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| AML & Causes |
Acute myelogenous leukemia (AML) is a malignancy that arises in either
granulocytes or monocytes which are white blood cells that battle infectious
agents throughout the body. AML is not inherited or contagious. It develops
when there is a defect in the immature cells in the bone marrow. Although
the exact cause of AML is unknown, exposure to benzene, cigarettes smoking,
and prior exposure to chemotherapy drugs are linked to the disease. The
effects of AML are:
1) the uncontrolled, exaggerated growth and accumulation of cells called
"leukemic blasts," which fail to function as normal blood cells, and 2) the
blockade of the production of normal marrow cells, leading to a deficiency
of red cells (anemia), and platelets (thrombocytopenia) and normal white
cells (especially neutrophils, i.e. neutropenia) in the blood.
Acute myelogenous leukemia is the most common type of leukemia in adults,
with an estimated 10,100 new cases of AML reported each year. Older people
are more likely to develop AML than children. In fact, the risk for
developing the disease increases about ten-fold from age 30 (1 case per
100,000) to age 70 (1 case per 10,000).
Acute myelogenous leukemia may be called by several names, including acute
myelocytic leukemia, acute myeloblastic leukemia, acute granulocytic
leukemia, or acute nonlymphocytic leukemia.
AML Subtypes
The subtypes of AML are classified based on the stage of development
myeloblasts have reached at the time of diagnosis. The categories and
subsets allow the physician to decide what treatment works best for the cell
type and how quickly the disease may develop.
(Designation / Cell subtype) -
M1, Myeloblastic, without maturation
M2, Myeloblastic, with maturation
M3, Promyelocytic
M4, Myelomonocytic
M5, Monocytic
M6, Erythroleukemia
M7, Megakaryocytic
AML is a very common form of leukemia in adults. More than 10,000 adults are
diagnosed each year in the USA. 65 is the average age of people diagnosed
with AML. Acute myelogenous leukemia affects more men than women, and is a
little more common among whites than blacks. AML accounts for just under
half of cases of childhood leukemia. Although leukemia starts in the bone
marrow, it can spread to the blood, lymph nodes, spleen, liver, central
nervous system and other organs. It does not usually form a solid mass or
tumor.
Prognosis, Survival Rates, and What to Expect
70to 80of acute myelogenous leukemia patients experience complete remission.
In total, about 20to 30of patients survive and are free of AML 5 years after
the diagnosis. AML patients who have not had a relapse during this time are
considered completely cured, because most relapses happen within 2 years of
the AML diagnosis.
Acute myelogenous leukemia patients who are under 60 years of age have a
better chance of survival than those patients that are older. This is due to
many factors including being able to stand the strong chemotherapy medicines
that are used to treat AML. With no treatment, AML leukemia patient life
expectancy is about 3 to 4 months.
Leukemia Symptoms and Diagnosis
Acute myelogenous leukemia (AML) symptoms result from the body not producing
enough healthy blood cells. Healthy bone marrow makes stem cells that grow
into the three types of blood cells: red blood cells, white blood cells, and
platelets. An AML patient's bone marrow makes too many blast cells (immature
white blood cells). Normal blast cells turn into a type of white blood cell
called granulocytes, but the leukemia blast cells do not. At the same time,
the marrow cannot grow enough normal red blood cells, white blood cells, and
platelets.
Someone with too few red blood cells (anemia) may:
- Feel tired
- Be short of breath
- Look pale
Someone with too few normal white blood cells and too many leukemia blast
cells may:
- Develop a lot of infections, for example, a sore throat
- Experience pain in the bones or joints
- Have a mild fever
Someone with too few platelets may:
- Bleed easily, such as swollen and bleeding gums, frequent nose bleeds or
cuts that bleed for a long time
- Bruise more easily than usual
- Develop pin-head sized spots under the skin
- Develop cuts that heal slowly or do not heal
Some people with AML, however, do not notice any symptoms. Their AML may be
discovered only during a blood test.
Leukemia Diagnosis
AML is diagnosed by examining bone marrow and blood samples under a
microscope. By examining the appearance of the leukemia cells, the sub-type
of AML can also be diagnosed. AML has seven sub-types, which are based on
the type of blood cells affected. The sub-type of AML is an important factor
in choosing the best cancer treatment for a patient.
High Risk Jobs / Benzene Exposure
A risk factor is anything that increases a person's chance of getting a
disease such as cancer. Environmental risk factors include benzene, smoking
cigarettes, and prior exposure to chemotherapy drugs.
Benzene Exposure and Acute Myelogenous Leukemia
Exposure in the work place to benzene use may cause Acute myelogenous
leukemia. While benzene has been banned in the United States for over 20
years, workers are still exposed to significant amounts of benzene poisoning
when working with petroleum products. Most workers come into contact with
benzene by breathing it into their lungs or absorbing it through their skin
when working with solvents. In the U.S. millions of workers are exposed to
significant amounts of benzene every year. Even small amounts of exposure to
benzene can cause Acute myelogenous leukemia cancer.
AML High Risk Jobs include:
Adhesive production
Barge Workers
Chemical Workers
Dock Workers
Gasoline distribution workers
Industrial plant workers who use solvents
Newspaper Press Workers
Offshore Workers
Painters
Paper and Pulp
Pesticide Manufacturing
Pipefittlers
Printers
Refinery Workers
Rubber Workers
Shoe / Leather workers
Synthetic Rubber Production
Tankermen
Truck Drivers
At Risk Benzene Exposure:
Benzene production workers include anyone who works around the following:
· Automotive gasoline Fumes
· Industrial Solvents
· Oil and Coal Emissions
· Paint
AML and Cigarettes:
Although many people know that smoking is responsible for most cancers of
the lungs, mouth, throat, and larynx, few realize that it can affect cells
that do not come into direct contact with smoke. Cancer-causing substances
in tobacco smoke are absorbed by the lungs and spread through the
bloodstream damaging normal cells and causing AML leukemia.
Prior Exposure to Chemotherapy Drugs
Patients with other cancers who are treated with certain chemotherapy drugs
are more likely to develop AML. The drugs most often associated with these
secondary (post-treatment) leukemias include mechlorethamine, procarbazine,
chlorambucil, etoposide, teniposide and to a lesser degree,
cyclophosphamide.
Combining these drugs with radiation therapy further increases the risk.
Most secondary leukemias are cases of AML and occur within 9 years after
treatment of Hodgkin's disease, non-Hodgkin's lymphoma, or childhood ALL.
Secondary leukemias sometimes occur following treatment of breast, ovarian,
or other cancers. Chemotherapy does not work as well for patients with
secondary Acute myelogenous leukemia.
I believe that the combination of PERC(Tetrachlorethylene), Benzene and
Radiation shifted my daughter's cells. This is what we know.
A Primer on Cytogenetics - Cytogenetics Determined my Daughter's DNA had
Mutated after Birth.
Cytogenetics is the study of chromosomes. Cytogenetic testing explores the
causes of abnormalities in the chromosomes
Chromosomes are found in the nucleus of cells. They contain all the genetic
information necessary to create a life form
Human cells have 46 chromosomes. The chromosomes consist of 22 pairs (one of
each type contributed by the mother and one of each type contributed by the
father), and two sex chromosomes, for a total of 46.
Genes are segments of chromosomes which contain particular genetic
information. The genes within our chromosomes contain the entire "blue
print" for the creation of human life. There are about 35,000 genes we know
about.
All chromosomes are made from DNA. DNA is a very long protein molecule.
These are the "building blocks" of life forms
Cancer can result when chromosomes become damaged or when chromosome
replication goes catywampus.
There are two major types of chromosomal damage: Numerical abnormalities and
Structural abnormalities.
Numerical abnormalities occur when cells lack the usual 46 pairs of
chromosomes. Structural abnormalities occur when cells have the usual 46
pairs of chromosomes, but the normal structure of the chromosomes has been
altered
Sometimes a chromosome will break into two pieces. This is called a
chromosome “break.” Sometimes one of the pieces is lost. This is called a
“deletion.” Either the long or the small arm of a chromosome can be deleted.
