule enters the cell, it binds to an aryl
hydrocarbon receptor, a receptor believed to facilitate certain types of cell detoxification. The
dioxin then binds to this site just as the site’s normal signal molecule would and the complex
formed between these two molecules journeys to the nucleus of the cell. Here it binds to the
cell’s DNA. This results in the facilitation of the transcription of cytochrome P450 and the
enzyme aryl hydrocarbon hydroxylase with which it is associated. In short, the dioxin causes a
naturally occurring process to happen more frequently (Zimpleman).
The actual threat posed by dioxins to the human population seems to be a topic of serious
debate in the scientific community. It is clear that at the molecular level dioxins pose a threat.
However, one must also look at the larger scale of dioxin exposure. Recall that the dioxin causes
the cell to produce the enzyme aryl hydrocarbon hydroxylase. Normally this enzyme is used to
break down fats and is not dangerous, but in excess it can pose a threat. Breaking down too much
22
fat can result in complications, one example being extreme loss of weight. However, this would
require a high exposure to dioxins. When considering the threat posed by dioxin, exposure level
must be considered.
There are many different sources of dioxins, and the amounts released by each source
changes with time (EPA). Dioxins are not intentionally manufactured for any purpose other than
research; they are a by-product of many industrial processes including waste incineration and
any industrial process using chlorine (Lester 1). In the past, the major releases of dioxin were
due to commercial and municipal waste incineration, manufacture and use of some herbicides,
and chlorine bleaching of pulp and paper. However, government regulations and voluntary
industrial action has led to drastic reduction from each of these sources. Today, the uncontrolled
burning of residential waste is considered to be one of the largest sources of dioxin production
(EPA). According to the EPA, only 50% of dioxin sources are currently known (Lester 1).
Due to the pervasive nature of dioxins in our environment, every human has some
diminutive amount of dioxin in their body that accumulates through low-level exposure build-up
in tissues. Although they are an environmental contaminant, most dioxin exposure occurs
through food consumption. Over 95% of dioxin exposure comes through dietary intake of animal
fats (EPA). It is also very common in meat, dairy products, and fish. (See table below for a
complete listing of where dioxin comes from and how much dioxin in humans comes from each
of these places. Note that TEQ means toxic equivalent factors, commonly called toxic
equivalents. TEQs assess the risk of an environmental sample contaminated with chemicals, in
this case dioxin. Ppt refers to parts per trillion, the equivalent of pg/gm TEQ.)
Table 4-1 Dioxin Levels in U.S. Foods (Clapp, table source: Schecter, 1994)
Food Type
pg/gm TEQ (ppt)
Food Type
pg/gm TEQ(ppt)
Ground beef
1.5
Bologna
0.12
Soft blue cheese
0.7
Cottage cheese
0.04
Beef rib steak
0.65
Beef rib/sirloin tip
0.04
Lamb sirloin
0.4
Chicken drumstick
0.03
Heavy cream
0.4
Haddock
0.03
Soft cream cheese
0.3
Cooked ham
0.03
American cheese sticks
0.3
Cod
0.023
Pork chops
0.3
Perch
0.023
Studies have shown that Breast-fed babies also have higher than average levels of dioxin in their
bodies (Lester 3). The EPA also advises that it is possible to receive small amounts of dioxin by
breathing in dioxin vapor, inadvertently ingesting soil-containing dioxins, or through skin
contact with anything that has dioxins in it (EPA).
There are many extreme examples of how dioxin exposure affected entire communities.
For example, the population of Seveso, Italy may have been harshly exposed to dioxin poisoning
because of the explosion at Hoffman-LaRoche chemical plant in 1976. Studies have shown that
23
these people exposed to dioxin in this area are showing signs of cancer. Because dioxin has the
ability to mimic specific hormones, it has the ability to cause cancers in many parts of the body.
Some studies have even linked dioxin exposure to soft tissue sarcoma (a malignant tumor that
begins growing in connective tissue such as muscle, bone, fat or cartilage) in humans. In the
Seveso region three different zones of dioxin contamination were distinguished, zones A, B, and
R. The people in the A zone were evacuated from the area because they would have been most
heavily affected by the dioxin. People in the B region were most damaged by the dioxin, and the
poison did not contaminate people in the R region. Using information from 1976 to 1986,
women in the B region have shown an increase in cancers of the gall bladder and biliary tract and
cancers related to the blood-forming system. In men located in the B region, only cancers in the
blood-forming system have occurred. Because cancer can form and become visible after a
period of ten years, more cancers or more severe cancers may have appeared at a later time in
these people, but the results were not recorded (Montague). The sex ratio of children born after
the Seveso accident (between 1977 and 1984) changed from an expected 106 boys per 100 girls
to 26 boys per 48 girls born. The explanation for this is possible recessive damage to the X sex
chromosome. This would be expressed in males as they only have one X- chromosome, while it
could be masked in females. The result would be that any damaged male embryos would die and
only female embryos with two damaged X chromosomes would be affected. However, this is
merely observed evidence, the actual cause of such possible damage to DNA is unknown.
(Zimpleman)
Of note is the correlation between dioxin exposure and cancer in humans. How dioxins
cause cancer seems to be unknown. We know that by facilitating transcription dioxins are simply
replacing a natural signal molecule and the cell’s DNA is not actually changed or damaged in
any way. In light of this, it has been theorized that dioxins may promote the growth of cancer
cells after they have been formed, but they do not actually cause the initial change in DNA
structure (Zimpleman).
Moreover, the amount of dioxin present in the body of an average American may harm
the immune system, causing some diseases to be more easily contracted than usual. This amount
of dioxin may also decrease the testis size in males and can also alter glucose tolerance in both
males and females. In one percent of Americans today, the dioxin level is high enough so that it
may cause endometriosis, the presence and growth of functioning endometrial tissue in places
other than the uterus. Endometrial tissue is the mucous membrane that usually lines the uterus,
but if the presence of this type of tissue moves to another place in the body, it causes severe pain
and possible infertility. A high amount of dioxin can also cause decreased sperm count in males
and the rates of hormonally linked cancers (those in the breasts, testes, and prostate) are
increasing (Dioxin homepage).
Another set of groups at risk for dioxin poisoning are those that live near or in areas
where industrial accidents involving dioxin contamination have occurred in the past. People that
live in Times Beach, Missouri; Jacksonville, Arkansas; Pensacola, Florida; are at a much higher
risk for dioxin poisoning because of the accidents that have occurred in these areas (Clapp).
Also, Vietnamese people are generally more at risk for dioxin poisoning because of the dioxin
contaminated Agent Orange used as a defoliant during the Vietnam War (Chang).
In 1999 the Belgium incident occurred, in which contaminated chicken feed caused
Europeans to be exposed to extreme amounts of dioxin. This amount of dioxin consumed
24
exceeded the limit for dioxin by 250 fold. Effects of this incident include chloracne (a severe
form of facial acne), elevated liver enzyme levels, pulmonary deficiency, and neurological
deficits (sensory changes and headaches) (Dioxin contamination and poisoning).
Dioxin is a powerful substance that has the ability to cause major and minor effects in
humans, no matter how much of the substance is present. It is hard to determine the exact effects
of increased dioxin poisoning in this country, but if something more is not done, all of the
diseases and problems that have occurred in the past will continue to occur. Cancers will
continue to form more regularly in humans and increased immune system problems, along with
lung problems and regulatory hormone alterations, will continue to occur. Fortunately there are
many organizations attempting to decrease the production of dioxins by Americans.
According to a Question and Answer Review of Dioxin put out by the U.S. Environmental
Protection Agency,
Over the last 20 years, EPA has aggressively looked for ways to reduce and control
dioxins in all environmental media in the United States. Collectively, these actions
have resulted in strict controls on all of the known and quantifiable major
industrial sources of dioxin releases (EPA).
Through these efforts, known and quantifiable dioxin industrial emissions have been reduced by
more than 90% since 1987. For example, municipal and medical waste incinerators were
estimated to have emitted nearly eighteen pounds and five pounds respectively of toxic dioxins
in 1987, but today that number is less than ½ and ¼ ounce per year.
The EPA also has strict standards for other dioxin sources. It monitors emissions in
conjunction with the Food and Drug Administration (FDA), the Food Safety and Inspection
Service (FSIS), and the Centers for Disease Control and Prevention (CDC) (EPA). These efforts
seem to be having an effect, as levels of dioxin are decreasing not only in the environment but in
our bodies as well (EPA). It is important that these agencies continue their work, for if it were
not for them, many people would be harmed everyday because of increased amounts of dioxin in
our environment. These agencies and organizations are attempting to keep our environment safe
and as free from dioxins as possible, increasing the safety of people living here in the United
States.
Works Cited
Chang, Raymond. Chemistry, 4th Ed. McGraw Hill: New York, pp 1063.
Clapp, et al. America’s Choice: The American People’s Dioxin Report.
http://www.safealternatives.org/report.htm Accessed 13 November 2005.
Dioxin Homepage. http://www.ejnet.org/dioxin Accessed 8 November 2005
25
Dioxin Contamination and Poisoning. Canadian Medical Association Journal. [Online]
Accessed 29 Mar 2005.
Environmental Protection Agency Homepage. http://www.epa.gov.
Greenfacts Homepage. http://www.greenfacts.org/dioxins/l-2/dioxins-1.htm#1
Lester, Stephen. How to Start to Stop Dioxin Exposure in Your Community. Accessed 15
October 2005. http://www.ejnet.org/dioxin/dioxin.html.
Montague, Peter. Dioxin Does Cuase Cancer in Humans. Rachel’s Hazardous Waste
News no 353. http://www.ejnet.org/rachel.rhwn353.htm. Accessed 2 Sept 1993.
Questions and Answers about Dioxins. U.S. Environmental Protection Agency. Updated
29 October 2004. http://www.cfsan.fda.gov/~Ird/dioxinqa/html#g11.
Zimpleman, Jeffrey M. “Dioxin, Not Doomsday.” Journal of Chemical Education. Vol.
76. No. 12. December 1999.
26
Vioxx:
The Phantom Menace of the Pharmaceutical World
Group: Niobium
Gregory Beauregard, Chelsea Duprey, Gavin Sangrey and Jennifer Soerensen
27
Rofecoxib, commonly known as Vioxx, is a nonsteroidal anti-inflammatory drug
(NSAID) used mainly for treatment of osteoarthritis, but also for acute pain, migraine headaches,
and menstrual pains. Vioxx was manufactured by Merck, one of the leading pharmaceutical
companies around the world, but was later withdrawn from the market because its risks
outweighed its benefits, an occurrence that spawned much controversy. The drug was approved
in May 1999 by the FDA after going through a six month long priority review and being taken
before the Arthritis Advisor Committee. The approval of the product was based mainly on the
safety of 5,000 patients on Vioxx who did not show any increased risks of very adverse or fatal
side effects (Statement…).
Vioxx consists of carbon, hydrogen, oxygen, and sulfur arranged into a specific chemical
structure, C17H14O4S. The chemical structure consists of two benzene rings which give the drug
better stability.
Photo 1
Photo 2
The Vioxx tablet contains either 12.5 mg, 25 mg, or 50 mg of roxecoxib and the following
inactive ingredients: croscarmellose sodium, hydroxypropyl cellulose, lactose, magnesium
stearate, microcrystalline cellulose, and yellow ferric oxide (Rofecoxib). A 5 mL dose of the
Vioxx suspension contains either 12.5 mg or 25 mg of roxecoxib and the following inactive
ingredients: citric acid, sodium citrate, sorbital solution, strawberry flavor, xanthan gum, and
purified water (Rofecoxib).
The Vioxx molecule is an enzyme inhibitor, but what exactly is an enzyme inhibitor?
For pharmaceutical enzyme inhibitors, the shape of the molecule is crucial to its success as an
effective therapeutic drug that can prevent the formation of harmful protein products. The
successful inhibitor must have a complementary shape that will competitively inhibit any
substrate from reaching the receptor site of the enzyme. If the molecule does not have
complementary shape, it will not be able to physically prevent the function of the enzyme, in this
case. Therefore, the mystery of the rofecoxib molecule lies in its shape, and the shape of the
molecule lies in its chemical composition. This is where the chemistry of the molecule and
electron geometry becomes crucial. Using basic Lewis structures combined with VSEPR and
valence bond theory, the elementary structure and shape of rofecoxib can be explained by
scientists. The Lewis structure of rofecoxib (above) reveals a basic planar tail surrounding a bent
center. The two benzene rings composed of 6 carbons are all attached to two fellow carbons and
a hydrogen molecule. The carbons are surrounded by three electron groups and embody the
trigonal planar model with 120 degrees between each bond. The odd ball within the rofecoxib
molecule is the 5-carbon ring structure which has an oxygen replacing a carbon within the ring.
As a result of the presence of this oxygen and of the singly bonded carbon, the ring of carbons
and oxygen is bent. The oxygen molecule as well as the neighboring carbon has a tetrahedral
28
geometry which repels the bonds to angles of 109.5 degrees, pushing the atoms out of the main
plane of the tail part of the molecule. At the end of one of the benzene molecules, there is a
tetrahedral shaped CH3 bonded to a trigonal planar SO2 molecule. Both of these additional groups
add to the uniqueness of the rofecoxib shape. This shape has been found as ideal for inhibiting
COX enzymes. To sum it up, the chemistry of the molecules defines its conformation and the
conformation determines its function (Vioxx…).
Vioxx belongs to a group of drugs known as coxibs. This group contains other antiinflammatory drugs such as celebrex, bextra, and naproxen. Coxibs reduce inflammation by
inhibiting the cyclooxygemase enzymes, COX-1 and COX-2. Unlike the other coxibs which
work as both COX-1 and COX-2 inhibitors, Vioxx works specifically as a COX-2 inhibitor.
Blocking COX-2 impedes the production of prostaglandins, consequently reducing pain and
swelling. However, COX-1 is an enzyme that protects the lining of the stomach, so blocking it
would increase the risks of stomach and intestinal problems including gastrointestinal toxicity.
In the clinical trials of Vioxx before the FDA’s approval, the risk of gastrointestinal side effects
was determined through a process called endoscopy. Endoscopy studies showed that using
Vioxx lowers significantly the risk of gastrointestinal ulcers when compared to ibuprofen
(Statement…). Therefore, gastronomically, Vioxx’s specificity inhibiting only COX-2 has more
positive results than the drugs that inhibit both COX-1 and COX-2.
The benefits of Vioxx relate mostly to osteoarthritis, an inflammation of the joints,
common in geriatrics. Vioxx also has been proven to help ease the pain of migraine headaches
and menstrual cramping as well. Vioxx’s versatility allows it to be taken by both men and
women at any age above eighteen (the safety and effectiveness of Vioxx on patients under
eighteen has not yet been evaluated, so it is not prescribed). Taken in either a pill or an oral
suspension, Vioxx is one of the most commonly used drugs world wide: two million people
were prescribed Vioxx at the time of its withdrawal in 2004 (Vioxx…).
Vioxx, like every drug, has side effects to it. Vioxx shares many of its side effects with
other nonsteroidal anti-inflammatory drugs. These effects include stomach upset, fatigue,
unexplained weight gain, severe headaches, muscle stiffness, cysts, fever, and mood changing.
More rare side effects include internal bleeding, abdominal pain, discolored stool, vomiting, and
liver disease (possibly fatal) (Side…). To reduce the risks of acquiring any of these side effects,
patients with a medical history of kidney disease, liver disease, heart attacks, stroke, blood clots,
blood disorders, alcoholism, or uncontrolled diabetes should stray away from taking Vioxx.
Also, in order to reduce any drug interactions, patients should not take Vioxx while taking other
coxibs or aspirin. Nevertheless, if Vioxx is taken with a stable medical history, not at the same
time as other coxibs, at the discretion of a physician, and responsibly, the chances of anything
happening are greatly minimized.
Of all the side effects associated with Vioxx, the most significant one is myocardial
infarct, a heart attack. According to certain studies, the drug seems to carry a very small risk of
heart attack, in the range of .3% to .5%, which is about one in three hundred patients (Brown). In
the VIGOR study, published in 2003, close to eight thousand patients with rheumatoid arthritis
were given either Vioxx or naproxen, another non-steroid anti-inflammatory drug. In the group
of people who took Vioxx, there were more than twice as many cardiovascular events than in the
naproxen group. The patients in the study with a history of cardiovascular disease were four
times more likely to have a cardiovascular event than the patients who took naproxen. An
29
analysis of this study results in a dilemma: either Vioxx increases the risk of cardiovascular
events or naproxen lowers it (Brown).
Annual rates of heart attack in patients taking Vioxx sheds even more light on how
dangerous the painkillers are. Of 48,000 patients, .5% of patients taking an inactive placebo pill
had a heart attack each year, while those who took Vioxx had a .80% chance (Brown).
In 2001, Merck began the APPROVe (Adenomatous Polyp Prevention on Vioxx) study, a
3 year study which would lead to Merck’s voluntary withdrawal of Vioxx from the market. The
trial’s aim was to evaluate the efficacy of Vioxx for treating colorectal polyps. Another aim was
to test more the cardiovascular safety of Vioxx (Vioxx…). The study was terminated when it
showed an increased risk of cardiovascular events occurring after 18 months of therapy. The
relative risk of these events between patients taking Vioxx and patients taking a placebo was
1.97. This study basically showed that the “long term use of rofecoxib resulted in nearly twice
the risk of suffering a heart attack or stroke versus patients receiving a placebo” (Vioxx…).
There are speculations as to why Vioxx has such adverse long-term cardiovascular
effects. Harvard University chemists Leleti Rajender Reddy and E.J. Corey have been
investigating the properties of Vioxx as a weak acid. Vioxx is the only COX-inhibitor that forms
a very reactive anion toward atmospheric oxygen when it releases its acidic proton. Maleic
anhydride and some -hydroxybutenolide are produced as a result of the weak acidic reaction.
Photo 3
Reddy and Corey have found that the maleic anhydride is not a metabolite for Vioxx. However,
some of this compound may survive in the body before being broken down long enough to react
with the nucleophilic groups of tissues and biomolecules. If this situation keeps up over many
months, the toxicity can accumulate and cause a heart attack. This idea also fits with the
observations that patients who only use Vioxx for a couple months do not have a higher risk of
heart attacks (Rouhi).
Another proposed reason for Vioxx causing cardiovascular problems has to do with its
lack of COX-1 inhibitors. In the case of cardiovascular events, the blocking of COX-2 increases
the formation of blood clots, however, the blocking of COX-1 suppresses the formation of blood
clots. In traditional coxibs which block both COX-1 and COX-2, a neutral effect occurs, but in
30
COX-2 specific Vioxx the absence of COX-1 creates an increased of a heart attack because the
blood clots formed from the blocking of COX-2 are not suppressed by the blocking of COX-1
(Rofecoxib).
Nevertheless, the drama of Vioxx is not only for the scientists in the lab--there has been a
huge controversy over the withdrawal of Vioxx from the market as well. The APPROVe study
was the biggest contribution to Vioxx’s withdrawal, as it concluded that the drug increases the
risk of cardiovascular disease. With heart disease already plaguing a vast majority of the nation,
this piece of news alarmed all peoples involved. From FDA officials down to prescribing
doctors and the patients, everyone was and is still voicing their questions, wondering, “why was
Vioxx approved and heavily marketed through direct-to-consumer advertising when its safety
wasn’t proven?” (Adams)
The main advantage of using Vioxx over other anti-inflammatory drugs was that VIOXX
was the first of a new class of “high-tech” drugs that would work like the old drugs, with fewer
side effects. With the extra hundreds of millions of dollars spent by Merck on advertising,
highlighting the benefits, Vioxx was prescribed in mass quantities. The profit made from selling
Vioxx was an astronomical amount, and even though the drug helped with inflammation without
causing stomach ulcers, the risk of heart problems was definitely a very crucial issue that had to
be dealt with. There have been multiple lawsuits against Merck, but other then court ordered
payments, the only compensation that Merck has provided has been that they buy back the
unused drugs from the consumer (Merck).
Photo 4
When Vioxx was finally taken off the prescription drug market in 2004, there were many
lawsuits for large sums of money. The first personal injury suit was won by Carol Ernst, widow
of a Texas man and Vioxx patient; she was awarded $229 million for punitive damages and $24
million for mental anguish and the loss of her husband (The Vioxx…). As of September, the
second such case against Merck was taking place in New Jersey. Frederick Humeston, a 60-yearold postal worker from Idaho, had a heart attack in September of 2001 due to (he says) taking
Vioxx. By the time Mr. Humeston’s case was in the courtroom, about 5,000 cases had been filed
against Merck, and lawyers expect that about 25,000 suits will be filed out of the more than two
31
million people who were prescribed Vioxx (Lawsuits). Currently there are also about 500 cases
in British courts in which claimants could win up to £30,000 each, which corresponds to about
$52,000 in the United States. British law firms are taking groups of Vioxx “survivors” and
turning them into group suits in which more claimants are likely to win their cases in front of the
juries. In addition, Congress has recently passed a law giving group cases of $5 million or more
to tougher courts, which some people feel is a cop-out for the pharmaceutical companies
(Green).
Aside from civil cases, Merck is under criminal investigation by the Federal Justice
Department for the marketing tactics used to sell and distribute Vioxx. The Food and Drug
Administration (FDA) is also doing an internal investigation into the research of its own doctors
to see if they did something wrong when the reports on safety and the approval of the drug took
place (Adams).
Recently, due to corporate greed, pharmaceutical companies have become more and more
untrustworthy. Their research is often faulty because they care more about making money than
about the safety of the consumers of their drugs. There is evidence from reports that Merck has
known since before Vioxx was put on the market that it had the potential to cause various
cardiovascular problems, and that the FDA chose to ignore this information initially. As more of
the information leaked, Merck appealed to the FDA to allow them to change their warning label,
which was permitted. A few years ago Merck did change the warning label to include side
effects related to heart attack, stroke, and blood clots. However, Vioxx should have been
removed from the market at that time because Merck obviously knew that it was unsafe for its
patients--but the company cared more about the bottom line profit than its customers’ lives and
safety (Adams).
Pfizer, the maker of similar COX-2 inhibitor Celebrex, recently took their medication off
the market as well, because a government-funded study came to the conclusion that Celebrex
was two and a half times more likely to cause a cardiovascular catastrophe than patients taking a
placebo. The same report also found that Celebrex was more likely to cause such an event than
Vioxx. Clearly Pfizer also knew about these side effects of the drug but chose to ignore them just
as Merck did. Another study done recently of Celebrex, Vioxx, and Bextra, another COX-2
inhibitor produced by Pfizer, found that patients taking Bextra were 53 percent more likely to
have a heart attack, 19 percent more likely if taking Celebrex, and 23 percent more likely if
taking Vioxx (Lawsuits).
Another agency whose trustworthiness is quickly fading is the FDA. The organization is
responsible for studying the effects of drugs on humans and animals, and clearly they chose to
overlook the cardiac-causing problems associated with Vioxx, Celebrex, and Bextr. Even after
FDA studies found that these three drugs were harmful to patients taking them, the organization
decided just to have Pfizer and Merck put more warning information on the prescription labels
and in the prescribing information. Instead of requiring that these three drugs be pulled from the
market, the FDA allowed each to stay on and even voted in favor of all three at a meeting of the
advisory panel to keep all of them available for sale (Lawsuits). This vote came after Vioxx was
off the market and shortly before the FDA required Bextra to be taken off the market because of
uncertainty as to its long-term side-effects.
