THE CONVERGENCE OF ENVIRONMENTAL INFLUENCES
AS POTENTIAL PRECIPITATING FACTORS OF
AML-M2
by
Meredith Tuttle
Submitted in Partial Fulfillment ofthe Requirements
for the Degree of
Master ofScience
in the
Chemistry
Program
SCHOOL OF GRADUATE STUDIES
YOUNGSTOWN STATE UNIVERSITY
JUNE 2000
THE CONVERGENCE OF ENVIRONMENTAL INFLUENCES
AS POTENTIAL PRECIPITATING FACTORS OF
AML-M2
Meredith Tuttle
I hereby release this dissertation to the public. I understand this dissertation will be
housed at the Circulation Desk ofthe University library and will be available for public
access. I also authorize the University or other individuals to make copies ofthis
dissertation as needed for scholarly research,
Signature:
lStudent /
)~ 7J 2-00<>/ (.
Approvals:
~_&--s;;committ~ember
'-'VL.UUu'ttee Member
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/ Date
Date
ABSTRACT
Acute myeloblastic leukemia is known as an insidious, often times fatal,
disease; however, its etiology has not been fully elucidated. This work was
conducted so as to explore the potential environmental influences that may
converge and precipitate a myelodysplastic event or even a leukemic
disease state. Environmental chemicals were the primary focus of this
investigation, including: the fertility drug clomiphene citrate, (Clomid); and
a combination of pesticides commonly applied to produce. Water samples
were extracted from Berlin Lake, as well, to gauge recreational water
contamination. The Berlin Lake water samples were found to contain a
number of hydrocarbon contaminants; with the main supplier of such
contaminants believed to be the 'fuel?dumping' of recreational crafts.
STATEMENT OF PROBLEM
This thesis attempts to marry two not unlike disciplines, pathology and
environmental chemistry; in that this work explores the
hematology/pathophysiology of acute myeloblastic leukemia (M2)-in
relation to this disease state's etiology. And it is within the etiology of AML
that this effort becomes totally intercalated with environmental chemistry.
Environmental chemistry, the term itself, quite often evokes ideas or
images of chemical pOllutants-what are they? Where are they? What
chemistry/reactions are they capable of?-an area of chemistry which is, by
many, never actually thought of in tandem with the medical arts. For if it
were, perhaps questions such as: What is the minimum lifetime level of
exposure for that compound? What chromosomal aberrations are
associated with such an exposure? Are there consequences to in utero
exposure? Will these compounds ever safely degrade? Would be more
closely associated with this discipline. It is just such questions that will be
brought to the fore in this thesis, regarding AML. The author would like to
not only introduce AML as a possible "environmental disease", but to also
present a somewhat rudimentary case study of a nine year old boy recently
diagnosed with AML M2; a diagnosis which was critically influenced by the
child's annual exposure to a contaminated water source.
TABLE OF CONTENTS
CHAPTER 1 How blood cells are produced????????????????1?7
CHAPTER 2 Description and function of blood cells???8?16
CHAPTER 3 Acute myelogenous leukemia....?.??.?...????17?23
CHAPTER 4 The pharmaceutical suspects????????????????24?29
CHAPTER 5 The environmental suspects??????????????????30?43
CHAPTER 6 The genetics?????????????????????????????????????????44?51
CHAPTER 7 Materials and methods?????????????????????????52?55
CHAPTER 8 Results?????????????????????????????????????????????????56?61
CHAPTER 9 Concluding remarks??????????????????????????????62?65
REFERENCES???????????????????????????????????????????????????????????66?69
APPENDIX 1 Medical Data??????????????????????????????????????70
Cytogenetics???????? ?????71
Flow cytometry reports???????????????????????72
Surgical pathology reports??????????????????73
Hematopathology???????????????????????????????74
APPENDIX 2 Blood values??????????????????????????????????????75
APPENDIX 3 Envi ronmental data????????????????????????????76
Map of Berlin Lake?????????????????????????????77
EPA documentation???????????????????????????78
APPENDIX 4 IR spectra??????????????????????????????????????????79
APPENDIX 5 Human Subjects Protocol
Review Form?????????????????????????????????????80
ii
Chapter 1: How Blood Cells are Produced
Hematopoietic Tissue
Blood cell production occurs at various points of or within the human
body during the course of development from embryonic through adult life.
Formation of the blood cells first begins within the yolk sac of the embryo;
later shifting to the liver and to a lesser extent the spleen-allowing these
organs to then become the dominant production sites between the second
and seventh months of gestation. The liver and spleen are then
superceded by the bone marrow-which then serves as the main and most
important site of blood cell production post-partem. Lymphocyte
production is the only exception to this; for their production occurs to a
greater extent in the lymphoid tissues post-partem. Hemapoietic tissue
occupies all of the cavities within the bones of the neonate; with
subsequent corporeal development however, this tissue becomes localised
in the cavities of the upper shafts of the femur, and humerus, the pelvis,
spine, skull and bones of the thorax. The total volume of hematopoietic
tissue within the adult body is between one and two liters. It is referred to
as red marrow primarily due to its macroscopic presentation; the bone
marrow within the more peripheral regions of the body/skeleton is
predominantly composed of adipose cells/adipocytes and is known as
yellow marrow. Yellow marrow claims a volume of between one and two
liters as well; serving as a reserve space into which hematopoietic tissue
can expand if, for example, the body should suffer an increased need for
blood cells and their production. Extramedullary hemapoiesis or
hemopoietic activity exclusive to the liver and spleen occurs in adult life
only in rather rare pathological conditions.1
Bone Marrow Structure
The red marrow, as found between or intermingled with the trabeculae
of bone within the marrow cavitiy, proper, houses specialized connective
tissue cells: reticulin fibrils, blood vessels, fat cells, nerves and
macrophages-along with cells of the lymphoid and hemopoietic series.
Fine reticulin fibrils help to create a supportive framework for the bone
marrow components. These fibrils extend/reach from the endosteum of
the bony trabeculae to the vascular sinusoids and are believed to be
produced by the adventitial reticular cell.
Adventitial Reticular Cell
The abluminal or adventitial surface of the marrow's vascular sinus
consists of reticular cells. These cell bodies are contiguous with the
vascular sinus, thereby contributing to a portion of its adventitial coat. The
adventitial reticular cell possesses extensively branched cytoplasmic
processes which enwrap the outer wall of the marrow's sinus-forming an
adventitial sheath.2
The reticular cells synthesize argentophilic fibers that, in conjunction
with their cytoplasmic processes, reach into the hemopoietic recesses of
2
the/ within the marrow; these fibers help to construct a framework upon
which hemopoietic cells rest. The cell bodies, their broad processes and
fibers help to compose the reticulum of the marrow.2 The membranes of
the adventitial reticular cells are known to contain high levels of alkaline
phosphatase; express COlO, C013 and class 1 HLA antigens; are positive
for the 6/19 antibody; express nerve growth factor receptors; differentiate
along the smooth muscle pathway; and contain alpha smooth muscle actin,
vimentin, laminin, fibronectin and collagens 1,3 and 4. These reticular
cells are commonly C034 antigen?negative.2
Fibronectin
Fibronectin is known to localize at the sites of hemopoietic cell and
marrow stromal cell attachment. Early erythroid progenitor cells attach
themselves to the cell?binding domain of fibronectin. Additionally,
adhesion of granulocyte hemopoietic cells to stroma is mediated for the
most part by fibronectin. Such a binding can be strengthened via protein
kinase C activators-phorbol esters, for example?thereby suggesting the
possible involvement of integrin receptors in the cell?attachment process.2
Collagen
Collagen types 1 and 3 are produced by fibroblasts within the
marrow and are associated with microvascular walls; type 4, however, is
confined to endothelial?type cells and their basal lamina. Marrow derived
fibroblasts along with stromal cells, synthesize collagens 1, 3,4,5, and 6.2
3
Laminin
Laminin is a multidomain glycoprotein with both mitogenic and
adhesive sites; it is a main component of the marrow extracellular matrix
and basement membranes. This glycoprotein reacts with collagen type 4
and assorted proteoglycans to regulate leukocyte chemotaxis. In a similar
manner, CD34 positive granulocytic progenitors, mature monocytes, and
neutrophils attach to laminin. Laminin is believed to have a part in
strengthening adhesive interactions with integrin receptors, specifically
receptors aSrn and a6p1-on the surface of hemopoietic cells within the
cytomatrix.2
Thus, it becomes apparent that marrow structure is critical for proper
hemopoietic activity; for it essentially provides a framework-as generated
by the adventitial reticular cell population, reinforced by the likes of
fibronectin, collagen and laminin-upon which or within which the
hemopoietic cell hierarchy is able to attach and differentiate. It is with this
structure then that the majority of the blood cell population, within the
general circulation of the body, is maintained.
With this juncture in the discussion, it becomes critical to recognize
and/or accept several generalisations concerning bone marrow, before
hemopoiesis-as involving blood cell production and differentiation-is able to
be considered. These generalisations are as follows:
1. in marrow there exists a hierarchy of hemopoietic cells;
4
with the primary or initial cell being referred to as the
multipotential stem cell;
2. stem cell differentiation is unidirectional and is closely aligned
with the restriction of any cell renewal capacity;
3. proliferation of the stem cells is wholly dependent upon contact
with the marrow's stromal cells;
4. the total overall proliferation and differentiation of stem cells is
regulated by local and systemic growth factors and their
accompanying inhibitors.3
Hemopoiesis
It is universally accepted that blood cells develop from a small
population of stem cells or progenitor cells within marrow; which maintain
their population via self-replication and also give rise to precursors of
various other blood cells.! The progenitor cells spend the majority of their
existence in an out-of-cycle Go phase; during this phase of the cell cycle
they are preoccupied with DNA repair and other forms of genetic
maintenance. Throughout the duration of this rather quiescent phase, the
cells are less susceptible to genetic damage by ionizing radiation,
alkylators, and viruses. As the number of cells reaching the terminus of the
Gl phase increases-stem cells are prepared to react within an approximate
thirty minute window to an array of stimuli; either carried to them via the
general circulation or as produced directly in the marrow.3
5
Following this post-GI accumulation and subsequent cellular activation
towards differentiation, proliferative activity progressively increases. It is at
this post GI accumulation that the blood cells are said to be in the
maturation compartment; in which a cascade of morphological changes
occurs without cell division-to yield the mature end-cell. The range of
different blood cell series which can develop from a particular precursor
progressively declines as the precursor comes to possess an increased
degree of differentiation.!
The Stem Cell
The stem cell or hemopoietic stem cell is often considered as an
example of the most primitive cell type. This fundamental cell is able to
divide; however a subset of the stem cell population will remain unmodified
during the maturation or stem cell phase. The cells that remain in this
"un-specified" state are/compose the pluripotential cell population.4
A small number of the cells in the maturation or stem cell compartment
are forever undergoing mitosis; this constant cell-set is responsible for
maintaining a relatively homeostatic blood cell population. For example,
when the demand for blood cells is intensified, the percentage of dividing
stem cells-both uncommitted and committed-increases. This stimulus to
differentiate for committed cells of each cell line, is mediated by
glycoprotein inducers or hemopoietins; including erythropoietin,
thrombopoietin and assorted leukopoietins.4
6
It is this complex cascade of hemopoietic events, as occurring within
the bone marrow, that produces the blood cells that sustain mammalian
life. Upon closer examination, however, there becomes apparent an
intrinsic fragility to this system of red blood cell (RBC), platelet, and white
blood cell (WBC) production; these cells-to be identified in the chapter
forthcoming-are not only at the very foundation of life, but, as it will be
shown, are also the first to fall victim to mutation and disease.
7
Chapter 2: Description and Function of Blood Cells
Red Blood Cells
The mature red blood cell is a rather unique development in cellular
evolution; for it has developed so as to exclude all biosynthetic organelles 
such as nucleus, ribosomes and mitochondria. Essentially, the rbc has
become a sort of hematologic minimalist, in that it possesses just enough,
biochemically speaking, to adequately fulfill its role of oxygen deposition
and carbon dioxide removal within the body. The rbc has developed into a
rather flexible biconcave torus shape?brilliantly formed so as to maneuver
through the blood vessels composing the body's microcirculation. The
mature rbc will travel in upwards of 1 million times through the body?
equaling a distance of about 300 miles. A normal, mature red blood cell
will measure approximately 7.8 J-lm in diameter, 1?7 J-lm in width and have
a volume of 94 ? 14 fL and a surface membrane area of 135 ? 16 sq J-lm.
Such a surface area enables these cells to not only endure the hydraulic
bending forces of non-laminar circulation, but adjust to various
instantaneous contortions without damage or retardation of progress.