Diagnosing Acute Myelogenous Leukemia
The latency period for benzene-induced leukemia is typically 1 to 20 years
after first exposure.
High Risk Occupations
Adhesive Production
Chemical Plant Workers
Gasoline Distribution Workers
Operators
Painters
Paper and Pulp Workers
Pesticide Manufacturing
Printers
Refinery Workers
Rubber Workers
Synthetic Rubber Production
Tankerman
Tire Plant Workers
Latency means the time from the initial exposure to a toxic chemical and the
eruption of a diagnosed cancer. For example, the latency period for
malignant mesothelioma, a tumor caused by asbestos, is between 15 and 40
years. That means that the interval between the initial exposure and the
development of a tumor is at the outside around 40 years and at the inside
about 15 years.
Leukemia has a much shorter latency period when compared to asbestos and
other carcinogens. Leukemias have been reported to arise in patients exposed
to benzene in only 8-9 months. The average latency period for refinery
workers is about 10 years. For Chinese shoe factory workers, latency period
from exposures to benzene and genesis of AML was just over 5 years.
The symptoms of leukemia and related bone marrow disorders are parallel to
many other diseases. During medical evaluation the physician will ask a
number of questions regarding recent and previous illnesses. If signs and
symptoms suggest acute myelogenous leukemia (AML), sample cells will be
taken from blood and bone marrow for laboratory testing.
A number of specialized physicians, including a pathologist, an expert in
disease diagnosis, and a blood specialist known as a hematologist will work
together to confirm the AML diagnosis.
Blood Test
A full blood count (FBC) or complete blood count (CBC) is the test that
provides all the cell information about your blood.
Two different counting methods will likely be used. Either an automated
analyzer or a hematology analyzer (a cell counter) will provide a very
precise measurement of normal cell levels. However, abnormal cells may be
identified incorrectly by both methods
A second count is manually performed to identify the number of blasts,
prematurely released white blood cells, that are in a patient's blood
Bone Marrow Aspiration and Biopsy
Patients with AML have low levels of red blood cells (erythrocytes), low
levels of platelets (thrombocytes), and high levels of white blood cells
(leukocytes) in their blood. When a high number of white blood cells or
blasts are found, a confirmed diagnosis of AML can only be obtained through
a sample of the bone marrow.
Bone marrow aspiration and biopsy procedures are more invasive and may
require pain killers to ease the discomfort.
A bone marrow aspiration is a procedure where approximately one teaspoon
amount of bone marrow liquid is suctioned from the back of the pelvic or hip
bone.
A second specimen, an estimated 1/16 inch cylindrical section of the bone
marrow is harvested from the same site and contains a solid piece of bone
and marrow. This is known as a core biopsy.
The bone marrow cells are evaluated according to their size, shape,
granule(s) content and maturity.
The mature cells are normal cells found in the circulating blood which
actively fight infection but can no longer reproduce.
Immature cells are undeveloped blood cells and poor infection fighters but
are capable of reproduction. These are known as 'blasts'.
Blasts percentages found in those with AML can escalate from 30 to 95
percent.
Cytology
Cytology is the examination of the peripheral blood (PB) and bone marrow
(BM) films by microscope.
Cytologists use the traditional Romanowsky-stained techniques as the
standard for hematology diagnosis.
Immunophenotyping
Immunophenotyping can determine at which stage of development the cell
became leukemic.
By testing for surface cell markers produced by each specific type of
leukemia the 7 subtypes of AML can be identified and classified.
Immunophenotypic analysis will establish if the blasts are myeloid or
lymphoid.
Blasts identified as myeloid return a diagnosis of AML.
The diagnostic accuracy achieved by immunophenotyping is a valuable tool for
developing a treatment program.
Cytochemistry
Cytochemistry is the branch of biochemistry that studies the chemical
composition and activity of cells.
Special chemical stains (dyes) are used on the cells from the original
sample and when applied the chemical stains cause the granules of most AML
cells to appear black in color or as black spots when observed through the
microscope.
The essential cytochemical tests are: myeloeroxidase (MPO) or Sudan black B
(SBB); non-specific esterase (NSE); or combined esterase (CE); and, Perls’
stain. www.pathologyoutlines.com
Flow Cytometry
Flow Cytometery is another accurate technique used to determine the exact
type of leukemia a patient has.
Special antibodies applied to the sample cells are passed in front of a
laser beam.
The laser will cause antibodies attached to the surface molecules to give
off light, which is measured and analyzed by the computer.
This method will allow groups of cells to be separated and counted.
Flow Cytometry is used to obtain an Absolute Lymphocyte Count (ALC) of white
blood cells, lymphocytes and T cells. ALC recovery serves as a powerful
predictor for survival of post-autologous stem cell transplantation Studies
are being conducted to determine if ALC can determine the prognosis and
survival rate of patients after induction chemotherapy
Cytogenetics
Cytogenetics is the study of chromosomes. Cytogenetic testing explores the
causes of abnormalities in the chromosomes.
Cytogenetics, the microscopic study of chromosomes, requires expert analysis
and identification of specific chromosomal abnormalities as it is used
increasingly to decide treatment.
Chromosomes contain DNA that control metabolism and cell growth.
Patients initially diagnosed with AML should have cytogenetic testing done
to analyze damage to chromosomes.
Patients with acute leukemia in remission will not benefit from cytogenetic
analysis because the procedure cannot adequately detect low levels of the
clone.
In some types of leukemia, two chromosomes may exchange or attach some of
their DNA to the other chromosome. This is known as translocation (i.e. part
of chromosome #1 is now located on chromosome #2).
Other chromosome changes are inversions, deletions, and additions.
Other Diagnostic Testing
FISH (fluorescent in situ hybridization) is a sophisticated test which aides
in the molecular genetic detection of translocations not seen under a
microscope of many subtypes of AML.
Gene-Expression Profiling is a experimental technique that creates a
fingerprint for some cancers but it is used to classify the various types of
AML into particular risk categories.
Imaging Studies (pictures of the inside of the body) are done when AML
patients have infections or medical problems not associated with their
cancer.
X-rays, CT scans, MRI(s), Gallium scan or bone scan and ultrasound are also
used by treating physicians.
What is a “Blast”
Stedman’s Medical Dictionary defines “Blast” as an immature, embryonic stage
in the development of cells or tissues.
When “Blast” is generically stated in diagnosing AML the writer is referring
to a “Blast Cell”, an immature precursor of a blood cell.
The healthy, normal bone yields less than 5 percent of blast cells.
If the percentage of blasts found in the bone marrow is at least 20 the
pathologist will likely return a diagnosis of acute myeloid leukemia.
The characteristics of blast cells in a patient play an important role in
diagnosing the correct leukemia subtype and AML sub-classification
Staging
Staging is used in most cancers to chart the course of the disease according
to the extent of the tumor. Because, leukemia normally spreads before it is
detected the disease is described as “untreated,” in “remission,” or
“recurrent.”
Cell classification systems are relied upon to identify the type and subtype
of leukemia. This system helps predict the prognosis and the probable
response to treatment of specific forms of leukemia.
Types & Subtypes of Leukemia
The two classifications of leukemia are based on the cell type; myeloid and
lymphoid.
Clinical behavior of the disease determines if leukemia is acute or chronic
and myelogenous versus lymphocytic.
For more than 20 years the French-American British (FAB) has been the
standard classification for leukemia; based on the cell morphology on
May-Grunwald-Giemsa (MGG) staining of peripheral blood and bone marrow
smears and basic cytochemical techniques.
The eight (8) subtypes of Acute Myelogenous Leukemia (AML) are:
1. undifferentiated AML (M0)
2. myeloblastic leukemia (M1)
3. myeloblastic leukemia (M2)
4. promyelocytic leukemia (M3 or M3 variant [M3V])
5. myelomonocytic leukemia (M4 or M4 variant with eosinophilia [M4E])
6. monocytic leukemia (M5)
7. erythroleukemia (M6)
8. megakaryoblastic leukemia (M7)
The World Health Organization (WHO) recommends the clinico-biological
classification of acute myeloid leukemia (AML) should include morphological,
cytochemical, cytogentic, immunophenotypic and molecular characterization of
the leukemia blasts.