32
An interview with one of the FDA’s officials that was instrumental in bringing VIOXX
off the market explains a little bit about the hair-raising situation. Dr. David Graham explains
that the FDA puts the interest of the pharmaceutical company before the safety and well being of
the American people when approving a drug. In fact, Congress passed the Prescription Drug
User Fee Act in 1992 by which drug companies pay the FDA to review their drug and approve it.
The FDA official explicitly says, “the FDA is not able to adequately protect the American
public” (Loudon). He mainly refers to high ranking officials that are in the structure of the FDA
and how the duality of their job descriptions puts them at the mercy of the industry. Therefore,
just because the FDA approves a drug does not mean that it is 100% safe for consumption or that
it will work better than other drugs that already exist. Every consumer should be concerned
about what is put into his or her body and should view the Vioxx upset not as something out of
the blue, but something that can and will happen time and again.
However, there are FDA spokesmen that defend the FDA and its actions. FDA director
Sandra Kweder of the Center for Drug Evalution and Research examines the issue of approved
drugs going bad in a speech in November 2004. She notes that it is important to understand that
all approved drugs have some risk factor in them—the risks are often identified in trials and are
listed on the product’s label. However, the FDA will not approve the drug if the drug’s benefit
does not outweigh its risk for the intended population. If FDA officials were prophets, this
philosophy would work perfectly, but FDA officials are indeed fallible and cannot know
everything about a drug. The clinical tests before the approval of a drug cannot anticipate all the
possible effects that a drug will have on a population. Not all adverse drug reactions can be
discovered from clinical trials. Sandra Kweder says also that “the issue of how to detect and
limit adverse reactions can be challenging; how to weight the impact of these adverse drug
reactions against the benefits of these products on individual patients and the public health is
multifaceted and complex, involving scientific as well as public policy issues”(Statement…).
So who really is to blame for the injuries and deaths resulting from Vioxx? Sandra
Kweder certainly makes the FDA sound very sorry and sincere, but it is also very true that the
FDA did not even push to get the drug off the market for the safety of the patients. Merck
somewhat made up for their wrongs by taking Vioxx off the market, but only after much
prodding from various groups, the media, and the people. In order to become a better company
both financially and ethically, Merck, and all pharmaceutical companies, should start caring
more about the welfare of patients and less about staying in the black and making lots of money.
Corporate greed has ruined the pharmaceutical industry, and has made it hard for patients to give
their trust. It is not easy for patients to put their lives in the hands of crafty businessmen and
voracious scientists working together. The only temporary solution is for patients to always
research the history of the drug before they use it, making sure to keep a watch out for all of the
studies and tests the drug is going through. However, it is also true that patients have to accept
that with every drug they take there is some risk. Medical science does not know everything yet,
but thankfully does learn from past mistakes.
Works Cited
Loudon, Manette. “The FDA Exposed: An Interview With Dr. David Graham, the Vioxx
Whistleblower.” http://www.newstarget.com/011401.html (accessed 10/15/05).
33
Brown, David. “Celebrex and Vioxx Increase Heart Disease Risk.”
http://www.mercola.com/2001/sep/5/celebrex_vioxx.htm (accessed 10/22/05)
“Statement of Sandra Kweder.” http://www.fda.gov/ola/2004/vioxx1118.html (accessed
10/22/05)
Rouhi, A. Maureen. “Investigating Vioxx Toxicity.” Chemical and Engineering News.
http://pubs.acs.org/cen/news/83/i02/8302vioxx.html (accessed 10/21/05)
“The Vioxx Recall Timeline.” Parker and Waichman. http://www.yourlawyer.com/vioxxrecall-timeline.htm (accessed 10/21/05)
“Merck Knew of Vioxx Heart Attack Risk Before Recall.” Yourlawyer.com.
http://www.yourlawyer.com/vioxx-heart-attack.htm (accessed 10/22/05)
“Vioxx Side Effects.” http://www.freewebs.com/vioxx-lawyer/vioxx-side-effects.html (accessed
10/22/05)
“Rofecoxib.” RxList. http://www.rxlist.com/cgi/generic/rofecox.htm (accessed 11/16/05)
“Vioxx Lawsuits.” Arthritis Drug Lawyers. http://www.arthritisdruglawyers.com/vioxx/
(accessed 11/10/05)
Green, David. “Taking Painkiller Ruined My Life.” BBC News. 24 Feb. 2005.
http://news.bbc.co.uk/1/hi/england/lancashire/4288535.stm (accessed 11/10/05)
“Vioxx—Rofecoxib.” World of Molecules. http://www.worldofmolecules.com/drugs/vioxx.htm
(accessed 11/15/05)
Pictures Used
Photo 1. World of Molecules. http://www.worldofmolecules.com/drugs/vioxx.jpg
Photo 2. World of Molecules. http://www.worldofmolecules.com/drugs/Rofecoxib.png
Photo 3. Chemical and Engineering News.
http://pubs.acs.org/cen/img/83/i02/8303Wnews2.ce.jpg
Photo 4. http://www.cohenandcohen.net/docs/vioxx_wt.jpg
34
The Essentials of Anthrax
Group: Manganese
Bethany Jenkins, Nathan Parsons, Natalia Souza and Jacob Thompson
35
An article entitled “Anthrax Claims Hundreds of Cattle; Experts Push Vaccination” might
cause some people to automatically link the deaths to bioterrorism. However, these cattle died
from anthrax causing bacteria growing naturally in the Great Plains of the United States.
Bacillus anthracis, the bacteria that causes the disease anthrax, is found in the form of spores.
These spores can “live in the soil for many years.” (CDC) After entering an organism, these
spores release several toxins into the cells that can be potentially fatal if left untreated.
Bacillus anthracis can be found many places around the world, even in the U.S. Given the
right conditions, it grows easily. However, it is most prevalent in poorer countries where health
care is least common. The Center for Disease Control and Prevention states that “anthrax is
most common in agricultural regions where it occurs in animals.”
As a disease, anthrax is relatively rare, affecting animals more than humans. According to
the National Institute of Allergy and Infectious diseases, “In the United States, only 236 anthrax
cases were reported between 1955 and 1999… most of those cases were occupational exposures
in people who work with animal carcasses or products.” However, during the anthrax scare of
2001, 22 people got anthrax, and 5 did not survive. Even more sobering is the knowledge that
“two hundred and twenty pounds of aerosolized anthrax spores sprayed from a nondescript truck
in any U.S. city would wipe out anywhere from 130,000 to 3 million people, the equivalent of a
hydrogen bomb” (MacDonald and Langreth). Anthrax is “odorless and tasteless”, and is hard to
distinguish from the flu. It can enter a person through a scrape, causing the skin to turn black. It
can also be contracted by eating infected food, or by inhalation, the most deadly form. Anthrax
clearly has the potential to be a major threat if used as a biological weapon.
Anthrax can be a naturally occurring spore forming bacteria, Bacillus Anthracis. It most
commonly occurs in wild and domestic lower vertebrates such as cattle, sheep, goats, camels,
antelopes, and other herbivores. When Anthrax infects humans it is usually from an occupational
exposure to the bacteria through exposure to dead animals and animal products from countries
where Anthrax is more common. Anthrax spores have the ability to stay alive for long after the
host animal is dead. On rare occasions anthrax has occurred in wild livestock in the U.S. though
it is much more common in the countries of South and Central America, Southern and Eastern
Europe, Asia, Africa, the Caribbean, and the Middle East. This is all pertaining to the naturally
occurring spores.
When used as a biological weapon a certain strain is grown for mass production. Because the
inhaled form is the most deadly, the spores of the strain are filed down to a size of a few
micrometers. This is the optimal size for inhalation. Ken Alibek is the former deputy head of the
Soviet Bio-weapons program. He says that the real secret of weaponising Anthrax is to blend the
modified spores with anti-caking chemicals that make them much more easily inhaled. The
reality of this is that it is easily done with readily available equipment. There was much
controversy in the 2001 anthrax scare, however, due to the fact that there was no traceable
evidence found from the spore-laden envelopes. Any slight mistake will leave traces in a lab that
is not air-filtered or will infect the person handling it. This suggests that there must have been a
professional working in a government lab who knew how to handle the bacterium.
Many countries have had their own bio-weapons programs including the United States. This
program was disbanded in 1969 and the anthrax that had been mass produced was destroyed.
36
Bacillus anthracis spores have several different ways they can affect humans. The resulting
anthrax disease can be contracted cutaneously, it can be ingested and infect the gastrointestinal
tract, or it can be inhaled and infect the bloodstream/body cells through the lungs. The fatality
rate of cutaneous and gastrointestinal infections is about 20-30%, while nearly all inhaled
infections result in death. Normal antibiotics are enough to subdue the skin and intestinal cases
of anthrax.
The cutaneous form of anthrax is most often obtained through infected animals and their hair
when the spores enter an open wound. “Skin infection begins as a raised itchy bump that
resembles an insect bite but within 1-2 days develops into a vesicle and then a painless ulcer,
usually 1-3 cm in diameter, with a characteristic black necrotic (dying) area in the center.”(CDC)
The gastrointestinal form of anthrax causes very severe problems when left untreated, including
vomiting, diarrhea and extreme abdominal pain. Though this form seems the least pleasant, it is
not the most fatal.
The inhaled form of anthrax is extremely deadly, though in its earlier stages is equivalent to a
common cold. When entering the lungs, the anthrax spores are ingested by macrophages and
subsequently release more spores as the infected macrophages move into the lymph nodes. The
spores release three proteins: protective antigen(PA), edema factor(EF) and lethal factor(LF).
PA binds with a receptor on cell surfaces and mutates to allow EF and LF to enter the cell
through endocytosis. Edema factor binds with calmodulin within the cell and creates a process
that swells the infected cells. Lethal factor cleaves six of seven signaling proteins within the cell,
rendering it unable to undergo mitosis. When the spores are able to contaminate the blood, the
spread of anthrax is very fast and usually unable to be stopped. “Combined PA and LF, known
as Lethal Toxin (LeTx), cause death when injected intravenously in animals.” (List Biological
Laboratories) Cell death through apoptosis or lysis often occurs within a few hours of its
infection.
It is said that only 18 occurrences of inhalation anthrax were accounted for before the anthrax
bioterrorism case in 2001 in the United States (Medline Plus). After 2001, The US Centers for
Disease Control and Prevention (CDC) counted 22 people who were infected in the postal
anthrax (JAOA Letters). Bacillus anthracis a rare but fatal disease which affects humans in
various ways. It is a bacterial organism that causes Anthrax, which is an infection. Fortunately
there are treatments in which to tend to this disease.
Anthrax can be transmitted in many ways through anthrax spores. These spores are defined
as inactive forms of the bacteria because when the bacteria sense their surroundings are no
longer livable they make a copy of their chromosome. Then Ed Lake says:
The rubbery cell membrane that surrounds the bacterial cell fluid beings
pinching inward around this chromosome copy, until there’s a little cell
within the large bacterial cell. This little cell are called the “daughter cell”
and the bigger, original one, what starts as the “vegetative cell” is now
called the “mother cell.” Next, the membrane of the mother cell surrounds
and swallows up the smaller cell, so that now two membrane layers
surround the daughter cell. Between these two membranes a thick wall
forms made out of stuff called peptidoglycan, the same stuff found in
bacteria’s rigid cell walls. Finally, a tough outer coating made up of a
37
bunch of proteins forms around all this, closing off the entire daughter cell,
which is now a spore. As the mother cell withers away or gets blasted by all
kinds of environmental damage, the spore lies dormant” (Lake, Ed).
Cutaneous anthrax, the most common, can be caught through touching animal fur or skin. It was
reported that, “Spontaneous healing occurs in 80 to 90 percent of cases. In 10 to 20 percent of
cases that go on to develop bacterium (massive bacterial infection of the blood), high fever and
rapid death follows” (National Vaccine Information Center). Lastly, there is gastrointestinal
anthrax which is acquired through eating undercooked contaminated meat.
Luckily there are treatments for the Anthrax disease. Antibiotics are normally given to those
infected earlier in order to make the other treatments like the vaccine successful. The prescribed
antibiotics include ciprofloxacin, penicillin, erythromycin, tetracycline, or chloramphenicol.
These must been taken by mouth for 4 weeks. Other forms of treatment are the anthrax vaccines
that are “93% effective against the infection” (Medline Plus). The Patient Education Institute
says:
The body produces natural antibodies that fight anthrax. However, when the
anthrax bacteria are too many, the body can not keep up with them.
Vaccination causes the body to produce the anthrax fighting antibodies
without actual exposure to anthrax. The vaccine includes the PA protein from
a type of anthrax that does not cause disease. The protein causes the body to
produce anthrax antibodies. After the vaccination, if the body is exposed to
anthrax spores, the body contains enough antibodies to fight anthrax
(MedlinePlus).
In some cases antibiotics can be too little for those people who were infected with inhalation
anthrax. They must use prophylaxis which is also used to treat small pox.
There is a great dilemma faced in the U.S. Most biological weapons of war are made in
response to the nuclear capabilities that the U.S. has and other countries are unable to obtain. So,
what does the U.S. do? If it dismantled all nuclear weapons, it would be unable to retaliate
against an act of war or even use nuclear weapons as a threat. There is no guarantee that if the
U.S. did dismantle all nuclear weapons that other countries wouldn’t simply make more to plan
for an attack that couldn’t be returned. Anthrax is a horrible weapon to use on other humans, as
are nuclear weapons that completely obliterate everything near them. Both weapons render the
area they effect uninhabitable as well. There is no real answer to this problem, but it is something
to consider nonetheless.
Works Cited
Fiala, Jennifer. “Anthrax Claims Hundreds of Cattle; Experts Push Vaccination”. DVM:
The Newsmagazine of Veterinary Medicine, Vol. 36 Issue 11, 2005.
Little, Stephen F. “Anthrax Vaccines”. Biodrugs, Vol. 19, Issue 4, 2005
Center for Disease Control and Prevention
(www.cdc.gov/ncidod/dbmd/diseaseinfo/anthrax_g.htm) (accessed October 2005)
38
(http://www.bt.cdc.gov/agent/anthrax/faq/signs.asp) (accessed October 2005)
National Institute of Allergy and Infectious Diseases,
(http://www.niaid.nih.gov/factsheets/anthrax.htm) (accessed October 2005)
List Biological Laboratories, Inc.,
(http://www.listlabs.com/Literature/171.htm) (accessed October 2005)
"Anthrax." Center for Disease Control. 25 Oct. 2005. National Center for Infectious Diseases. 15
Nov. 2005
(http://www.cdc.gov/ncidod/dbmd/diseaseinfo/anthrax_g.htm#How%20common%20is%20anthr
ax%20and%20who%20can%20get%20it) (accessed October 2005)
Mackenzie, Debora. "Anthrax bacteria likely to be US military strain." New Scientist. 24 Oct.
2001. New Scientist print edition. 15 Nov. 2005
(http://www.newscientist.com/article.ns?id=dn1473) (accessed October 2005)
American Osteopathic Asso. "The Journal of the American Osteopathic Association." JAOA
Letters. 2004. (http://http://www.jaoa.org/cgi/reprint/104/11/452) (accessed October 2005)
"Anthrax." MedlinePlus. 11 Oct. 2005.
(http://http://www.nlm.nih.gov/medlineplus/tutorials/anthrax/htm/_no_75_no_0.htm) (accessed
October 2005)
"Anthrax." Wikipedia The Free Encyclopedia. 1993.
(http://http://en.wikipedia.org/wiki/Anthrax#Treatment_and_prevention) (accessed October
2005)
Lake, Ed. "What is "cross contamination"?" Spores, Folds, Glove Boxes and Mail Boxes. June
2003.
(http://http://www.anthraxinvestigation.com/spores.html(accessed October 2005))
Fisher, Barbara. "Biological Warfare and Anthrax Vaccine." National Vaccine Information
Center. Dec. 2001. (http://http://www.909shot.com/History/Newsletters/spanthrax.htm)
(accessed October 2005)
39
Methamphetamine:
The Chemical Nature and Human Impact of the
Drug
Group: Ruthenium
Jaime Dalrymple, David Kleberg, Danny Pabon, and Laura Tyrell
40
Most people have heard of the drug Methamphetamine.
The fact that its use has been fluctuating over the last
decade or so is not surprising to anyone. But as far as its
chemical makeup, people just don’t know what makes
Meth what it is. By studying its chemistry, we can further
understand its effects on the body, as well as foresee any
potential hazards in its production. As a sort of introduction
to the information at our fingertips, the following table
gives some base knowledge into Meth’s chemical makeup:
TABLE 1.1: Methamphetamine
Now, this information by itself does nothing without
any sort of analysis of the procedure of making this
(S)-N-methyl-1-phenyl-propan-2substance or its effects on the body (which follow shortly),
amine
which can be inferred by its examination. It really is of
CAS
assistance in understanding what the drug actually does, as
537-46-2
number
its chemistry dictates its properties in regards to the body.
But it is helpful to realize that this is just another chemical, ATC code N06BA03
and as such, is relatively easy to understand from a Chemical
C10H15N
scientific viewpoint. All of this information can be cross- formula
referenced in order to find similar substances and make SMILES CC(CCl=CC=CC=Cl)NC
correlations to the different properties they might share.
Molecular
The more base information we can obtain about this drug,
149.24 grams
weight
the easier it will be for people to understand just how
harmful it can be. It is imperative that we get to the point Melting
175 °C
where we have enough mastery of its chemistry that we can Point
combat the epidemic at its source. This is only hoped for,
however, in the midst of a very difficult situation. This understanding would help in the
regulation of substances used in the drug’s production, but the simplicity of producing Meth
makes this information only useful as a starting point. Methamphetamine consumption in the
U.S. seems to be decreasing, but it is a problem. The accessibility of the substance, the dangers
caused by producing it, and the severity of the effects it has on users all make methamphetamine
a very dangerous substance (wikapedia.org).
Methamphetamine, more commonly known as Meth, is a powerful drug that affects humans
physically and psychologically in both detrimental and beneficial ways. However, the beneficial
effects are short lived and are far outweighed by the lasting adverse effects. The short term
beneficial effects include increased brain activity, alertness, and awareness. Because
methamphetamine stimulates the central nervous system, it gives the user the illusion of having
more energy. Meth, as opposed to other stimulants like cocaine, stays present in the brain for
several hours (stopmethaddiction.com). Thus, the feelings of alertness and energy are prolonged.
This is often why Meth is so popular among college students. Weight loss and heighten sexual
stimulation are additional physical effects of Meth that are often viewed as positive or beneficial.
The harmful physical effects of methamphetamine far outnumber the beneficial ones. These
effects range from tooth decay and mood swings to stroke and death. The most common and
harmful effect of Meth is physical dependence on the drug. The first use produces the most
extreme high, but over time a tolerance is built and the same level of feeling is not reached again.
41
Therefore, many users spend their time trying to recapture that first experience and become
easily addicted.
Using Meth once can cause significant damage, but once a user is addicted, the damaging
effects become far worse. Methamphetamine use can cause damage to the nerve receptors in the
brain and cause permanent damage to serotonin and dopamine-producing brain cells. The
immune system and the cardiovascular system are also affected. With chronic use,
methamphetamine can cause the lining of the heart to become inflamed, as well as cause damage
to small blood vessels in the brain. Hyperthermia (elevated body temperature) also results from
Meth use and can cause the body to convulse, eventually leading to death or severe mental
impairment (stopmethaddiction.com). Sexual disorders such as erectile dysfunction can also
develop over time. STDs are common among Meth users due to reckless behavior while
intoxicated. (wikipedia.org). Methamphetamine use during pregnancy has been linked to severe
birth defects, premature birth, and abnormal behavioral patterns in infants
(stopmethaddiction.com).
The effects of methamphetamine are not purely physical, they are psychological as well.
Again, the positive effects are far outweighed and outnumbered by the negative ones. The
positive mental effects include the user’s ability to focus and pay attention while high. Users feel
motivated to complete tasks and feel as if they have the energy and ability to do so. Depending
on the method of use (consumption, injection, etc.), either an intense rush or prolonged high is
felt by the user (stopmethaddiction.com). Over all, methamphetamine use produces a feeling of
bliss and euphoria because it elevates dopamine levels in the brain.
In contrast to the pleasure felt while high, extremely adverse psychological consequences
follow Meth use. Psychological addiction to the drug, hallucinations, paranoia, mood
disturbances, and psychosis are all common results of prolonged Meth abuse
(stopmethaddiction.com). Psychosis results from both physical brain damage from drug use and
the emotional damage of addiction. Psychosis as a result of Meth, often referred to as
“amphetamine psychosis,” includes delusions (such as the feeling of insects crawling on the
body), panic attacks, anxiety issues, bipolar behavior, and extreme phobias (wikipedia.org).
Meth users have also been known to exhibit fits of rage and violent behavior often resulting in
homicidal and/or suicidal behavior. Meth addicts are often overwhelmed by feelings of
nervousness, depression, confusion, and isolation. Insomnia is also experienced by many who
abuse Meth, as is the tendency towards repetitive motor activity. Eventually, getting high is a
Meth users only form of comfort or joy, and they can therefore no longer enjoy things that
people would normally find pleasurable. Being caught in a cycle of depression and addiction
often drives many Meth users to commit suicide. Methamphetamine addiction leads to moral,
spiritual, emotional, and often physical death.
Meth users can be identified by many obvious signs. Not all of these signs are conclusive, but
they can be useful indicating when/if a person could be using. The Stop Meth Addiction web
sight lists the following key signs in identifying a user:
increased heart rate, blood pressure, and respiration, flushed or tense appearance,
dilated pupils, bloodshot eyes, a chemical odor on their breath, excessive
sweating, rapid speech, inability to sleep or eat, severe weight-loss, rotting teeth,
42
scars and open sores, repetitive behavior, memory loss, teeth grinding,
restlessness, and tremors. (stepmethaddiction.com)
Meth users that mainline the drug (i.e. injecting it in liquid form) may also have needle marks or
scars on various parts of their bodies. These signs are not concrete evidence that a person is in
fact using Meth, but they are reason to give rise to suspicion.
Part of the methamphetamine problem is how easily it can be made. The extreme
accessibility to the tools and chemicals necessary to create Meth is one of the factors
contributing to the danger of the drug. Methamphetamine can be made with a lava lamp, red
phosphorous, iodine, and distilled water. The directions for methamphetamine production are
widely available on websites and they read as follows. First, obtain ephedrine or
pseudoephedrine. This can be easily found in dugs like Sudafed. Pills work best because they are
easy to clean. After cleaning the pills, chop them and mix with muriatic acid and hydrogen
peroxide and let sit for 12 hours. Next, wash with water, dry it and let stand for one day. Now,
mix with distilled water, red phosphorus and iodine. Pour this solution into lava lamp and screw
the top of the lamp back on. Plug the lamp and let solution cook for 48 hours making sure the
temperature is within a range of 90-100 C. Allow the product to crystallize then dissolve in
water and filter. Place the product into a jar and add a non-polar solvent mixing it well. Let this
solution stand for 15 minutes. Now discard the top layer. When the solution has cooled to room
temperature, add 25% lye solution in small increments until the solution stays milky white. After
15 minutes remove and save the top layer. Add the non-polar solution and lye solution again and
pull off the top layer again. Now gas the top layers you have save with sulfuric acid and salt,
then filter. Now use ice-cold dry acetone and alcohol to wash the product. The product of this
reaction is crystals of Methamphetamine (neonjoint.com).