Additionally, the biconcave shape of these corpuscles allows for a quite
favorable surface area to volume ratio; thereby allowing them to travel
across and/or through cylindrical capillaries only 5 J-lm in diameter, via the
adoption of an umbrella shape transverse to the direction of blood flow.3
8
Membrane Properties
The structural elements of the red blood cell membrane that make the
aforementioned progress possible include:
1. a lipid bilayer, composed of phospholipids and non-esterified
cholesterols; providing a semipermeable barrier between the
internal cell cytosol environment and the external environment of
the blood stream, proper;
2. transmembrane proteins;
3. a membrane skeleton that essentially sheathes the internal or
cytosolic side of the cell-affording it (the cell) a high degree of
structural stability or integrity.2
Composition
The vast majority of the membrane's phospholipids are
phosphoglycerides-consisting of a glycerol backbone; the hydrophobic long 
chain fatty acids are anchored to glycerol's first two carbons. The
residues, which determine phospholipid specificity are linked to the third
carbon of glycerol by means of phosphoester linkages and are exposed at
one of the lipid bilayer surfaces. The involved phosphoglycerides are of the
following mix: 27% of the total phospholipids-phosphatidylethanolamine;
28%-phosphatidylcholine; 13%-phosphatidylserine, along with
phosphatidylinositol. Sphingomyelin constitutes the other phospholipid
contributor; it consists of a hydrophilic moiety identical to that of
9
phosphatidylcholine; however, the hydrophobic region is composed of
ceramide. It is important to note that ceramide contains sphingosine along
with a fatty-acyl side chain attached to sphingosine's amino group. In
addition, cholesterol fits into the membrane in its unesterified form.2
Cell Surface
The surface of the rbc is fortified via neuraminic acid residues, which
impart a negative surface charge to the cell. Any deviation in cell surface
charge is anything but salubrious in regards to the health of the
erythrocyte. The red blood cell surface antigens are found on the
glycolipids; ie the glycosphingolipids or upon the externally exposed
portions of transmembrane proteins or their carbohydrate side chains.2
Membrane Permeability
The normal erythrocyte membrane is virtually impermeable to
monovalent and divalent cations. This helps to maintain a high potassium,
low sodium, low calcium cellular content. Anions, however, are exchanged
via the anion transport protein. The rbc cell membrane is also known to
contain at least one water channel protein that facilitates the rapid
movement of water molecules across the membrane; because of these
channels, the erythrocyte behaves as a perfectly, or very nearly so, run
osmometer. Glucose is carried via a glucose transporter protein, while
larger, charged molecules do not travel across the rbc cell membrane.2
10
Red Blood Cell Function
The ultimate design of the erythrocyte is the ability to transport oxygen
and carbon dioxide, the respiratory gases. Hemoglobin picks up oxygen in
the pulmonary capillaries and delivers it, via the rbc, to tissue capillaries;
within the tissues, oxygen is exchanged for carbon dioxide-a byproduct of
cellular metabolism. A human, at rest, consumes approximately 250mL of
oxygen and exhales around 200mL of carbon dioxide, every minute.
Dissolved as a gas in plasma water, only about 5mL of oxygen can be
delivered to needy tissues each minute. Whole blood is capable of
delivering 200 ml of oxygen/liter, due primarily to red cell hemoglobin, to
tissues within the body. For this oxygen delivery to occur, hemoglobin
must bind oxygen with an intensity that allows it to be removed from
pulmonary capillaries at high oxygen tensions; while still being able to
deliver/unload oxygen at the decrease oxygen pressure of the tissues;
hemoglobin must meet/attach to oxygen with flawless affinity.3
Platelets
Platelets are formed in the Golgi region of the cytoplasm of
megakaryocytes and are released into the blood via cytoplasmic
fragmentation. Thrombocytopoiesis is under the dictate of thrombopoietin.
Although the majority of the blood's platelets are produced by
megakaryocytes within the bone marrow, a small number is believed to be
11
derived from pulmonary megakaryocytes.4 Platelets store a number of
molecules that influence platelet function, vascular tone, fibrinolysis and
wound healing; these compounds are released upon platelet activation.2
The mean diameter of platelets is variable; generally the platelet is
between 1.5 and 2.5 Jlm across, only about 1/3 to 1/4 the diameter of rbc's.
Platelets have even been observed to possess filopodia-or long, thin
processes extending outward from the platelet body proper.2 Platelets
possess a glycocalix, which extends 14 to 20 Jlm from the cell surface.
This 'coat' is believed to consist of membrane glycoproteins, glycolipids,
mucopolysaccharides and adsorbed plasma proteins. The platelet surface
is host to a network of indentations, thought to represent openings of the
cell's open canalicular system, a complex channel system that
communicates through out the cell. In addition, platelets, in an electric
field, react or move as is they were influenced by a net negative surface
charge. This net negative surface charge is created, in part, by sialic acid
residues attached to proteins and lipids along the cell-surface. The overall
electrostatic repulsion created via this charge, is believed to aide in the
prevention of at?rest platelets from adhering to others or the negatively
charged cells of the endothelium.2
12
Membrane Properties
The plasma membrane is a trilaminar unit consisting of a bilayer of
phospholipids within which is embedded cholesterol, glycolipids and
assorted glycoproteins. This membrane is believed to house the Na+ and
Ca+2 ATPase pumps, which are integral in controlling the platelets' ionic
environment. The phospholipids, which help to create and stabilize the
plasma membrane, are distributed in a rather asymmetrical pattern; with
those negatively charged phospholipids, phosphotidylserine in particular,
are known to accelerate the coagulation cascade. Additionally, select
membrane phospholipids are enriched with arachidonic acid; thereby
providing a repository of arachidonic acid ready for release and subsequent
conversion into thromboxaneA2, often referred to as TXA2.2
Organelles
The sol-gel zone or platelet interior, houses two types of granules: the a.
granule and the dense bodies; along with sparse mitochondria and
glycogen deposits. The a. granules outnumber the dense bodies within the
platelet; are contained by a membrane and hold hydrolytic enzymes 
including acid phosphatase, ~-glucuronidase, and cathepsin; the dense
bodies are enriched in serotonin and derived from a.-granules.4 They also
contain ATP and ADP in a 2:3 ratio respectively. Storage of these adenine
nucleotides is believed to be done via a vertical stacking of the molecules'
rings. The planar hydroxyindole rings of serotonin may also aide in the
13
construction of these aggregates.4 Decrease of the contents of the dense
granules, from activated platelets, is part of a fundamental positive
feedback reaction for platelet aggregation; based upon ADP being a rather
strong platelet agonist and serotonin a weak agonist.4
Function
The platelet, in response to strong activators, such as: adhesion to
exposed collagen with blood vessels following a vascular trauma; adhesion
to atherosclerotic blood vessel walls following plaque rupture; thrombin
and/or elevated collagen concentrations2; undergoes a biochemically
prescribed sequence of events. This sequence includes: a distortion of
shape; adhesiveness; primary aggregation; secondary aggregation; and
release reactions. The sequence realizes completion if the inducer is
requisitely strong with no accompanying inhibitors. If the inducer should
be weak, however, with subsequent activation of one or more inhibitors,
then the response can stop and actually reverse. The inducer also helps to
predict whether the response sequence is followed in its entirety. This
hemostatic process is inclusive of/to the activation of the blood coagulation
response, as well.4
White Blood Cells
Classification of Lymphocytes
14
Mature lymphocytes, although originating from a common parent cell,
are divided into several functional types. These functional types include: T 
cells, B cells and the intriguingly titled natural killer (NK) cells; however,
the scope of this discussion will be narrowed to include only T and B-cells.2
T-cells
T-Iymphocytes are the predominant lymphocyte in blood and lymph. In
the lymph nodes, T-Iymphocytes are known to localize within the dense
corona of lymphoid follicles in addition to congregating in the interfollicular
and subfollicular zones; within the spleen, they are found within the outer
mantle of the periarteriolar sheath. When sensitized T-cells are activated,
they produce Iymphokines; furthermore, upon activation, T-cells are able to
behave as effectors, helpers and/or suppressors. Effector T-cells are
integral in the delayed hypersensitivity reaction along with the graft-verus 
host reaction; whereas helper T-cells promote or enhance antibody
production by B-Iymphocytes; and suppressor T-cells inhibit antibody
production by B-cells.4
T-cells possess C02, C04 and COB receptors; these receptors are
simply adhesion molecules and/or signal transducers. The C02, C04 and
COB receptors react with a number of cell surface ligands, including the
lymphocyte function-associated antigens (LFAs), LFI and LF3. As an
example of this relationship, consider the following: the conjugation of C02
to LF3 ligands promotes nonspecific adhesion of T-cells to antigen
15
presenting cells (APCs) and by doing so, facilitates antigen recognition and
T-cell activation. In complement, the interplay between C04 or COB
receptors with MHC (major histocompatibility complex) proteins reinforces
the bond strength of specific T-cells to APCs. Following this contact, T-cell
recognition by the T-cell antigen receptor (TCR) and APC binding through
MHC complementarity induces lymphocyte effector function; for example,
cytolysis, or Iymphokine production. Following this biochemical
crescendoing, the T-cell involved, disengages from the APC, creating a
vacant site for the attachment of additional antigen-specific resti ng T-cel~.3
B-cells
B-cells are relatively short-lived, and originate from within the bone
marrow. They have a number of surface immunoglobin receptors, (lgM,
IgA, IgO. IgG, IgE), and fundamental in the construction and maintenance
of the humoral defense system.4 B-cells have developed so as to be able to
recognize a seemingly infinitesimal number of potential antigens; and
following contact with the antigen, they convert to plasma cells; with the
function of the plasma cell ultimately being antigen-secretion. When a B 
cell is activated, via antigen contact with an Ig receptor, a clone of
antibody-secreting plasma cells is produced. A minority of the activated
cells divide only briefly; however, they will survive as 'long-lived memory
cells'.3
16
Chapter 3: Acute Myelogenous Leukemia (AML)
Pathophysiology of AML
In prefacing the definition of AML, acute myeloid leukemia, it is
necessary to define the cancer, leukemia. Leukemia is a malignancy of the
blood?forming cells; occurring when immature or mature cells multiply
uncontrollably within the bone marrow. This condition is identified as
lymphocytic or myeloid depending upon which cell?line is altered.
Leukemia is then considered to be acute or chronic; acute leukemia being
characterized by a disease in rapid progression with a predominance of
blastic or highly immature cells; whereas chronic leukemia signals a
disease developing at a much slower rate with an increased number of
mature cells.l More specifically then, acute myeloid leukemia is identified
as the rapidly progressing neoplastic growth of immature myeloid cells or
myeloblasts; and because the nonlymphoid cell?lines are involved, this
malignancy is equally recognized as acute nonlymphocytic leukemia or
ANLL (ACS). Briefly then, the myeloid cell lines include the following
sequences of cell maturation within the bone marrow:
*stem cell ~ myeloid stem cell ~ erythroblast ~ reticulocyte ~
erythrocyte
*stem cell ~ myeloid stem cell ~ megakaryoblast ~
promegakaryocyte ~ megakaryocyte ~ thrombocyte
17
*stem cell ~ myeloid stem cell ~ myeloblast ~ basophiI
*stem cell ~ myeloid stem cell ~ myeloblast ~ eosinophil
*stem cell ~ myeloid stem cell ~ myeloblast ~ neutrophil
*stem cell ~ myeloid stem cell ~ monoblast ~ promonocyte ~
monocyte ~ macrophage.2
Thus, surveying the number of rather complicated cell-differentiation
schemes, it becomes increasingly clear that there exists a rather extensive
list of site combinations where a perversion of cell-development can occur.
For example, a derangement in the myeloid cell line at a
pluripotential/stem cell, gives rise to a disease sequelae of vastly different
dynamics than would a derangement occurring further along the
differentiation scheme.3 However, any sort of renegade or neoplastic
proliferation of cells such as myeloblasts, erythroblasts and the like, not
only encourages genetic misprints in these unchecked cells-but by the
sheer numbers of cells being 'over-produced'-healthy marrow cells are
dislodged. This usurping of cell position, within the marrow matrix,
manifests itself within the patient as anemia, neutropenia and
thrombocytopenia.2
Anemia-a reducti'on in the quantity of the oxygen-carrying pigment or
hemoglobin, within the blood; the main symptoms include:
excessive tiredness and fatigability, breathlessness on
exertion and poor resistance to infection.
18
Neutropenia-a decrease in the number of neutrophils in the blood;
resulting in an increased susceptibility to infections.
Neutrophils-a variety of white blood cell,
distinguished by a lobed nucleus and the presence in its
cytoplasm of fine granules that stain purple with
Romanovsky stains. The neutrophil is capable
of phagocytizing bacteria and contributes to the
body's defense against infection
Romanovsky stains?a group of stains used
in the microscopic examination of blood cells,
consisting of variable mixtures of thiazine dyes; such
as azure B with eosin. Romanovsky stains
communicate characteristic patterns, on the basis of
which blood cells are classified. This group of stains
includes stains of: Leishmann, Wright, May-Grunwald,
and Giemsa.