Based on available data WHO suggests classifying AML into four main groups:
1. AML with recurrent cytogenetic translocations
2. mAML: Multilineage AML
3. Secondary AML
4. Morpholocical and Immunophenotyping classification (necessary for those
that do not fit within the preceding categories)
Using these homogeneous categories (as explained in the Glossary section)
would allow for further development and refinement of current and future
treatment strategies.
What are clinical biomarkers?
Biomarkers are clinical tests that are specific to an occupational or
environmental exposure or illness. In 1982, biomarkers were defined by The
National Research Council, with respect to their clinical utility as
follows:
EXPOSURE biological markers reflect an exogenous substance or its metabolite
that is measured in a compartment of the body
Biological markers of EFFECT refer to the measurable alterations that can be
seen as established or potential health impairment.
SUSCEPTIBILITY biological markers gauges a person’s ability to respond to an
xemobiotic (foreign substance) challenge.
How Benzene is Metabolized by the Body
Benzene is metabolized by the body via two different pathways; inhalation
and skin absorption.
The complete metabolism of benzene takes hours after its entry into the body
via an inhalation exposure route.
Urinary products are normally eliminated rapidly.
Occupational exposure levels have a third, more slowly exchanging section.
Benzene is present in the blood and expired in the breath for extended time
periods.
Use of White Blood Cell Counts for Occupational Screening
The minimum mandatory observations to be made from a peripheral blood smear
are (1) differential white blood cell count; (2) description of the
appearance of abnormalities in the red blood cells; (3) platelets
abnormalities charted; and (4) thorough search of each blood smear for
immature white cells.
Unexplained elevations of white blood cells are regarded as evidence of
benzene exposure and the employee must immediately vacate the work area to
prevent any further exposure to benzene vapor.
Suppression of Absolute Lymphocyte Count
Lymphocytes are any one of a group of white blood cells that are crucial to
the body’s immune system. Some of them are known as B-cells and T-cells.
The T-lymphocytes in a donor’s bone marrow or blood can cause a harmful
reaction known as graft versus host disease.
Prior to transplant the collection of marrow or blood can be treated with
agents that will decrease the number of T-lymphocytes that are to be infused
with the stem cells.
Acute vs. Chronic Leukemia
While both Acute and Chronic Leukemia are usually cancers of the white blood
cells, the distinction between them is based upon their "untreated"
behavior.
Acute leukemia affects growing cells very early in cell life causing the
cells to remain immature and unable to function. Patients with acute
leukemia are more likely to suffer from infection, bleeding and anemia.
Acute leukemia can be fatal within months if immediate treatment is not
pursued.
Chronic leukemia affects the more mature cells which can retain much of
their normal function. The chance of bleeding and infection are less likely
and patients may live for many years without treatment.
A chronic leukemia can sometimes convert to an acute variety known as
Richter’s syndrome.
Martyn Smith Ph.D.
Dr. Martyn Smith is a professor of toxicology, School Public Health, at the
University of California at Berkeley. Dr. Smith has published hundreds of
articles, many dealing with benzene toxicity. His lab focuses on leukemia
and lymphoma and is funded by the National Institutes of Health. According
to Dr. Smith:
There are four types of leukemias, all common mechanisms of pathogenesis.
AML is one. AML subdivided morphologically into seven subtypes, but
subtyping has clinical significance but “no proven etiological or
epidemiological relevance.”
Three causes of leukemia: benzene, ionizing radiation, and chemo drugs.
Studies prove benzene metabolites cause genetic changes in human stem cells
which cause leukemia. “There is no real dispute among scientists that
benzene causes human leukemia, including AML. This has been accepted since
the late 1970s.”
In the 1970s, epidemiological studies clearly established benzene as cause
of leukemia.
The factual bases for Dr. Smith’s opinion that benzene w/i RDMP caused AML
in a plaintiff:
1. history of occupational exposure to benzene containing products and other
toxic chemicals,
2. other risk factors for AML ruled out
3. AML had a clonal inversion of chromosome 16, which is characteristic of
secondary leukemias arising from exposure to quinone topoisomerase
inhibitors (the plaintiff had AML at young age and was treated with
chemotherapy).
Smith applies Bradford Hill Criteria (consistency, strength, bio
plausibility, temporal association and dose response) to support his
causation opinion.
"The most probably mechanism by which benzene induces AML is via inhibition
of the enzyme toposomerase II and the production of chromosome
rearrangements" (in particular, chromosome rearrangement inversion 16).
There is no safe threshold for benzene induced AML. This is policy of
OSHA/NIOSH/EPA. Distinguish from aplastic anemia, also caused by benzene,
but that disease has an exposure threshold. Note: in benzene induced
leukemia, only one stem cell is permanently changed, but in aplastic anemia
“all the stem cells in the bone marrow are either destroyed or prevented
from dividing.”
No safe occupational exposure threshold because there is plenty of
background benzene (air pollution, gasoline, smoking), adding on more
exposure in workplace would be dangerous.
Not possible to reconstruct accurate cumulative exposure level for given AML
patient-worker, because it is not subject to routine monitoring and diverse
work schedule. But plaintiff describes episodes of exposure exceeding OSHA
permissible exposure level (PEL)[1 ppm 8-hour standard] and the 5 ppm short
term (15 minutes) exposure level (STEL). Estimates cumulative life time
exposure level greater than 2 ppm-years.
Review of epidemiology in Australian petrochemical workers. Studies discuss
toxic effects on white blood cell counts among workers at various levels of
exposures (ppm). Smith has published in Science that "hematotoxicity occurs
in workers exposed to less than 1 ppm benzene" which would raise questions
about US exposure standards. (Have to add background exposure levels to
workplace levels).
Reiterates point that clinically there are AML subtypes but the latter has
no relevance to causation. Defense strategy to force toxicologist to base
opinion on epidemiology study showing association between AML-subtype with
inversion 16 specifically. No scientific basis. The epidemiology studies on
AML do not break down the AML by its subtypes. [Like sarcomotoid vs
epithelial vs. Biphasic vs. Desmoplastic mesothelioma].
"There is no published epidemiology study showing a statistically
significant relationship between any specific cytogenetic change and benzene
induced AML." The studies which confirm benzene causes AML did not attempt
to detect specific cytogenetic tests like inversion 16. Presence or absence
of specific chromosome change not required to prove benzene causation.
Leukemia most strongly associated with benzene exposure in 15 years prior to
diagnosis. (This patient was not exposed to cancer drugs or ionizing
radiation prior to diagnosis and stopped smoking in 1983).
Affidavit, February 1, 2005, Martyn T. Smith, Dr.P.H., State of California.
Dr. Peter F. Infante
Dr. Peter Infante is an epidemiologist who from 1983 to 2002 was the
director of the Office of Standards Review for OSHA, the primary agency
charged with reviewing and revising OSHA health standards based on risk
assessments and epidemiologic, toxicologic and industrial hygiene data. He
has been recognized for his outstanding work towards greater understanding
of the toxic effects of benzene on humans.
Corporate Medical Knowledge
Benzene has been known as a powerful bone marrow poison since 1897. In 1928,
the first published case of benzene-induced leukemia was reported.
Researchers at the time recommended substitutes for benzene because it was
so toxic.
In 1943, in a confidential report on the toxicity of benzene for Shell
Development Company, the report states: "While prolonged exposure to any
concentration of benzene is dangerous, there is a marked variation in
susceptibility of individuals" so that some will get leukemia and others
won't.
In 1948, the American Petroleum Institute (API) issued a report on the
Toxicology of Benzene: "inasmuch as the body develops no tolerance to
benzene and there is a wide variation in individual susceptibility, it is
generally considered that the only safe concentration for benzene is zero."
in 1965, Browning reported 65 cases of benzene induced leukemia, concluding
that it was an established fact that benzene causes leukemia and that all
cell types of leukemia could be caused by benzene.