Methamphetamines labs are covered in vapor from the process of making the drug. There are
methods by which law enforcement personnel may detect the presence of the substance on
property and clothing. The Fourier Transform Infra-Red Spectroscopy is one form of detection
that uses infrared light to determine the chemical nature of a substance through analysis of the
structure. The gas chromatograph/ mass spectrometer allows for detection of a small
concentration of methamphetamine in a sample of air from a lab (nlectc.org).
The labs in which methamphetamine is produced are extremely dangerous. It is common,
especially in rural parts of the country, for people to produce Meth in home labs. This makes
meth production even more dangerous. Meth labs have been uncovered in every state in
America, mostly in the west, southwest, and Midwest portions of the country. Thousands of
clandestine Meth labs are found each year by police (Newsweek). Although some chemicals
used in the Meth-making process are dangerous, most of the chemicals used to make Meth are
not particularly harmful by themselves. Many Meth ingredients are simply household products or
easily obtained chemicals. However, when they are combined and heated, they become a threat
to the safety of everyone involved.
The dangers of producing Meth at home are seemingly innumerable. The vapors emitted
during Meth production can cause severe damage to the respiratory system of those who inhale
them. The lungs can even become burned, depending on the type of vapor or gas inhaled. One
such emitted gas is phosphine gas, an extremely harmful substance (stopmethaddiction.com).
There are large amounts of chemical waste produced by Meth production. Residue from Meth
43
lab chemicals can remain at the site and on clothing for years after the lab is shut down. The
effects of these chemical residues can include respiratory problems, as well as cardiovascular
problems. Long term exposure to Meth lab chemicals can result in liver and kidney damage,
cancer, and neurological damage. (stopmethaddiction.com). If a child is exposed in utero to Meth
lab chemicals, the child may be born with lesions on its heart and/or brain. (Keltner). Burns from
chemicals and Meth lab fires are also very common. Home labs are often operated by people not
properly trained in chemistry or chemical safety procedures. Incompatible chemicals are often
mixed, or combined chemicals are heated too high or left unattended. These factors can result in
chemical burns, fires, and explosions. It is not uncommon for Meth labs to simply explode, not
only causing death and injury from the explosion, but also from the spread of harmful
substances. Explosions are the reason behind 15% of Meth lab discoveries as well as the reason
behind the many fatalities in Meth labs each year (ojp.usdoj.gov ).
According to the FDSS, U.S. federal authorities seized a total of 2,807 kilograms of
methamphetamine in 2001 compared to 3,373 kilograms in 2000. Although this may indicate
that Methamphetamine use is declining on a federal level, there is still a major problem in rural
areas where Methamphetamine labs are abundant. Producing Meth in such isolated areas makes
detection much more difficult for authorities. In places like Montana and Alaska it is very
difficult to find Meth labs concealed in wilderness hunting cabins. Most of the methamphetamine
produced in the U.S. is made in household labs in rural areas of the south, west, and Midwest and
it is estimated that thousands of labs remain undetected in these areas. Meth is abused most
commonly by people ages 18-25 as a party drug.
Although there is much work to be done, it appears that the problem is getting better. The
Methamphetamine Anti-Proliferation Act was passed in July 2000. This law toughened
sentencing guidelines and supplied more funding for authorities and anti-drug education. A
major development in working towards a solution was the choice of many stores to place certain
cold medicines (such as Sudafed) behind the counter to help control the availability of ephedrine
or pseudo ephedrine. This is expected to limit the quantity of Meth ingredients available to those
who produce it.
A stimulant with mainly negative side effects, methamphetamine has easily become the drug
of choice for a new generation. From these effects to the immense danger of mass-production,
one may wonder why this drug has gained much massive popularity. People will constantly look
for another “buzz” or “fix” for their pleasure or to help them push themselves farther than is
naturally allowed. Why one would risk serious injury or death to obtain or continue the use of
this drug is testimony to the harm it is wreaking on society. There are some people who feel that
the use of certain substances is a necessity in everyday life. One of the more interesting quotes
we have heard reiterates this with alcohol as the substance of choice. This is a sad realization
about today’s society: people refuse to accept that they have a need that can only be filled by a
Savior, and choose to stuff this specific void full of obtuse abuses, like a child trying to force
puzzle pieces in where they don’t fit. It is absolutely imperative that society as a whole comes to
realize that we do not need to alter our state of mind in order to function day-to-day. They need
to understand that their momentary high will eventually fade, and they will be left empty once
again, their addiction eventually becoming a self-destructive cycle ultimately leading to
incarceration, injury or death.
44
Works Cited
<.http://www.dea.gov/pubs/states/montana.htm>. (accessed November 16, 2005)
< http://www.dea.gov/pubs/states/alaska.htm>.(accessed November 16, 2005)
16 Nov. 2005 <http://www.dea.gov/pubs/states/massachusetts.html>.(accessed November 16,
2005)
"Dangers To Children Living at Meth Labs."
<http://www.ojp.usdoj.gov/ovc/publications/bulletins/children/pg5.html>.(accessed November
16, 2005)
"Federal Trafficking Penalties." DEA. DEA. <http://www.dea.gov/agency/penalties.htm>.
(accessed October 21, 2005
Feinstein, Dianne, and Jim Talent. "A Remedy for the Meth Epidemic." Washingtonpost.com. 30
Apr. 2005. Washington Post. <http://www.washingtonpost.com/wpdyn/content/article/2005/04/29/AR2005042901368.html>. (accessed October 21, 2005
"How to Make Meth." Neonjoint Drug Recipes.
<http://www.neonjoint.com/drug_recipes/chapter3.html>.(accessed October 21, 2005)
"Identifying a Meth User." Stop Meth Addiction. Narconon Southern California.
<http://www.stopmethaddiction.com/id-meth-user.htm>. (accessed October 22, 2005
Keltner, Lelia, Carolae Chervenak, and Theodoraae Tsongas. "Clandestine Meth Labs: Risks to
Children." Epidemiology. 06 July 2004. Lippincott, Williams & Wilkins
<http://www.epidem.com/pt/re/epidemiology/fulltext.00001648-20040700000217.htm;jsessionid=DcHLNqis5bDGZdp4qGd21kLxxQm9deAGEifrGAepq2aliU1CeKo5!352798717!-949856145!9001!-1>.(accessed October 22, 2005)
"Methamphetamine Detection." Justnet. National Institute of Justice. >.(accessed October 22,
2005)<http://www.nlectc.org/assistance/meth.html>.
"Meth Lab Exposure: Health Risks." Boulder County Colorado Government Online Public
Health. Boulder County Colorado.
<http://www.co.boulder.co.us/health/meth/healthImpacts/labs.htm>. (accessed October 22, 2005)
Shenfeld, Hilary, Andrew Murr, Arian Campo-Flores, Sarah Childress, Catharine Skipp,
Susannah Meadows, Dirk Johnson, Jessica Silver-Greenberg, and Anne Underwood. "America's
Most Dangerous Drug." Newsweek Society. 2005.
<http://www.msnbc.msn.com/id/8770112/site/newsweek/>>.(accessed November 16, 2005).
Wikipedia The Free Encyclopedia.
<http://en.wikipedia.org/wiki/Main_Page>.>.(accessed October 21, 2005)
45
Methamphetamine: Fun, Cheap, Deadly
A new epidemic in the war on drugs
Group: Scandium
Daniel Finn, Sean Lafferty, Alana Sellers and Amanda Wagers
46
There are many new drugs in today’s society. Many of these drugs give whoever takes
them a “get-away high”, a high which seemingly removes them from their current pains and
troubles. Among these new drugs is methamphetamine. Methamphetamine, also referred to on
the street as crystal meth, glass, ice, P, or Tina, is a synthetic stimulant drug and it is highly
addictive as the following article attests.
[T]his drug has a unique, horrific quality. In an interview, Stephan
Jenkins, the singer in the band Third Eye Blind, said that methamphetamine
makes you feel 'bright and shiny.' It also makes you paranoid, incoherent and
both destructive and pathetically and relentlessly self-destructive. Then you will
do unconscionable things in order to feel bright and shiny again (David Sheff,
"My Addicted Son," New York Times Magazine, February 6, 2005, p. 44).
Methamphetamine addiction has been blamed for increases in crime rates in many
communities across the United States, especially theft either to obtain funds for the purchase of
the drug, or to obtain ingredients for the synthesizing of the drug. This paper will discuss the
chemical make up of methamphetamine, the process of synthesizing it and the dangers that
process entails, the effects of the drug on the human person, the effects of meth use on the
greater community and the response of the federal government to this growing problem.
Chemical Makeup and Synthesizing
Methamphetamine, as it most frequently appears is a colorless crystalline solid. It is an
alkaloid similar in structure to MDMA (ecstasy) and is available in 5mg or 10mg doses, usually
in the form of pills. It is a simple molecule, and its natural chemical state is an oily liquid. Before
the drug can be used meth cooks must convert the oil to methamphetamine hydrochloride (a salt)
in their labs. The chemical formula for methamphetamine is C10H15N with a molecular weight of
149.24 g/mol and a melting point of 175 ˚C. This melting point is very interesting in that it
makes the production in a lab fairly easy.
Methamphetamine is highly illegal in the U.S., and the making of the drug can give the
manufacturer up to 10 years in prison. Despite the penalty for being found producing
methamphetamine, or meth, access to information on manufacturing meth is readily available on
the internet. Meth manufacturing has gone through several changes as laws have been
established that place regulation on over the counter drugs, in which meth is based from. For a
while the main chemical in meth was ephedrine, which is common in most cold and asthma
medicines. New regulations on cold medicines containing ephedrine have shifted manufacturers
to buying cold medicines with pseudo ephedrine. The cold medicines are processed to remove
buffers from pseudo ephedrine to get ephedrine. Red phosphorous and iodine are added to the
mixture, and are readily available for manufacturers because there are no laws regulating the
purchase of these chemicals. This substance is then filtered to remove any red phosphorous and
iodine; this process makes the meth even more pure. Other chemicals such as sodium, potassium,
lithium, or anhydrous ammonia are added to the mixture, and left to dry. When the anhydrous
base is evaporated a crystalline powder is left; this is meth at its purest state. Before sale, a
manufacturer will dilute the pure meth most commonly with MSM, a common cutting agent that
is sold at many pet supplies stores.
47
Methamphetamine labs are not only dangerous because of the consequences of being
caught, but the byproducts of the process are toxic and explosive. The dangers in producing
methamphetamine are primarily due to the highly volatile chemicals involved which can easily
explode with great force. Many meth cooks are inexperienced which frequently leads to the
mishandling of chemicals and therefore, explosions. Many injuries thus occur just from
producing this drug, let alone using the drug after production.
Other injury in the production stage can come simply from handling the necessary
materials, many of which are poisons. The raw materials in the production for methamphetamine
involve many household items such as: Freon, ether (starting fluid), toluene (paint thinner),
pseudo ephedrine (cold medicine), sulfuric acid (drain cleaner), anhydrous ammonia, iodine,
muriatic acid, and lithium (camera batteries).
Law enforcement must have special training and take many precautions when
dissembling a meth lab with the knowledge that the chemicals they are dealing with are lethal if
breathed in or touched. Numerous meth labs are found in homes that have children, and the
children have easy access to the lab and the toxic wastes. Also, many manufacturers dump the
byproducts into the nation’s streams, rivers, and sewage systems to cover up their illegal
activities.
The Effects of Methamphetamine on the Addict
Methamphetamine is very desirable drug because of its effects on the body. It helps the
socially awkward feel accepted, heightens the sense of euphoria especially in the party scenes,
and contributes to quick weight loss. The majority of users are drawn in by these enticing
attributes, and because of meth’s nature they soon become addicts. Unfortunately treatments for
such a drug are difficult and long term, resulting in low recovery rates. It affects all aspects of a
persons’ life. Interestingly enough methamphetamine can have positive effects on a person. It
once was used in lower doses to aid patients suffering with ADD and Narcolepsy, but the
characteristics of the drug and its abuse have caused it to be made illegal.
Methamphetamine is a stimulant, causing increased energy in users. As a result jerky
movements (Athetosis), incessant talking, increased physical activity and grinding of teeth are
usually observed in an addict. A personal interview was done with Beth (last name withheld), 19,
an addict now in recovery. In the interview, Beth described the urge to “do
something…ANYTHING…homework, drawing, typing, talking, fixing, cleaning…” In more
extreme cases this leads to tremors and convulsions. (Other short term side effects include
hyperthermia, brain damage, and even death.) Long term effects on the body may be the results
of common withdrawal. Sores in the mouth or loss of teeth due to incessant grinding are also
common as is restlessness and again, death. When asked how it affected Beth’s physical health,
she explained, “It makes your body tired and weak. When you come down off of it you feel like
[expletive]. Your stomach hurts real bad, muscles ache, head hurts, jaw hurts from clenching it
so hard.” One thing to remember, however, is that the physical parts are most likely the easiest to
get over.
The mental affects methamphetamine has on people most often include increasing
paranoia, passing euphoria, restlessness, irritability leading to aggression, anxiety, stereotypy
(OCD like behaviors) and hallucinations. In the interview done with Beth, she described a period
48
of time in which she lived with her boyfriend, Jeremiah, whose paranoia increased greatly in the
short time she knew him.
“…he ended up getting addicted to the drug and eventually started cooking it
himself...He got real paranoid and thought he had cameras all inside his house,
outside his house, UNDERNEATH the house (he thought the cops were under
his house listening to him talk to people about meth and trying to bust his lab.)
He also thought that the FBI was in the trees outside, he thought they were
getting into his car and hiding in the truck so that when he was driving they
would be listening to his conversations. He’d drive faster to try to get away
from the men in his trunk.”
Unfortunately, one night while under the influence of the meth, in a similar
situation Jeremiah lost control of his car and passed away.
Cognitive and Behavior Interventions as well as Thinking/Expectation Altering Therapy
are the two most common therapies used today. Many people are also involved in training to
improve their coping skills, as well as therapies to increase self-esteem. Treatment for
methamphetamine addiction is complicated, however, due to the extreme withdrawal symptoms
as well as social pressures. Many people have difficulties changing their stereotypical behaviors,
fighting biological symptoms and resisting influences from their friends. Unfortunately there is
no absolute way to free oneself from meth addiction. In the words of Beth, “Nothing good comes
from doing meth…nothing at all…it will take away everything from you, and you never realize it
until it’s too late.” These effects of individuals have drawn greater attention in recent years from
the federal government which will be discussed in the next section.
Methamphetamine and the federal government
Until the past 20 years, methamphetamine use was considered as a minor drug problem and
not many people were aware of its existence. However, from 1992 to 1999 the amount of meth
labs seized increased by 580% due to increased scrutiny from the government following a sharp
increase in meth use. It is estimated that one meth manufacturer teaches on average ten people
how to make meth. While many are trying to raise awareness of the effects methamphetamine is
having on the nation, the position of President Bush is that marijuana should be the main concern
of the government. Bush states that marijuana is the starter drug which leads people to use more
dangerous drugs, such as methamphetamine. In spite of this stance, the Bush administration is
taking some action to fight the methamphetamine epidemic. One step that the government is
planning on taking is placing a purchase limit of 3.6 grams per a transaction for retail sales of
over the counter pseudo ephedrine products. Since pseudo ephedrine is the main ingredient in
meth production, this should make it more difficult for meth cooks to obtain sufficient supplies
for the synthesizing the drug. Also, the federal government wants to have a law regulating all
products containing ephedrine or pseudo ephedrine, as well as require all importers of pseudo
ephedrine to get Drug Enforcement Administration approval if there is a change to the
shipment’s original purchaser. The President's 2006 drug control budget is $12.4 billion, with
increases in areas vital to the fight against methamphetamine—including treatment programs,
domestic law enforcement, and international efforts.
Conclusion
49
Methamphetamine is a growing epidemic in the United States as well as throughout the
world, and local communities to this point have had to shoulder most of the burden alone.
Fortunately, this problem is starting to be discussed at higher levels of government. Several
outcomes are possible from this increase in interest in the methamphetamine epidemic by the
federal government. The first is that more funding and training will be made available to local
communities for their police and medical. Obviously this would be a good thing, though it will
not be enough. A greater outcome will also fund the training for medical professionals to
operate long-term recovery centers for meth users. Furthermore, the federal government needs
to train and equip the FBI to assist local law enforcement in the apprehension of meth producers
as well as to increase the scrutiny of organized crime syndicates which have begun to be
involved in the production and distribution of meth. If the federal government turns full
attention to combating this epidemic on all its fronts, from large scale raids and arrests, to the
long process of changing the behaviors of meth users, it may yet be possible to prevent
methamphetamine use from reaching the extremes of the cocaine epidemic in the 70s and 80s.
For the government to make these changes it is necessary for voters to be aware about the
problem and bring it to their attention of our elected representatives. Then we will begin to see
progress on this problem.
Works Cited
Sources used for this paper include the following:
http://www.whitehousedrugpolicy.gov/news/press05/meth_factsheet.html (accessed October
2005)
http://www.stopmeth.com/made.htm (accessed October 2005)
http://www.foxnews.com/story/0,2933,166209.html (accessed October 2005)
http://www.thevillagefamily.org/metharticle.html (accessed October 2005)
http://en.wikipedia.org/wiki/Methamphetamine (accessed October 2005)
http://www.idph.state.ia.us/eh/common/pdf/hseess/meth_lab_cleanup.pdf (accessed October
2005)
http://www.dhfs.state.wi.us/eh/ChemFS/fs/MethClnUp.htm (accessed October 2005)
http://www.nevamo.com/meth.htm (accessed October 2005)
http://www.the-center.org/pdf/Meth%20Epidemic.pdf (accessed October 2005)
www.dea.gov (accessed October 2005)
50
Over the Counter Killers
Group: Rhodium
Amanda Cayton, Suzanne Poole and Shannon Stanley
51
In September of 1982, a tragic event occurred. Seven people in the Chicago area died
suddenly after taking Extra Strength Tylenol capsules. This Tylenol was later found to be
contaminated with cyanide poisoning. Johnson & Johnson, the makers of Tylenol, were forced
to pull the product from shelves. They discovered 8 bottles total that had been contaminated. It
was apparent that it had not been a mistake on the company’s part because all 8 of these bottles
had come from different factories and all of the deaths had occurred in the Chicago area (1).
Eventually the FBI ruled it to be an act of terrorism. Since this time, the FDA has established
stricter regulations on the packaging of over-the-counter drugs.
The chemical cyanide is anything that has a carbon atom and a nitrogen atom bound by a
triple bond (2). This chemical’s poisonous ion is usually found in combination with other
elements such as sodium cyanide, hydrogen cyanide, and potassium cyanide. In coalition with
hydrogen, it is a colorless gas that carries with it the faintest smell of almonds. When combined
with sodium or potassium it is presented as a white solid which also has the almond smell
characteristic, which can be detected on a person’s breath after being ingested. Although this
chemical can be found and used in many ordinary places, it is also can be used as a lethal
substance.
Cyanide was most commonly remembered as the gas used by the Nazis in their death
camps during the Holocaust. This form, Zykon B, works by distributing hydrogen cyanide into
the air. The gas chambers in the United States also use a form of cyanide in its gas chambers (2).
Cyanide, in salt form, has also been a popular form of suicide weapon because it is easily
ingestible and its effects are rapid.
Cyanide is naturally found in many foods, plants, bacteria, fungi, and algae. It is found in
cigarette smoke and can also be produced in the burning of plastics and other synthetic materials.
This chemical is used in the textile and paper industries and is used in developing photographs
and dealing with different metals and mining processes. Cyanide is also used for fumigation.
Cyanide, since it is found in nature and used in everyday materials, is present in the
environment. It is found in its gaseous form, hydrogen cyanide, in the air and on the surface of
water. It is also in soil because of the plants that produce it and as a result of industrialization.
The cyanide found in the soil, if toxic enough, could contaminate water sources, which could
lead to human exposure to the chemical.
Exposure to the deadly cyanide ion can occur through breathing, soil, contaminated water
supply, cigarettes, and certain cyanide containing foods. The effects of exposure are dependent
upon the amount of time the person is exposed, how much the person is exposed to, and the form
of cyanide the person comes in contact with. If a person has a single encounter with an extremely
minute amount of cyanide the effects are not lethal. They can include seizures, nausea and
vomiting, difficulty breathing, and anxiety. If a person comes in contact with a small amount of
cyanide repeatedly then the results worsen. These can envelop an increase of the blood’s content
of cyanide, difficulty in the movement of phalanges and appendages, vision trouble, hearing loss,
thyroid enlargement, headaches, low blood pressure, and chest pain. Irritation and sores can also
be a result if the person’s skin comes in contact with cyanide. When cyanide is encountered in
large amounts the result is either fatal and the effects can be seen in minutes, can cause lung
failure leading to death in the near future, or serious disabilities including lung injury, heart
problems, or brain damage. It is most dangerous in its gaseous state when it is unable to diffuse
52
and disperse into an open area. It rises due to its density being inferior to that of oxygen. These
two characteristics allow it to have substantially less harmful effects when it is found outside.
Cyanide, although fatal, is not a carcinogen, which means it does not cause cancer.
Instead the effects of cyanide on the body are a result of its ability to inhibit cellular respiration.
It interrupts the electron transport chain and does not allow oxygen to pull the electrons towards
itself, which is the key to the whole process. This prevents the cells from receiving oxygen and
causes them to die. The brain and the heart are the first parts of the body affected because they
are in need of the most oxygen. If not effective immediately, the first signs of cyanide poisoning
are difficulty breathing, seizures, and loss of consciousness. There is no known difference
between the reactions of children and those of adults when exposed to this harmful chemical, and
it is also not known if it causes birth defects directly, though it was a result of rat testing.
There are a few tests to determine whether or not someone has cyanide poisoning or has
been exposed to this dangerous chemical. These tests are able to detect the amounts of cyanide in
the urine and blood, but they are not one hundred percent accurate. Noticeable symptoms and the
scent of almond on the breath are the best indicators for exposure to cyanide.
Cyanide is most notably remembered in the Tylenol incident of 1982. This act of
terrorism caused Johnson & Johnson, the makers of Tylenol, to rethink their packaging
techniques and take affirmative action in response to this tragedy. They immediately pulled all
Tylenol capsules from the shelves and offered consumers an exchange of their capsules for
tablets, which are much harder to poison. The company even offered a $100,000 reward for the
criminal. Since this put America into such a state of shock, the company set up a toll-free hotline
for consumers to call and get their questions answered about the product. Because the company
shared all the details of this incident and what they were doing to help prevent it from happening
again, the media was kind to them and viewed the company in a good light. “When experts talk
about crisis management, the most positive case usually cited is that of the McNeil/ Johnson and
Johnson Tylenol tampering incident, even though, at the time, the company did not have a
formal crisis plan in place… In fact, the Tylenol crisis management has become the gold
standard by which all crises are now measured.”(3).