Thrombocytopenia-a reduction in the number of platelets within the
blood. This condition results in bleeding into the skin, spontaneous
bruising, and prolonged bleeding after injury. Thrombocytopenia
may result from failure of platelet production or their excessive
19
destruction.5
Clinical Presentation of AML
The general clinical signals that may indicate the development of AML,
within a patient, include: pallor, fatigue, weakness, palpitations and
dyspnea (heavy or laboured breathing) upon exertion-all being symptoms
which communicate anemia. Whereas, easy bruising, petechiae (red skin
spots signifying bleeding into the skin), epistaxis (nosebleed), gingival
bleeding, conjunctional hemorrhages and prolonged bleeding following
superficial skin injuries, are symptoms characteristic of thrombocytopenia.
In addition, fever is present in the majority of patients upon diagnosis; as is
palpable splenomegaly and/or hepatomegaly.1
Although there are many combinations of/profiles of symptoms at
diagnosis, perhaps the most accurate and fail-safe infrastructure to
construct a diagnosis around is the hematological findings/CSC numbers
and the initial personality of the bone marrow.
A bone marrow biopsy of a patient suspected of developing AML, will
always contain leukemic blast cells.2 Myeloblasts are identified within the
biopsy via three pathognomonic features: reactivity with a series of
histochemical stains; the presence of Auer rods within the cells; and/or
reactivity with specific monoclonal antibodies against epitopes found on
the surface of the myeloblasts.2 Additionally, normal erythropoiesis,
20
megakaryocytopoiesis and granulopoiesis are significantly reduced or non 
existent within the biopsy. The aspirate of marrow may also contain
isolated clusters of erythroblasts or megakaryocytes.2
The blood values of a patient suspected of developing AML-often
communicate a suspicious WBC level; many times being either
superelevated or subnormal. The myeloblast population within the blood is
not necessarily valuable in determining the extent of leukemic cell
infiltration into the body, but is valuable in gauging disease progression.
Blast counts in excess of 100,000 cells/J,lL indicate the potential for a
terminal progression and scream of the risk of the formation of 'Ieuko 
occlusions' within blood vessels of the lungs and brain. Such CNS vessel
occlusion, by gummy accretions of sticky myeloblasts, contributes, if not,
precipitates, life-threatening neurological damage; for example, fatal
cerebral hemorrhage.3
Types of AML
Acute cases of myelogenous leukemia are classified according to the
French-American-British (FAB) identification scheme. The type of AML is
assigned a label of M1-M7; accompanying each designation is a set of
hematological thresholds that must be met to allow for such a diagnosis.
The categories and hematologic criteria conform to the following:
AML M1-Myeloblastic leukemia: At least 30% of the nonerythroid
cells within the marrow are recognized as myeloblasts;
21
with a minimum of 3% of blasts staining for
myeloperoxidase or granule phospholipid via
treatment with Sudan Black.
AML M2?Myeloblastic leukemia with maturation: At least
30% of the nonerythroid marrow cells are
myeloblasts; promyelocytes account for more
than 10% of the population and monocytic
elements more than 20%.
AML M3?Promyelocytic leukemia (APL): The majority of
marrow cells are abnormal hypergranular
promyelocytes; Auer rods may be present
within a small percentage of these promyelocytes.
AML M4?Myelomonocytic leukemia (AMML): At least 30% of
the nucleated marrow cell population are blasts;
with granulocytics accounting for more than
20% of the nonerythroid marrow cells.
AML M5?Monocytic leukemia (AMoL): At least 30% of the
entire nonerythroid marrow cell population are
monoblasts, promonocytes or monocytes. In
the M5A subtype, a minimum of 80% of all
monocytic cells are monoblasts.
22
AML M6-Erythroleukemia (AEL): A minimum of 50% of
the nucleated marrow cell population are
erythroid precursor cells; in addition, at
least 30% of the remainder of nonerythroid
cells are blasts.
AML M7-Megakaryoblastic leukemia (AMegL): The marrow
biopsy displays at least 30% of the cells present
to be of megakaryocytic lineage.3
As mentioned within the preface, a specific case of pediatric AML M2 
myeloblastic leukemia with maturation-will be the primary focus of this
discussion.
23
Chapter 4: The Pharmaceutical Suspects
What was the precipitating factor/s to the
development of AML in this case study?
As spoken to within the preface-this thesis, ultimately, is an expanded
case study; the focus being a then nine year old male, diagnosed with AML
M2. Having characterized the disease state in chapters preceding, the
question of HOW? arises. More precisely, how exactly is a child at risk for
developing leukemia-myelogenous leukemia at that? The first possibility to
be explored is maternal/paternal chemical exposure, followed by infant
chemical exposure.
When analysing the chemical exposure of the diagnosed young man and
his parents, it becomes obvious, quite rapidly, that two pharmaceutical
agents are of paramount importance to this discussion; sulfisoxazole and
clomid (clomiphene citrate). Sulfisoxazole is somewhat suspect in that, as
an infant, this young man received 18gm, in <5 days, as treatment for
otitis media; 18gm, in <5 days, in a pediatric context, is considered an
overdose.6 Of equal, if not greater, suspicion is clomiphene citrate or
clomid, a fertility drug taken by the mother, to induce ovulation. Clomid
regimens, as will be presented, are notorious in their ability to encourage
fetal/neonatal structural malformations; in conjunction with chromosomal
abnormalities and leukemia within the neonate'?
24
Clomid
Clomid, is identified by its manufacturer, Hoechst, as an orally
administered, nonsteroidal, ovulatory stimulant; chemically identified as 2 
[p?2(chloro-l,2-diphenylvinyl-phenoxy]triethylamine citrate. Clomid or
clomiphene citrate, is a mixture of two geometric isomers,
[cis(zuclomiphene) and trans(enclomiphene)] containing from 30-50% of
the cis?isomer.7
Clomid has the potential to interact with those tissues rich in estrogen 
receptors; these tissues include, but are not limited to, the hypothalamus,
pituitary, ovary and endometrium. This drug may also compete with
estrogen for estrogen-receptor binding sites and may retard the renewal of
intracellular estrogen-receptors. Essentially, clomid initiates an endocrine
cascade ending in a preovulatory gonadotropin surge, pre?empting
follicular rupture. The first event in this cascade is a marked increase in
the release of pituitary gonadotropins. This increase encourages
steroidogenesis and fo/liculogenesis; thereby promoting the growth of the
ovarian follicle and increases in circulating estradiol /evels.7
Although such an endocrine cascade may be the exact desired result-a
number of the risks and contraindications may unfavourably skew the
benefit/risk ratio of clomid therapy. The outward or obvious upon
parturition, malformations which are experienced by the subject of this
study, include: undescended testicles, inguinal hernia and umbilical hernia.
25
All three of these structural abnormalities are specifically cited within the
physician's package insert for clomid, as possible risks. In addition, the
risk of neoplasms and chromosomal disorders are cited: the neoplasms
listed directly include neuroectodermal tumour, thyroid tumour,
hepatoblastoma, and most importantly for this discussion, leukemia. It is
also worthy of mention, that clomiphene citrate is contraindicated for
women known to suffer from organic intracranial lesions-such as pituitary
tumour.7 In the instance of the nine year old subject, his mother has been
diagnosed with just such an intracranial lesion, a pituitary tumour; her
diagnosis preceded her c10mid therapy.
In addition to the mother's anovulatory condition, the child's father was
identified as suffering from oligospermia. The parameters for oligospermia
are between 0.5-20 million sperm/mI8 ; with normal serum gonadotropins
and testosterone. However, although clomid/clomiphene may be taken at
doses up to 100mg/day, in treatment of male infertility, due to a
miscommunication, the child's father took two times the prescribed dose
during treatment. It has been suggested that extremely high or low
concentrations of clomid/c1omiphene negatively impact both sperm
motility and fertilising capacity.9 Please consider the risks that begin to
intensify for the fetus-considering that both parents are
26
receiving clomiphene therapy and one is receiving two times the prescribed
dosage. If there was "acceptable risk" with exclusively mother receiving
fertility therapy, did the line between benefit and risk become a bit
muddled when father began treatment, and two times the treatment at
that?
Sulfisoxazole
Sulfonamides
Sulfonamides, the general category of pharmaceuticals to which
sulfisoxazole belongs, are synthetic derivations of p 
aminobenzenesulfonamide. A benzene ring with a sulfonamide group and
a primary amino group para to the sulfur side-chain, impart antibacterial
activity to the compounds. Substitution of the N4 ?amino group with groups
e.g. radicals, that may be easily converted to a free amino group within the
body, allow the compound to retain antibacterial activity. Furthermore, any
substitutions within the N1?amide group produce compounds different in
solubility, protein binding, tissue distribution, and rates of metabolism and
excretion. The most effective sulfonamides are those obtained via
substitution of heterocyclic groups in the N1 position.6
Sulfonamides are principally bacteriostatic; in that they directly disrupt
bacterial utilization of p?aminobenzoic acid (PABA) within the biosynthesis
of tetrahydrofolic acid cofactors. This interference is possibly due to
sulfonamides being structural analogs of p?aminobenzoic acid; thereby
27
being capable of competitively inhibiting dihydropterate synthase.
Dihydropterate synthase catalyses dihydropteric acid formation from PABA
and pteridine. Dihydropteric acid is a tetrahydrofolic acid precursor. The
bacteriostatic potential of the sulfonamides is only realised against
microbes that synthesize their own folic acid.6 Thus sulfonamides are
effective against gram positive bacteria, including: strains of Staphylococci,
Streptococci, Bacillus anthracis, Clostridium tetani, Clostridium pertringens,
along with a number of strains of Nocardia asteroides and Nocardia
brasiliensis. The gram negatives which thay are effective against include:
Enterobacter, Escherichia coli, Klebsiella, Proteus mirabilis, Proteus vulgaris,
Salmonella and Shigella.6
Sulfisoxazole
Sulfisoxazole, the sulfonamide specific to this discussion, shares the
actions and uses of the sulfonamides. However, there exist a number of
adverse reactions with this sulfa drug, as with many others. The most
pertinent, here, being the sulfonamide-induced blood dyscrasias:
agranulocytosis, hemolytic, aplastic or megaloblastic anemia, leukopenia,
thrombocytopenia and eosinophilia.lO The blood dyscrasias are believed to
be provoked by both an immunologic reaction, involving haptene formation
and destruction by antibodies, and an idiosyncratic mechanism. It has
been demonstrated that such toxic effects, from sulfa drug therapy, occur
after a latent or window period, anywhere from 2 to 36 months, following
28
treatment.ll Please consider the course of sulfa drug treatment taken by
the subject: 18gm, <5 days, powder form, in a pediatric context; it is of
vital importance, when analysing this therapy, to recognise that not only
does this scenario constitute an overdose-but the sulfisoxazole was not
prepared in the pharmacy, as the prescribed suspension. The prescription
was however, filled and given to the patient's parents with minimal
instruction; not enough instruction to allow them to realise that
sulfisoxazole is not/should not be administered as a powder-to be
sprinkled over a patient's cereal! Such miscommunication and negligence
could only endager this child, and most probably set him up for an
increasing susceptibilty to a hematologic event, such as leukemogenesis!
29
Chapter 5: The Environmental Suspects
Environmental chemical exposure of both parents and child is perhaps
best divided into two distinct groups of chemicals: Berlin Lake water
contaminants and fruit and vegetable contaminants. The Mahoning River
Basin plays a key role in this case study due to the child's repeated annual
exposure to Berlin Lake water via swimming, diving and boating. Whereas
preservative chemicals, common to fruits and vegetables are integral in
that the child's father has worked in the produce department of a local
grocery chain for nearly thirty years.
Berlin Lake
Appendix C, of the EPA's May 1, 1996 report on the Mahoning River
Basin, catalogues over 495 known spills into the basin and its tributaries,
between 1983?1994. Before discussing some of the more serious spills, it
is essential to note that the level of sophistication or better yet, exactitude
in identifying what exactly spilled and in what volume, is of an incredibly 
even frightfully low level. For example, entries of spills of "waste water?
quantity unknown" or "sewage?quantity unknown" or "unknown white stuff?
quantity unknown" or "suspended solids, yellow material, orange stuff,
illegal dumping, junk/trash"-all recorded "quantity unknown"-are
representative of how the government has documented spills into a
waterway, known of and used in almost exclusively a recreational capacity.
30
Some chemicals that have been recorded as spilling into this waterway
in excess of thousands of gallons, include: 1,3-butadiene, assorted fuel oils,
asbestos, ethylene glycol, propylene glycol, and 2,4,6-trinitrotoluene.12
The first, most obvious and unfortunately the most frequently spilled
chemicals, are those, as previously mentioned, which belong under the
heading of hydrocarbons or petroleum distillates. The petroleum distillates
have increased toxic effects when they are aspirated into the
tracheobronchial tree than when they are ingested; ingestion of between
500-1000mL may cause minor symptoms, whereas aspiration of just ImL
can lead to lethal chemical pneumonitis.8 Pesticides, camphor,
halogenated compounds and metals, if dissolved in petroleum distillates,
can significantly increase this toxicity.8
Petroleum distillates are recognised as fat solvents, capable of altering
nerve function, potentially leading to depression, coma and convulsions.