Acute Myelogenous Leukemia (AML) caused by benzene
The most commonly associated leukemia to benzene is acute myelogenous
leukemia (AML). The four AML subtypes are caused by benzene, they are not a
separate disease for causation purposes. The large epidemiology studies
which prove that benzene exposed workers have a significant 4 to 5-fold risk
of contracting AML did not subdivide cases of AML into categories based on
specific cytogenetic (chromosome) abnormalities.
The literature indicates that benzene exposure causes a variety of
chromosomal abberations that may lead to or contribute to leukemia, but
there does not appear to be a unique pattern in benzene-induced leukemias.
There is no basis in science for requiring an AML patient to produce
epidemiological evidence showing an elevated risk from benzene for his
particular AML subtype with the chromosomal aberration inversion 16. Benzene
induced AML occurs both with and without detected chromosomal abnormalities.
Low dose exposure to benzene can cause leukemia. Published articles show
that for workers historically exposed to an average benzene leel of less
than 10 ppm, the relative risk for all blood cancers combined was 2.2. For
the group of workers with AML or with it's precursor myelodysplastic
syndrome (MDS), who were exposed to constant average benzene level of less
than 10 ppm, the relative risk was 3.2 (statistically very significant).
Shell Oil's medical director agrees that MDS is a precursor to AML.
Major Epidemiology Studies: no safe level of exposure
Workers with less than 10 ppm constant average of benzene exposure, down to
1.2 ppm with a mean cumulative benzene exposure of 6.7 ppm years, have a
statistically significant 3.2-fold risk of contracting leukemia or MDS.
Studies in 2003 show the risk of leukemia was increased for all cumulative
exposures above 1 ppm-years. Leukemia risk is being reported at lower and
lower levels.
There is no evidence of a threshold for benzene exposure and leukemia.
Short term exposures can produce abnormal changes in white blood cell
counts, as measured in blood tests (Pliofilm study). "There was no evidence
for a threshold effect for the hematologic effects of benzene exposure,
suggesting that even exposure to relatively low level of benzene, e.g., less
than 5 ppm, may result in hematologic suppression" (Ward).
All lines of white blood cells and blood platelets significantly reduced
among workers exposed to atmospheric benzene levels less than 1 ppm. Earlier
progenitor cells more sensitive to benzene's toxicity than more mature blood
cells. (Lan, 2004).
In 2004, a European group of scientists recommended the occupational
exposure limit for benzene be reduced to 40 ppb, which is 25 times lower
than the current OSHA permissible exposure limit (PEL) of 1 ppm. (billion vs
million).
Gasoline-Benzene Exposure
Benzene is found in gasoline. Complying with OSHA's PEL for gasoline vapor
does not protect against exceeding OSHA PEL for benzene (standards for
benzene in liquid form and vaporous form).
Hazards of benzene in gasoline first reported in medical literature in 1928.
Numerous cases of leukemia among gasoline workers, auto mechanics and gas
service station workers. Service station workers have 3 fold greater risk of
contracting leukemia than general population.
Studies show significantly elevated risk of leukemia for children living in
homes neighboring auto repair shops and gas stations. (very high for AML:
relative risk of 7.7). There is a high risk of AML with very low benzene
exposure levels (evaporated from gasoline).
Benzene causes leukemia by damaging genes which regulate blood cell
production and proliferation. Low levels of benzene exposure (between 1 ppm
and 2.5 ppm) produce chromosomal damage to the lymphocytes of bone marrow
cells. (1980, Dow toxicologist).
Inhalation of 1 ppm benzene for a single 6 hour period causes significant
excess of chromosomal breakage in lab animals. (Erexson, 1986). Exposure to
1 ppm of benzene for a short time can cause genetic lesions that may
adversely effect susceptible workers.
Chromosomal breakage in T and B lymphocytes in granulocytos of workers
exposed to low-level benzene. (2002).
Swedish study in 1996 of workers exposed to gasoline found damage to
chromosomes of blood cells at low benzene exposure levels of 0.1 ppm and 0.3
ppm.
Assessing Exposure Levels
Can the worker smell benzene? Detection threshold is between 61 ppm and 97
ppm. (the mean detection level for benzene is 61 ppm and the level at which
the average person knows they are actually smelling benzene is 91 ppm).
A strong odor of benzene in the air represents a benzene level of 700 ppm.
If worker smells gasoline, the estimated constant exposure level is 1.3 ppm
benzene. The gasoline odor threshold is 140 ppm.
Did worker get headaches? If worker has headaches when working around
benzene, the estimated exposure level was between 500 and 1500 ppm.
If worker passed out from benzene exposure, the estimated exposure level was
7500 ppm.
No scientific evidence that cumulative dose has been validated as proper
method for assessing a dose response relationship between benzene exposure
and leukemia.
Peak and intermittent exposures to benzene augment the toxicity of the
cumulative benzene does and present the greatest risk of genetic damage.
Research supports premise that intermittent peak benzene exposure episodes
carries greater risk of developing leukemia than the same cumulative benzene
dose accumulated by a more even mode of exposure.
Can toxicologist rule out other causes of AML in patient with AML who was
occupationally exposed to benzene?
Affidavit, February 1, 2005, Peter F. Infante, Dr.P.H., State of Virginia.
Dr. David Egilman
Dr. David Egilman is a clinical associate professor of community medicine at
Brown University. He is board certified in Internal Medicine and
Preventive-Occupational Medicine. Dr. Egilman studied at the National
Institute of Occupational Safety and Health and the NIH. He has published
over 40 articles including multiple articles on the subject of dose
assessment. He teaches and continues to publish on the topic of development
of scientific knowledge of the workplace in the 20th century and the
corporate, governmental and scientific response to those hazards, including
benzene.
Unequivocal scientific evidence shows that benzene causes AML and doubles
the risk of contraction of AML at very low doses. This relationship has been
generally accepted in the scientific literature for at least 30 years.
Dose estimates used in epidemiology to determine exposures to groups of
workers – not individuals.
Numerous studies show increased ratio > 2 for incidence of leukemia or a
Standard Mortality Ratio > 200 demonstrating that the risk of contracting
leukemia, and specifically AML, after exposure is more than double than
those without exposure. Rate ratio of two not required to establish
causation as causal factors as “relatively low rate ratios” may be equally
or more important than strong associations from a public health perspective.
Benzene exposure precedes AML.
Benzene exposure has specifically been associated with chromosomal changes.
Most petrochemical facilities do not maintain adequate exposure monitoring
programs or do not publish exposure estimates for particular tasks involving
high exposure to benzene or gasoline with benzene.
Quantitative analysis based in part on description of odor and an
understanding of the odor threshold for benzene. Industries use odor
threshold as means of calculating exposure to benzene of their workers.
Consensus that no safe level of exposure has been established for benzene.
Every U.S. government agency looking into the issue of benzene and AML has
determined this dose-response relationship has no threshold . . there is no
level of exposure to benzene that does not raise risk of developing AML.
Smith et al. reported statistically significant excesses of hematotoxicity
in workers exposed to levels of benzene below 1ppm.
The mechanistic and biologic facts concerning benzene and AML are consistent
with the known theories of AML induction accepted in scientific community.
The Mechanism of Benzene-induced Leukemia (Smith, M. Environ Health
Perspectives. 1996 Dec; 104 Suppl 6:1219-25).
The scientific community and regulatory agencies having read the medical and
scientific literature on benzene and leukemia (approximately 80of adult
leukemia is AML.) have uniformly accepted and determined that benzene
exposure causes AML.
Affidavit, February 1, 2005, David Egilman, M.D. Norfolk County,
Massachusetts
Chinese Shoe Factory Study
A study funded by the National Cancer Institute encouraged Chinese and
American scientists to collaborate on a study of the effects of benzene
exposure below 1ppm, the current OSHA Permissible Exposure Limit.
Beginning in 2000, 240 Chinese factory workers who were routinely exposed to
benzene-laced glue in a shoe factory were studied for changes in their blood
cells as a result of benzene exposure.
In the Dec. 3, 2004 issue of Science, the scientists conducting this study
published findings that 109 workers exposed to less than 1ppm benzene
exhibited on average 15-18fewer white blood cells than unexposed workers.
Aside from a decrease in white blood cells, the progenitor cells in the
exposed workers bone marrow were less able to grow and reproduce than those
cells of unexposed workers.