This was an awful incident that happened, but it made people more aware to the
possibility of other people tampering with the products they were buying. This incident caused
over-the-counter products to become safer and harder to break into. Johnson & Johnson
reintroduced extra-strength Tylenol onto the market with a new triple-safety-sealed tamper
resistant package. Although for a while it seemed as though the company might never recover,
the new tamper resistant package helped Americans feel safer about the Tylenol product.
Johnson & Johnson was able to restore the public’s trust in their products, and within three
months after the tragic event, the sales were back by eighty percent and the new and improved
capsule even exceeded the forecasted sales by fifty percent (3). By creating the new package,
Johnson & Johnson showed that even though they were not the cause of this problem; they were
trying to fix it. It showed that they cared about their consumers, and that they wanted them to be
happy with the purchase they had made.
This incident helped to raise awareness about safety issues among over-the-counter
drugs. In 1983, the Federal Anti-Tampering Act was passed outlawing the tampering of any
consumer product or its container. The FDA passed regulations requiring manufactures to use
53
tamper-resistant packaging for most over-the-counter drugs, oral hygiene products, and even
some cosmetics. The FDA’s definition of a tamper-resistant package is a package with one or
more indicators or barriers to entry which if breached, or missing, can be reasonably expected to
provide visible evidence to consumers that tampering has occurred. Some products are even
required to have 2 barriers (4) Even though the regulations placed on over-the-counter drugs are
rather strict, the FDA still stresses the importance of consumer awareness. If the package looks
suspicious or if anything seems out of the ordinary, then the product should be returned to the
store where it was bought. It is important to read the label, which will describe the products
tamper-evident features. Most importantly, never take any medicine that is discolored or that has
a strange odor (4).
Cyanide’s fatal effects can clearly be seen in the tragic events that occurred in the homes
of so many innocent people in the Chicago area in 1982. When the Tylenol capsules were
ingested, the cyanide immediately took affect on the victim’s body and resulted in death. The
company of Johnson & Johnson dealt with such an unfortunate event, even though it was not
directly their fault, with affirmative action. Although the deaths of the innocent were tragic, it led
to a positive reform in the safety mechanisms now applied to the packaging of over-the-counter
drugs and other products. It also raised consumer awareness and opened the eyes of all those
who so easily trusted in the reliability of medicinal products.
Literature Cited:
1.“1982 Chicago Tylenol Murders” Wikipedia, the free encyclopedia. 18 October 2005.
21October 2005. <http://wikipedia.org/wiki/Tylenol_scare.>
2.“Cyanide” Wikipedia, the free encyclopedia. 11 Nov. 2005.
http://en.wikipedia.org/wiki/Cyanide.
3. Murray, Eileen, and Saundra, Shohen. ”Lessons from the Tylenol Tragedy on Surviving a
Corporate Crisis.” Medical Marketing & Media 1 Feb. 1992.
4. . Cramer,Tom. “Look Twice: How to Protect Yourself Against Product Tampering”.
FDAConsumer. Oct. 1991.
5.Agency for Toxic Substances and Disease Registry. 22 Nov. 2004. “ToxFAQS™ for
Cyanide”. 11 Nov. 2005. http://www.atsdr.cdc.gov/facts8.html.
6. Centers For Disease Control and Prevention.
27 Jan. 2004. “Facts about Cyanide” 11
Nov. 2005. http://www.bt.cdc.gov/agent/cyanide/basics/facts.asp.
7. Fandray,Dayton. ”Ethical Company”.Workforce. Dec. 2000: 74.
8.. Greenberg, Eric J.D.”Product Tampering” 27 April 1999. 4 Nov. 2005.
http://www.facsnet.org/tools/ref_tutor/tampering/framework.php3.
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55
Encephalitis: a Chemical Swelling of the Brain
Group: Iridium
Zachary Coursen, McKenzie Garvey, Claire Munro and Nilda Ramos
56
Encephalitis, a condition that is talked of little in our society, is an inflammation of the
brain that can lead to many health related complications and even death. This paper will seek to
provide a general overview of the disease and discuss the causes, symptoms, prevalence,
diagnosis, treatments, as well as the chemical processes involved when encephalitis is
contracted.
More then a hundred viruses can cause encephalitis. Encephalitis is simply a primary
response of swelling in the brain. The swelling can be a result of a variety of viruses, fungus,
and/or bacterial parasites that enter the body and travel through the blood stream to the brain.
Swelling is a natural response to foreigners that arises with an increase in vasodilatation and
fluid concentration in the area affected by the virus in order to “flush out” the infected cells.
This response – encephalitis- is a mechanism by which the body locates the infected cells and
increases the concentration of defense reagents, usually leukocytes, including white blood cells
and macrophages, to the location of the infection. One may wonder how these responses are set
in action; the answer is in the chemistry of the body. This will be discussed shortly (6,7).
While there are many ways of contracting this rather rare disease, the most common is
through a virus. This broad term, ‘virus,’ could come from a range of problems including a
childhood sickness, the herpes-simplex virus, ticks/lime disease, mosquito bites and bacterial
infections (1,2). More and more causes are discovered that lead to encephalitis, and in this way
the disease is still a mystery. Without any concrete cause or warning of the disease it is hard to
prevent it from happening.
Encephalitis has as many symptoms as it does causes. Each cause of the virus may
produce a variety of symptoms, but most forms of the disease have a few commonly occurring
symptoms that could help identify the disease in its early stages. Like most other diseases
encephalitis may start out as a mild problem but can balloon into much more if it is not dealt
with promptly. Common symptoms may include things such as fevers, headaches, and lack of
energy but as the disease progresses the symptoms may begin to also include seizures,
hallucinations, memory loss, hearing loss, severe confusion and even comas (1,2). Babies who
are diagnosed with encephalitis have symptoms such as excessive crying, a large bulging soft
spot, vomiting and body stiffness.
Babies, older people, and others with weakened immune systems (such as HIV+ patients)
have the greatest risk of contracting encephalitis. The type of encephalitis that is contracted due
to a weak immune system is often referred to as secondary encephalitis (2). As previously
mentioned, the disease is rather rare in that it affects a mere one person out of two hundred
thousand people according to hospitals (1). The prevalence is thought to be a lot larger than this
because sometimes symptoms are so mild that people feel that there is no need to seek medical
attention (1).
Early diagnosis of encephalitis is crucial, for its symptoms can appear suddenly and
escalate rapidly to severe stages. The most brutal stages of the disease last for approximately a
week but may require many months in recovery; depending on how much, if any, damage is
done to the brain (1). There are several tests that can help identify the presence of infection and
inflammation. The first step would be to perform a neurological examination. Such an
examination involves a series of tests meant to assess performance of the patients’ nerve, sensory
57
and motor functions, as well as hearing, speech, vision, coordination, balance, mental status, and
changes in mood or behavior.
Next, the doctor would perform a series of more in depth tests that would present
scientific evidence of the presence of a bacteria and inflammation in the brain. Analysis of the
blood, urine and body secretions of the patient would help detect and identify infections as well
as the presence of antibodies and foreign proteins. Furthermore, analysis of the cerebrospinal
fluid that surrounds the brain would help detect infections, inflammation and other diseases
specifically located in the brain. This fluid can be obtained from the patient through a procedure
know as a spinal tap, or lumbar puncture, in which a special needle is inserted in the lower back
and the cerebrospinal fluid is removed. The fluid is then tested for the presence of bacteria or
blood which is normally not present in the fluid if the person is healthy. Computer-assisted
imaging such as CT scans or MRI can also be used for detection and diagnosis of this uncommon
disease. Lastly, the electroencephalography, or EGG, is used to monitor electrical activity in the
brain through the skull and can therefore identify abnormal brain waves.
Other than being careful to avoid some of the causes of encephalitis (by checking for
ticks, etc), and maintaining a healthy immune system, a person should be aware if the food they
eat and the water they consume is tainted. Also, they should keep up personal hygiene (7). There
is no real prevention of all types of this disease since some vaccines have been developed for
specific causes of encephalitis but not for others. The treatment of the disease is rather specific
to the symptoms that are caused. If the patient contracted the disease due to the herpes simplex
virus, then anti-viral drugs may be helpful. Women who are pregnant and have herpes
encephalitis will probably have to take anti-viral drugs, or they might have to have a C-section to
avoid exposure to the baby (7); but in the case of many other patients the disease is broken down
into symptoms to treat, such as problems with headaches are treated with aspirin, and are
monitored closely. Most people with encephalitis may also consider taking a corticosteroid to
reduce the swelling of the brain (1).
One common method of treating any type of inflammation is through the use of
corticosteroids. These naturally occurring steroids are produced, and released from the adrenal
cortex. When corticosteroids are taken for health reasons in addition to the naturally made ones,
they are said to “reduce swelling and decrease the body's immune response” (4). One may
logically look to corticosteroids to help reduce the swelling in the brain, but no solid evidence
has yet to be found in support of this practice (6).
The West Nile virus is one of the causes of encephalitis that is generally caused by a
mosquito bite which transfers the virus with the bite. When the virus is allowed to enter the
body and grow, it will head for the central nervous system where it eats at the tissue in the brain
and brainstem. As the virus enters the CNS, inflammation (encephalitis) occurs as a natural
reaction to the virus in order to warn the body, both outside and in, that something has gone
severely wrong (3).
Treating encephalitis, doctors often prescribe an antibiotic right away because there are
so many forms of encephalitis. Another way to treat encephalitis, if herpes are presumed to be
the cause, is acyclovir. This can help with healing, but it doesn’t cure herpes encephalitis. If the
antibiotic doesn’t work, then doctors will know it is not caused by bacteria. If the patient has
enterovirus or arbovirus, the doctors will only be able to treat the symptoms. A patient will then
58
be put into a dark room in case of headache. Pain medication is given, but only sparingly,
because they can change the brain’s natural defense solutions (5). A drug may also be
administered for the swelling such as a steroid like dexamethasone.
Looking for a cure means looking at the problem in detail; getting at the chemistry of
encephalitis should help in the search for a common cure. As previously mentioned, encephalitis
is a primary defense response against invaders in the body. The swelling of the brain acts more
as a ‘signal’ rather than a ‘symptom’ to warn the body of the problem. The signal is given off
through chemical means released from the mast cells present in the area of the body that is most
affected. Mast cells (which are just leukocytes/WBC’s) have receptors on them that work to
recognize other cells in the body. Normal body cells don’t have a problem being recognized by
these, but when they come upon a cell that doesn’t contain the same information as other body
cells they recognize it as an invader; a threat to life (8).
As soon as the receptors are activated these cells release chemicals such as histamine,
interleukins and other chemicals that are sent to places like the adrenal medulla where hormones
and other chemicals can be released in the “fight-or-flight” response to the bacteria or virus.
These responses include previously mentioned responses such as vasodilatation, and an increase
in fluid volume (8).
Although the mast cells are vital in triggering other responses, sometimes they will get
directly involved in the fighting and act as macrophages or lysosomes which contain many
varieties of potent enzymes in order to break up alien substances. Lysosomes themselves
involve chemistry because their enzymes cannot work in high pH areas. Thus, they tend to
engulf the cell into their own structured vesicle in order to work at the appropriate acidity to
break apart the harmful cell (8). Without the chemistry in these cells and others that work to
protect the body we would have little hope in warding off foreign invaders into our bodies.
As briefly reviewed in this paper, encephalitis is an autoimmune response to a harmful
foreigner in our bodies. These foreigners may include bacteria, parasites, fungus, and viruses in
that inhabit the brain. As a defense mechanism, swelling will develop wherever the foreigners
are present. There are many ways the inflammation will affect the brain; from slight problems
such as a fever or headache, to more serious complications like brain damage and death.
Responding quickly to encephalitis is crucial before letting the infection escalate further and
before swelling causes neuronal death. There are only a few cures that are known for
encephalitis, but thankfully enough is known about the disease that some prevention has proved
to be helpful. The body has a naturally good defense against foreigners, but with encephalitis this
can prove harmful because of the limits in cranial space. In the bodies fight against the initial
problem many chemical mechanisms are important in signaling and responding to these harmful
substances. The body is a complex and amazing structure that incorporates many chemical
reactions, some of which can be seen in encephalitis; the chemical swelling of the brain.
Works Citied
1) Kids Health, Infection Encephalitis,
http://kidshealth.org/parent/infections/bacterial_viral/encephalitis.html, copyright 1995-2005,
The Nemours Foundation.
59
2) Richard Robinson, www.healthatoz.com/healthatoz/atoz/ency/encephalitis.jsp, Copyright
2005, medical network Inc.
3) Encephalitis Information Resource,
http://www.encephalitis.info/TheIllness/WhatisEncephalitis.html, (last modified 6/26/05),
Copyright the Encephalitis Society 2002.
4) www.dictionary.com, (Accessed 11/12/05)
5) HealthLink Medical college of Wisconsin, The facts about Encephalitis,
http://www.healthlink.mcw.edu/article/1031002417.html, (Article Created 2004-09-22), (Article
reviewed 2004-09-22), Copyright 2003 Medical College of Wisconsin.
6)Clase Ac and Banfield BW, Corticosteroids Are Unable To Protect against Pseudorabies
Virus-Induced Tissue Damage in the Developing Brain, J Virol, 2003, Vol. 77, p. 4979-4984.
7) Quinn C. Thomas, Infectious Diseases,
http://www.ehealthmd.com/library/encephalitis/ENC_whatis.html, Copyright 2002-205.
8) Chai, Joshua, What exactly is encephalitis and how do you get it?
http://www.madsci.org/posts/archives/dec2001/1008703844.Vi.r.html, Copyright 2001,MadSci
Network: Virology.
60
The Mortality of the Immortal:
The true cause of death of the great emperor
Napoleon Bonaparte
Group: Tellurium
Sarah Cunlifffe, Alida D’Angona and Andrew Mathews
61
It was a long held belief that Napoleon Bonaparte, the great conqueror and selfproclaimed emperor, died of a stomach ulcer that developed into stomach cancer. The doctors
who performed the autopsy on Napoleon’s corpse after his death came to the conclusion of death
by stomach cancer, but did Napoleon, the great emperor, die in such a helpless way or was he
poisoned? “‘The lesions to the stomach described by Francesco Antommarchi (the doctor who
performed the autopsy) were not the cause of death,’ [Paul Fornes] told the conference” (News in
Science 1). If he were poisoned, it would not be far fetched to believe that Napoleon could have
been poisoned; he had many enemies in Britain and even among his so-called friends. What
evidence exists that Napoleon was poisoned and why is it credible?
Napoleon Bonaparte had a very engaging personality and accordingly charmed almost
everyone he met. Yet this trait might have just been the catalyst to cause the death of the great
Napoleon. When Napoleon was exiled to St. Helen four of his closest friends accompanied him,
two with their wives. However, one of the wives, the Countess deMontholon, left St. Helen in
1819 with her baby girl, Napoleana. It is believed that the Countess was actually a mistress of
Napoleon and that her newborn child was fathered not by the Count but by Napoleon. The Count
deMontholon was also close personal friends with some of Napoleons worst enemies, such as the
Duke of Artois who later became Charles X. Also the Count was to inherit the vast majority of
Napoleon’s estate upon the emperor’s death, even helping Napoleon draft his final will. Finally,
the Count deMontholon had access to Napoleon’s personal wine. This wine was consumed
exclusively by Napoleon, so this could have been the most likely source for the small amounts of
arsenic to be administered over a long period of time. The Count had many reasons to kill
Napoleon, but is there proof that Napoleon was actually murdered?
Even years after a person has dead it is still possible to find whether or not there are
certain chemicals in their system, such as poison. Using a technique called atomic absorption
spectrophotometry (AAS) it is possible to find what elements are in certain materials. A small
sample of the material, in this instance Napoleon’s hair, is weighed than dissolved using very
strong acid. “A minute quantity of the liquid sample solution, about 0.01–0.02 the size of a
raindrop (20–50 μL), is sprayed into a nitrous oxide–acetylene or air–acetylene flame, which
vaporizes the solution, releasing metal atoms from their chemical compounds and converting
them into their elemental forms” (Chemistry 1). A wavelength of light that is suitable for a
certain element is shown through the flame, and a detector on the other side measures the
intensity of the light. The amount of light absorbed is proportional to the concentration of the
element in the solution, thus the concentration in the original object. Every element in a sample
must be measured one at a time and compared to the original element, so the process is a slow
one but very accurate. It can measure trace elements to the parts per million. This is all very
useful in finding some chemicals in the corpses of long dead persons. Figure 1.1 shows how
atomic absorption spectrophotometry works.
62
Figure 1.1 Atomic Absorption Spectrophotometer (AAS)
When Napoleon died his hairs were cut and his head shaven, as was a custom in those
times. His hairs were than distributed to family and friends, so his hairs were tracked down and
samples were used from those. Pascal Kintz, a toxicologist, Ben Wilder, a Canadian Napoleon
enthusiast, Sten Forshufvud, a dentist and amateur toxicologist, all are strong proponents of the
poisoning theory and ran the tests on Napoleons hairs. “ ‘The analysis showed there was major
exposure, and I stress 'major', to arsenic,’ said Pascal Kintz, a toxicologist who studied five
samples of Napoleon's hair preserved since his death in exile on the island of St Helena in 1821”
(News in Science 1). Kintz also said that the accepted limit of arsenic concentration in the hair is
one nanogram per milligram of hair, but one of the samples had a concentration of 38
nanograms. A group of three hundred in eastern France who had drunk water contaminated with
arsenic had a lower concentration than was found in Napoleon’s remains. Also Hamilton Smith,
of the University of Glasgow, along with Sten Forshunfvud tested Napoleons hair for arsenic and
found higher than normal levels. They sliced up the hair and, upon the basis that hair grows at
the rate of three inches per month, examined each section to correlate the arsenic levels with
precise dates. They utilized Marchand’s diary, Napoleon’s faithful valet who stayed with the
emperor during most of his stay on St. Helen, to correlate the levels.
“The conclusion reached by Weider and others is that the arsenic, in combination with the
antimony and mercury-based purges and emetics given to Napoleon (the mistaken but common
medical practice of the time) plus Napoleon's consumption of large amounts of a sweet drink
called orgeat (to slake his thirst from the arsenic) all combined to kill him. On top of the
arsenic, antimony and mercury, orgeat is made from the tincture of apricots which contain
prussic acid -- hydrocyanic acid” (The Death of Napoleon 6).
So how did Napoleon die? This question has proven itself to be a mystery for decades.
While it is almost undebateable that the cause of Napoleon’s death was due to arsenic, the
mystery lies in whether arsenic was used as a murder weapon, or if it was long-term exposure to
arsenic that killed him. Although there could potentially be an incentive to kill such a figurehead,
there is a myriad of evidence that counter the argument. Ultimately since there is no conclusive
63
answer to this mystery it is necessary to look at the evidence and deduce a logical conclusion
based on that evidence.
Napoleon was exiled to St. Helena in 1815, which is where he also ended up dying. It is
imperative to note that Napoleon felt ill five weeks prior to his exile there. He complained of
pain in his stomach on the right side. It was thought that Napoleon died of stomach cancer,
which was what both of his sisters and his father died of. This correlation begs the question, was
the stomach cancer hereditary or was another outside factor causing it? Could that factor be
arsenic? Arsenic was present in many substances in Napoleon’s time. In addition, doctors that
preformed the autopsy on Napoleon failed to take into account the general wasting of the body
that occurs with cancer. Many symptoms of arsenic poisoning can mirror those of cancer.
Supposing arsenic does cause one to develop stomach cancer symptoms, the next logical
question is how and where would Napoleon come into contact with enough arsenic to kill him if
he did not have a murderer? The evidence is actually quite abundant; arsenic was found in a
wallpaper sample, bed drapes, and very common in ailments and medicines.
Napoleon’s wallpaper in St. Helena was tested positive for Scheele’s Green (this is a
solution of copper sulfate and sodium arsenite). The green dye was also present in the drapes on
his bed. In 1893 a study was done on Scheele’s Green, which indicated that in the presence of
moisture (from the air for example) a mold from the dye causes the copper arsenite to convert
into arsenic trimythal. Arsenic Trimythal is a very toxic vapor when inhaled, enough to kill a
person if over exposed. Napoleon would have constantly been inhaling these vapors while on the
island, especially in his last two years because he was often confined in his room. (Who killed
Napoleon 6).
In addition to this evidence, Scheele’s Dye was also found on the drapes of his bed prior
to his exile in St. Helena. The fumes from this alone could be enough to be toxic and kill him
slowly over time. This could help explain why he was feeling ill a few weeks prior to his exile.
If this evidence is still not conclusive enough it is also important to note that arsenic was
a common ingredient in medicines and ailments during Napoleon’s time. Although we do not
have absolute proof that he ingested any of these medicines it is very probable that he would
have. He was a wealthy, prominent head-figure, thus it is logical to conclude that if he were sick
he would be given medicine to ease his pain.
In the time of the emperor it was common practice to use arsenic to slow the effects of
balding, so Napoleon could have been using arsenic as a hair care product. Another source of the
arsenic could have been from the food he was eating. Food often can become contaminated
through the soil and if the kidneys are not functioning properly to eliminate the excess arsenic, it
could have potentially poised a problem. Napoleon had a long list of disorders ranging from
dysuria and chronic skin disease neurodermitits to weeping fits and rages, all of these could have
weakened his system making him more venerable to the influences of the naturally occurring
arsenic around him. (Who killed Napoleon 9).
Those who are proponents of the theory that Napoleon was murdered use the fact that an
overwhelming amount of arsenic was found in Napoleon’s hair as evidence to his murder. This
evidence however does not prove he was murdered. There were substantial traces of arsenic
found in the roots of his hair, but it is foolish to suggest that the only way the arsenic could have
64
been found here was due to poisoning. Traces of arsenic would appear in the hair samples
regardless of how the arsenic entered his body. An interesting point to also make here is that
during Napoleon’s time, it was a common practice to take locks of hair from famous people; in
order to preserve the hair arsenic was put on them. (Who killed Napoleon 12).
Another source that could have potentially obstructed getting a clean sample was that
Napoleon’s body was lying in soil for a good long time before it was dug up. His corpse could
have become saturated with arsenic from the ground then. This could account for the arsenic
found in his hair. All of these are speculations, but it is almost undeniable that Napoleon came
into contact with arsenic that eventually lead to his death, whether unintentionally or on purpose.
So what effects does arsenic actually have on the body, causing the doctors to mistake it for
stomach cancer?
The effects of Arsenic on the body are quite pernicious. Arsenic poisoning “kills by
massively disrupting the digestive system, leading to death from shock” (Arsenic Poisoning).
Symptoms of arsenic poisoning include violent stomach pains, vomiting and delirium. Arsenic
poisoning is usually a long drawn out process since it usually ingested in small doses
accidentally over a long period of time. Its symptoms mirror those of cholera, which made it a
handy murder weapon during earlier centuries when cholera was more prevalent. Arsenic is also
known to be a cause of lung and skin cancer in humans.
Elemental arsenic is not used in
poisoning. Heating of ores of arsenic produces a form of arsenic called arsenic trioxide (As4O6).