Benzene contaminants of the distillates, may potentiate adverse effects on
liver, kidney and bone marrow function.13 Laboratory findings, based upon
exposed individuals, tell of reduced RBC counts, bone marrow hypoplasia
and the presence of protein and RBC's in the urine.13
1,3-Butadiene
1,3?Butadiene is produced during petroleum processing. It is the 36th
highest volume chemical produced in this country. 1,3-Butadiene is
31
recognised by the DHSS as a human carcinogen. Exposure to this
compound is possible via: urban or suburban air in or around chemical,
plastic or rubber facilities; air contaminated from car/truck exhaust or
waste incineration; cigarette smoke; drinking/swimming in water near
production or waste sites; and skin contact with gasoline.14 The
occupational exposure limit, as established by OSHA, for 1,3-buatdiene, is
lOOOppm of air.IS
Fuel Oils
Fuel oils are, obviously, a veritable hydrocarbon cocktail, produced
directly from crude oil petroleum; and include kerosene, diesel fuel, jet
fuel, range oil and home heating oil. Fuel oils, when spilled into water are
not degraded into more benign or eco-friendly compounds, quite the
contrary. Rather, these petroleum by-products may dissolve in water
and/or eventually be deposited in the waterway's sediment. Furthermore,
fuel oils, of any sort, are recognised as bioaccumulators?simply meaning
that they accumulate in the adipose of any exposed creature-fish, bird,
human, or otherwise. One of the most direct routes of exposure is the
immersion or consumption int%f contaminated water. Unfortunately,
prolonged and/or repeated exposure to such compounds adversely effects
kidney function and interrupts the prothrombin and fibrin sequences within
the blood; thereby significantly increasing clotting times.14
32
Used Mineral-Based Crankcase Oil
This compound differs from unused oil in that it contains additional
chemicals formed via high temperature and high pressure exposure within
an engine. It also contains an assortment of metals from engine parts, in
addition to gasoline, antifreeze and byproducts of spent gasoline.14 When
such a mixture invades the environment, it acts in much the same way as
fuel oils. They find their way through waterways, accumulating in low-layer
sediments, animals, fish and humans. Therefore, exposure to
contaminated water or soil would be possible delivery routes into the body.
And once an individual has suffered such a repeated exposure,
hematological events, such as anemia, become increasingly likely to occur.
In addition, used oil contains PAH's or polyaromatic hydrocarbons-which
are recognised carcinogens.14
Contaminants, other than the petroleum distillates, which have been
spilled into the Mahoning River Basin/Berlin Lake, include: asbestos,
ethylene glycol, propylene glycol and 2,4,6-trinitrotoluene.12
Asbestos
The term asbestos is applied to any mineral that decomposes into
fibres. Chrysotile, the most common form, is fibrous serpentine, a
magnesium silicate containing 40% silica. Its fibres are tubular in cross 
section and as small as O.015~m in diameter. Crocidolite, another form, is
fibrous riebeckite, a sodium ferro-ferrosilicate, which is 41% silica. Its
33
fibres can be as minute as 0.08Jlm in diameter. A third form, amosite, is
fibrous grunerite, a magnesium ferrosilicate, 49% silica. Amosite fibres
are as little as O.lJlm in diameter. Asbestos also includes anthophyllite
and termolite-actinolite. Uses for the various forms of asbestos include:
cloth production, brake linings, cement products, paper, flooring, gaskets
and paint; a total of 3 million tonnes is produced annually in the United
States.16 Asbestos does not readily degrade within the environment, it
merely settles-in water, soil, and within animals. Asbestos is capable of
bioaccumulation. Inhalation of asbestos fibres increases the risk for lung
cancer and mesothelioma, which is a cancer of the pleural membrane.
Whereas, ingestion of such contaminated water, has been shown to elevate
the risk for stomach, intestinal, esophageal, pancreatic and kidney
cancers.17 The EPA has set a limit of 7 million fibres/L as the highest
concentration of long fibres acceptable within drinking water.14
Ethylene and Propylene Glycol
Ethylene glycol and propylene glycol are clear, colourless, liquids-best
described as 'syrupy' at room temperature. Both glycols are main
components of anti-freeze and de-icing solutions for cars, boats and
airplanes; and are used in the manufacturing of polyesters-also as solvents
in the plastic and paint industries.12
The fatal dose of ethylene glycol is approximately 100g. Whereas the
exposure limit for particulate ethylene glycol is 10mg/m3 ; 50ppm for
34
vapour.18 Ethylene glycol and its esters are distributed with metabolic
water and are metabolised to oxalic acid within the body; it is this
conversion that is believed to be involved in some of its toxic effects.19 The
ethers of ethylene glycol, although not degraded to oxalic acid,
idiopathically produce brain and kidney damage.18 The majority of the
glycols produce profound acidosis.19
The pathology of a glycol poisoning may include congestion and edema
of the brain, focal hemorrhagic necrosis of the renal cortex, along with
hydropic degeneration of the liver and kidneys. Commonly, calcium
oxalate crystals are found within the CNS (brain and spinal cord) and
kidneys.18 The primary pathway of or to exposure, excluding direct
contact, is via contact with contaminated water or soil.12
2,4,6?Trinitrotoluene
As is commonly known, trinitrotoluene is used as an explosive. The
acute fatal dose is between 1?2g; while the exposure limit is O.5mg/m3.20
In an exposed organism, TNT injures almost every cell it contacts; in
particular, those cells of the liver, bone marrow and kidney. Pathological
findings of a TNT poisoning would most likely tell of acute, yellow atrophy
of the liver, bone marrow aplasia, petechial hemorrhages and toxic
nephritis. Bone marrow involvement is communicated via laboratory
findings of depressed RBC counts, in conjunction with anisocytosis and
poikilocytosis; there may be relative lymphocytosis, as well.2o
35
TNT enters the environment via waste-waters and solid waste products
of the armament industry. This compound, like so many others, is able to,
and all too frequently does, migrate via surface water and soils into
groundwater. Trinitrotoluene also displays bioaccumulative capabilities;
with the most likely route of exposure being contact with contaminated
surface and/or ground waters.12
Produce Pesticides/Paternal Exposure
Paternal chemical exposure via three decades of produce handling
includes, but may not be exclusive to, the following chemicals. Please note
that following each chemical is a list of associated health effects linked to
exposure to that particular chemical.
Acephate-found on cranberries
-carcinogenic; damages brain and nervous system
Azinphos Methyl?found on apples
-damages brain and nervous system
Captan-found on strawberries
-carcinogen; damages reproductive system; causes birth
defects; damages brain and nervous systems; damages
the immune system
Carbaryl?found on peaches and oranges
-carcinogen; damages reproductive system; causes birth
defects; damages brain and nervous system; interferes
36
with hormones
Chlordane-Cis-found on summer squash and winter squash
-carcinogen; damages reproductive system; causes
birth defects; damages brain and nervous system;
interferes with hormones
Chlordane-Trans-found on summer squash and winter squash
-carcinogen; damages reproductive system; causes
birth defects; damages brain and nervous system;
interferes with hormones
Chlorothalonil-found on string beans and onions
?carcinogen; damages brain and nervous system
Chlorpyrifos?found on peaches
-damages brain and nervous system
DCPA-found on broccoli, turnip greens, turnips, lettuce romaine
-carcinogen
DOE-found on spinach and potatoes
-carcinogen; damages reproductive system; causes birth
defects; damages brain and nervous system; interferes
with hormones
DOE, P,p1?found on broccoli, turnip greens, lettuce romaine
-carcinogenic; damages reproductive system; causes
birth defects; damages brain and nervous system;
37
interferes with hormones
DDT-found on spinach
-carcinogen
Dicloran?found on peaches
?health effects unknown
Dieldrin?found on winter squash
?carcinogen; damages reproductive system; damages
brain and nervous system; interferes with hormones;
damages the immune system
Endosulfan I?found on summer squash
?damages brain and nervous system; interferes with
hormones
Endosulfan 2?found on summer squash
-damages brain and nervous system; interferes with
hormones
Endosulfan Sulfate?found on watermelons, cucumbers, summer
squash, winter squash
?damages brain and nervous system; interferes
with hormones
Ethion?found on grapefruit
-damages the brain and nervous system
Imazalil-found on bananas and oranges
38
-carcinogen; causes birth defects; damages brain and
nervous system
Iprodine-found on peaches
-carcinogen
Methamidophos-found on string beans and tomatoes
-damages brain and nervous system
Omethoate-found on tomatoes
-health effects unknown
Oxamyl-found on tomatoes
-health effects unknown
Permethrins-found on spinach and tomatoes
-carcinogen; interferes with hormones
Thiabendazole-found on potatoes, apples, bananas, grapefruit
-causes birth defects; damages brain and nervous
system
Trifluralin-found on carrots
-carcinogen; damages reproductive system;
causes birth defects; interferes with hormones;
damages immune system21
Of these 26 chemicals, many are classified as cholinesterase inhibitor
pesticides: acephate, azinphos, chlorpyrifos, ethion, omethoate-are
39
recognised as being organic phosphates; whereas, carbaryl and oxamyl
are recognised as carbamates.22
Cholinesterase inhibitors are most commonly employed in agriculture to
control soft-bodied insects. The organophosphorous derivatives act via
combining with and subsequently inactivating acetylcholinesterase.23 This
combination is believed to occur according to the following reaction:
AChe + (ROhPO => ROH + (RO)2PO(AChe) => (RO)2PO(OH) + Ache
The pace of this reaction and stability of product, the cholinesterase 
phosphate combination, are rather dependent upon the structure of the
phosphate ester.22
The action of the carbamates is similar in mechanism, although the
combination is reversible.22
The inactivation of cholinestrase, by these pesticides, permits
acetylcholine to accumulate. This neurotransmitter build-up is not without
consequence; it contributes to a rather complex sequelae. First, there
exists the possibility of/for the potentiation of postganglionic
parasympathetic activity; such eNS activity is corporeally expressed as:
constricted pupils, stimulation of intestinal muscles along with salivary and
sweat glands; constriction of bronchial muscles, contraction of the urinary
bladder, slowing of the sinus node and blockage of the AV node. This initial
excitation is followed by the extended depolarization of the skeletal
muscles; ultimately resulting in paralysis. In conjunction, there is a
40
depression of the eNS, precipitating inhibition of the inspiratory center 
effectively terminating respiration. The final component is variable
ganglionic stimulation or blockage, expressed as either a rise or fall in bp
and/or dilation or constriction of the pupils.23
In addition to the cholinesterase inhibitor pesticides, the
aforementioned 26 pesticides also include a number of chemicals that are
recognised as endocrine/hormone disrupters; including carbaryl, DDT,
metabolites of DDT, dieldrin, endosulfan, permethrin and trifluralin.24
Hormone or endocrine disrupters are chemicals recognised to have the
ability to interfere with the endocrine system of animals and humans; the
compounds are able to block or even mimic the body's natural hormone
signals. Thereby sending false hormone messages, interrupting real
hormone messages, preventing the synthesis of the body's true hormones,
and even accelerating the degradation and elimination of the true
hormones. Obviously then, a number of health effects have been
associated with endocrine disrupters, including: reproductive disorders,
dysfunction of the immune system, cancer (breast, prostate, testicular),
neurological effects, attention deficit and compromised short-term
memory, decreased/low IQ's. Furthermore, it has been suggested that
these chemicals may pose a very specific threat to both the developing
fetus and young children; with exposure in-utero and via breast milk.24
41
It is just such early chemical exposure that is believed to be
contributing to some rather disturbing trends in childrens' health, and in
the reproductive health of adults. Please consider the following:
1. Childhood cancers, cancers in children <15 years of age, have risen
10% between 1974 and 1991 in the United States; cases of ALL-acute
lymphoblastic leukemia, rose by 1% per year in the US from 1973 to
1994. The rate of brain cancer has increased 2% per year during the
same time frame.25
2. A number of studies have confirmed the trend of American girls entering
puberty earlier than was found in past research. There is believed to be
a chemical contribution to this change: for in a recent study, it was
substantiated that girls, whose mothers had the highest level of PCB's
and DDE in their system while pregnant, entered puberty 11 months
earlier than girls whose mothers had significantly lower levels of the
pesticides.26
3. The ratio of male to female births has dramatically declined in recent
decades. Although a number of theories of explanation have been
offered, parental exposure to endocrine disrupters appears most likely.