Partial List of Benzene Containing Products
Products Uses
WD-40
Penetrating Oil
Liquid Wrench
Penetrating Oil
Rust-Ban 392
Penetrating Oil
Sunoco Household Oil
Penetrating Oil
3-In-One Electric Motor Oil
Penetrating Oil
3-In-One Household Oil
Penetrating Oil
Gardner Blacktop Driveway Sealer
Driveway Sealer
Gardner EZ STIR Filler Sealer
Driveway Sealer
Parks Furniture Refinisher
Paint/Finish
Parks Adhesive Remover
AD. Remover
Parks Mineral Spirits Paint Thinner
Mineral Spirits
Parks LacquerThinner
Thinner
Parks Brush Cleaner
Brush Cleaner
Parks PRO Liquid Paint Stripper
Stripper
Parks Liquid Strip
Stripper
Parks Lacquer Thinner 6/13/97
Thinner
Parks Adhesive Remover 9/4/98
AD. Remover
Parks Liquid Deglosser 9/4/98
Deglosser
Gumoutregane Premium Gas Treatment
Automotive
Gumoutxtra 1 Tank Carb Cleaner
Automotive
Gumouttune Up Spray
Automotive
Gumoutcarb/Fuel Injector Cleaner (Aerosol)
Automotive
Gumoutcarb/Fuel Injector Cleaner (Liquid)
Automotive
Gumoutdiesel Fuel System Cleaner
Automotive
Gumoutcold Weather Diesel Treatment
Automotive
Gumoutliquid Intake Cleaner
Automotive
Classic Aerosol Wax
Automotive
Champion Carb. Cleaner
Automotive
Champion Flush Off Degreaser
Automotive
Champion Brake Cleaner
Automotive
Champion Cold Galvanize
Automotive
Champion Galv Off?
Champion CS?
Champion N/F 4 Way Penetrating Oil
Penetrating Oil
Champion Stainless Steel Cleaner
Cleaner
Champion X It Out Vandal Mark Remover
Cleaner
Champion Super Lubricant
Lubricant
Champion Spray Paint
Paint/Finish
Champion Flying Insect Killer
Insecticide
Champion Fire Ant Killer
Insecticide
Champion Multi Insect/Lice Killer
Insecticide
Champion Indoor Insect Fogger
Insecticide
Champion Ant & Roach
Insecticide
Champion Metered Insecticide
Insecticide
Bonide Grass, Weed & Vegetation Killer
Yard
Ortho Weed-B-Gone
Yard
Staffel’s Screwwork Compound-U.S.
Formula M 62Insecticide
Dr. Roger's Screw Worm Smear Formula
No. 62
Insecticide
Martin's Formula No. 62 Screw Work Smear
for Horses and Mules
Insecticide
Thoroseal Redi Mix Paint
Paint/Finish
Naptha
Industrial/Lab
VM & P Naptha
Industrial
Benzene levels in Toluene Products
Products Uses
Ethylbenzene
Industrial
Toluene
Industrial/Lab
Toluene Xylene Industrial
Xylene
Industrial
Benzene levels in Organic Solvents
Products Uses
Butadiene
Industrial/Lab
Butene
Industrial/Lab
Cumene Industrial/Lab
Cyclohexanol Industrial/Lab
Cyclohexanol C Industrial/Lab
Dichloropentadiene Industrial/Lab
Isoprene Industrial/Lab
Monochlorobenzene Industrial/Lab
Piperylene Industrial/Lab
Hexane Industrial/Lab
Hexane C
Industrial/Lab
Benzene levels in Solvents and Products.
Products Uses
Asphalts
Construction
Calibrating Fluid
Automotive
Charcoal Lighter Fluid All
Contact cements
C9 Aromatics Industrial/Lab
Dicyclopentadiene Industrial/Lab
Elastomeric Adhesives Industrial/Lab
Ethylbenzene Industrial/Lab
Hexane Industrial/Lab
Hydraulic Fluds Industrial/Lab
Kerosene All
Ink Markers Printing
Lacquer Thinner All
Lantern Fuel & Gas Stove All
Leather Black and Stain Woodworking
Liquid Polish
Liquid Wrenc Automotive
Mineral Spirits All
140* Flash Aliphatic Industrial/Lab
140* Flash Aliphatic: Solvent Industrial/Lab
Paste Polish
Rubber Cement All
Rubber Solvent
Shell DAN
Shell Rubber solvent
Shell Sol Bj-77BG
Shell Sol BJ-19EG
Spray Lubricant
Slop Oil
Solvasol
Solvasol 2
Stoddard Solvent
Trimethybenzene
Unland screen developer
Varnish Makers
Vinyl Thinner
VM & P napthol
Coke Ovens
Companies alleged to have produced benzene:
Age Refining, Inc.
Allied Corporation
Amerada Hess Corporation
Apex Oil Company
Aristech Chemical Company
Arkema, Inc.
AroChem International Inc.
Ashland Chemical Company
Ashland Oil, Inc.
Ashland Petroleum Company
Ashland, Inc.
Atlantic Richfield Company
Atofina PetroChemicals, Inc.
Aux Sable Liquid Products
BASF Corporation
BP America, Inc.
BP Amoco Corp., individually and as successor by merger
to Amoco Corporation;
BP Corporation North America, Inc.
BP Products North America, Inc. f/k/a Amoco Oil Company
Chevron Chemical Company
Chevron Corporation
Chevron Phillips Chemical Company, LLC
Chevron Products Company
ChevronTexaco Products Company
CITGO Petroleum Corporation
Coastal Eagle Point Oil Co.
Coastal Refining and Marketing, Inc.
ConocoPhillips Company
Crown Central Petroleum Corporation
Dow Chemical U.S.A.
El Paso Corporation
EPEC Corporation
EPEC Oil Company
EPEC Polymers, Inc.
Equilon Enterprises, LLC n/k/a Shell Oil Products US
Equistar Chemicals, LP
Exxon Chemical Company
ExxonMobil Corporation
Fina Oil and Chemical Company
Fina, Inc.
Hess Oil Virgin Islands Corp.
Hoechst Celanese Corporation
HOVENSA, LLC
Huntsman Corporation
Huntsman Petrochemical Corporation
Kalama Chemicals, Inc.
Kerr-McGee Corporation
Koch Industries, Inc.
Koch Petroleum Group, LP
Koch Refining Company
Lyondell Petrochemical Company
Lyondell-CITGO Refining Company, Ltd.
Madison Industries, Inc.
Marathon Ashland Petroleum LLC
Marathon Oil Corporation
Mobil Chemical Company
Mobil Oil Corporation
Motiva Enterprises LLC
NOVA Chemicals, Inc.
Occidental Chemical Company
Occidental Petroleum Corporation
Oxy Petrochemicals, Inc.
Phibro Energy USA, Inc.
Phillips Petroleum Company
Phillips Puerto Rico Core Inc.
Quantum Chemical Company
Salomon Inc.
Shell Chemical Company
Shell Oil Company
Southwestern Refining Company, Inc.
Sun Refining and Marketing Co.
Sunoco, Inc.
Texaco Chemical Company
Texaco Inc.
Texaco Refining and Marketing, Inc.
The Coastal Corporationv
Companies alleged to have supplied benzene
Abbott Laboratories
Aceto Corporation, New York
Admiralty Specialty Products Eastern Chemicals
Agrevo U.S.A. Company
Ajay North America, LLC
Akrochem Chemical Co.
Akzo Nobel Coatings Inc.
Albemarle Corporation, Louisiana
Albright & Wilson Americas Inc.
Aldrich Chemical Co. Inc.
Alemark Chemicals - Amsysn Inc., Connecticut
AlIied Signal Inc. (Engineered Materials)
Alliance Chemical
Amber Synthetics - Amsyn Inc., Connecticut
Amerada-Hess Corporation. (Corporate Headquarters - New York)
Amoco Chemical Co., Illinois
Amvac Chemical Corporation
Anderson Development Co.
Angus Chemical Co.
Apollo Colors Inc.
Apollo Scientific Ltd.