It has very little smell or taste, so it is undetectable. It is called white arsenic because when it is
oxidized it becomes a white color, instead of its naturally occurring grey
color. The first person to obtain white arsenic was an 8th century Arab
alchemist, Jabir ibn Hayyan. It had many uses through out the ages, a
pendent to keep the wearer from infection during the plague. It was used
during the Victorian ages by women that thought it would improve their
complexion, and it was believed that small amounts taken of a long period
of time would improve breathing over time, and a solution containing 1%
Arsenic Trioxide
potassium arsenite was used for many conditions such as asthma. Arsenic Figure 1. 2
th
compounds were used as pharmaceutical antibiotics up until the mid-20
century. Arsenic is found in many places including food, soil, and dishware materials; exposure
is inevitable, but if exposed to in large amounts or small amounts over long periods with out
being treated can be lethal.
Hallmarks of arsenic ingestion include skin lesions, peripheral neuropathy and anemia
(Case Studies in Environmental Medicine: Arsenic Toxicity). The main problem in dealing with
arsenic is that it readily changes valence states and forms species with varying toxicities.
However, according to Elson M. Hass M.D., “arsenic may even be essential and functional in
humans in very small amounts” (Arsenic). On average there is about 10-20 mg of arsenic in the
body. Its when this level begins to rise that a problem occurs. The kidneys are usually able to
handle arsenates found naturally in foods. It can be treated somewhat with EDTA, however it is
important to resolve it as quickly as possible to ensure maximum health. Figure 1.3 on the
following page shows the effect that arsenic has on the Krebs Cycle.
65
When arsenic enters the tissues it combines with sulfhydryl groups and prevents the
oxidation of dihydrolipoate to lipoate. The formation of acetyl-CoA is enabled with Lipoate, so
arsenic blocks the Krebs cycle and interrupts oxidative phosphorylation. This depletes the
amount of ATP formed and thus causes the death of a metabolizing cell. Arsenic also inhibits the
formation of
ATP by substituting its anions for phosphate in the reaction of ADP to ATP and ADParsenate is formed, and the high energy phosphate bonds cannot be utilized
Figure 1.3- Effect of Arsenic compounds on the pyruvate dehydrogenase reaction.
There are many theories surrounding the death of the infamous Napoleon Bonaparte.
People can and will hypothesis upon his death for many more years to come. There are facts that
we can be certain on though; Napoleon was exposed to arsenic, and his symptoms mirrored those
of one suffering from arsenic poisoning. Could arsenic have been the cause of the death of the
great emperor? Well, based on the knowledge about the subject it can now be assumed that
arsenic contributed to his death, but the ultimate cause of his death continues to be ambiguous.
Napoleon Bonaparte had many enemies, but were any brave enough to take the life of such a
prominent and powerful man? There are many questions surrounding the subject, but very few
conclusive answers for those questions. Even with all the evidence presented, in the end all that
can be said is that Napoleon died a questionable death but lived a powerful life.
Bibliography
Arsenic. 2 November 2005.
http://www.portfolio.mvm.ed.ac.uk/studentwebs/session2/group12/arsenic.htm.
Arsenic (Inorganic). 25 October 2005. http://cerhr.niehs.nih.gov/CERHRchems/arsenic.html.
Arsenic Poisoning. 24 October 2005. www.wikipedia.org/arsenic_poisoning.
Atomic Absorption Spectrophotometry (AAS). 25 October 2005.
http://www.thebritishmuseum.ac.uk/science/text/techniques/sr-tech-aas3-t.html.
66
Case Studies in Environmental Medicine: Arsenic Toxicity. 27 October 2005.
http://www.atsdr.cdc.gov/HEC/CSEM/arsenic/.
Chemistry 101: Atomic Absorption Spectrophotometry. Nancy McGuire. 25 October 2005.
http://www.chemistry.org/.
The Death of Napoleon. Aiuto, Russell. 1 November 2005.
http://www.crimelibrary.com/terrorists_spies/assassins/napoleon_bonaparte/3.html.
Who Murdered Napoleon? Probably Nobody! Blair, Victor. 2 November 2005.
http://www.napoleon-series.org/research/napoleon/c_arsenic.html.
67
Was Napoleon Poisoned?
Group: Titanium
Angela Langlais, Rachael Page, Andrew Pierce and Matt Schneider
68
Napoleon Bonaparte was a man of noble power. His great leadership skills and mastery
of military techniques made him a man to be greatly esteemed and feared. With such great
power, Napoleon was also a man who had many enemies. Exiled at the end of his life, he died
separated from civilization. Once conquering the world, Napoleon was left to end his life in
solitude on the island of St. Helena. Away from the public eye, his death has left many mystified.
Some say that his death was natural, caused by environmental factors and genetics, while others
are convinced that he was murdered. Understanding the life of this great man and the state of his
body after his death is the only way to uncover the true cause of his demise.
Napoleon Bonaparte was born August 15, 1769, in Corsica. His family was of minor
Corsican nobility. As a child, Napoleon went to the school of Autun where he learned French,
although he did not quite master it. He then went on to the military academy at Brienne. After
studying there for five years, he went on to the elite military school, École Royale Militaire, in
Paris. Napoleon studied artillery and completed a two year course in one year. After graduating,
he was commissioned to second lieutenant of artillery at the age of 16.
When the Revolution broke out, Napoleon returned home and stayed there for several
years. While at home, he was promoted to the position of lieutenant-colonel. Then in June
1793, because of conflict between the Bonaparte family and the conservative nationalist leader
Pasquale Paoli, Napoleon and his family was forced to flee to France.
Soon after, the family moved to France. Napoleon was appointed as artillery commander
in the French forces besieging Toulon, which was occupied by the British. It was here that
Napoleon first demonstrated his military genius. He drove out the British and recaptured the
city. He was promoted to brigadier-general and made a close associate of Augustin Robespierre,
the younger brother of a revolutionary leader named Maximilien Robespierre.
In 1795, Napoleon was given command of the improvised forces to put down the uprising
of the royalists and the counter-revolutionaries. Napoleon put down the protesters easily. This
sudden triumph earned him immediate fame and wealth, as well as becoming romantically
involved with Josephine de Beauharnais. He married her in 1796. Shortly after his marriage,
Napoleon was promoted to commander of the French “army of Italy.” He then made a series of
victories including: driving the Austrians out of Lombardy, conquering Rome, conquering
Venice, and other parts of Italy.
Following this Napoleon made numerous other victories and conquered a large amount of
land. He became a very wealthy and famous man. In 1804 Napoleon uncovered an assassination
plot against him. He had the offenders executed and used this incident to set himself up as the
emperor of France. After this self appointment, Napoleon conquered more nations but he kept
losing more and more troops as he went along. Countries started allying against Napoleon until
there was enough troops to drive him back to France.
Napoleon was finally defeated on the 18th of June, 1815. He was imprisoned and then
exiled to the island of Saint Helena by the British. While on the island he wrote out his will as
well as several codicils. He died on the 5th of May, 1821.
It was on this small island that the once great emperor died, leaving others to decide how
such an event occurred. New research involves the presence of arsenic poison. There are many
theories supporting and attempting to disprove the theory of Napoleon’s poisoning. It is
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important to be aware of all of the evidence on both sides of the controversy in order to
formulate an educated opinion. It is also important to examine and determine the reliability of the
testing used.
It was long believed by many historians that Napoleon died of stomach cancer. This was
the verdict of an autopsy carried out after his death by his personal physician Francesco
Antommarchi and witnessed by five other doctors. Stomach cancer had also killed Napoleon's
father. Swiss researchers say that his trousers show a loss in weight prior to his death, confirming
that he had cancer. Scientists from the anatomical pathology department of the University
Hospital in Basel and the Institute of Medical History at the University of Zurich found the pair
of trousers he wore just prior to his death had significantly shorter weight measurements than
other pants of his. By researching the correlation of measured waists and weights of healthy and
stomach cancer patients, it was estimated that Napoleon lost between 11 and 15 kg in the last six
months of his life.
Still others claim it was the treatments given to Napoleon in an attempt to cure him that
actually killed him. He was given regular doses of antimony potassium tartrate, or tartar emetic,
a poisonous colorless salt which was used to make him vomit. He was also given regular enemas.
The researchers, led by forensic pathologist Steven Karch, say this would have caused a serious
potassium deficiency, which can lead to a potentially fatal heart condition called Torsades de
Pointes in which rapid heartbeats disrupt blood flow to the brain. They say the final straw is
likely to have been a 600 milligram dose of mercuric chloride, given as a purge to clear the
intestines two days before his death. This was five times the normal dose, and would have
depleted his potassium levels still further, they say.
It wasn’t until the 1950's when amateur Swedish toxicologist Sten Forshufvud pioneered
research, that the idea of Napoleon being poisoned entered the scene. Later, in 1982, the topic
received more publicity when Ben Weider and David Hapgood published The Murder of
Napoleon. Ben Weider later went on to write six books about Napoleon Bonaparte and requested
the most recent study into Napoleon’s death. The International Napoleonic Society responded to
Weider’s request and headed the investigation. Pascal Kintz, the President of the International
Association of Forensic Toxicologists, claimed to have found traces of arsenic in the few strands
of hair of Napoleon’s that have been preserved. This finding was also supported by previously
recorded results.
There have been several other occurrences that have sparked such recent and sudden
interest. In 1995, the FBI and Scotland Yard discovered that clippings Napoleon’s hair
(purchased at a Paris auction in 1975) were traced with poison. This discovery used Graphite
Furnace Atomic Absorption Spectroscopy to find traces of arsenic of three hairs that had been
given to Betsy Balcombe in 1818.
In addition to this recent preliminary investigation, there are many other pieces of
evidence that would lead one to believe that Napoleon’s murder had a motive and means. History
plays a large role in setting the state for a motive. After being defeated at Waterloo, Napoleon
was banished to the island of St. Helena. The British and French did not want to risk a second
comeback of Napoleon as French emperor, and had reason to fear this as he had previously
returned to power after his exile to Elba. The fear of his return to power gives basis for a motive
for his murder. There also has been, and still is, constant criticism regarding the cruelty with
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which Napoleon was treated by the British. Britain controlled the island of St. Helena, and there
seemed to be tension between Napoleon and the governor of the island, Sir Hudson Lowe.
The written documentation of Napoleon’s last years are also a valid piece of evidence to
be taken into consideration. Napoleon clearly stated in his will, “I die prematurely, murdered by
the English oligarchy and its hired assassins.” When taken literally, this is an outright accusation
of murder, sanctioned by the English government. In addition to Napoleon’s first-hand account,
the memoirs of Louis Marchand, Napoleon’s loyal chief valet, were published in the 1950's.
They provided detailed accounts of what Napoleon ate and drank nearly everyday, which is
essential in determining the means by which Napoleon was poisoned. Marchand also included an
autopsy report in his memoirs. Henri Bertrand, Grand Marshal of the palace, also documented an
autopsy report that was published during the 1950's. It could be speculated that these men were
trying to point something out.
Not only do we have written evidence, but actual scientific evidence reveals traces of
arsenic in Napoleon’s hairs. The testing was conducted by Dr. Hamilton Smith at the University
of Glasgow, using irradiation testing procedures. The testing occurred in the Harwell Nuclear
Research Laboratory of London. This new evidence is backed by previous findings that are
similar. The new interest, stimulated by Canadian author and Napoleon expert Ben Weider,
served to support previous arguments and reignite interest in the controversy. The scientific
evidence is far more reliable than the written testimony. There have been more than one test
conclusion that has revealed the presence of arsenic in Napoleon’s hair. The strongest arguments
are the combinations of the eyewitness accounts of symptoms paired with the scientific evidence
that supports the written accounts.
There are several theories as to who murdered Napoleon. Weider and Forshufvud, who
recently compiled a book on this topic, place the blame on his most trusted French aid on St.
Helena-Count Charles-Tristan de Montholon. They claim that the Count was following orders of
the Count d’Artois, brother of the French King Louis XVIII and future King of France, to ensure
that Napoleon didn’t reclaim the throne. These authors have researched and have determined that
Napoleon was given arsenic over a period of the six years that he was on St. Helena (18151821). The arsenic weakened his immune system and created frequent sickness, later giving him
the poison that ultimately ended his life. Montholon controlled everything that Napoleon ate and
drank, which gave him unlimited opportunity and means to poison Napoleon. Montholon also
was out-of-favor with Napoleon, and only joined with him suspiciously at the last minute before
his exile.
The majority believe that Napoleon was poisoned over a long period of time, which
ultimately lead to his demise. Weider and Forshufvud point out that Napoleon was still popular
with the French (particularly the French army) at the time of his exile. Making his murder blatant
and sudden might have sparked an uprising. In addition, Napoleon’s son was still alive in Austria
and ready to takeover the throne upon Napoleon’s death. Clearly, the French wanted to avoid
this.
Many experts believe Napoleon Bonaparte's death would have been much quicker if the
poison was taken orally. They said the emperor's body contained some 15 parts per million of the
poison, where the maximum safe limit is only three parts per million. Following their
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investigation, the experts said they believed the emperor had absorbed the toxin over a long
period of time and cited such things as hair products, wallpaper, ash from wood fires or glue as
being the slow-poisoning culprits.
Therefore, there is reason to believe that the arsenic was not take orally or from any other
individual. During the 19th century there had been a number of cases of arsenic poisoning that
had rather puzzled everyone. In 1893 an Italian Biochemist called Gosio discovered what this
could be attributed to. A coloring pigment called Scheele’s Green had been used in fabrics and
wallpapers from around 1770. It was easy to make and reflected a bright green color. However, it
contained copper arsenite. Gosio discovered that if wallpaper containing Scheele’s Green
became damp and molded, it could chemically convert the copper arsenite to a vapor form of
arsenic. Breathing in the deadly vapor results in an ugly case of arsenic poisoning.
Sure enough, a documented sample of the wallpaper in Napoleon’s room on the island
that had been handed down to Shirley Bradley was offered. The wallpaper showed a single star
with the principal colors of green and brown. It is believed that the brown is indeed a faded gold
color because green and gold were the imperial colors. By the same scientific tests that originally
found the arsenic in Napoleon‘s hair, the green pigment on the wallpaper sample was also found
to contain arsenic.
Only after fully delving into the different theories and aspects of Napoleon’s death can
we make an educated conclusion. No one can be exactly certain as to how he died or who was
responsible, but by piecing together all of the information that is available, we can make some
excellent inferences.
If arsenic was influential in Napoleon’s death, it is important to recognize the
characteristics of this amazing element. With an atomic number of 33 and the classification of a
metalloid (Bentor), arsenic may be best known as a poison. Therefore, many may be surprised to
discover that it is actually a naturally occurring element in the earth’s crust. It is not uncommon
for scientists to find traces of arsenic in the dust released by volcanoes or in the eroded materials
that now exist as mineral deposits (Navy Environmental Health Center). The natural existence
of arsenic is coupled with the discharge resulting from human industrialization. Arsenic is
especially easy to release when certain substances, such as oil, coal, and gas, are burned. Arsenic
is most often used in the production of wood preservatives. Once in our environment, arsenic is
unable to deteriorate. However, like many other elements, it is able to transform its structure to
form a variety of molecules.
Rarely occurring in its pure form, arsenic may form both organic and inorganic
compounds. Inorganic forms, which are most commonly found with molecules of oxygen, sulfur,
or chlorine, are usually the toxic structures that have disabling effects on the environment and
human bodies (NSC.Org). Most forms of arsenic are odorless, flavorless and colorless, making it
very difficult to discover if one has been exposed or not (BBC News). Napoleon was exposed to
a form of this toxic element known as copper (III) arsenite (Ball). This particular form is also
odorless, but may be seen as a yellowish-green powder. In the past, this copper arsenite was used
as a pigment, insecticide, fungicide, and had medicinal uses for animals. Unlike many other
forms of arsenic, copper arsenite has not yet been labeled as a carcinogen. This fact, however,
does not diminish its toxicity. It can easily enter your body and is especially dangerous because
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of it is easily soluble by lipids (Graziono 2004). It is most likely to enter one’s body by being
absorbed into the skin or simply breathed in.
Irritation, in the form of rashes and burns, can result from exposure. Elevated and
frequent contact has severe effects on a human’s nervous system and results in vomiting,
abdomen discomfort and severe diarrhea (New Jersey Department of Health and Senior
Services). This severe gastrointestinal discomfort is caused by the deactivation of the enzyme
groups of sulfhydryl within our bodies. Arsenic tends to bind to these enzyme groups to form a
stable compound. The result of this formation is that fluid passes easily through the cell
membrane into our stomach and intestines (Graziono 2004). Besides the obvious side effects,
arsenic will eventually build up and will be overwhelmingly present in one’s hair, nails, nervous
tissue, bones, muscles, and skin (Graziono 2004). These build ups provide doctors with one way
to easily test for the poison. Arsenic poisoning is far from being a problem of the past or simply a
conspiracy theory about Napoleon’s death. The fact is that 1000 cases of arsenic poisoning are
reported annually (Graziono 2004).
The violent nature of Napoleon’s life would lead many to accept the idea that he was
murdered. However, we have decided that the most credible theory actually lies in the
environment in which he was confined. We have two undeniable pieces of information about the
last days of Napoleon’s life. One is that Napoleon died with a large build up of arsenic in his
hair. Second, scientists now have an actual sample of wallpaper from Napoleon’s home. This
wallpaper was found to contain Scheele’s green pigment, which is now known to contain the
compound copper arsenite. Becoming damp and moldy, this pigment would release a vapor form
of arsenite spreading throughout Napoleon‘s room. These are the most credible facts regarding
Napoleon’s death. Therefore, we conclude that Napoleon did die of arsenic poisoning. However,
this poisoning was unknown to all present in his home. Napoleon’s death was an unintentional
result of his surroundings.
Reference List
Ball, Hendrik. The Strange Story of Napoleon’s Wallpaper.
http://www.grandillusions.com/napoleon/napol1.htm (accessed 10/22/05), as part of Hendrik
Ball’s Grand Illusions. http://www.grand-illusions.com/index.htm (accessed 10/22/05).
Ball, Hendrik. Arsenic and Napoleon’s Death. http://www.victorianweb.org/history/arsenic.html
(accessed 11/15/05), published 1/14/02.
Bentor, Yenin. Periodic Table: Arsenic. http://www.chemicalelements.com/elements/as.html
(accessed 11/15/05).
Bloy, Marjie. What was the cause of Napoleon’s death?
http://dspace.dial.pipex.com/town/terrace/adw03/c-eight/france/napdead.htm (accessed
10/22/05), as part of Marjie Bloy’s A Web of English History. http://www.historyhome.co.uk/
(accessed 10/22/05).
Graziono, Dr. Christopher. Toxicity, Arsenic. E-Medicine: instant Access to the minds of
medicine. http://www.emedicine.com/med/topic168.htm#section~author_information (accessed
11/15/05), published 10/4/04.
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Hooker, Richard. Napoleon.
https://exchange.gordon.edu/exchweb/bin/redir.asp?URL=http://www.wsu.edu:8000/~dee/REV/
NAPOLEAN.HTM (accessed 10/15/05), published 6/6/99.
Kauffman, Jean-Paul; The black room at Longwood: Napoleon’s exile on Saint Helena; Four
Walls Eight Windows: New York, 1999.
Napoleon ‘killed by his doctors’. http://news.bbc.co.uk/2/hi/health/3913213.stm (accessed
10/22/05), published 7/22/04 by BBC News.
Trousers tell why Napoleon died. http://news.bbc.co.uk/2/hi/health/4512289.stm (accessed
10/22/05), published 5/4/05 by BBC News.
Tests Show Napoleon ‘Not Murdered’. http://www.napoleonguide.com/naparsenic.htm (accessed
10/22/05), as part of Napoleonic Guide. http://www.napoleonguide.com/index.htm (accessed
10/22/05).
Napoleon poisoning theory revived. http://www.abc.net.au/science/news/stories/s308382.htm
(accessed 10/22/05), published 6/6/01 by ABC.
Arsenic Poisoning. http://news.bbc.co.uk/1/hi/health/medical_notes/459078.stm (accessed
11/15/05), published 9/27/99 by BBC News.
Arsenic. http://www.nsc.org/library/chemical/arsenic.htm (accessed 11/15/05), as part of
National Safety Council. www.nsc.org (accessed 11/15/05).
What is Arsenic? http://www.nehc.med.navy.mil/downloads/ep/Posters/arsensml.pdf (accessed
11/15/05), published January 2003 by Navy Environmental Health Center.
Hazardous substance Fact sheet: Copper Arsenite.
http://www.state.nj.us/health/eoh/rtkweb/0530.pdf (accessed 11/15/05), published December
2002 by the New Jersey Department of Health and Senior Services.
Chemistry: WebElements Periodic Table: Professional Edition: Arsenic.
http://www.webelements.com/webelements/elements/text/As/key.html (accessed 10/23/05).
Arsenic. http://en.wikipedia.org/wiki/Arsenic (accessed 10/23/05).
Arsenic. http://www.scescape.net/~woods/elements/arsenic.html (accessed 10/23/05).
https://exchange.gordon.edu/exchweb/bin/redir.asp?URL=http://www.lucidcafe.com/library/95a
ug/napolean.html
https://exchange.gordon.edu/exchweb/bin/redir.asp?URL=http://www.napoleanguide.com/leader
s_napolean.htm
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The Secret Behind
Anastasia Romanov
Group: Molybdenum
Brittany Armstrong, Lauren Enright, Evan McDermott and Nikki Reynolds
75
There has been a lot of controversy surrounding one person in the history of the
Romanov family. Her name is Anastasia Romanov. The major controversy is based around
some people’s beliefs that she was never even a person, just a myth and some thought that she
lived through the assassination of her family. Because of these rumors DNA tests were done on
any people who claimed they were Anastasia. MtDNA and cloning were also a part of
determining the frauds.
There has been much controversy over whether or not Anastasia Romanov was actually
murdered along with the rest of her family, or if she managed to survive the massacre and escape
to safety. There are a few causes for this controversy, including the fact that the bodies of the
Romanov family were never found (until 1991) and in February of 1920 a woman named Anna
Anderson came forward claiming to be the Duchess Anastasia herself. With a surprisingly strong
knowledge of Anastasia’s background and similar physical characteristics to Anastasia, Anna
Anderson had many people wondering whether or not she was the true Anastasia.
Aside from the claims of Anna Anderson being Anastasia, another very big piece of
evidence causes controversy as to whether or not this Grand Duchess was killed along with the
other members of her family. In 1991, nine sets of bones were found at the burial site of the
executed Romanov family. Through the analyzing of the size and shape of the bones, scientists
came up with evidence that claimed that the bones of the two youngest Romanov children were
missing: Anastasia and her younger brother Alexei. Along with the bones, scientists also
discovered mitochondrial DNA that belonged to Anastasia’s parents, the Czar and the Czarina.
Using this evidence later on, scientists compared the evidence of the Romanov family DNA to
the woman claiming to be Anastasia (Anna Anderson), and found that the results did not match.
Despite the DNA evidence, many people still argued that Anastasia could still have
survived, and Anna Anderson could’ve indeed been her. Also, because the Romanov family had
been buried for so long, and their bones were outside in nature where natural effects could’ve
easily altered the accuracy of the DNA, the outside world was led to believe that there was still a
chance that the results of the DNA matchings could’ve been false.