The endocrine disrupter theory is supported by a study conducted in
Seveso, Italy; where large volumes of dioxin were released into the
environment, following an industrial accident. Eight years after the
42
accident, 12 daughters and ?sons were born to nine couples
recognised to have had the highest levels of dioxin exposure.27
4. Testicular cancer has increased an astonishing 55% in England and
Wales between 1979 and 1991; with the diagnosis of 1,137 new cases
in 1991 alone. The development of this particular form of cancer is
believed to be strongly influenced by developmental aberrations of the
testes in utero-with endocrine disrupters suspected as initiating such
aberrations.28
5. Oligospermia or decreased sperm count, is becoming increasingly
common in men of all age brackets, throughout Europe and the US. 28
6. Breast cancer has been on the increase 1% per year since the 1940'sin
the US; and between 1945 and 1980, Denmark experienced a 50%
increase in this form of cancer. A number of studies have drawn a
direct relationship between breast cancer and exposure to endocrine 
disrupting chemicals-such as DDT, dioxin and PCB's.28
7. In England and Wales, prostate cancer has increased 40% from 1949 to
1991.28
43
Chapter 6: The Genetics
It has been suggested that every recognized cancer is the result of some
genetic event or better yet, genetic damage. Of course, implicit to this
statement is the recognition that assaults upon an individual's DNA are
possible via x-rays/radiation, chemicals-misperscribed/misadministered
pharmaceuticals-environmental pollutants, and viruses; for there must be
some sentinel event that initiates this "cascade." When studying the
cytogenetics of this particular case of AML-M2, it is not unlikely that
genetic aberrations were integral in allowing disease progression (Appendix
I-cytogenetic data).
The anomalies for this leukemia patient include the following:
1. consistent hypodiploidy;
2. random, nonclonal chromosomal loss;
3. loss of V-sex chromosome;
4. translocation between the long arms of chromosome 11 at l1q13
and 15 at 15q22;
5. translocation involving the long arms of chromosome 8 at 8q24.1
and Y at Yq12;
6. the presence of two cell lines within the bone marrow.
44
Table 6-1
Glossary of Cytogenetic Terminology29
Centromere-The constriction along the length of the chromosome
that is the site of the spindle fibre attachment. The position of the
centromere dictates whether chromosomes are X-shaped
(metacentric) or V-shaped (acrocentric).
Karyotype-Arrangement of chromosomes from a particular cell
according to an established system such that the largest
chromosomes are first and the smallest ones are last. A normal
female karyotype is represented as 46, XX; a normal male karyotype
is represented as 46, XV.
Translocation-A break in a minimum of two chromosomes with an
exchange of material.
Deletion-A segment of a chromosome goes missing as a result of a
single break (terminal deletion) or two breaks with loss of the
intervening segment (interstitial deletion).
Inversion-Two breaks occur in the same chromosome with a rotation
of the interim segment. If both breaks occur on the same side of the
centromere, it is known as a paracentric inversion; if the breaks are
on opposite sides, it is known as a pericentric inversion.
45
The genes that are suspected of contributing to the development of
leukemia are commonly divided into five classes:
1. those genes that carry growth-stimulating signals from the cell
nucleus;
2. genes that activate transcription or RNA synthesis within the
nucleus;
3. genes responsible for the promotion of cell differentiation;
4. genes involved in apoptosis-referring here to the programmed cell
death experienced by blood cells upon completion of their
functions;
5. "anti-oncogenes" or those genes that suppress tumour
development, under normal biochemical/genetic
conditions.3o
47
Table 6-2
Primary Cytogenetic SUbgroups in Acute Myelogenous Leukemia31
Translocation FAB/lncidence
t(8;21) -20% of M2; 6?10% of de novo AML
Clinical Morphology: auer rods, hypergranulated myelocytes, durable
remissions.
t(15;17) -99% of M3; approx 10% de novo AML
Clinical Morphology: consumptive coagulopathy (DIC), durable
remissions with all-trans-retinoic acid and additional chemotherapy;
hypergranular variant w/coarse azurophilic granulation; microgranular
variant with decreased granulation and nuclear constrictions.
Inv(16); t(16;16) ->90% of M4Eo; 7-10% de novo AML
Clinical Morphology: marrow eosinophilia w/coarse irregular basophilic
granules.
t(11q23; variable) -approx 5% de novo M4 and M5 AML
approx 5% t?AML
Clinical Morphology: variable morphology but w/a monocytic
component; associated w/t-AML and a generally poor prognosis.
48
Table 6-3
Prognostic Impact of Selected Chromosome Abnormalities in de novo AML
Karyotypic Abnormality Complete Remission Rate Length of CR
Inv(3) low short
-S/Sq low short
-717q low short
t(8;16) low short
t(8;21) high long
+8 variable variable
t/del (11q23) variable short
t(lS;17) high long
inv(16) high long
+21 high variable
After digesting the aforementioned genetic information and data, some
troubling aspects to this particular case of AML M2 come to the fore.
1. The identification of at least two cell lines indicates that
karyotypic evolution has occurred-if the karyotypes are related;
however, if the two karyotypes are unrelated, this could indicate
49
the occurrence of two independent leukemogenic events
(Alimena).
Multiple clones occur more frequently in those patients with
secondary leukemia (77.9%), compared to patients with ANLL de
novo (10.8%). Slightly more than 33% of all cases with multiple
clones had losses of part or even all of chromosome #5 and lor
chromosome #7?as a first step change. However, 9:10 patients
with secondary leukemia and multiple clones had involvement of
the chromosomes. The second step chromosomes most often
involved include #9, #17 or #21. Those patients found to
express t(8;21) in addition to multiple clones, most often had
loss of a sex chromosome.32
2. There is a subset of ANLL patients, characterized by the presence
of t(8;21) in bone marrow cells. At the Second International
Workshop on Chromosomes in Leukemia, 40 such patients were
reviewed, and it was recognized that:
A. the occurrence of the translocation was intimately related
to the morphologic diagnosis of FABM2 (acute
myeloblastic leukemia with maturation);
B. the loss of a sex chromosome was frequently associated
with this translocation;
50
C. the rate of both remission and survival were recognized as
relatively good, most notably in cases with some normal
metaphases; whereas the association of a missing sex
chromosome with t(8;21) carried a poor prognosis;
D. there was some geographic difference in the occurrence of
t(8;21).33
Of particular interest in this case: consistent hypodiploidy, loss of the Y 
sex chromosome, secondary chromosomal rearrangements consistent with
having received chemotherapy, and a relatively low number of observed
metaphases. Furthermore, the initial or diagnostic cytogenetics, do not
communicate any necessarily inherited (maternal/paternal) chromosomal
anomalies (breakpoints, etc); thereby raising the question of what exactly
was the sentinel event in this child's life-that could have provoked a
leukemogenic event? The possible suspects, in this case, are quite
unfortunately becoming the usual suspects in the development of
childhood cancers: pharmaceuticals (in-utero, neonate exposure, or both),
and the external environment (exposure to contaminated food, water, soil).
51
Chapter 7: Materials and methods
The portion of this case study concerned with assessing any external
environmental influence was initiated on 10.22.98, 12 days after the
patient's admission to hospital; under the original diagnosis of
pancytopenia/aplastic anemia. This data was collected over seven days;
and includes water samples from Berlin Lake (Appendix 3), and soil
samples from the lawn of the patients home (Appendix 3).
Materials
All of the solvents used within the context of this study were pesticide
grade (Fisher Scientific, Fairlawn, NJ). Additional reagents included: 100?
mesh silicic acid (MalJinckrodt Chemical Works, St. Louis, MO); 80-200
mesh alumina, anhydrous sodium sulfate (Fisher Scientific, Fairlawn, NJ)
and sodium chloride (VWR Scientific, Westchester, PA). The analytical
standards used within this case-study, were purchased from Supelco, Inc
(Bellefonts, PA) or Ultra Scientific (North Kingstown, RI). The helium and
nitrogen were ultra pure carrier grade. The filters employed for the
preparation of the water samples were type GMF grade filters, 47mm,
(Whatman, Maidstone, England); the accompanying polyurethane foam
plugs were purchased from Graseby Anderson (Cleveland, OH).
52
The water filters were precleaned via baking at 450?C for a minimum of
20h in a muffle furnace; they were then wrapped in 'cleaned' aluminum foil
and sealed in plastic bags. The polyurethane foam plugs were prepared for
use via soxhlet extraction, I8h in acetone; followed with soxhlet extraction
in petroleum ether, I8h. Upon completion of the cleaning protocol, the
polyurethane foam plugs were dried, via low heat, in a dry seal dessicator;
following which they were stored in glass jars with teflon-lined lids. The
silicic acid was 'cleaned' via baking at 140?C, 24h; and before its use, it
was deactivated with 1.7% water. The adsorption alumina was 'cleaned'
via overnight baking at 450?C; prior to its use, it was deactivated with 6%
water and stored in a glass jar with a teflon-lined lid. The anhydrous
sodium sulfate was prepared in a similar manner, with overnight baking at
450?C and stored in a glass jar with a teflon-lined lid. Any sodium chloride
crystals used, were prepared via a petroleum ether rinse, followed-up with
a dichloromethane rinse; and then dried at 140?C. Boiling chips, used
throughout this protocol, were prepared by soxhlet extraction with
petroleum ether in a cellulose thimble, 12h; they were then dried at 140?C
and stored in a glass jar with a teflon-lined lid.
Sample Collection and Work-up
Soil
The lawn sample was collected 10.22.98; stored in cleaned aluminum
foil within a labeled plastic bag at 4?C until further work-up was possible.
53
The soil, was later thawed and manually mixed, to promote
homogeneity. Approximately 15.721g of the soil was mixed with sodium
sulfate to remove any water. The dried soil was spiked with 452ng PCB?
103, transferred to a 'clean' cellulose thimble and extracted, via soxhlet
with dichloromethane, 24h. The extract was then reduced via rotary
evaporation, transferred into hexanes and concentrated under nitrogen, to
2ml.
The extract was then cleaned via an alumina column composed of a
glass wool plug, on top of which was 2g AI203 and 1cm Na2S04. The
alumina column was pre-prepared with 5mJ of 5% dichloromethane in
petroleum ether. The sample was then added to the column and eluted
with 20ml 5% dichloromethane in petroleum ether. The resulting eluent
was then concentrated and solvent exchanged into iso-octane under
nitrogen.
Water
Water samples were collected in cleaned 4L solvent jugs, from locations
in and around Berlin Lake (Appendix 3). The samples were stored at 4?C
until extraction was possible.
The polyurethane foam plugs were extracted via soxhlet, in petroleum
ether, for 24H. The filters, prior to use, were refluxed in dichloromethane
for 18h.
54
The water samples were transferred into individual stainless steel
canisters (Coca-Cola Bottling Company of Northern Ohio, Youngstown,
Ohio). The water samples were pushed, via nitrogen pressure, through a
47mm GMF water filter, in attempt to remove any particulate matter; each
sample required several filters, due to high levels of particulate matter.
The water filters were then wrapped individually in cleaned aluminum foil
and stored in plastic bags at -lOcC.
The filters were soxhlet extracted with dichloromethane 24h. The
extracts were then reduced to 5-l0ml and solvent exchanged into iso 
octane via rotary evaporation. The entire sample inventory was reduced
individually to lml under nitrogen. The samples were cleaned using a
silicic acid/alumina column; a glass column was dry-packed with a first
layer of 3g silicic acid (1.7% water added), followed by a second layer of 2g
adsorption alumina (6% water added), and a third layer of 2cm anhydrous
sodium sulfate.
55
Chapter 8: Results
The spectra, as collected for this particular case study, may be found in
Appendix 4. The following analyses of the data were made possible
through these references: (it is important to note that IR analysis done in
this manner is non-specific)
? The IR Wizard on the web;34
? Spectrometric Identification of Compounds 5th ed.
Appendix C: Characteristic Group Absorptions.
R.M. Silverstein, G.C. Bassler, J.C. Morrill;
John Wiley and Sons, Inc. New York: 1991.35
K-Soil
*collected 10.22.98
*sample run 4.29.99
*peaks of interest: 1300-1050 em-I possible functional groups include
esters and/or lactones;
2900 em-I possible functional groups include -CHO, -
CH3, ?CH2.
K-soil
*collected 10.22.98
*sample run 4.30.99
*peaks of interest: 1300?1050 em-I possible functional groups include
esters and/or lactones;
56
2900 cm-! possible functional groups include -CH3, -
CH2.
Filter 3-8 Feed
*collected 10.22.98
*sample run 5.3.99
*peaks of interest: 2354 cm-! possible functional groups include -NH2+,
-NH+, =NH+, P-H.
Syringe 8 Feed
*collected 10.22.98
*sample run 5.3.99
*peaks of interest: 2945.6 cm-! possible functional groups include -CH3,
-CH2;
1100 cm-! possible functional groups include P?O-alkyl,
-COH, ROCOCOR, C=S, S=O.
Filter 4 8 Feed
*collected 10.22.98
*sample run 5.2.99
*peaks of interest: 2400 cm-! possible functional groups include NH2+,
NH+, =NH+, P?H.
57
Filter 2 B Feed
*collected 10.22.98
*sample run 5.3.99
*peaks of interest: 2350 cm-l possible functional groups -NH2+, NH+, P?H.
Filter 1 B Feed
*collected 10.22.98
*sample run 5.2.99
*peaks of interest: 2900 cm-l possible functional groups include -CH3, .
CH2;
500 cm'l possible functional groups include C?I alkyl.