Aristech Chemical Corporation
Ashland Distribution, Ohio
Ashland Oil Inc., Kentucky
Austin Chemical Co. Inc.
Avecia Inc. (US Headquarters)
Aztec Peroxides, Inc. (Laporte Group)
B I Chemicals Inc Henley
B.F. Goodrich Chemical Group
BASF Corporation, New Jersey
Bayer Corporation
Bedoukian Research, Inc
Bell Flavors & Fragrances Inc.
Bethelehem Steel Corp., Pennsylvania
Biddle Sawyer Corporation, New York
Bimax, Inc
BioTherm Inc.
Boliden Intertrade Inc.
Borregaard Synthesis Inc. (Production & Sales Office)
BP Chemicals Inc.
Browning Chemical Corp
Cambridge Isotope Laboratories Inc.
Capital Resin Corporation
Carbolabs Inc. (Head Quarters)
Cardinal Industries Inc.,Wisconsin
Cardolite Corporation
CDR Pigments & Dispersions
Cedar Chemical Corporation
ChemDesign Corporation (Headquarters)
ChemFirst Inc.
Chemol Inc.
ChemPacific Corporation
Chemsyn Laboratories
Chevron Chemical Company (Aromatics & Olefins Division)
Chevron Phillips Chemical Company LP
Chino Mines Company
ChiraChem International Chemicals Co.
Chiragene Inc.
Chirex Ltd.
Ciba Specialty Chemicals (Performance Polymers Division)
Ciba Specialty Chemicals (Textile Dyes Division)
Ciba Specialty Chemicals Corp. (Additives Division)
Ciba Specialty Chemicals Corp. (Consumer Care)
Ciba Specialty Chemicals Corporation (Pigments Division)
Ciba-Geigy Corporation
Citgo Petroleum Corporation
Coastal Rafining & Marketing Inc.
Conatus Corporation
Condea Vista Company
Consep Inc. (Speciality Chemicals)
Contract Chemicals, Inc., Virginia.
Cookson Pigments Inc.
Crompton Corporation (Global Corporate Headquarters)
CTC Organics
Cytec Industries Inc.
D & O Chemicals, Inc
Davos Chemical Corporation
Daychem Laboratories Inc.
Deepwater Iodides, Inc.
DeForest Enterprises Inc.
Deltech Corporation
Detrex Corporation
Diaz Chemical Corp., New York
Diaz Intermediates Corp, Arkansas
Drexel Chemical Company
DSM Fine Chemicals Inc.
DSM Pharma Chemicals
Dye Specialties, Inc
Dynamic Sysnthesis
Eastman Chemical Company
El Paso Corporation, Texas
Elan Chemical Company
Elf Atochem North America Inc. (Organic Peroxides Division)
Emkay Chemical Co.
Engelhard Corporation
Enzyme Technologies, Inc., Oregon
Equistar Chemicals, LP, Texas
Esprit Chemical Company, Florida
Esprix Technologies, Florida
Expo Chemical Company, Inc., Texas, USA Expo Chemical Company, Inc.
Exxon Chemical Co.
FabriChem, Inc
Fairmount Chemical Co. Inc.
Ferro Corporation (Grant Chemical Division)
Fina Oil & Chemical Co.
First Chemical Corporation
Flint Hills Resources, LP
FMC Lithium (Headquarters - North America)
Frinton Laboratories Inc.
Frinton Laboratories, Inc., New Jersey
Gelest Inc.
General Electric Co. (Plastics Division)
Generichem Corp
Georgia Gulf Corporation
GFS Chemicals, Inc.
Givaudan Fragrances Corporation (Fragrance production)
GNC Group Inc., North Carolina
Goodyear Tire & Rubber Co. (Chemical Division)
Great Lakes Chemical Corporation (World Headquarters)
Greenwood Products Inc.
Guardian Environmental Technologies, Inc., Connecticut
H.W. Sands Corp.
Hampford Research, Inc
Harcros Chemicals Inc
Hardman Inc
Har-Met International Inc.
Hart Products Corporation
Hatco Corporation
Hawks Chemical Company Ltd.
Henkel Corporation (Organic Products Group)
Hercules Incorporated
Highside Chemicals Inc.
Hilton-Davis Co
Hoechst Celanese Corporation
Honeywell Burdick & Jackson
Howard Hall International, Connecticut
Huntsman Corporation, Utah
Huntsman Petrochemical Corporation
Huntsman Polymers
Hurley Chicago Co., Inc.
ICC Chemical Corporation, New York
ICI Americas Inc
Independent Chemical Corporation
Inolex Chemical Company
Inspec U.S.A. Inc.
International Flavors & Fragrances Inc.
International Specialty Products Inc.
InterSpex Products, Inc, California
Intertrade Holdings Inc., Tennessee
Isotec Inc. (Sigma Aldrich)
J. T. Baker (Division of Mallionkrodt Baker Inc. - Corporate Headquarters)
James River Corp
Jarchem Industries Inc
JBL Scientific Inc
JLM Chemicals Inc. (JLM Industries Inc.)
JLM Industries Inc. (Corporate Headquarters)
Kalama Chemical Inc.
Karl Fischer Export GmbH
Kenrich Petrochemicals Inc.
Kincaid Enterprises, Inc
Kingchem Inc.
King's Laboratory Inc.
Kira Corporation
Koch Chemical Company, Kansas
Lancaster Synthesis Inc.
LANXESS, Pennsylvania
Lever Brothers Co. (Business Unit)
Lidochem Inc.
LignoTech USA, Inc. (Sales Office)
Lobeco Products Inc.
Lonza, Inc
Lord Corporation
Lyondell Chemical Company
Lyondell Petrochemical Company, Texas
Magruder Color Co. Inc
Mallinckrodt Inc., Missouri
Man Corporation, Utah
Marathon Ashland Petroleum LLC
Mayzo Inc.
McINTYRE Group, Ltd.
Midac Corporation, California
Miljac, Inc, Connecticut
Millennium Specialty Chemicals Inc. (Jacksonville Plant)
Mitsui & Co. (U.S.A.) Inc
Mobil Chemical Company (Petrochemicals Division)
Molecular Rearrangement, Inc
Monomer-Polymer & Dajac Labs, Inc, Pennsylvania
Monomer-Polymer and Dajac Laboratories Inc., Pennsylvania
Monsanto Co.
Montco Research Products Inc.
Morre-Tec Industries, Inc, New Jersey
Mytech, North Carolina
Neuchem Inc.
NIPA Hardwicke Inc.
Noah Technologies Corporation, Texas
Nobel Chemicals, Inc.
Norman, Fox & Co.
Norquay Technology Inc.
Norse Laboratories
NovaChem Corporation
Novartis Crop Protection Inc.
NSC Technologies (Unit of Monsanto Company)
Oakwood Products Inc.
Occidental Chemical Corporation (Petrochemicals Group)
Occidental Chemical Corporation
Olympus Services LLC. (HQ & Customer Service)
Optima Chemicals Group LLC
Organics Division - Witco Corporation
Otsuka Chemical Co. Ltd.
Para-Chem
PCL Group Inc.
Pechiney World Trade (USA) Inc., Connecticut
Penta Manufacturing Co., (ME), New York
Petra Research, Inc.
Petrobras Petroleo Brasileiro S.A. (New York Office)
Pfaltz & Bauer Inc., Connecticut
Pfister Chemical Inc.
Pharmrite, North America Corp.
Phibro Energy USA Inc.
Phillips Chemical Company
Phillips Puerto Rico Core Inc.
PHT International Inc. (Corporate Headquarters)
Pierce Chemical Co.
Pilot Chemical Company
PMC Global Inc.
PMC Specialities Group Inc.
Polymer Applications Inc.
Polysciences Inc.
PPG Industries Inc., Louisiana
Pressure Chemical Co.
R S A Corp, Connecticut
R. W. Greeff & Co. Inc.
R.T. Vanderbilt Co. Inc.
Rainbow Chemicals Company, Lake Bluff, Illinois
Regis Technologies, Inc.
Reichhold Chemicals Inc.