Many have said that the story told by Anna Anderson of being Anastasia was so accurate,
that it seemed almost impossible that she wasn’t really her. Through the claims of this woman
who called herself Anna Anderson and the questioning of the DNA no longer being accurate
after so many years, the outside world is led to believe that the murder of Anastasia Romanov
was in fact only a myth.
Was there actually a girl within the Romanov family named Anastasia? Anastasia
Nicholaevna Romanov was a real person, a daughter to Nicholas and Alexandra Romanov. She
was also the youngest daughter of the royal family. She was not what many people would think
of as a person of a royal family because she was known to be spunky, care free, and to be
rebellious at times, smoking at the age of sixteen. She liked to make practical jokes and did
everything possible to avoid going to school classes. She even had two dogs named Jimmy and
Shvybzik. On July 16, 1918 the Romanov family was assassinated by a group of Bolshevik
soldiers. The bodies were dragged off to be buried and two of the bodies went missing. One of
the bodies was Anastasias and the other was her brothers. Once this knowledge of the missing
bodies reached the public the rumors began.
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There were many women who proclaimed themselves as being Anastasia, but they were
easily rejected and seen as imposters. There came one person proclaiming to be Anastasia who
no person could prove she was not Anastasia. Anna Anderson looked just like Anastasia and
that’s all the public needed for information to believe that Anna Anderson was truly Anastasia.
Even though people believed she was Anastasia and people could not prove her wrong at that
time, was she truly Anastasia? The answer to that is no, Anna Anderson was not the real
Anastasia. Before DNA tests were able to be produced a young woman from Berlin wrote to a
German newspaper stating that the supposed pictures in the paper of Anastasia were really
pictures of her former room mate who was a Polish farm worker. At that point it could not be
proven true or false so it was dropped and seen as false. She was then proven to be a fraud by a
group of German and British forensic scientists. They recently compared a forty-three year old
blood sample and a piece of Anna Anderson’s intestine to DNA retrieved from Nicholas and
Alexandra Romanov’s bones. The results showed that Anna Anderson DNA showed no
resemblance to the Romanov family’s DNA.
Even with the DNA proving Anna Anderson as not being Anastasia many people believe
she was. Many people think that the DNA from a forty-three year old sample is not able to be
completely accurate, and that it would not make sense for Anna Anderson would not spend that
much effort trying to prove she was something she was not. Even thought Anna Anderson was
not the long lost Anastasia there was a real Anastasia. And to this day no one is sure what
happened to her after the assassination. Most people believe that the jewels sewn into her dress
may have saved her life by reflecting the bullets and that she had fainted and not died. Then a
one of the assassins took pity on her and took her away to be his wife while she never
remembered her past. Although all these rumors had been produced no one really knows what
had happened to Anastasia, all that we know is that she had once lived as a daughter to the Royal
Romanov family.
Chemistry is connected to DNA through the proteins in the DNA. Tissues, muscles, and
organs are formed, because one can "trace the pathway of life from the macromolecule known as
DNA to the formation of cells, tissues, organs, and ultimately, to complete organisms." DNA
plays a major part in mystery of Anastasia’s life because of her family background. The Bible
says, "Two eyewitnesses were required to convict a person of a crime under Hebraic law" (Deut.
17:6), since the murder of the Romanov family was not to go unnoticed in the world of the 20th
century.
Forensic DNA testing was extremely effective in the mystery behind the Romanov family
in Russia because it proved with biological evidence that Anastasia did not exist in the name of
Anna Anderson. When Czar Nicholas II and family of Russia were murdered by the Bolsheviks
at Yekaterinburg in 1918, only nine skeletons were buried, but two were missing. Alexei and
Anastasia were the missing links of the family. Anna Anderson claimed to be Anastasia. A
television reporter, Maurice Philip Remy said, "Perhaps anticipating science, Anderson requested
she be cremated, since the genetic secrets of her body could not be derived from ashes, it seemed
as if the mystery would never be solved, but at last we can say that this woman, who was
supported by champions throughout her life, was not Anastasia." Anna Anderson did not want to
die in a measly old town; "she wanted to come out into the world, wanted to become an actress something special because her fiancé was killed in World War I on the Western Front. The
77
destructible disease of depression sunk into her when she killed a foreman in a factory with a
grenade.
In 1920, a woman tried to commit suicide by jumping off a bridge in Berlin, Germany.
That woman is Anna Anderson who in the 1920, was proved by the German court that she was
not Anastasia, and was only a Polish peasant of the Schanzkowska family. After Anna Anderson
died in 1984, a DNA experiment in 1994 occurred with Anna Anderson’s DNA and Anastasia’s
grand nephew, Prince Philip, Queen Elizabeth’s husband DNA. DNA can be found in blood,
bones, and hair. Dr. Gill of the British Home Office Forensic Science Service carried out the
DNA tests. The results showed that she was not related to the Romanov family which quieted
downed the debates and confusion over the mystery. The royal families of England, Austria, and
Russia had such familiar relations that a DNA comparison could be done. The background of
Anastasia becomes even more interesting because Queen Victoria of England was Anastasia’s
great grandmother.
Mitochondrial DNA analysis was important in the fate of the Revolution of the Russian
royal family. Published in Nature Genetics in 1994, after the analysis was taken. From the DNA
analysis, some discrepancy was between the mitochondrial DNA of the Tsar and his relative. The
Tsar had two bases of C and T at position 16169, which is heteroplasty. This could only occur if
there were two types of mitochondrial DNA with C at one point, and T at another point. At the
1994 testing of DNA, all of the relatives had T at position 16169. The question still remains
whether Anastasia died with her family that cruel night of July, 16th or did she escape and have a
pleasant life with hidden secrets of her past kept to herself.
DNA tests were an attempt to prove whether or not Anna Anderson was actually
Anastasia. Scientists in England were asked by the Russians to work with them with the new
DNA technologies. There were specifically three DNA tests that were used to confirm the
identity of Tsarina and her children (Nature Genetics, 1). They looked at mtDNA (mitochondrial
DNA) that is passed on from women to their children; it cannot be inherited from the father.
Scientists use mtDNA to link children to their mothers and other ancestors generations apart.
Analyzing the mtDNA, it was found that skeleton four, the Tsar, was alike of two of his living
relatives. There was one exception. The bone sample had a mixture of matching T and
mismatching C bases (Guyer, 1). Cloning experiments were done and indicated that the mixture
was due to heteroplasmy within the Tsar. Heteroplasmy is “the situation in which, within a
single cell, there is a mixture of mitochondria (energy producing cytoplasmic organelles), some
containing mutant DNA and some containing normal DNA” (Genetics Home Reference, 1).
This mismatch drove a lasting controversy with the authenticity of the remains. They came to
the conclusion that a final report could not go out until there was more DNA evidence.
Further testing was done on the skeleton of the Tsar’s brother, Georgij Romanov, to get a
handle on the occurrence and segregation of the heteroplasmic mtDNA in the Tsar’s family.
After some testing it was found that the mtDNA of Georgij was a match of the Tsar’s and was
also heteroplasmic leading to the confirmation of heteroplasmy within the Tsar’s lineage and
confirming the identification of the Tsar. There was a shift from heteroplasmy to homplasmy
(mitochondrial genomes are identical) which was consistent with the difference in heteroplasmic
ratios of the brothers showed mtDNA segregation. While the heteroplasmic mtDNA was being
reviewed, cloning experiments were done to rid the final product of any technical error. Through
all the DNA tests performed, it was not proven that the family was the Romanovs (Guyer, 1).
78
However, with the location of the grave, the bones found, the fillings found from the teeth, and
the relationship of DNA among the family all gave strong evidence that the bones were indeed
those of the Romanov family (Guyer, 1).
Works Cited
Anastasia. http://www.webcom.com/~lpease/collections/disputes/anastasia.htm. Accessed
2005.
Biochemistry, Genetics, and Replication of DNA.
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Cancer Dynamics-Musing from the Coalface in a research lab modeling cancer as a complex
system. http://cancerdynamics.blogspot.com/. Accessed 2005.
Constitutional Rights Foundation, Forensic Evidence, The Riddle of the Romanovs.
http://www.crf-usa.org/bria/bria133.html. Accessed 2005.
Fowler, Rebecca J. The Virginia Pilot. http://scholar.lib.vt.edu/VA-news/VAPilot/issues/1994/vp941006/10060504.htm. Accessed 2005.
Genetics Home Reference. http://ghr.nlm.nih.gov/ghr/glossary/heteroplasmy. Accessed
2005.
Guyer, Ruth Levey, Ph.D. DNA’s Role in Tales From the Crypt. http://scienceeducation.nih.gov/nihHTML/ose/snapshots/multimedia/ritn/Romanov/Romanov1.html.
Accessed 2005.
HIH Grand Dutchess Anastasia Historical Society. http://www.concentric.net/~Tsarskoe//.
Accessed 2005.
Molecular Genetics. http://opbs.okstate.edu/~melcher/MG/MGW1/MG1374.html. Accessed
2005.
Nature Genetics. Mitochondrial DNA Sequence heteroplasmy in the Grand Duke of Russia
Georgij Romanov establishes the authenticity of the remains of Tsar Nicholas II. Accessed
2005.
The Romanov Massacre. http://members.tripod.com/~Pharaoh30/index-13.html. Accessed
2005.
Images follow
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Websites for Pictures Used
http://www.fortunecity.com/victorian/hornton/890/romanovpics/anastasia.jpg
http://worldroots.com/brigitte/gifs/romanov59b.jpg
http://www.angelfire.com/biz5/romanovs/album2.html
http://en.wikipedia.org/wiki/Anna_Anderson
http://ntap.k12.ca.us/whs/projects/history/himages/anastasia1.jpg
http://www.alexanderpalace.org/anastasia/
http://www.best.com/users/~samsloan/czarbone.htm
http://www.peterkurth.com/ROMANOV%20BONES.htm
http://members.tripod.com/~Pharaoh30/index-13.html
http://scienceeducation.nih.gov/nihHTML/ose/snapshots/multimedia/ritn/Romanov/mitochondrion.html
ANASTASIA AND FAMILY
1. ANASTASIA (young)
.
2. THE ROMANOV FAMILY (1916)
(from left to right) Tatiana, Anastasia, Maria, Olga, Nicholas II, Alexandra, Alexei
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ROMANOV REMAINS AND DNA EVIDENCE
.
3. THE CZAR’S AND HIS FAMILY’S BONES THAT WERE DISCOVERED IN 1991
4. EXAMPLE OF THE TYPE OF DNA THAT WAS EXTRACTED FROM THE ROMANOV
FAMILY’S REMAINS AND USED AS EVIDENCE
(MITOCHNODRIAL DNA)
ANASTASIA ROMANOV vs. ANNA ANDERSON
5. NASTASIA
6. ANNA ANDERSON(ANASTASIA IMPERSONATOR
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The Bright Side of Fireflies: Bioluminescence
Group: Indium
Erik Boyer, Tim Ehle and Abby Marstaller,
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To set the record straight, lightning bugs and fireflies are the same creature. Fireflies are
nocturnal members of the Lampyridae Family of the Beetle Order. There are more than twothousand species of fireflies on this earth. Fireflies are a delight to be around while they are out at
night because they give off small yet radiant flashes of light as they fly about. They do this by a
chemical reaction inside themselves called bioluminescence. Bioluminescence is a process that
allows certain organisms to produce light through chemical reactions within their bodies. Fireflies
use these chemical reactions to attract mates. Each species of fireflies has its own unique series of
flashes that it uses to make sure there is no crossbreeding between species. The different flash
patterns range from a continuous glow to a series of rapid flashes. Each firefly is born with a
particular flash, unique to its species, encoded in its brain.
Much like the varying flash patterns, the male and female ability to glow also differs from
species to species. Within certain species of fireflies neither male nor female glows. These fireflies
come out during the day and attract mates using chemical attractants also known as pheromones.
The most common scenario, however, is the species where both male and female flash. The
following is the mating ritual for these most common species: First, the male firefly will soar
through the air flashing his designated flash pattern for all to see. While this is going on, the female
firefly waits patiently in the grass below until she feels she is ready to mate. When she is ready and
she sees a series of flashes that she recognizes, she will flash back using the same pattern. While
flying through the air, the male firefly watches the ground carefully for this return signal. When he
spots the response, he will flash back, all the while flying closer and closer to the spot where his
prospective mate waits for him. They continue this flash-dialogue until the male reaches his mate
and if all goes well there will soon be a new nest of firefly larvae which will grow into adult fireflies
come spring.
Firefly larvae, also known as glowworms, emit light also. Their purpose for glowing is to
warn off possible predators. The glowing informs the predators of the larvae’s bitter taste and warns
that they could be toxic. This warning keeps predators from eating the firefly larvae and ensures that
the larvae will grow up to become fireflies.
The light given off by fireflies starts as a series of chemical reactions that take place in a
region of the firefly’s abdomen called photocyte cells. The two chemicals needed to produce the
light are luciferin and luciferase. Luciferase is the catalyst or promoter in the process while oxygen
provides the energy to keep the process going. The process begins when the oxygen through
respiration circulates to the photocytes which is where the reaction occurs. The oxygen, luciferin,
and luciferase react with magnesium and adenosine troposphere (also known as ATP) which are
already waiting in the photocytes. When Luciferin combines with oxygen and ATP, it turns into a
very unstable high-energy chemical. It is so unstable that as it converts back to its natural form,
energy is released. The energy released causes the bioluminescence, or the glow. The firefly can
regulate the chemical reaction and therefore the intensity of light by controlling the amount of
oxygen that it lets into its abdomen.
After the chemical reaction is complete, nitric oxide regulates the bioluminescence or flash
pattern. Cells that line the airway of the firefly produce the nitric oxide. When produced, the
mitochondria shuts down, which in turn causes the release of an enzyme that, along with released
oxygen, causes the bioluminescence.
Most organisms that use bioluminescence give off light at wavelengths between 420 and 479
nanometers known as blue light. This is because most bioluminescent animals live in the depths of
the ocean where blue light penetrates further than all others. Fireflies on the other hand give off
83
light closer to a 500 nanometer wavelength in the yellow-green area of the visible spectrum. Certain
animals, such as squid, can even change the wavelength of the light they emit.
Fireflies are not the only animals that use bioluminescence. Many ocean faring organisms
possess this ability as well as species of tree living fungus known as foxfire. A few examples of
these glowing, ocean-dwellers are: bobtail squid, marine hatchet fish, the barreleye, and the
cookiecutter shark. These animals use bioluminescence for the same reason as the firefly larvae do:
to protect against predators. While living in the deep dark sea, it may sound dangerous for an animal
to try to protect itself from predators by glowing; however, the method of defense actually works
very well. This is because the fish that use this defense mechanism are often silhouetted against the
bright sky which makes them an easy target for predators lurking below. By making themselves
bright, they are camouflaging themselves against the bright sky and are harder for their predators to
spot. Another sea creature that uses bioluminescence as a means of survival is the angler fish. The
angler fish has a glowing appendage that dangles from its head. This attracts small fish to swim
directly in front of the hungry angler’s mouth, thus providing him with food.
Bioluminescence has interested mankind for many years yet scientists have only recently
begun to understand it and duplicate its results in the laboratory. The process has been used in the
laboratory to track cells and gene products and has also been used most commonly in glow sticks.
The earliest use of bioluminescence dates back as early as World War II when the Japanese gathered
large amounts of fireflies and ground them into a powder. In places where it was too dangerous to
light a match or have another light source, soldiers would take a little of the powder and dampen it to
get a glow. By doing so they were able to read maps or instructions in places where it would have
been impossible to do so otherwise.
Scientists can also create luciferin and luciferase in a laboratory and can genetically
introduce it into plants. These plants can then be turned into medicines that can track bacteria. For
example, after introducing it into the blood or urinary tract, doctors can take samples and if bacteria
is present the samples will glow. Also, blood that has been donated will go bad after a period of
time because as red blood cells age they can rupture and render the blood no longer useable.
Luciferin and luciferase could be added to the collected blood so that when the cells begin to decay it
will start a chemical reaction that causes the bad blood to glow notifying doctors that it is no longer
useable.
There are many other uses scientists have discovered for these chemicals. Some of the most
notable ones are the chemical’s ability to detect if food has gone bad or bacteria is present. This
detection is possible when an enzyme called apyrase is added to the food along with the
bioluminescent chemicals. If bacteria is present the food will glow. This test can be performed
rapidly, while normal tests can take days to get results as the bacteria often needs to be cultured first.
Bioluminescence has also been used to detect hypothermia in livestock which has saved the industry
millions of dollars by prolonging the lives of cattle and swine. In addition to aiding farmers by
testing for frostbite in animals, bioluminescence has also helped astronauts by detecting electricity in
spacecrafts. When even a small amount of ATP is detected in the air, a flash of light is given off
which allows scientists on earth to record the signal. Bioluminescence has been used in everything
from waste water treatment, to environmental protection, to anti-biotic testing, and even genetic
research. Scientists are hoping that some day they will learn how to tag cancer cells or the AIDS
virus so they can observe how these diseases spread. This information could lead to better
understanding of the illnesses, better treatment for patients, or could even lead to cures.
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Bioluminescence is such a valuable process to study and understand because of its wide
variety of uses. Portable, self-sufficient lighting would be useful to soldiers over seas or even a
camper lost in the dark woods. Because bioluminescence has helped advance medical knowledge
tremendously, it is a topic that should be studied further. Better understanding of this process could
lead to a better understanding of the microscopic killers that dwell inside many citizens of the world
today. Because the AIDS virus is a prominent issue, any advancement in the understanding of this
illness would be worth spending tax dollars on. Fireflies used bioluminescence to insure the survival
of their future generations and by the looks of recent laboratory findings, bioluminescence could be a
factor in providing the human race with stronger, healthier, and more equipped future generations as
well.
Works Cited
Chemistry of Bioluminescence. 2005. The Bioluminescence Web page. 19 Oct. 2005.
http://www.lifesci.ucsb.edu/~biolum/chem/
How do Fireflies Light Up? 2005. How Stuff Works.com. 19 Oct. 2005.
http://science.howstuffworks.com/question554.htm
Provonsha, Arwin. General Information on Fireflies. University of Purdue Entomology Dept. 17.
Nov. 2005. http://science.howstuffworks.com/question554.htm
Tally, Steve. 1999. Fireflies: Science Lesson in a Jar. University of Purdue.18 Oct 2005.
http://www.purdue.edu/UNS/html4ever/980626.Turpin.fireflies.html
Trigger of a Firefly’s Flash Discovered. 2001. USA Today.com. 18 Oct. 2005
http://www.usatoday.com/news/science/2001-06-28-fireflies.htm
Fireflies. 2005. Wikipedia.org. 19 Oct. 2005. En.Wikipedia.org/wiwi/fireflies.
85
Bioluminescence in the Firefly
Group: Vanadium
Adam Brooks, Annie Cameron and Kimberly Prior
86
Bioluminescence is light formed from a chemical reaction within a living creature.
Bioluminescence has fascinated people throughout history but it is only recently that the chemistry
involved in the process has been analyzed and used to benefit mankind. The benefits provided by
the advancement of gene therapy are important, but are they worth the ethical implications that may
result from such advancements, such as testing on animals?
There are many different bioluminescent organisms, however, most of them are found deep
in the ocean and use their light both to see and to scare away predators. Anglerfish have a small ball
filled with bioluminescent bacteria that hangs in front of their faces. The Pacific Black Dragonfish
is unique in that its entire body lights up. Many squid and jellyfish are also bioluminescent.
However, bacteria are by far the most numerous bioluminescent organisms. Dinoflagalates are
single-celled algae that are found to light up as boats create a wake in the water. One of the most
amazing examples of bioluminescence is the “milky sea” phenomenon, where vast areas of the
ocean light up. Boats in the Indian Ocean report having sailed through water that glows a pale
bluish light for hours. This amazing phenomenon is even visible by satellite in space. There are
only a few bioluminescent organisms found on land, including some glowing fungus on trees and a
few families of insects, like the firefly. The firefly’s contribution to the learning of bioluminescence
will be detailed in this section of the paper. Some organisms such as squid and a few species of fish
require photoprotein along with luciferin and luciferace in the reaction but most, including the
firefly, do not.
The bioluminescence in fireflies is produced by photogenic organs. The light organ is called
the lantern, and it is positioned on the lower abdomen of the firefly. Thousands of photocytes
clustered together in groups called rosettes are arranged throughout the lantern. Oxygen, which is
crucial to the bioluminescence reaction, passes through the tracheal air supply. There is a tracheal
air supply at the center of each rosette and each of these air supplies are surrounded by tracheolar
end organs. Mitochondria within the photocytes regulate the oxygen flow to the peroxisomes.
When the oxygen is allowed through the mitochondria to the peroxisomes, a chemical reaction
between luciferin, luciferace and the oxygen takes place. Luciferin is the chemical that creates the
light and luciferase is the chemical that catalyzes or starts the reaction. ATP (adenosine
triphosphate) is required as a cofactor within the reaction. The chemical reaction in fireflies is as
follows; luciferin + luciferace + ATP_ luciferyl adelylate-luciferace + pyrophosphate. The products
then undergo another reaction, shown here; luciferyl adenylate-luciferace+O2_ oxyluciferin +
luciferase + AMP + light. Luciferase catalyzes the oxidation of luciferin and light is produced.
Oxyluciferin is an inactive byproduct. (Branham, online)
Scientists have sought for years to understand the reason why fireflies flash. It is now clear
that fireflies most likely use bioluminescence for more than one single purpose. One reason is to
signal to predators that it does not taste good because it contains defensive chemicals. When
disturbed, fireflies flash faster and more vibrantly to warn away predators. More evidence was
added to this hypothesis when it was shown that animals learn to avoid glowing objects when they
are associated with a bad tasting object. (Branham, online) Another reason for bioluminescence in
fireflies is for mating purposes. Each species of fireflies has a specific flash pattern that signals to
fireflies of the opposite sex that they wish to mate. With most species the male flies around flashing
his lantern while the female waits perched on a piece of foliage. If the female sees a male that she
likes than she will flash her own lantern to signal the male. Without bioluminescence, fireflies
would not be able to sufficiently defend themselves or mate.
87
There are several different theories as to how the firefly controls this mechanism; however,
there are two theories that are readily accepted by most scientists, one being the “Oxygen Control
Theory.” This theory hypothesizes that the firefly turns its light on and off by controlling the oxygen
supply to the photic organ where it is used in the chemical reaction with luciferin and luciferase.
Another theory known as the “Neural Activation Theory” hypothesizes that the firefly has control
over tracheal end cells which after being stimulated, releases a molecule that acts as a messenger to
begin the chemical reaction. This molecule is composed of nitric oxide, which passes from the
tracheolar cells to the peroxisomes. Nitric oxide is a colorless and poisonous gas that is small and
diffusible enough to pass through cell membranes. (www.bio.davidson.edu)
However, one theory being right or wrong is inconsequential. The primary theory remains
that without oxygen the chemical reaction can not take place and light will not be produced. When a
lantern is dark it is said to be in “quiescent.” The lantern remains dark because no oxygen is allowed
to reach the peroxisomes. Instead the oxygen is consumed by the shield of mitochondria. How the
flash is created has already been discussed, but it is also very important to take into account that the
firefly itself is in direct control of its own bioluminescence and the frequency of the flashes. The
procedure begins with quick bursts of neural activity. This electrical excitation in the ventral nerve
and the brain induce action within the firefly’s lantern.