C?Feed
*collected 10.25.98
*sample run 4.30.99
*peaks of interest: 2900 cm-l possible functional groups include -CHO, .
CH3, ?CH2;
1300?1050 cm'l possible functional groups include
esters and/ or lactones.
Filter 1 B Feed
*collected 10.25.98
*sample run 5.4.99
*peaks of interest: 2250 cm-l possible functional groups include aromatic
ketones;
58
1640 cm-! possible functional groups include o-amino or
o-hydroxyarylketones, 6?membered rings (-NCON-).
Filter 2 B Feed
*collected 10.25.98
*sample run 5.3.99
*peaks of interest: 2960 cm-! possible functional groups include -CH3, -CH2
Section A/Dam Water
*collected 10.25.98
*sample run 5.18.99
*peaks of interest: 2250 cm-! possible functional groups include aromatic
ketones;
1640.9 cm-! possible functional groups include o-amino
or o-hydroxyarylketones, 6-membered rings (-NCON-).
Dam Water
*collected 10.25.98
*sample run 5.18.99
*peaks of interest: 2250 cm-! possible functional groups include aromatic
ketones;
1640.9 cm-! possible functional groups include o-amino
or o-hydroxyarylketones, 6-membered (-NCON-).
59
Beyond Dam
*collected 10.25.98
*sample run 5.4.99
*peaks of interest: 2080.9 cm-1 possible functional groups include -N=C=S;
1640.9 cm-1 additional possibilities include C=N
(conjugated cyclic), C=N and/or -C=C-C=N-.
C Feed
*collected 10.25.98
*sample run 4.29.99
*peaks of interest: 2950 cm-1 possible functional groups include -CH3,  
CH2;
1500-1030 cm-1 possible functional groups include
esters and/or lactones.
Syringe C Feed
*collected 10.25.98
*sample run 5.3.99
*peaks of interest: 2950 cm-1 possible functional groups include -CH3,  
CH2;
1050 cm-1 possible functional groups include P-O-alkyl,
C=S, S=O, C-OH, ROCOCOR.
60
Please note when reading the data collected, that the main objective of
the collection/analysation of such samples was to provide further evidence
for the presence of these chemicals; these chemicals/functional groups are
already recognised contaminants of the Mahoning River Basin (EPA).
Therefore, this summary is presented to merely lend support to the casual
correlation between chemical contaminants and AML. It is this correlation
that is being discussed within this thesis.
61
Chapter 9: Concluding Remarks
It would be virtually impossible, as well as completely academically
irresponsible, to compose a definitive statement as to how this case of
pediatric AML-M2 arose; however, as this thesis is a single case-study, it is
able to contribute several documented casual-although perhaps not so
casual-links to chemical exposure and increased risk for leukemogenesis
If the reader goes beyond the necessarily limited focus of this single
case-study, he/she will be able to find scores of articles/recent
publications that are able to claim direct links between chemicals and
cancer. Thus, if this study's documentation should be met with any degree
of incredulity, it may behoove the reader to consider the following:
1. Children whose homes and/or yards were treated with pesticides are
believed to be at a greater risk for developing childhood cancer,
according to a study published February 27, 1995 in The American
Journal of Public Health. The researchers, involved with this study,
compared home pesticide use in >52 cases of childhood cancer in
Denver, CO, between 1976 and 1985 with those of 222 healthy
children with similar demographic profiles. Children from birth
through 14 years of age, whose yards were routinely treated with
herbicides and/or insecticdes, had a 4-fold increased risk of soft
tissue sarcomas and malignant tumours of the connective tissues-
62
compared to their healthy contemporaries. Furthermore, the study
found that in?utero exposure to pest?strips, during the 3rd trimester
of pregnancy, increased a neonate's risk for developing leukemia
three times (University of N. Carolina www.enn.com).
2. A review of 61 studies, published in BioEssays 1999, concluded that
the sharp decline in average sperm density, in the western world,
may be even more dramatic than previously believed. For the
University of Copenhagen, 1992, found a 50% decline in sperm
density between 1938 and 1990. A later reanalysis of this,
conducted by the University of Missouri?Columbia, proposes that the
decline most likely exceeds 50%. It is believed that this startling
trend may be attributable, in part, to inadequate amounts of
available estrogen; realising of course, that estrogen is necessary for
the production of healthy sperm (www.cnn.com).
3. High blood levels/concentrations of organochlorines (DDT, DOE,
PCB) have been associated with gene mutations identified in patients
diagnosed with pancreatic cancer. Patients with a formal diagnosis
of pancreatic cancer were 5?10 times more likely to display elevated
organochlorine blood levels-compared to those patients hospitalized
for medical conditions other than cancer. Additionally,
concentrations of both DDT and DOE were most elevated in those
patients expressing mutations in the gene K?ras; K?ras is suspected
63
of being a target for carcinogens. In Spain, where this study was
conducted, 78?100% of analysed meat samples were found to
contain DOE; while 50% of the fish samples contained PCB (Lancet
1999; 354:2125?2129).
4. The organophosphate pesticide, chlorpyrifos, is one of 40 such
compounds, currently being reviewed by the EPA; in attempt to
determine the health risks it may represent, primarily for children.
Chlorpyrifos, produced by Dow Chemical Co., is recognised on the
market as Dursban and/or Lorsban; Dursban and Lorsban are found
in over 800 products with applications inside of homes and
hospitals. The EPA estimates that 20 million to 24 million pounds of
this chemical are applied annually. A recent study of 993 adults
found that 8 in 10 urine samples contained quantifiable amounts of
chlorpyrifos. Even more alarming, is the finding that of 89 children
studied, 9 of 10 urine samples tested positive for chlorpyrifos-in
quantifiable amounts, as well (www.MSNBC.com).
The ubiquitous character of chemical contamination is absolutely
alarming; misplaced, misused chemical compounds dominate our lives and
more importantly, the lives of our children. Forty percent of all human
deaths are directly linked to some sort of environmental influence:
radiation, air pollution, soil pollution, organochlorines, endocrine
disrupters. To deny this control that chemical contaminants exact upon
64
the globe is simply foolhardy. Quite simply then, exposure to chemicals
damages DNA; and damaged DNA misreads coding signals; genetic
misreads precede genetic mutations and genetic mutations precede
cancer-this much is indisputable.
65
REFERENCES
66
1. Firklin, Frank, etal. DeGruchy's Clinical Haemotology in Medical Practice
5th ed. 1997.
2. McKenzie, Shirlyn. Textbook of Haemotology 2nd ed. Williams and
Wilkins: Baltimore, 1996.
3. Jandl, James. Blood: Pathophysiology. Blackwell Scientific Publications:
Oxford, 1991.
4. Miale John. Laboratory Medicine Haemotology 6th ed. The C.V. Mosby
Company: London, 1982.
5. The Bantam Medical Dictionary rev. ed. Bantam Books: New York, 1990.
6. Physicians' Desk Reference. Medical Economics Company, Inc.: New
Jersey, 1989.
7. Hoechst Marion Roussel-information insert for Clomid (clomiphene
citrate tablets USP): prescribing information as of February 1996.
8. The Merck Manual 14th ed. Merck & Co, Inc. New Jersey: 1982.
9. Chan SYW, Wang CCL & Tang LCH: Effect of clomiphene citrate
on human spermatozoal motility and fertilizing capacity in vitro.
Fertil Steril 1985; 43:773.
10. PaIva IP & Koivisto 0: Agranulocytosis associated with
trimethoprimsulphamethoxazole. Br Med J 1971; 4:301.
11. Pisciotta AV: Drug induced leukopenia and aplastic anemia.
Clin Pharmacol Ther 1971; 12:13.
12. www.e.pa.com
13. Couri D & Milks M: Toxicity and metabolism of the neurotoxic
hydrocarbons n?hexane, 2-hexanone, and 2,5-hexanedione. Annu
Rev Pharmacol Toxicol 1982; 22:145.
14. www.atsdr.cdc.gov
15. www.mentor.net
16. Leineweber JP: Fiber toxicity. J Occup Med 1981; 23:431.
67
17. Anderson HA & Selikoff IJ: Biological effects of mineral fibers and
particulates. Environ Hel Perspect 1980; 34:1.
18. Jacobsen D etal.: Studies in ethylene glycol poisoning. Acta Med
Scand 1982; 212:11.
19. Brown CG etal.: Ethylene glycol poisoning. Ann Emerg Med 1983;
12:501.
20. Rickert DE et al.: Dinitrotoluene: Acute toxicity, oncogenicity,
genotoxicity and metabolism. CRC Crit Rev Toxicol 1984; 13:217.
21. www.foodnews.com
22. Lotti M & Becker CE: Treatment of acute organophosphate poisoning.
J Toxicol 1982; 19:121.
23. Barrett DS et al: A review of organophosporous ester?induced
delayed neurotoxicity. Vet Hum Toxicol 1985; 27:22.
24. Colburn T & Clement C (1992) Chemically Induced Alterations in Sexual
and Functional Development: The Wildlife/Human Connection. Princeton,
New Jersey: Princeton Scientific Publishing.
25. Schmidt CW: Childhood cancer: A growing problem. Env Heal Persp
106: A18?A23.
26. Herman?Giddens ME etal.: Secondary sexual characteristics and
menses in young girls seen in office practice. Pediatrics 99; 505:502.
27. Davis DL et al. Reduced Ratio of male to female births in several
Industrial countries: A sentinel health indicator? JAMA 279:
1018?1023.
28. Skakkbek NE etal.: Germ cell cancer and disorders of
spermatogenesis: An environmental connection? APMIS 106: 3?12.
29. Rowley JD. (1989) Chromosome Abnormalities in Human Cancer.
Practice and Principles ofoncology 3rd ed. Lippencott.
30. Cline MJ: NE J Med. 330:5; 528?529.
68
31. Geddes AA, Bowen DT, Jacobs A. Clonal karyotype abnormalities and
Clinical progress in the myelodysplastic syndrome. Br J Haemotol.
1990; 76: 194-202.
32. Alimena G (1984) Cancer Genetics: Cytogenetics 11:300?351.
33. Hagemeijer A et al. (1984) Cancer Genetics: Cytogenetics 11: 280?
290.
34.The IR Web Wizard?sponsored by DanetGmbH
35. Silverstein RM, Bassler GC, Morrill JC: Spectrometric Identification
Of Components 5th ed. Appendix C: Characteristic group absorptions.
John Wiley and Sons, Inc. New York: 1991.
69
APPENDIX 1
Medical Data: Cytogenetics, Flow cytometry reports, Surgical pathology
reports, Hematopathology reports
70
CYTOGENETICS
71
NORTHSIDE MEDICAL CENTER
TOD CHILDREN'S HOSPITAL
BEEGHLY MEDICAL PARK?orUln
HEALTH
DEPARTMENT OF LABORATORY MEDICINE
CYTOGENETICS AND MOLECULAR GENETICS LABORATORY
(330) 740-3765 / 3756
CYTOGENETICS REPORT
PATIENT--? ..., ?
DATE OF BIRTH :5/31/89
HOSPITAL NUMBER :0272192
ACCESSION NUMBER .. : 10 -11 - 2 31M - 9 8
LOCATION
DOCTOR :
REFERRAL : Pancytopenia/ AML
SPECIMEN TYPE : Bone Marrow
SPECIMEN COLLECTION DATE : 10/11/98
SPECIMEN RECEIVED DATE : 1 0/1 1/98
PRELIMINARY DATE: 11 /9/98 " ~
FINAL DATE: 11 /10/98 .~
<45 45 46 47 >47 Total
5 4 1 1 0 0 20
STAINING METHOD : GTG
CULTURES ANALYZED: 4
CELLS KARYOTYPED : 4
RESOLUTIOl\ : 475 Bands
CYTOGENETIC DIAGNOSIS : 45,X,-Y[3]/46,XY[17]
COMMENTS:
All observations were made from direct, overnight, and T-cell and B-cell stimulated cultures. Two cell lines
were detected in this specimen. The first cell line (3/20) contained a modal number of 45 chromosomes
including one X chromosome. However, each cell in this line was missing the Y chromosome. Although loss of
the Y has been shown to be a normal age-related phenomenon in older males, this finding is not common in a
patient of this age. Loss of the Y has been described in AML, often as a secondary change. The second cell line
17/20) was the normal male karyotype.
I!
I
12;97)
'WSw'"' p, f. 'fie
~Medical Director, Cytogenetics
500 Gypsy Lane'Youngstown, Ohio 44501 . Phone (330) 740-3767 . Fax (330) 740-3790
WESTERN RESERVE CARE SYSTE:.:..;.M'---_
Forum Health / Northside Medical Center
Department of Cytogenetics
Patient Narne~
Accession No.:lO-11-231M-98
Karyotype Designation:
Date of Birth:5/31/89
Referring Doctortllllllllllllll
Doctor Drawn~  
Slide List:6A 173.7x4.6 (2) kary
Resolution:500 Bands
2 3 4 5
~~ ~~ ~n XI a" r" 3ftl
6 7 8 9 1 0 1 1 1 2
r. r~ .41 'i ~e\ .~ a~ ,.,14
1 3 1 4 1 5 1 6 1 7 1 8
&i tir. :c(~ ... .... I." I( ...,.