Rhodia Inc. (Fine Organics Division)
Rhodia Pharma Solutions, New Jersey
Rhone-Poulenc Inc. (Surfactants & Specialties)v
Richman Chemical Inc., Pennsylvania
Ricon Resins Inc.
Rieke Metals Inc.
Rit-Chem Co Inc, New York
Rohm & Haas Co.
RSA Corp.
Rubicon Inc.(joint venture), Louisiana
Ruetgers-Nease Chemical Co., Inc.
Ruger Chemical Co. INc
Rutgers Organics Corporation
Ryte Products Inc.
Salsbury Chemicals Inc.
Sartomer Company
Sattva Chemical Co.
Schenectady International Inc.
Schweizerhall Inc
Scott Specialty Gases Inc. (Detroit Area)
Service Chemical Inc.
Shell Atlantic Services Company
Shell Chemical LP (Sales Office)
Sigma Chemical Inc.
Sigma-Aldrich Corporation
Silar Laboratories
Sithean Corp.
Skymart Enterprises Inc.
Sloss Industries Corporation, Alabama
SmithKline Beecham
Solutia Inc.
Southern Texas Chemical Corp.
Sovereign Chemical Company
Specialty Industrial Products Inc.
Spectrum Chemicals & Laboratory Products, California
SPS Alfachem
SST Corporation
Standard Chlorine Chemical Co. Inc.
Star Enterprise
Stepan Company
Sterling Chemicals Holdings, Inc.
Strem Chemicals Inc.
Sun Chemical Corp.
Sun Company Inc.
Sunoco Chemicals
Synasia Fine Chemicals Inc., New Jersey
Synchem Inc.
Syntech Labs Inc.
Synthetech Inc.
Synthon Corporation
Teva Pharmaceutical USA
Texaco Refining & Marketing Inc.
The Chemical Company, Rhode Island
The Dow Chemical Co., Michigan
Tiarco Chemical
Tilley Chemical Co. Inc.
Time Products
Tomen (America) Inc.
Total Specialty Chemicals, Inc., Connecticut
Transammonia, Inc., New York
Transworld Chemicals Inc.
Tri Quest LP
TR-Metro Chemicals Inc.TR-AMC Chemicals
Tulstar Products Inc.
Ultramar Diamond Shamrock Corporation (Merger of Valero Energy Corporation
(Valero Marketing & Supply Company)
Ungerer & Co. Inc.
Union Carbide Corporation
Uniroyal Chemical Corporation
United Phosphorus Inc. (North American Headquarters)
Unitex Chemical Corporation
Universal Preservachem Inc.
UOP
UPT Chemicals Inc.
US Chemicals Inc., Connecticut
Velsicol Chemical Corporation
Vilax Corp.
Vivion Inc.
Wall Chemical Corp.
Warner-Lambert Company
Westco Chemicals Inc, California
Westlake Styrene Corporation
Wilshire Chemical Co. Inc.
Witeg Scientific
Wm E Phillips Co.
Wyckoff Chemical Co., Inc
Zeneca Ag Products
Zeneca Specialties
COMMON DEFENDANTS
3M manufactured and distributes benzene containing adhesives and consumer
products.
Ameripol Synpol Corporation manufactured and supplied synthetic rubber
products containing benzene.
BP Amoco Chemical Company manufactured and distributed benzene containing
polymers.
BP America Production Company manufactured and distributed benzene
containing oils and fuels.
Chase Product Company manufactured and supplied benzene containing
automotive and other home-products such as cleaners, disinfectants and
paints.
CIBA Specialty Chemicals Corporation manufactured and supplied chemicals
containing benzene for use in automobiles, textiles, plastics, paper and
home and personal care products.
CPS Chemical Company, Inc. manufactured industrial organic chemicals
containing benzene.
The Dow Chemical Company manufactured chemicals and plastics containing
benzene for the following industries: adhesives and sealants, automotive,
chemical processing, oil, gas, mining, paints plastics and rubber
Dow Corning manufactured products containing benzene serving industries
including automotive, aviation, aerospace, beauty and personal care,
chemical manufacturing, compound semiconductor, construction, household and
cleaning, imaging, industrial assembly and maintenance, mold making, oil and
gas, paints and ink, photonics, plasma, plastics, power and utilities,
pressure sensitive, pulp and paper, rubber fabrications, solar, textiles and
leather.
E.I. DuPont de Nemours and Company manufactured chemicals containing benzene
to be used in industrial end products and consumer end products, including
abrasives, additives, adhesives, building and construction, carpet and
flooring, cleaning products and chemicals, coatings, consumer products,
container resins, displays, fabric, fibers, films, flocculants,
flouropolymers, food, fuel cell components, fungicides, herbicides,
industrial chemicals, inoculants, insecticides, laminates, licensing, paint
and coating, personal protection, PET technology, plastics, polymers,
polyerethanes, printing and proofing, refractory, seed, specialty chemicals,
and transformers.
Ethyl Corporation manufactured and distributed benzene-containing diesel
cetane improver and gasoline performance additives.
GATX Terminals Corporation received and supplied benzene or benzene
containing petroleum products.
Gulf Oil Limited Partnership manufactured and distributed oil products,
kerosene and motor fuels.
Honeywell International Inc. manufactured and supplied chemicals containing
benzene.
Huntsman manufactured, produces and distributed base chemicals including
benzene and cyclohexane.
Lyondell Petrochemical Company manufactured and marketed chemicals and
polymers containing benzene for automobile parts, home building materials,
household products, carpeting, furniture, wall coverings, fabrics and
personal grooming aids.
National Starch and Chemical Company manufactured and distributed benzene
containing glues and adhesives.
Pharmacia Corporation, f/k/a Monsanto Company, manufactured benzene
containing products including lawn care weed control products.
Pre-Coat Metals manufactured benzene containing building materials.
Radiator Specialty Company manufactured benzene containing products
including Liquid Wrench and Valvemedic.
Sinclair Oil Corporation manufactured and distributed benzene containing
petroleum products and lubricants.
South Hampton Refining Company manufactured and distributed benzene
containing petrochemical products.
Sun Chemical Corporation manufactured benzene containing inks and coatings.
Sun Oil Company manufactured and distributed benzene containing
petrochemical products and chemical intermediates.
Turtle Wax, Inc. manufactured benzene containing car care products.
Union Carbide Corporation manufactured benzene containing chemicals and
polymers. Union Carbide chemicals and polymers are found in paints and
coatings, packaging, wire and cable, household products, personal care,
pharmaceuticals, automotive, textiles, agriculture and oil and gas.
United States Steel Corporation manufactured benzene containing raffinate
used in oils and lubricants.
What Are the Risk Factors and Causes of Childhood Cancer?
Many pediatric cancers occur very early in life and many parents want to
know why. Some of these cancers are the result of a familial predisposition
(cancer runs in family). Radiation exposure, Toxic Exposure and Pesticides
contribute to certain types of childhood cancers. Unlike cancers of adults,
childhood cancers are not significantly related to lifestyle-related risk
factors such as tobacco or alcohol use.
National Cancer Institute Research on Childhood Cancers
In the United States in 2005, approximately 9,510 children under age 15 will
be diagnosed with cancer and about 1,585 children will die from the disease
(1). Although this makes cancer the leading cause of death by disease among
U.S. children 1 to 14 years of age, cancer is still relatively rare in this
age group with, on average, 1 to 2 children developing the disease each year
for every 10,000 children in the United States.
Among the 12 major types of childhood cancers, leukemias (blood cell
cancers) and brain and other central nervous system tumors account for over
one-half of the new cases. About one-third of childhood cancers are
leukemias. The most common type of leukemia in children is acute
lymphoblastic leukemia. The most common solid tumors are brain tumors (e.g.,
gliomas and medulloblastomas), with other solid tumors (e.g.,
neuroblastomas, Wilms’ tumors, and sarcomas such as rhabdomyosarcoma) being
less common.
Over the past 20 years, there has been some increase in the incidence of
children diagnosed with all forms of invasive cancer, from 11.5 cases per
100,000 children in 1975 to 14.6 per 100,000 children in 2002. During this
same time, however, death rates declined dramatically and 5-year survival
rates increased for most childhood cancers. For example, the 5-year survival
rates for all childhood cancers combined increased from 55.9 percent in
1974–1976 to 78.6 percent in 1995–2001 (2). This improvement in survival
rates is due to significant advances in treatment, resulting in cure or
long-term remission for a substantial proportion of children with cancer.