Scientists hope that with further study of bioluminescence, they may be able to use luciferase
to detect which cells are active in specific genes. With this technology, scientists will then be able to
transfer a potentially therapeutic gene and be able to tell if the transfer is successful. To simplify the
explanation of genetics, it is safe to say that all organisms are controlled by DNA (deoxyribose
nucleic acid). Different combinations of the chemicals that make up DNA (adenine, thymine,
cytosine, and guanine) are called genes. Each gene determines what type of protein will be
produced, which in turn determines various traits expressed in organisms. When dealing with the
study of bioluminescence, the term gene expression is often used. It is important to understand this
concept in order to understand the possible medical benefits of studying bioluminescence. Each cell
in an organism contains the entire genetic code for the entire organism. However, not all of the
genes are expressed in every cell of the organism; otherwise all of the cells in the organism would be
identical. Thus, in specific cells, some genes are expressed while others are suppressed. This
concept is better explained by Neil Campbell and Jane Reece as follows:
[T]he cells of multicellular organisms must continually turn certain genes on and off
in response to signals from their external and internal environments. In addition,
gene expression must be controlled on a long-term basis for cellular differentiation,
the divergence in form and function as cells become specialized during an organism’s
development[…] The enzymes that transcribe DNA must locate the right genes at the
right time, a task no easier than finding a needle in a haystack (Campbell, 362).
Also crucial to the study of bioluminescence is an understanding of gene therapy. “Gene
therapy is a technique for correcting defective genes responsible for disease development”
(www.ornl.gov). Gene therapy is the process by which a faulty gene (one that is coding for an
incorrect protein and thus causing a genetic disease) is removed and replaced by the correct gene.
The process of gene therapy is as follows:
A carrier molecule called a vector must be used to deliver the therapeutic gene to the
patient's target cells. Currently, the most common vector is a virus that has been
genetically altered to carry normal human DNA. Viruses have evolved a way of
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encapsulating and delivering their genes to human cells in a pathogenic manner.
Scientists have tried to take advantage of this capability and manipulate the virus
genome to remove disease-causing genes and insert therapeutic genes. Target cells
such as the patient's liver or lung cells are infected with the viral vector. The vector
then unloads its genetic material containing the therapeutic human gene into the target
cell. The generation of a functional protein product from the therapeutic gene restores
the target cell to a normal state (www.ornl.gov).
Though all of this biological information seems relatively unrelated to bioluminescence, it
actually is quite crucial to the study. The study of bioluminescence could potentially be crucial in
the study of various genetic diseases as well as illnesses such as cancer that develop later on
(www.news-service.stanford.edu). Diseases like cancer are often caused by mutations in genes. At
times, genes will randomly mutate, causing the production of cancerous cells. Other times mutations
are stimulated by environmental sources, such as certain chemicals or x-rays. Cancer-causing genes
are called oncogenes (Campbell, 369). If scientists are eventually able to locate specific oncogenes,
cancer may be able to be eliminated at its source. It is possible that the study of bioluminescence
could aid scientists in this study.
Scientists study the way organisms can turn on and off the gene that controls
bioluminescence in the hopes of it possibly shedding some light on the concept of gene therapy.
Scientists believe that they may be able to use luciferase, the chemical used in bioluminescence, to
detect which specific genes organisms are activating in certain cells. Recently, medical scientists
tested this idea on mice. Borrowing glow-in-the-dark chemistry from fireflies, scientists have
developed a technique enabling them for the first time to observe gene activation as it occurs in a
living mammal. In a series of experiments performed at the School of Medicine in mice and rats, the
researchers used ultrasensitive cameras to detect light emitted when certain genes were turned on,
even deep inside the animals' bodies (www.news-service.stanford.edu). This technology may
eventually enable scientists to determine which genes are affected by a specific genetic disorder so
that that gene could potentially be replaced by a normal gene. “The new technique will help
researchers know when they have succeeded in transferring a potentially therapeutic gene into lab
animals” (www.news-service.stanford.edu).
Thus far, humans have not reaped the medical benefits of such research. There have been
instances in which humans have participated in experimental treatments of gene therapy, but the
government has not yet approved large clinical use of the process.
The Food and Drug Administration (FDA) has not yet approved any human
genetherapy product for sale. Current gene therapy is experimental and has not
proven very successful in clinical trials[…] FDA's Biological Response Modifiers
Advisory Committee (BRMAC) met at the end of February 2003 to discuss possible
measures that could allow a number of retroviral gene therapy trials for treatment of
life-threatening diseases to proceed with appropriate safeguards. FDA has yet to
make a decision based on the discussions and advice of the BRMAC meeting
(www.ornl.gov).
An important aspect of the study of bioluminescence is to consider how the experiments
themselves are conducted and whether or not anything or anyone is harmed because of them. Many
ethical questions are asked when animals are used in conducting medical experiments such as in the
study of bioluminescence. Is it ethically right to be risking the lives of living organisms in order to
retrieve information? How important is this information to the study of human medicine? Do the
89
pros of the experiment balance out the cons in terms of the mistreatment of the animals used? Could
the experiment be done without using animals?
In the case of bioluminescence, the gene that makes fireflies glow (luciferase), is being
implanted into the cells of lab mice so that they too, glow like fireflies. This helps medical
researchers see inside the animals and more easily determine whether the drugs they are testing are
successful. For example radiologist David Piwnica-Worms of Washington University School of
medicine in St. Louis injected the luciferase gene that makes fireflies glow into his mice. Then by
measuring the amount of yellow coming from within the mouse, he was able to decipher how well
the mouse was reacting to the new drug. The molecule in which they targeted the luciferase gene to
is one on the surface of cells called IKK. IKK, or Ikappa kinase, is a regulator of pathways into the
cell and, if not regulated properly, is a trigger for the changes of cell processes and activity levels of
genes which often cause diseases such as cancer. Piwnica-Worms explains:
You can think of that the same way the gears and pulleys of some sort of machine
might be able to mechanically transmit a signal from one area to another. One of
those pathways is known at the NF-KappaB pathway. It's a very important signaling
pathway that senses external stimuli and the cells respond to that. It generally has a
pro-inflammatory or pro-proliferation signal, which means telling the cells to
respond by dividing, by growing.
So in this particular case, Piwnica was using mice to test a cancer drug that was supposed
prevent tumors from growing larger or faster than they would without it. Without luciferace, the
experiment would have been conducted by injecting a certain amount of the drug being used and
then waiting to see whether the cancerous tumor grows. Clearly, this method creates a high potential
of harming the mouse because if the drug being tested is unsuccessful and does not work, then the
mouse is left with a large tumor and is necessarily killed. "Then you no longer have that animal to
study to find out if the therapy was effective, so you need many more groups of animals in order to
evaluate efficacy," Says Christopher Contag, the acting assitant professor of pediatrics and director
of bioluminescence research at Stanford. Even if the end results of the experiment is positive, and
the tumor stopped growing, there are two other important negative aspects to consider when looking
at this kind of experiment. David explains, "You still never knew if the drug was acting on the tumor
in the way you’d designed it to. The end result–the tumor stopped growing–is helpful; but you’d still
have to wait to days and weeks to find that out."
The use of luciferase with these kinds of drugs has dramatically changed the way in which
these experiments are drawn out. Before bioluminescence was used, researchers had to destroy the
animals in order to look inside of them. Studies have now shown that less mice are needed and less
harm is done to them. With the use of the bioluminescence, only parts of the cell of affected by the
lucerifase gene, and it is much easier to decipher how well the drug is working and what dose works
best. This enables them to fine tune the drug and dosage for the maximum benefit. Not only so, but a
traditional study would have required six months and over 300 mice to complete the experiment.
Now, the procedure is performed over a five day period with less than 30 mice.
Many other experiments such as this have been performed on mice and rats, and other
mammals in laboratories across the country. And although some may argue that animal testing
should not ever be used in research, the fact of that matter is, that it most likely will always happen.
But, contrary to popular belief, by using bioluminescence and the gene that comes from fireflies, it is
possible to reduce the amount of animal. Contag reiterates this. "You can reduce the number of
animals used for experiments tenfold while getting more information more quickly. This will help
90
streamline development of many types of therapies, including DNA-based gene therapies and gene
vaccines." Therefore, for those opposed to the mistreatment of animals in chemical science, this
method of using bioluminescence is really improving that issue. And with so many medical
advances being produced from this kind of light, it would be difficult for anyone to say that this
process was unethical.
Besides being used for medical experimentation, this light from fireflies is also important in
multiple other ways. Bioluminescence and the light emitted from these fascinating creatures is
actually quite unique. Take a regular light bulb for example; Only 10% of the energy emitted from
this bulb comes off as visual light. The majority of the energy (90%) is given off as heat. Nearly
100% (99.5) of the energy emitted from this luciferase come off as light. This can be extremely
useful to us as humans today. Already special electronic detectors have used the chemicals from
these fireflies in order to help find earth-life forms in outer space. People have also begun to use this
light to help warn them when milk, food, or water may be bacteria contaminated. There are other
uses for this cold light produced from the enzymes in these fireflies, and more and more
advancements are made each year and researchers are discovering new ways to use this light with
every experiment they use.
The study of fireflies and their unique and fascinating bioluminescence is being used in
chemical research and is helping in making strides forward in the medical world today. Scientists
and researchers are slowly discovering more ways to incorporate bioluminescence into their
experiments and have so far been made major strides forward with their results. Although success
rates are not currently very high, with time, chemists expect bioluminescence to become a crucial
part of their studies in gene therapy, as well as other medical research. Bioluminescence is also being
used in other areas of the technological world today and the unique gene is becoming more popular
as a light source for many scientists and chemists across the globe. Also, a positive aspect of the use
of this bioluminescence is the fact that more animals’ lives are being spared and less animals are
being used for research because of the amazing abilities of this bioluminescence luciferase gene. In
conclusion, the advancements that are being taken because of bioluminescence are very important
and chemists should continue to reap the benefits of these fascinating fireflies.
Works Cited
Branham, David. Bioluminescence. http://iris.biosci.ohio-state.edu/projects/FFiles/biolum.html. (13
November 2005).
Campbell, Neil A. and Jane B. Reece. Biology: 6th Edition. Boston: Benjamin Cummings, 2002.
Carswell, Lindsay. Firefly Pharmaceuticals.
http://www.sciencentral.com/articles/view.php3?article_id=218392650&cat=1_2. (15 November,
2005).
Chris, Dennis. Lightening Bugs and Fireflies.http://worldkids.net/critters/QnA/messages/409.html.
(15 November 2005).
Gene Therapy. Human Genome Project Information.
http://www.ornl.gov/sci/techresources/Human_Genome/medicine/genetherapy.sht ml. (9 November
2005).
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Jenssen, B. R. Bioluminescence in Fireflies.
http://www.bio.davidson.edu/people/midorcas/animalphysiology/websites/2004/J enssen/. (17
November 2005).
Stephens, Tim. “Living Mice Glow When Genes Turn On.” Stafford Online Report. http://newsservice.stanford.edu/news/1997/october15/miceglow.html.(14 November 2005).
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The Venus flytrap
Group: Rhenium
Sarah Mattingly, Jessica Roberts and Sam Sereda,
93
Variations between Carnivorous and non-Carnivorous plants
Although it would seem obvious to most that the differences between carnivorous and noncarnivorous plants would be immense, there are actually only few differences between the different
types of plants. The carnivorous plant and the non-carnivorous plant both photosynthesize, or
produce glucose to use as energy throughout the plant and release oxygen into the atmosphere.
However, carnivorous plants photosynthesize using their traps in place of leaves to collect sunlight
(Answers). This stunts their growth, because their traps cannot simultaneously be an efficient place
to catch prey, and absorb light. The main difference between carnivorous and non-carnivorous plants
is that normal plants do not have these traps to capture insects. Carnivorous plants capture small
insects, and use these insects to get essential nutrients they cannot get from their environment, like
nitrogen and calcium. Normal plants do not have these structures, probably because normal plants
did not have to evolve in such a harsh environment (Wikipedia).
Another difference between carnivorous and non-carnivorous plants is that carnivorous
plants can live in environments where non-carnivorous plants would have no chance of surviving.
Their insect-catching traps allow them to survive in environments with extremely low amounts of
nitrogen and phosphorus, in bogs and swamps. Although they spend large amounts of energy on the
traps, it makes it possible for the carnivorous plant to stay alive in its bleak environment. However,
carnivorous plants do not survive as well as non-carnivorous plants in areas with high amounts of
nutrients because their traps take up so much energy that they are not able to compete with the
normal plants. The traps are only profitable to the plant when there is high nutrient strain on the
plant (Gould). These extra appendages on the carnivorous plants are essentially the only difference
between them and the more normal photosynthesis-only plants. The Venus flytrap is one of the most
intricate carnivorous plants, its ability to live in such an extreme environment and the fact that is can
close and trap its prey make it the most intricate carnivorous plant.
How the Trap Moves
The mystery of the Venus Flytrap’s (Dionacea muscipala) speed is one that has captivated
scientists since its original discovery. The mechanism by which it achieves the lightning fast snap for
which it famous has eluded those same scientists for almost as long. However, in the recent January
27th edition of Nature two scientists proposed an explanation with its roots in basic geometry and
simple botany.
Mahadevan and his fellow colleagues began investigating this age-old problem of how a
plant with no ‘active muscle fibers’ reacts so quickly to stimuli (Blackwell). The answer lies in the
shape that the trap holds while not catching its prey. The scientists began their investigation by
painting fluorescent ink dots all over the outside of the open, non-feeding trap (Weiss). They utilized
high-speed video and photography to trace the movements of the dots as the traps were stimulated,
and then snapped shut. What they discovered is that the normal mode of plant movement is only half
the story.
The undisturbed flytrap has an outward-curving, more convex shape, as Darwin himself
noted in Insectivorous Plants. It has also been known for a while that when a fly lands it stimulates
tiny hairs on the inside of the trap’s surface. This signals for the transportation of fluids to the outer
cells. Past here however, things are a bit of a mystery. So this is where Mahadevan, Forterre, and
others took up the case. They noted that when fluid built up in the outer cells, the resulting change in
cell shape put pressure on the interior cells. However, the original configuration of the trap resists
94
this new pressure, to a point. After about a second of buildup that initial shape loses its stability and
the whole thing flips inwards, into the concave cup which holds the prey (Weiss). This more
mechanical mode of movement is easily demonstrated using a curved piece of plastic or thin metal,
even a plunger. The original shape resists the new pressure up to a point and then snaps into the new,
opposite, configuration, meaning it’s ‘bistable’, or has two stable configurations (Summers). This
gradual change, and quick reaction are also shown in the experimental evidence. They showed that
the leaves did not move at a consistent rate or speed. The leaves moved about 20% of their total
motion in a so-called ‘phase one,’ at a rather slow speed. Then in ‘phase two’ the most rapid motion
occurs, covering 60% of the total distance. Phase three covers the final 20% of the distance, and is
once again much slower than the intermediate phase two. The trap can be in the process of closing
that final 20% for several hours. This marriage of biochemistry and simple geometry shows how
diverse the world can be, and how this carnivorous plant can obtain its fast and difficult to catch
meal.
What They Eat
This meal can consist of many different things, though not, as is commonly thought, humans.
The most common types of prey are flies, spiders, caterpillars, slugs, crickets, and some larger
carnivorous plants even eat small frogs and amphibians. Another misconception, and common
mistake made in fables, is that the traps can be fed hamburger meat. The nutrients that the plant
receives can only come from insects. (Meeker-O’Connell) The Venus flytrap does not have a brain,
and therefore has no control over what it does and does not catch. It can only decipher between
living and non-living. This is achieved once again by mechanical means. Any living organism it
catches lands in the trap, and sets off the hairs. However, it then continues to move even after this
initial contact. It is this continued stimulation that triggers the final closing of the trap, and the
beginning of digestion. If say, a leaf, or a rock, or a wind blown seed were to enter the trap, the first
and second stages would commence. But without continued movement, the final stage would not
occur. Instead the leaf would, over a lengthy process of over 12 hours return to its original convex
shape (Meeker-O’Connell). This takes so long because the new stable shape must be overcome, and
return to the initial convex configuration. The object inside will then either fall out, be blown out, or
simply sit there, because the trap lacks the ability to ‘spit’ it back out.
How the Venus flytrap digests its prey
The Venus flytrap lives in unique environments with low amounts of nutrients in the soil.
The bogs of South Carolina contain many of these carnivorous plants because few other plants are
able to grow. Because it lives in such a harsh environment, it has developed a process to get certain
nutrients from its prey. It traps insects, mostly flies, and breaks them down into the nutrients it
needs. The soil in these bogs contains immeasurable amounts of nitrogen and calcium (Carnivorous
plant answers). This is extremely difficult for the plant to live in because it needs nitrogen for
essential protein synthesis and calcium for cell wall stability. The bogs in which the Venus flytrap
dwells also contain low amounts of phosphate for nucleic acid synthesis and iron for chlorophyll
synthesis (Gould). These are imperative if the plant wants to survive. Ammonium (NH4NO3) exists
in large amounts in the soil, and the plant can harvest some of its nitrogen from this source. But
increased amounts can easily kill the flytrap. The best way for the flytrap to get its nitrogen is
through capture of prey. Once the Venus flytrap catches its prey, it does not secrete digestive
enzymes right away. Instead it secretes these enzymes slowly only after further movement and
stimulation, to avoid being fooled by drops of water and random material falling in its trap. Uric acid
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(C5H4N4O3) is known to activate digestive enzymes, because of the low amount of excretion still left
on the hairs of the fly. (Gould).
The main enzymes the plants use to digest their prey are closely related to enzymes animals
use to break down the food they eat. All plants need amino acids (nitrogen-containing compounds),
to make the proteins they needs to mature and survive. In Venus flytraps, protease cleaves the bond
between a carboxyl group (-CO2H) and an amino group, (-NH2). Protease then breaks down the
insect material to give the plant enough amino acids to manufacture its essential proteins.
(Wikipedia) With out these amino acids, the tRNA in the plant has nothing to combine into proteins.
Another group of enzymes that breaks down the prey are phosphatases. A phosphatase hydrolyzes
phosphoric acid (H3PO4) from the insect to make DNA in the plant. Another important digestive
enzyme is chitinase. It breaks down the tough chitin shell of the various insects it may catch, and
makes important sugars. All of these enzymes are held is the plants’ many lysosomes. These small
structures in the plants’ cells store unusually high amounts of enzymes in the Venus Flytrap,
compared to other plants, because it needs to break down the more complex proteins found in
insects. These enzymes allow the Venus flytrap to obtain nutrients it cannot derive from other
sources in the environment.
The different types of the Venus flytrap
The Venus flytrap, or Dionaea muscipula, has only one species. However, there are several
different cultivars that have been created by horticulturists. The term cultivar is a contraction of the
term “cultivated variety.” These different varieties in the original species are the same as a pedigree
plant, somewhat like a show plant. There are several different cultivar registries in which you can
look up a plant to find the different cultivar names. The company in charge of researching and
cataloging each plant and its different cultivars, and specifically for carnivorous plants (like the
Venus flytrap), is the International Carnivorous Plant Society. They hold all authority over the area
of registering each plant in the carnivorous genre. When looking up or registering a plant in a
cultivar registry book, you will find the scientific name of the plant, followed by the cultivar names
in single quotes. For example, if you were to look up a Venus flytrap that was red, it would be listed
as Dionaea muscipula, ‘Red Dragon.’
Within the cultivars, there are different cultivar groups. In these groups are different cultivars
that share similarities with other cultivars of the same plant. If, when working on a specific cultivar,
you were to find a cultivar with similar details, you would register them as the same group, but with
separate names.
The major cultivars of the Venus flytrap are listed below:
Dionaea ‘Dentate Traps’, has short, tooth-like traps. (pictured above)
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Dionaea ‘Jaws’ the trap spines are short and pointy, while the traps are large. It gets its name from
the shark-like appearance when the plant has just closed its lobes.
Dionaea ‘Sawtooth’, which has saw-like edges to the trap. (pictured above)
Dionaea ‘Red Dragon’ is also known as Dionaea ‘Akai Ryu’, and is a dark red. (pictured above)
Dionaea ‘Red Piranha’ has the color of the ‘Red Dragon’, and also the spines around the
traps similar to the ‘Dentate Traps’.
There is also one cultivar group within the Venus flytrap genus, which is the Dentate Traps
Group. This contains all the varieties that have tooth- or saw-like spines along the traps.
Dormancy
‘The most common dormancy signs of the Venus Flytrap are: very slow growth; many of the
traps turn black and die; the few traps and leaves left may become slightly dried and brown by the
edges; and the healthy traps left may be sluggish when closing or may not close at all” (“Growing
Cycle of Dionaea Muscipula”, Dr. Samuel Vergio Miensinompe, paragraph 9). Generally, Venus
flytraps are active from May to October, and lie dormant during the winter months. However, as Dr.
Miensinompe discovered, not all plants are subject to this schedule. As he explained in his article the
most likely reason for this was an alteration to their biological timing rhythm, which had probably
been thrown off by a late dormancy (Botanical society). However, in most cases, the plants will go
through dormancy in the winter months, when the temperatures drop. As was stated in the quote
above, most, if not all of the plant’s leaves will die, and its growth rate will be greatly reduced. It
should be kept at a temperature range of 40 to 55 degrees Fahrenheit, 45 to 50 degrees being the
most effective. If the plants are kept outside, especially in a severe drop of weather (much like that in
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New England), the plants should be covered in mulch until spring. This keeps the plants from
freezing and thawing repeatedly, which can kill them. Another possibility in order to keep a Venus
flytrap alive is to remove the bulb, spray it with fungicide and, wrapped in sphagnum moss, kept in
the refrigerator for the months it is dormant. During this time, the plant should not be exposed to
frost.
Although there is plenty of information about how to care for a plant while it is dormancy, it
is hard to determine why carnivorous plants, specifically the Venus flytrap, goes into dormancy at
all. There are several speculations on the process, however. The one that makes most sense is that,
considering that it relies on small insects for nourishment, it has adapted to the climates in which
these insects survive. Since the insects tend to hibernate in the winter months, it is plausible that the
plant had to change the way it survives, and “hibernate” as well. While many other opinions are
realistic as well, the one we have mentioned seems to make more sense.
Works Cited
Black, Harvey. “Carnivorous Plants.” Chem Matters. December 1993.
URL=<http://www3.district125.k12.il.us/chemmatt/93/93_12_t/931204t.pdf
“How does a Venus flytrap sense prey?” The Carnivorous Plant FAQ. May 2002.
URL=<http://www.sarracenia.com/faq/faq2135.html>
“How many kinds of Venus flytraps are there?” The Carnivorous Plant FAQ. May 2002.
URL=<http://www.sarracenia.com/faq/faq2680.html>
“Latest News- Venus Gets Physical: How the Trap is sprung.” Blackwell Plant Science. February 6, 2005.
URL=<http://www.blackwellpublishing.com/PlantSci/latest/article.asp?id=127>
Leoalpha. “Venus Flytraps.” h2g2. December 29, 2004. URL=<http://www.bbc.co.uk/dna/ww2/A2982404>
Meeker-O’Connell, Ann. “How Venus Flytraps Work.” How Stuff Works. 1998-2005.