1 9 20 2 1 22 X Y
Forum Health / Northside Medical Center
Department of Cytogenetics
ltient Name:I 8cimen #3)
:cession No.:11-9-252M-98
lryotype Designation:46,XY[1]
lte of Birth:5/31/89
~ferring Doctor:
Jctor Drawn:
.ide List:8A 137.5x22.1(1)kary
~solution:500 bands,
~{ ~~
K~ ?11 .~t'~~ ?.
2 3 4 5
}{}( ,--- lt~ ~~ J\~ ~ ,--- t.. It" ...,, f .
6 7 8 9 1 0 1 1 1 2
A,. ftt'\ ~" f' )f, \I. ., :..~ ii ........
1 3 1 4 1 5 1 6 1 7 1 8
1 9
"1l
20 2 1 2 2 x y
Page I 0
. CHILDREN'S CANCER GROUP
CYrOGENETICS REPORTING FORM
To be completed by the Institutional Cytogeneticist
and submitted to the Group Operations Center.
t:lT.It.,.~ T.:II.R.1i!T, nF.~F.
STUDY 10: 2981 - E - 10
REG#. 50095
PTNAME: /r .
(E/10)
LLI Sex
12 Male
2= Female
"
Lab case No.: _
DatcJtime specimen collected:
Date/time specimen received:
I-LLLU2J.1J.3.J..:('M MOD Y Y
1_'_~\....Q...LLL2J-lJ
M MOD Y Y
\ ,30 ~M~
__,_3_0__ ,A~I/?)
Type ofspecimen: check all that apply (fill out separate form for each type of tissue)
I v1 bone marrow aspirate
LI bone marrow biopsy
LI peripheral blood
LI lymph node
LI other (specify) _
If unsatisfactory results, check boxes
c.' <:> I-\-ed10:,poor sample (c1011ed, hypocellular, contaminated, etc.)
interphase nuclci prcscnt but fcw or no llIctaphascs
poor quality metaphascs and/or inadcquatc banding (Note: even though unsatisfactory results,
plcase fill in the processing information on the back of the page).
~I o
LI
Notc: Evcn if t11e study was inadequatc, please fill in t11C processing information on t11e back ofthis page.
Additional Comments
V'c-h-?-t-h. " .....~\- ~ r W<!>3
~ C\Y"\ ~'"'\ Co d ...c.e. ~v
C.1.:Y'\.H <t s ,x - Y /4b,XY "4c..
.,...,..,.e. ~he~e...s C (, ~ J).
(0(Y) l-k:ul th -T(
Name of Institution
I
rt715
eeG 3/28/97
CHILDREN'S CANCER GROUP
CYTOGENETICS REPORTING FORM
. PLACE LABEL HERE
,..40 ......... Tn
SWDY ID: 2961 - E - 10
REG#. 50005
PT NAtv1E.
(E/10)
rage 2 of.
?PROCESSING INFORMATION (Fill inlhc nwnocr ofcells obtainco from each processing mclhod A, B, C, or D.)
A B C D TOTAL NO.
NORMAL D 0 i I
CLONE-I
CLONE-2
CLONE-3
ABNOIUvtAL
NONCLONAL
TOTAL NO, 0 0 \ 0 I
Specify type of processing ano the tn>e ofoanding uscd for cach ofthe Icllcrcd boxes above.
A. v? (C d- _ (..lr...
B. OJSY'V\",CjI.,:: (L'6-
C. B- C e\ \ .sf, "",,,",I ~-kd - CrTC--
D. 1 :: l. e [I '), h M '"' (?.4?d - 6-I G-
List kaI)'otypcs of each donal ano nondonal cell (ISCN 1995. DO NOT include cclls \ViUI random loss as nonclonal
abnonllal cells.)
NORMAL: 4-'0 i xy C.i J
CLONE-I:
CLONE-2:
CLONE-3: _
NONCLONAL-l: _
NONCLONAL-2: _
NONCLONAL-3: _
GGG 3128/97
NORTHSIDE MEDICAL CENTER
TOO CHILDREN'S HOSPITAL
BEEGHLY MEDICAL PARK-- $0nun
HEALTH
DEPARTMENT OF LABORATORY MEDICINE
CYTOGENETICS AND MOLECULAR GENETICS LABORATORY
(330) 740-3765 / 3756
CYTOGENETICS REPORT
PATIENT
DATE OF BIRTH : 5/31/89
HOSPITAL NUMBER :0272192
ACCESSION NUMBER : 11-23-268M-98
LOCATION
DOCTOR :
REFERRAL : AML
STAI~I:"IG METHOD: GIG
CULTURES ANALYZED: 1
CELLS KARYOTYPED : 1
RESOLUTION : 525 bands
CYTOGENETIC DIAGNOSIS : 46,XY[1]
SPECIMEN TYPE : Bone Marrow
SPECIMEN COLLECTION DATE: 11/23/98
SPECIMEN RECEIVED DATE: 11/23/98
PRELIMINARY DATE : 1 2/9/98
FI:"IAL DATE: 12/10/98
<45 45 46 47 >47 Total
0 0 1 0 0 1
COMMENTS:
Ten cultures were initiated on this specimen including direct. overnight and T- and B-cell stimulated
cultures. Only one metaphase was observed in the T-cell stimulated culture and was apparently the normal
male karyotype. However, due to poor growth of the specimen, the possibility of chromosomal mosaicism
involving abnormal cell lines cannot be excluded.
--"-'McdicalDirector, Cytogenetics
500 Gypsy Lane? Youngstown, Ohio 44501 . Phone (330) 740-3767 . Fax (330) 740-3790
;12/97) WESTERN RESERVE CARE SYSTEM
.. .. v <, ,. ~. '.,' , .'~' ~ ? ? ? - f. ':....,-;' ~ : ...' ", .. "l- ' ? ~:
NORTHSIDE MEDICAL CENTER
TOD CHILDREN'S HOSPITAL
BEEGHLY MEDICAL PARK-- $orum
HEALTH
DEPARTMENT Of LABORATORY MEDICINE
CYTOGENETICS AND MOLECULAR GENETICS LABORATORY
(330) 740-3765 / 3756
CYTOGENETICS REPORT
'ATIENT
)ATEOFBIRTH :5/31/89
IOSPITAL NUMBER : 0272192
~CCESSION NUMBER : 12-9-277M-98
~OCA nON ===::::-.....)OCTOR :.
~EFERRAL : AML
iTAINING METHOD : GIG
:ULTURES ANALYZED :3
:ELLS KARYOTYPED : 4
{ESOLUTION : 550 bands
CYTOGENETIC DIAGNOSIS : 46,XY
SPECIMEN TYPE : Bone Marrow
SPECIMEN COLLECTION DATE : 1 2I 9 I 98
SPECIMEN RECEIVED DATE: 12/9/98
PRELIMINARY DATE : 1 /7I 99
FINAL DATE: 1111 199
Cells counted
<45 45 46 47 >47 Total
0 6 1 6 0 0 22 t'--
":
;.'
COMMENTS:
'Jormal Male Karyotype.
~II observations were made from T and B cell stimulated cultures. Please note that although 6/22 cells were
lypodiploid, all displayed random, nonclonal chromomal loss. !;
I
No chromosome abnormalities were demonstrable at this level of resolution,
Please remember that this analysis does not eliminate the possibility of single cell defects, chromosomal mosaicism
involving abnormal cell lines of low frequency or small chromosomal structural abnormalities.
Medical Director, Cytogenetics
.....
Forum Health / Northside Medical Center
Department of Cytogenetics
Patient Name
Accession No.:12-9-277M-98
Karyotype Designation:46,XY
Date of Birth:5/31/89
Referring Doctor:
Doctor Drawn:
Slide List:6A 152.4xl0.5kary(2)
Resolution:550 bands
5
x y
1 8
1 2
w6
A
4
17
1 1
1 6
1 0
;., -. Si~ ~ , ~ ~~
1 9 20 21 22
rr , f f
2 3
fJ ~ " ?,
~, .,.~
6 7 8
Qt ~ ~ ~ e
1 3 1 4 1 5
~orurn NORTHSIDE MEDICAL CENTERTOD CHILDREN'S HOSPITALBEEGHLY MEDICAL PARK
HEALTH .
DEPARTMENT OF LABORATORY MEDICINE
CYTOGENETICS AND MOLECULAR GENETICS LABORATORY
(330) 740-3765 I 3756
CYTOGENETICS REPORT
PATIENT :"., =.z:~:-=. -:: .'-~
DATE OF BIRTH : 5/31/89
HOSPITAL NUMBER : 0272192
ACCESSION NUMBER : 12-30-294M-98
LOCATION
DOCTOR :
REFERRAL : AML
STAINING METHOD : GIG
CULTURES ANALYZED :2
CELLS KARYOTYPED: 4
RESOLUTION: 550 Bands
CYTOGENETIC DIAGNOSIS : 46,XY,
COMMENTS:
SPECIMEN TYPE : Bone Marrow
SPECIMEN COLLECTION DATE: 12/30/98
SPECIMEN RECEIVED DATE : 12/30/98
PRELIMINARY DATE: 1/15/99
FINAL DATE: 1/18/99
Cells counted
<45 45 46 47 >47 Total
0 3 17 0 0 20
Normal Male Karyotype. All observations were made from T cell stimulated cultures.
No chromosome abnormalities were demonstrable at this level of resolution.
Please remember that this analysis does not eliminate the possibility of single cell defects, chromosomal mosaicism
involving abnormal cell lines of low frequency or small chromosomal structural abnormalities.
--.-.Medical Director, Cytogenetics
500 Gypsy Lane? Youngstown, Ohio 44501 ? Phone (330) 740?3767 ? Fax (330) 740-3790
(12/97) WESTERN RESERVE CARE SYSTEM
~. ? ". ~",,~'.,' , '. ~. '. I. , ? ? '....,. ? ~ .. ??~ or-
Forum Health / Northside Medical Center
Department of Cytogenetics
Patient Name:~-~ --- ,
Accession No.:12-30-294M-98
Karyotype Designation:46,XY
Date of Birth:5/31/89
Referring Doctor? ............
Doctor Drawn:
Slide List:6A 129.2x5.8 (2) kary
Resolution:575 Bands
y
I
x
1 2
t"(
1 8
t
11
lf ({
t' "4 5
'f{. ,), i'~ 11 1r
tl
1 3 1 4 1 5 1 6 17
i~ ,c ... , \?6-?
19 20 21 2 2
:;('C 4
171
6{{
NORTHSIDE MEDICAL CENTER
TOO CHILDREN'S HOSPITAL
BEEGHLY MEDICAL PARK$orum
HEALTH
DEPARTMENT OF LABORATORY MEDICINE
CYTOGENETICS AND MOLECULAR GENETICS LABORATORY
(330) 740-3765 I 3756
CYTOGENETICS REPORT
PATIENT
DATE OF BIRTH :5/31/89
HOSPITAL NUMBER :0272192
ACCESSION NUMBER : 2 - 18 - 37M - 9 9
LOCATION : Pediatric Oncology
DOCTOR :.........
--~FERRAL : AML
SPECIMEN TYPE : Bone Marrow
SPECIMEN COLLECTION DATE : 2/1 8/99
SPECIMEN RECEIVED DATE : 2/1 8/99
PRELIMINARY DATE :3/18/99
FINAL DATE :3/18/99
Cells counted
STAINING METHOD : GIG
CULTURES ANALYZED : 8
CELLS KARYOTYPED : 6
RESOLUTION : 550 Bands
CYTOGENETIC DIAGNOSIS : 46,XY
<45 45 46 47 >47 Total
2 1 1 7 0 0 20
COMMENTS:
Normal Male Karyotype.
All observations were made from direct, overnight and T and B cell stimulated cultures. Although not clonal,
several structural abnormalities were detected in the T-cell stimulated cultures which included: one cell
'th an apparent translocation between the long arms of chromosomes 11 (at band 11 q13) and 15 (at band
_."22) and loss of the Y chromosome; and one cell with a translocation involving the long arms of
chromosomes 8 (at band 8q24.1) and Y (at band Yq12). Rearrangements involving chromosomes 8 and Yare
often seen as secondary changes in AML, and are not specific to any particular FAB subtype. Clinical
correlation is necessary.
No chromosome abnormalities were demonstrable at this level of resolution.
Please remember that this analysis does not eliminate the possibility of single cell defects, chromosomal mosaicism
involving abnormal cell lines of low frequency or small chromosomal structural abnormalities.
lrector, Cytogenetics
edical Director, Cytogenetics
500 Gypsy Lane' Youngstown, Ohio 44501 . Phone (330) 740-3767 ? Fax (330) 740-3790
(12/97) WESTERN RESERVE CARE SYSTEM
Forum Health / Northside Medical Center
Department of Cytogenetics
Patient Name.