Long-term trends in incidence for leukemias and brain tumors, the most
common childhood cancers, show patterns that are somewhat different from the
others. Childhood leukemias appeared to increase in incidence in the early
1980s, with rates in the preceding years at fewer than 4 cases per 100,000.
Rates in the succeeding years have shown no consistent upward or downward
trend and have ranged from 3.7 to 4.8 cases per 100,000 (2).
For childhood brain tumors, the overall incidence rose from 1975 through
2002 (from 2.3 to 3.5 per 100,000), with the greatest increase occurring
from l983 through l986. An article in the September 2, 1998, issue of the
Journal of the National Cancer Institute suggests that the rise in incidence
from 1983 through 1986 may not have represented a true increase in the
number of cases, but may have reflected new forms of imaging equipment
(magnetic resonance imaging or MRI) that enabled visualization of brain
tumors that could not be easily visualized with older equipment. Other
important developments during the 1983–1986 period included the changing
classification of brain tumors, which resulted in tumors previously
designated as “benign” being reclassified as “malignant,” and improvements
in neurosurgical techniques for biopsying brain tumors.
The causes of childhood cancers are largely unknown. A few conditions, such
as Down syndrome, other specific chromosomal and genetic abnormalities, and
ionizing radiation exposures, explain a small percentage of cases.
Environmental causes of childhood cancer have long been suspected by many
scientists but have been difficult to pin down, partly because cancer in
children is rare, and partly because it is so difficult to identify past
exposure levels in children, particularly during potentially important
periods such as pregnancy or even prior to conception. In addition, each of
the distinctive types of childhood cancers develops differently—with a
potentially wide variety of causes and a unique clinical course in terms of
age, race, gender, and many other factors.
A monograph based on data from the National Cancer Institute’s (NCI)
Surveillance, Epidemiology, and End Results (SEER) Program was published in
1999 on U.S. trends in incidence, mortality, and survival rates of childhood
cancers. In the monograph, information about known, suspected, and possible
risk factors is summarized in more detail. It is available at
www.seer.cancer.gov on the Internet. More
up-to-date incidence, mortality, and survival information for children (<15
and <20 years of age) is available at
www.seer.cancer.gov on the Internet, in
sections 28 and 29.
Results of Recent Studies Supported by the NCI
For several decades, the NCI has supported national and international
collaborations devoted to studying causes of cancer in children. Some of the
key findings from recent studies include:
High levels of ionizing radiation from accidents or from radiotherapy have
been linked with increased risk of some childhood cancers;
Children treated with chemotherapy and radiation therapy for certain forms
of childhood and adolescent cancers, such as Hodgkin’s disease, brain
tumors, sarcomas, and others, may develop a second primary malignancy;
Low levels of radiation exposure from radon were not significantly
associated with childhood leukemias;
Ultrasound use during pregnancy has not been linked with childhood cancer in
numerous large studies;
Residential magnetic field exposure from power lines was not significantly
associated with childhood leukemias;
Certain types of chemotherapy, including alkylating agents or topoisomerase
II inhibitors (e.g., epipodophyllotoxins), may cause increased risk of
leukemia;
Pesticides have been suspected to be involved in the development of certain
forms of childhood cancer based on interview data. However, interview
results have been somewhat inconsistent, and have not yet been validated by
physical evidence of pesticides in the child’s body or environment;
No consistent findings have been observed linking specific occupational
exposures of parents to the development of childhood cancers;
Several studies have found no link between maternal cigarette smoking before
pregnancy and childhood cancers, but increased risks were related to the
father’s prenatal smoking habits in studies in the United Kingdom and China;
Little evidence has been found to link specific viruses or other infectious
agents to the development of most types of childhood cancers, though
investigators worldwide are exploring the role of exposure of very young
children to some common infectious agents that may protect children from, or
put them at risk for, developing certain leukemias;
Recent research has shown that children with AIDS, like adults with AIDS,
have an increased risk of developing certain cancers, predominantly
non-Hodgkin’s lymphoma and Kaposi’s sarcoma. These children also have an
additional risk of developing leiomyosarcoma (a type of muscle cancer);
Specific genetic syndromes, such as the Li-Fraumeni syndrome,
neurofibromatosis, and several others, have been linked to an increased risk
of specific childhood cancers.
NCI’s Current Research on Childhood Cancer
NCI is currently funding a large portfolio of studies
(www.researchportfolio.cancer.gov) looking at the causes and most
effective treatments for childhood cancers at an estimated cost of $166
million for Fiscal Year 2004. Ongoing investigations include:
Studies to identify causes of the cancers that develop in children
The Children’s Oncology Group (www.childrensoncologygroup.org) is
evaluating potential risk factors for a variety of childhood cancers. Very
large studies of childhood acute lymphoblastic leukemia, acute myeloid
leukemia, non-Hodgkin’s lymphoma, primitive neuroectodermal tumors of the
brain, astrocytoma, and neuroblastoma have recently been completed, while
investigations of germ cell tumors are ongoing. These studies have included
evaluation of diverse categories of suspected and possible risk factors
including exposures linked to infectious agents (e.g., enrollment in
daycare, spacing of siblings, and infectious diseases contracted during the
first 12 months of life); parental occupational exposures to radiation or
chemicals; parental medical conditions during pregnancy or before
conception; parental, fetal, or childhood exposures to environmental toxins
such as pesticides, solvents, or other household chemicals; maternal diet
during pregnancy; early postnatal feeding patterns and dietary factors;
reproductive history and other reproductive factors; and familial and
genetic factors.
The role of maternal exposures to oral contraceptives, fertility drugs, and
diethylstilbestrol (DES) is being investigated in several ongoing studies.
Researchers are looking at the role of familial and genetic disorders.
The cancer risk of HIV-infected children is under investigation.
The Childhood Cancer Survivor Study (see below) is evaluating the risks of
second cancers related to radiation therapy and chemotherapy received by
survivors of childhood cancer as part of treatment for their primary cancer.
Monitoring of U.S. and international trends in incidence and mortality rates
for childhood cancers
By identifying places where high or low cancer rates occur, researchers can
uncover patterns of cancer that provide important clues for further in-depth
studies into the causes and control of cancer.
Studies to better understand the biology of childhood cancer, with the hope
that this understanding will lead to new treatment approaches that target
critical cellular processes required for cancer cell growth and survival
Researchers are investigating fundamental cellular processes, such as signal
transduction, cell cycle control, transcriptional regulation, and tumor
suppressor gene inactivation, to develop new prevention and treatment
strategies.
Projects designed to improve the health status of survivors of childhood
cancers
A major component of NCI’s survivorship research efforts is the Childhood
Cancer Survivor Study (CCSS), which was created to learn about the long-term
effects of cancer and its therapy on childhood cancer survivors
(www.cancer.umn.edu). This knowledge may be useful in
designing future treatment protocols and intervention strategies that
increase survival and minimize harmful health effects. In addition, CCSS
serves to educate survivors about the potential impacts of cancer diagnosis
and treatment on their health. CCSS includes 14,000 childhood cancer
survivors diagnosed with cancer before the age of 20 between 1970 and 1986,
and approximately 3,500 siblings of survivors who serve as control subjects
for the study. The CCSS cohort was assembled through the efforts of 27
participating centers in the United States and Canada and has been
coordinated by investigators at the University of Minnesota. Funded by the
NCI, the study was initiated in 1993 and completed in 2004.
Articles Related to the Probable Causes
of Childhood Cancer and the Disease
Cell Mutation and Translocation Types
Protecting Your Health - List of Diseases and their known Causes
More on Leukocytosis - Caylee had
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National Superfund Sites
MMR & Leukemia Reports
Dog Bites and Staph Infections
The Importance of CBC Tests and what they can determine
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Danyal Ali |
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Paul Tungol |
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Caylee Cepero |
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Robyn Nemitz |
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Brittany Zipter |
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