URL=<http://science.howstuffworks.com/venus-flytrap2.htm>
Miensinompe, Dr. Samuel Vergio. “Growing Cycle of Dionaea Muscipula.” The Venus flytrap. 1998, 2000.
URL=<http://www.strato.net/~crvny/sa03005.html>
Schulze, W., Schulze, E.D., Schulze, I. and Oren, R. “Quantification of insect nitrogen utilization by the
venus fly trap Dionaea muscipula catching prey with highly variable isotope signatures.” Journal of
Experimental Biology. December 5, 2000. URL=<http://jxb.oxfordjournals.org/cgi/content/full/52/358/1041>
Summers, Adam. “Biomechanics.” Natural History Magazine. June 2005.
URL=http://www.naturalhistorymag.com/master.html?http://www.naturalhistorymag.com/0605/0605_biomec
hanics.html
“The Mysterious Venus Flytrap.” The Botanical Society of America.
URL=<http://www.botany.org/bsa/misc/carn.html>
Weiss, Peter. “In a Snap: Leaf Geometry Drives Venus Flytrap’s Bite.” Science News Online. January 29,
2005. URL=<http://www.sciencenews.org/articles/20050129/fob5.asp>
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“What makes carnivorous plants different from other plants?” The Carnivorous Plant FAQ. May 2002.
URL=<http://www.sarracenia.com/faq/faq1080.html>
“What should I feed my Venus flytrap? Hamburger meat?” The Carnivorous Plant FAQ. May 2002.
URL=<http://www.sarracenia.com/faq/faq2160.html>
“Venus Flytrap Growing Guide.” Dangerous Plants.
URL=<http://www.dangerousplants.com/grow_traps.asp>
“Carnivorous plants” “Answer for Carnivorous plants, June 2003
URL=<http://www.answers.com/topic/carnivorous-plant-2>
“Venus Flytrap” Wikipedia September 20, 2005 URL=<http://en.wikipedia.org/wiki/Venus_flytrap>
“Carnivorous plants” Scientific American, Life at the Edge. James Gould, Carol Gould. 1989, W.H.
Freeman and Company, New York.
99
Presidential Award for Green Chemistry,
Optimyze and Its New Paper Recycling Technology
Group: Antimony,
Lucien Bisson, Tricia Chan, Katherine Ells and Matthew Gorgol,
100
A simple definition of chemistry is the study of matter and the changes it undergoes. Many
of the processes through which chemists change matter have negative impacts on the environment by
producing hazardous materials. In our industrialized society the effect of hazardous byproducts has
become an issue at the forefront of chemistry. This problem gave rise to the field of Green
Chemistry which seeks to reduce the hazardous effects of chemical processes.
Green Chemistry is the science of reducing the harmful effects of chemical processes on the
environment and the human population. Unlike other methods, which seek to reduce pollution by
cleaning it up once it has been produced, Green Chemistry seeks to eliminate waste before it is
created. This is accomplished by studying processes that produce pollution and developing new
chemicals and catalysts for these processes that have less impact on the environment.
Green Chemistry is important because pollution is such a big problem in our overcrowded
cities and industrial plants. Every year in America the chemical industry releases three billion tons
of chemical waste into the biosphere and spends 150 billion dollars trying to clean it up (Green
Chemistry). This is daunting number, but Green Chemists hope to bring this number down. The
beauty of this field is that it creates less waste while not hindering industrial businesses. Many
programs that reduce pollution do so by enforcing regulations on how much waste can be produced.
The only way factories can reduce waste is by reducing the amount of product they produce, which
lowers revenue. Green Chemistry solves this problem by developing new chemicals that reduce
waste, and are sometimes increase productivity, a great boost to many businesses.
There are three main points Green Chemistry tackles to reduce pollution and increase
productivity. Green chemists look to develop processes that increase the amount of product
produced from an equal amount of reactant and solvent. This is key because industrial businesses
will look to buy such products that increase efficiency and revenue. This process also reduces waste.
Chemists also look to design safe and pollution free solvents to catalyze chemical processes. This is
the heart of Green Chemistry. There will never be a totally safe and environmentally friendly
chemical, but the closer chemists can get the closer we get to eliminating pollution. Green
Chemistry also looks to develop energy efficient processes. Reducing the consumption of electricity
and other non renewable sources of energy is a main concern of Green chemists.
As recycling is a major factor in environmental concern, it is a key focal point of green
chemistry. Paper recycling is becoming particularly important in order to counter the damage done
by the paper industry. Chemicals such as chlorine compounds and other toxic solvents are employed
in the production of paper, making the industry a major contributor to pollution. Other negative
aspects of paper production include the use of massive amounts of energy, water, and the output of
solid waste (Environmental).
However, recycling steps are being taken to remedy this growing problem. With deforestation
becoming more of an issue in our era, discovering ways to eliminate contamination of recycled paper
has become a very important issue. According to ecocycle.org; recycling saves natural resources and
animal habitat, reduces the amount of trash produced, generates less air and water pollution, and
consumes less energy than using virgin materials.
•
Recycling 1 ton of paper saves 17 trees, 2 barrels of oil (enough to run the average car for
1,260 miles), 4,100 kilowatts of energy (enough power for the average home for 6 months),
3.2 cubic yards of landfill space, and 60 pounds of air pollution.
101
•
Recycling also helps to slow the build-up of greenhouse gases (because it saves energy) and
reduces the pollutants that contribute to acid rain, along with many other contributions to the
environment (Recycling).
•
If we recycled all of the newspapers printed in the U.S. on a typical Sunday, we would save
550,000 trees--or about 26 million trees per year.
The good news is, Americans are responding to the ecologists’ plea for recycling, and recycling rates
in the United States nearly doubled from 1990 to 2000.
While recycling is definitely a positive impact on the environment, there are occasionally
obscure drawbacks to the recycling process. Factories create millions of pounds of solid waste each
year. The Toxic Release Inventories revealed discharges of approximately 14 million pounds of
known toxic substances in 1996. Certain types paper contain non-recyclable materials such as inks,
dyes, coatings, pigments, staples, and “stickies” which include tape or adhesives, coatings, plastics,
and other contaminants. These contaminants that are mixed in with the paper fiber make low-grade
paper that rips easily, effectively removing more than half of reusable paper (CWAC). Instead, they
are thrown away as waste solids during the recycling process, adding to the landfill. Another
problem evolves when these stickies must be cleaned from equipment during the recycling process.
Chemical solvents are often used to dispose of the contaminants, but they themselves raise health
issues, and are non-recyclable. These solvents also add to the air pollution dilemma (Alternative).
In 1945 a small company started in Memphis, Tennessee with four employees and one fiftygallon process vessel, this is the beginning of Buckman Laboratories. Now the company that was
once based on controlling the growth of microorganisms has grown to make five hundred different
products with seventeen hundred employees in more than seventy countries. Buckman Laboratories
today works at providing chemical treatment technologies to solve industrial problems. These
problems can range from improving productivity and improving profit margins to complying with
environmental regulations.
In Buckman Laboratories’ Environmental mission statement they state that they will try to
push the envelope in environmental protection and always keep the highest standards. This idea was
first brought up in Buckman in 1992. The Bulab Holdings board of directors created the
Environmental Policies Committee to oversee Buckman’s global environmental program. Since that
time Buckman Laboratories has strived to be safer and healthier to the environment. By the year
2000 Buckmman had reduced their operational emissions by forty percent while increasing
production by forty percent.
Buckman Laboratories manufactures products in many different areas of business.
Agriculture, wood treatment, coatings and plastics, water treatment, leather, and pulp and paper are
just a few of these product lines. In the pulp and paper line they can do most anything. They make
paper, help you make paper, and will solve any problem you throw their way. One of the biggest
problems they are currently struggling with is the pollution caused by paper recycling (“About
Buckman”).
The United States Environmental Protection Agency (EPA) founded the Presidential Awards
for Green Chemistry in order to recognize individuals, groups, or companies for their technological
contributions to bettering the environment. “The Presidential Green Chemistry Challenge Awards
Program provides national recognition of outstanding chemical technologies that incorporate the
principles of green chemistry into chemical design, manufacture, and use, and that have been or can
be utilized by industry in achieving their pollution prevention goals” (“Green Chemistry”). Since
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1996, each year, the EPA presents The Presidential Award for Green Chemistry in several
categories. These categories include the use of alternative synthetic pathways for green chemistry,
the use of alternative reaction conditions for green chemistry, and the design of safer chemicals
(“Green Chemistry”).
In 2004, the Presidential Green Chemistry Award for Alternative Solvents/Reaction
Conditions was presented to Buckman Laboratories International, Inc. for their development of new
ways to deal with this sticky recycling situation. The company released a new enzyme called
Optimyze. Optimyze is used to remove stickies from recyclable paper in order that it can be reused.
According to the American Forest and Paper Association, stickies cost the industry $650 million a
year, largely in non-recyclable paper. This was a huge step in increasing the efficiency and
cleanliness of paper-producing (NHHA).
Optimyze works by removing polyvinyl acetate, the major glue component of stickies, from
recyclable paper. The company found an appropriate enzyme that could degrade the polymers. The
enzyme catalyzes hydrolysis of the vinyl acetate materials, converting them to water-soluble vinyl
alcohols and acetic acid that are later removed. Optimyze has reduced chemical use by 600,000 lb
per year and has increased production by 6%. Overall, paper mills have saved millions of dollars by
using this fascinating product. Optimyze is now being used in more than 40 paper mills worldwide.
Buckman Laboratories plans to continue its exploration of enzymes for other applications. A
representative of Buckman has stated that "there are not many other companies utilizing enzymes in
the paper industry at this point. We expect to use enzymes a lot more in the future" (Ritter).
References:
“About Buckman.” Buckman Laboratories International, Inc. 2005.
<http://www.buckman.com/eng/about.html.>
“Alternative Solvents/Reaction Conditions Award.” US Environmental Protection Agency.
<http://www.epa.gov/greenchemistry/ascra04.html>
Anastas, Paul T.,and Williamson, Tracy C. Green Chemistry. Washington DC: American Chemical
Society, 1996.
Challener, Cynthia A. “Green Chemistry for Sustainability” May 23, 2005.
<http://www.chemalliance.org/Columns/050520.asp.>
“Environmental Impacts of the Paper Industry.” Clean Water Act Council. 15 Nov 2005
<http://www.cwac.net/paper_industry/>
“Foundations for Healthy Communities.” New Hampshire Health Association. April 1998.
http://www.healthynh.com/nhha/state_law/environment/stats/he_stat_apr98.php
“Green Chemistry.” US Environmental Protection Agency. 16 Nov. 2005. 2005.
<http://www.epa.gov/greenchemistry/>
“Recycling.” US Environmental Protection Agency. 15 Nov 2005.
<http://www.epa.gov/epaoswer/non-hw/muncpl/recycle.htm>
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“Recycling and Environmental Facts.” Eco Cycle. 15 Nov 2005.
<http://www.ecocycle.org/tidbits/index.cfm.>
Ritter, Stephen K. Green Innovations. 2004.
http://pubs.acs.org/cen/coverstory/8228/8228greenchemistry.html
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The Crisis at Bhopal
Group: Hafnium:
Mbong Azang-Njaah, Brittany Howell, Ivana Moffitt, and Jason Lefever
105
On December 3rd, 1984, a disaster occurred that made the world question the ethics of having
large production plants in third world countries. Nations like India, struggling to find a place in an
industrialized society, often fall victim to environmental destruction due to chemical production.
Some feel that the larger world powers exploit third world countries by taking advantage of their
inexpensive production costs, land, and labor. All the while, the people and the environment of said
countries are put in harm’s way due to the hazard of the products that are manufactured. The purpose
of this study is to explore the chemicals involved in the crisis at Bhopal, the subsequent response, the
disrepair of the facility, and the effects of producing chemicals in third world countries.
The Union Carbide plant in Bhopal was originally established for the importing, packaging,
and distribution of raw fertilizer and pesticides to parts of India and East Asia. Due to budget cuts,
Union Carbide decided to use the plant to manufacture pesticides in the early 1980s. However, the
plant was inadequately equipped to contain the chemicals involved in pesticide manufacturing. By
1984, exposure to deadly chemicals injured forty-five workers (Riddle, 12, 17). One particular
chemical, methyl isocyanate (MIC), caused major harm to the citizens of Bhopal. This chemical was
used in the production of the pesticide sevin (Riddle, 14). MIC is a volatile and toxic chemical that
can cause severe irritation to the nose and throat. When MIC reacts with water, it produces
methylamine and carbon dioxide, as seen in the following equation:
CH3NCO + H2O ––> CH3NH2 + CO2
In the case of the Bhopal disaster, the gas produced by the above reaction along with excess heat
caused the pressure within the tanks to rise. As a result of these hazardous conditions, the tanks
ruptured (Barrens, 1). Once the gas escaped, it spread quickly into the surrounding area, subjecting
the residents of Bhopal to severe bodily damage.
On the night of the accident, plant workers were assigned to clean the pipes containing MIC.
While cleaning, they noticed that the pressure within the pipes was alarmingly high and rapidly
climbing. By the time the workers notified their supervisor, the pressure had already caused the
pipes to crack, releasing the deadly gas. Plant employees tried desperately to contain the leak but it
was escaping too fast to be completely contained (Riddle, 20-22). A warning siren sounded but it
was quickly disabled in an attempt to minimize the spread of panic among the residents (“Bhopal”).
Unaware of the disaster unfolding at the Union Carbide plant, the residents of Bhopal began to wake
up coughing. Soon their eyes began to burn and swell shut, and they had difficulty breathing. Many
citizens died before they could reach medical help. One resident recounted her experience, “My eyes
were now so swollen that I couldn’t see out of them. So about an hour after I first felt the gas, we left
the house, my daughters-in-law held me by the hands. The streets were full of corpses. The skins of
people were full of blisters. Nobody could be recognized” (Riddle, 35).
The local officials were not prepared to deal with a disaster of this magnitude. Prior to this
incident, very little was known about methyl isocyanate. What was known about MIC dealt mainly
with the chemical properties of the gas, not its toxic nature. “No material safety data sheets (MSDS)
were available to workers at the plant” (standard protocol in U. S. Industry). Very little was known
about the exact composition of the gas cloud that formed over Bhopal, simply referred to as the
“Bhopal gas,” because it dissipated within hours. Biopsies of victims revealed characteristics
attributed to cyanide poisoning, one of which was cherry-red blood. These findings suggest that
somehow cyanide was mixed with MIC in the vapor cloud (Kim, 249).
The severity of the Bhopal incident may have been reduced had there been greater awareness
and more efficient responses on the local and international scale. Many of the steps necessary to
106
prevent a disaster of this proportion were overlooked. While the aftermath of the incident fails to
associate blame with one particular institution, it is clear that whatever plans were in place did not
allow for proper use and upkeep of the facility as well as reaction to emergency situations.
Consequently, the response fell short of the aid that the situation required.
Local authorities were uninformed as to the potentially devastating repercussions of housing
such a chemical facility. India’s willingness to build this chemical facility is yet another example of
a third world country seeking economic growth with little knowledge for the environmental
ramifications. Even after the facility was operational, it did not bring the economic success expected.
With a decline in sales came the dismissal of staff members. The lack of proper staffing and poor
facility maintenance left the site vulnerable to disaster. Cutbacks in laborers resulted in a weakened
core for safety checks, which were at best, few and far between.
A few months prior to the disaster, scientists within the Union Carbide Corporation
expressed concern over findings of probable danger. The facility was insufficient for housing
hazardous chemicals. The plant’s record of industrial accidents was on the rise as more and more
workers had fallen victim to the effects of MIC. However, the senior staff paid little attention to
these warnings. In fact, local authorities knew nothing of the impending danger. Had the senior staff
shown more concern for addressing certain concerns within the facility, the incident could have been
thoroughly contained.
The surrounding towns, already vulnerable to exposure, were inundated in a cloud of gas.
While a medical response was made, it was insufficient. Medical personnel were not properly trained
to treat victims exposed to MIC. Victims suffering from pulmonary edema showed symptoms like
labored breathing, and desperately needed advanced treatment like loop diuretics (Bhopal). Instead,
they were given cough medicine. Clearly such a primitive method of treatment illustrates the fact
that no one was prepared to face the lethal effects of exposure to deadly chemicals.
According to patrons of the pesticide plant, Union Carbide aid was instantaneous and
recurrent (Union). In addition to an initial aid of $2 million, the Corporation claimed to have
provided medical personnel, equipment, and various supplies. Further attempts to give aid included
funds to build a hospital. However, the Indian government promptly rejected subsequent Union
Carbide funds for aid.
Digging deeper, several root issues ultimately led to the incident in Bhopal. “Developing
countries, such as India, are particularly vulnerable as they lack the infrastructure required to
maintain technology but are nevertheless, eager to set up and maintain industrial plants” (TED, 1).
Perhaps this lack of infrastructure doomed the facility to such a fate from the beginning. At one point
in this investigation, Union Carbide attempted to call the incident a case of sabotage brought about
by an unhappy employee. “Independent investigation by engineering and consulting firm Arthur D
Little, Inc., concluded that the gas leak could only have been caused by deliberate sabotage;
someone intentionally connected a water hose to the gas storage tank” (Union). However, the
disrepair and lack of general organization in the plant could not have been the work of a single
person; the state of the facility was the result of many people neglecting their duties in the upkeep of
equipment. A close examination of the plant conditions and maintenance reveal this to be true.
Looking further at the meaning of a lacking infrastructure, it is evident that the facility did
not have appropriate maintenance, safety, and emergency procedures in place to operate, contain,
and respond to the production, and any possible accidents. Several pieces of equipment in the factory
were damaged or defective. The storage tanks for MIC had faulty pressure and temperature gauges.
As a result, employees ignored warnings from the gauge levels since they gave inaccurate readings.
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When the pressure or temperature did reach dangerous levels as it did on the night of the incident,
the tanks’ warning system failed to trigger.
Investigations have shown that employee negligence or carelessness also had an impact on
the situation. The storage tank for MIC was filled beyond the recommended capacity. In addition, a
reserve tank that was supposed to hold excess MIC was already full. With an excess of gas and no
extra holding tanks, the facility was not prepared to contain a spill. Not only was it incapable of
containing a spill, the facility was also unprepared to neutralize one. Ideally, escaping MIC would be
neutralized by a gas scrubber. A gas scrubber is meant to neutralize the gas with Caustic soda, a
derivative of sodium dioxide. The Caustic soda would bring the toxicity of the gas to a safe level.
However, the gas scrubber was waiting for maintenance and therefore not operational. One of the
flare towers was shut off for maintenance as well. Had this piece of machinery been operational, it
would have burned the escaping MIC, preventing it from spreading to the environment. A water
curtain that was also meant to impede the leaking gas was too short to cover the entire flare tower
where the leak occurred. Even if the curtain was not capable of containing all of the escaping gas, it
was not long enough; therefore, there was no chance of containing the leak in the first place.
The list of defects, poor maintenance record, and examples of employee negligence
demonstrate a poor system for hiring skilled employees, training those employees, and keeping them
accountable for their work. The staff that was working at the time did not maintain the facility in a
way that kept it in operating condition. The employees did not even take heed to the warning signals
present. However, they are not to be fully credited with the blame. The deeper issues remaining
clearly show that the facility was not built and maintained in line with a safety code, the employees
were not trained to adequately and quickly repair the faulty equipment, and there was no emergency
procedure established to deal with accidents. The incident at Bhopal was the result of “a complete
absence of community information and emergency procedures” (TED, 3).
The Bhopal incident was not the first of Union Carbide’s industrial accidents. The tunneling
of a hydro-electric project just east of Charleston, West Virginia became known as the Hawk's Nest
Incident. Thousands of workers died within the year because they had not been supplied with masks
to protect themselves from silica dust. This incident is analogous with the Bhopal tragedy in
illustrating Union Carbide’s negligence of maintaining safe work environments, which essentially
created disaster-prone situations.
Incidents like the one in Bhopal create a difficult controversy. The United States must face
the issue of continued association with Corporations like Union Carbide. Although India is the
fourth largest power purchasing parity (a number used to compare the standards of living within a
country) and has the fourth largest coal reserve, national poverty is just as prevalent (CIA). Due to a
relatively less stable economy, it is significantly cheaper for the U.S. to operate under India’s lenient
industrial laws.
Bhopal residents continue to experience the effects of the disaster today. After three thousand
people died immediately in 1984, ten thousand more have died due to diseases brought on by the
hazardous gas. Not only have the first-hand victims suffered from the disaster, many infants have
died in spontaneous abortions since the Bhopal incident. In 1989, Union Carbide agreed to give $470
million to compensate for the damages and to aid the families affected. At the same time, clean-up
procedures for the current state of Bhopal have yet to be determined.
Warren Anderson, the Chairman on Board and Chief Executive Officer of Union Carbide,
responded very quickly to the Bhopal disaster. He was involved in every political, economical, and
industrial decision for the Bhopal plant (Account). Anderson was notified and immediately rushed to
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the plant the night of the disaster. However, due to his position, the Indian government held him
responsible for the disaster and placed Anderson under house arrest. Specifically, Anderson’s
charges include manslaughter, grievous assault, poisoning and the killing of animals (Clemens). His
prosecutors will seek to indict him based on the Union Carbide documents (found in 2002) in which
Anderson authorized the exportation of hazardous chemicals. The International Campaign for Justice
in Bhopal has asked the United States to relinquish custody of Anderson as he has not been tried to
date.
Although people like Warren Anderson want to forget this catastrophic event, organizations
such as the International Campaign for Justice in Bhopal will not let the issues at hand be silenced.
Justice demands Union Carbide to accept responsibility and pay the price of neglect and oversight.
While financial compensation can never reverse the agony suffered by victims and their loved ones,
it can purchase the means to end the environmental damage oppressing the people of Bhopal. The
necessity to act is great, as a renewed environment of safety will lower the death count and allow
inhabitants to live in toxic free lands.
Works Cited
Account on the Web. Urban Carbide. 8 Nov. 2005. http://www.bhopal.com/chrono.htm>.
Barrans, Richard E. “Pesticide Reaction and Water.” Harold Myron. Newton BBS, United States of
America: Department of Energy. 30 October 2005
http://www.newton.dep.anl.gov/askasci/chem99/chem99589.htm
“Bhopal Disaster.” Wikipedia Encyclopedia. 4 October 2005. Wikipedia Encyclopedia. 10 October
2005 <http://en.wikipedia.org/wiki/Main_Page>.
CIA Website- http://www.cia.gov/cia/publications/factbook/geos/in.html
Clemens Work: Inside story of Union Carbide's India Nightmare, U S News & World Report, Jan.
21, 1985
Kim, Jim Yong, Joyce V. Millen, Alec Irwin, and John Gershman. Dying for Growth: Global
Inequality and the Health of the Poor. Monroe: Common Courage Press, 2000.
Riddle, John. Bhopal. Philadelphia: Chelsea House Publishers, 2002.
TED Case Studies: Bhopal Disaster. Http://www.american.edu/TED/bhopal.htm
Union Carbide Corporation: Chronology of Key Events Related to the Bhopal Incident.
Http://www.bhopal.com/
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