Accession No.:2-18-37M-99
Karyotype Designation:46,XY
Date of Birth:5/31/89 .Referring Doctor:
Doctor Drawn:
Slide List:1A 156.3x20.6(2) .kary
Resolution:550 Bands
KX ~ ? J'! 1< It Jt A /It ,.'-; ...., ., ;-.....' " ,~, ,,-
1 0 11 1 2
I)f"-\., "fa t\ fl ;c..." ~ .'\ A~~
1 3 1 4 1 5 1 6 17 1 8
J' ?? . ... .... .. ..;" , ? /'>II"",
1 9 2 0 2 1 2 2 X Y
FLOW CYTOM ETRY REPORTS
72
.? ' ~.J
, i" l
I "
-- ........, ..., r..I__iilHi.:toP" .......~_ .... ~_~ ???_._ ?.?
UGI-cc-tltl IHU lU:qc Hi'i rUKUi'i I'jll\" ~tiIHULUu'y H\K ~~:if1~d~I~l.Jj/j~/A
NORTHSIDE'MlmrCAl CENTERantm
TOO CHILO~~~~'HOSPITALBEEGHLY MEtJIOA[ PARK
H E A L T H<:'!;:j.",?
DEPARTMENT OF LABORATORY MEDICINE
r. U<i
"', 1""\ ~J Y" ',I '.j)UI
T307B (TOD 3)
BBlBO X7
1798-0460
S9B-13175
0272192
002721920011
PAT LOC:
CPT CODE:
ACCESS NO:
R.EFERE)lCl:l NO,
HOSP NO:
ACCOUNT NO:
FLOW CYTOMETRY CONSULTATION
PATIENT:
SURGEON:
RESIDENT:
ATTEND PH'll ??? 21 ...
COpy TO PHY:
DATE OF OPERATION: 10/11/98
DATE 0' ACC~SSION: 10/11/98
DATE OF REPORT: 10/17/98
\I
~,.
- -J}{
PREV Ace: F98-0416 598-13470 598?13175 X98-30aa 594?07494 S89-09860
,.:.
S~EC~N SUBMITTED: 1\: BONE MARROW
Numbar of cells ex~ined: 0,12 million/cc .~
Description: Marrow smeara ehow emall numbers of ~ematopoietic cells withdyapoietic features. Light scatter studies show indistinct marrow cell
population with decreased maturation of myeloid cells. A" distinct and
moderately heter~geneous lymphoid population is seen.
CD19
Kappa light. chain
Lambda light chain
T-cell Antigens
C02
CD]
CDS
CD7
Myeloid Antigens
CD13'
CDH'
CO]],
Other Antigens
CD45
COlO (CALlJ\)
CD34
Dual posit.ivit.y
CD19 and CD10
CDH and CD7
\' p0E!i!:ive
22
Non-specific binding
Non,specific binding
\' positive
56
35
38
70
\ positive
16
11
39 ,.
t positive
100
1
23
\' positive
1
22
','
:~.
" 
"
IfOlt/l' UJ7l
500 Gypsy Lane' Youngstown. Ohio 44501 ' Phone (330) 740?3767 ' FalC. (330) 740?3790
WESTERN RESERVE CARE SYSTEM
lS&lW!!lUl!iWMUS::dJa WldiZl& & &ZiditEi2:z.dtZa a
...,
j?
!t~
FLOW CYTOMETRY CONSULTATION
PATIENT: ',.:.,'-_, __ ,
ADDRESS:
10/16/98
10/16/98
10/16/99
??j t
F98-04'16
598?134700272192'
002721920011
T307B (TOO 1)
88180 XS
DATE OF OPZRATION:DATI or ACCESSION:
DAft OF REPOR.T:
ACCESS NOI
stUERENCE )TO:
HOS' )10:
ACCOtnn' NO:
PAT LOC:
CPT CODE:
S9~-07~94 589-09860599-13470 598?13175 X9B-30B8
SURGEON!
RESIDENT:
ATTEND PH'llCOpy TO PHY:
PREV ACC:
AGE/SEX: 91 M
BIRTHDATF.::05!31!1989SOC SEC: e. ??
SPECI~N SOBMITTEDI A: LEFT RETROPERITONEAL LYMPH NODE,
NEEDLE BIOPSY
C019 and COlO 0.3
B-c~ll Antigens \- ,Positive
Dual positivity ~ .1lositlve
i'"
:',.
~ t
y
r.,.
~'"
~ ..
to
~ ?,
;.
'.f,,-'.
I':
s.
r.,
I.
. ,
"Ii.
ii
~
\
::':{I
I
...,
I'
I,.
'.,
.-.,
Method;
COMMENT: OUQ to small sample size a limited study was performed. No'
monoclonal lymphoid population was identified. A more adequate sample is
recommended for diagnostic evaluation. See also surgical pathology r~port
598-13470.'-'.
INTER.PRETATION:
LEFT RETROPERITONEAL LYMpH NODE, NEEDLE BIOPSY, FLOW CYTOMSTRIC
IMMUNOPHENOTYPIC ANALYSIS, MCNOTYPIC LYMPHOID POPULATION NOT IOiNTIFIEO,
SEE COMMENT.
jt
C045 9COlO
(CALLA) 0.6
C019 0.4
Kappa light chain 0.2
Lambda light chain 0.1
Other Antigens t positive
Viability; gO\-
Number of cells examined: 0.05 million/cc
Description: Cell suspension show. fQw lymphoid calls intermixed with
moderate amount of red blood cells. Light scatter studies show no diatinct
l~nphoid population. '
!FO't1 (11197)
600 Gypsy lane ?Youngstown, Ohio 44501 . Phone (330) 740..3767' Fax (330) 740?3790 .-.r
~',
......~III _ -..?XS_?. '.:::~'I'~-
t"'. Uti
-'I'?? " r??6 ,
':";.. : 't \"
[ LL.. ....
NORTHSIDE MEDICAL CENTER
TOO CHILDREN'S HOSPITAL
BEEGHLY MEDICAL PARK
OCT-23-9b Fkl IU:U3 AM ~UKUM NMG PAIHULUGl
$orum
HEALTH
DEPARTMENT OF LABORATORY MEDICINE
1
FLOW CYTOMETRY CONSULTATION
PATIENT;
ADDRESS: .-.
AGE/SeX: 9Y M
BIRTHDATE:OS/3l/1989soc
SEC:
ACCBSS NO: F9B-0492
JUlPBRBNCZ NO:
HOSP NO: 0272192
ACCOUNT NO: 002721920011
PAT LOC: T307B (TOO 3)CPT conK:
BB190X~
SURGEON:
RESIDENT:
ATTEND PKY:
COpy TO PH'{:
PREV Ace: 598-13539 F98-047G
S94-07494 589-09860
DATE or OPBKATION; ~O/20/9a
DATE OP ACCESSION: 10/20/98
DATE or REpORT: 10/22/98
--ew
598-13470 F98-0460 S9B-13175 X98-308S .;-
.~.
Number of cells examined:
A: BONE MARROW AND PERIPHERAL BLOOD
a-cell Antigens
COl9
Xappa light chain
Lambda light chain
T-cell Antigens
Method: FACS Lyse
t positive
3.2
Non-specific
Non-specific
t positive
t positive
11.1>
Non-:specitic
Non-specific
!....:positive
C02
C03
CDS
C07
68.1
56.5
56.4
91.5
63.5
56.S
56.4
80.4
Myeloid Antigeng
CDl)
COB
CD33
Other Ant:igens
CD45
COlO (CALLA)
CD34
~ pogitive
12.6
2.2
27.7 (gated)
\- positive
93.2
1.5
16.3
,positive
14.7
9.1
29.5
\- positive
99.5
<1
14 .1
, (12197)
500 Gypsy Lane'Youngstown, Ohio 44501 ? Phone (330) 740-3767 ? Fax (330) 740?3790
WESTERN RESERVE CARE SySTEM
.'f
Ii.
NORTHSIDE MEDICAL CENTER
TOO CHILDREN'S HOSPITAL
BEEGHLY MEDICAL PARK~ __~$orun1
':'"::H--::E~A~L~T~H~---
DEPARTMENT OF LABORATORY MEDICINE
1
FLOW CYTOMETRY CONSULTATION
PATIENT:
ADDRESS:
\ t;
OPERATION: 02/18/99
ACCESSION:_~2/18/~~~
REPORT: ~::~:~~~~
898-16359 F98-0543
898-13639 F98-0476
889-09860
ACCESS NO: L99-0068
REFERENCE NO:
HOSP NO: 0272192
ACCOUNT NO: 0027219 94
PAT LOC:
CPT CODE: -.;::..~u..tlo~:C::...._ ....
DATE OF
DATE OF
DATE OF
898-17346 X98-3909 F98-0564
X98-3394 R98-00245 F98-0482
898-13175 X98-3088 894-07494
F98-0591
X98-3529
F98-0460
AGE/SEX: 9Y M
BIRTHDATE:05/31/1989
SOC SEC:
SURGEON:
RESIDENT:
ATTEND PHY:
COpy TO PHY:
PREV ACC:
898-15570
898-13470
SPECIMEN SUBMITTED: A: BONE MARROW
Method: FACS lyse
Number of cells examined:
B-cell Antigens
CD19
Kappa light chain
Lambda light chain
T-cell Antigens
CD2
CD3
CD5
Myeloid Antigens
CD13
CD14
CD33
Other Antigens
CD45
CDIO (CALLA)
CD34
Dual positivity
CD19 and CDIO
% positive
1
Non-specific staining
Non-specific staining
% positive
4
7
4
% positive
6
8
18
% positive
41
<1
2
% positive
<1
500 Gypsy Lane? Youngstown, Ohio 44501 . Phone (330) 740-3767 ? Fax (330) 740-3790
WESTERN RESERVE CARE SYSTEM f_.__
~ Ukt_Z4-0;:;;;;&;;;97)??Jij?US4dW iUtiJWtUSS_
SURGICAL PATHOLOGY REPORTS
73
SURGICAL PATHOLOGY REPORT
r, UO
PATIEN'l':
ADDR.lSSS:
AGE/SEX: 9Y M
BIRTHDATEIOS/31/1989
SOC SEC:
ACCESS NO:
HOSP ~O:
ACCOON"l' NO:
PAT LOC,
CPT CODE:
598?13175
02'72192
00272l9200ll.
'1'3079 (TOO 3)
09305/88311/66313 X2
~~:'- {-
-; .
~ ~:
"i:'
-\
"
St1R.GEON:
R.ESIDENT:
ATTEND PHY:COpy TO PUY:
PRE 01' DX:
OPERATIONl
POST OP OX:
HISTORY:
R/O HiTS.
BIOPSY
ALL, RiO MATS.
POSS. ALL
DATE OF OPERATION: 10/11/9A
DATE O~ ACCESS10N, 10/12/99
DATE OE' RBPOR.T: 10/17/96
? -.AnS "
PRi:V Ace: X98?3088 SH?074H 589?09960
TISSUES REMOVED: A: LT. PSIS eM SIOPSY AND
ASPIRATION
INTRA/EXTRA CONSULT: INTRA
FINAL DIAGNOSIS:
BONE MARRO~. BIOPSY, MILD PANHYPOPLASIA WITH
OYSPOIESIS. SUGGESTIVE OF
TOXIC MtELOPATHY. SEE: COMMENT.
COMMENT: Sec~ions of bone marrow biopsy rQvaal
a generous segment of marrow
Ghowing 30% cellularity. There are moderate artifactual
~d degenerativQ
changes of the marrow presumably due to prolonged
marrow storage in R.PMI
~olution. All cellUlar components
appear represented but there is a moderato
shift to the left with moderate dyspoietio features
of all three cell lines.
Occasional small aggregates of lymphoid cells
are-noted which appear to have
atypical morphology. Also noted scattered within
the marrow ate increased
numbers of histiocytic cells. Thera also appears
to be a focal increase in
reticular fibrosis. No blastic infiltrates. or
granulomata are noted. Bony
trabeculae appear unremarkable. Stainable iron
stores are essentially absent.
The histologic f~atures are somewhat obscured
by ~rtifacts induced by
prolonged storage in RPMI solution. The overall
left shift in maturation.
dy~poietic features, and hypocellularity
suggest the possibility of a toxic
myelopathy. No evidence for acute blastic leukemia
or aplastic anemia is
present. A repeac bone marrow biopsy and bone
marrow aspiration for flow
cytometric immunophenotypic analysis is recommended
for more definitive
evaluation if pancytopenia persists. See also
Flow Cytometry immunophenotypic
analysis report F98-0460.
GROSS: ~. Received is a cylindrical fragment
of firm tissue measuring 3.3 x
0.2 x 0.2 em, The specimen is eubmitted
entirely in 1 cassette. OG/NSN/adb
jki
500 Gypsy lane'Youngstown, Ohio 44501 . Phone (330) 740?3767 ?
Fax (330) 740?3790
WESTERN RESERVE CARE SYSi'EMII
"?I?Dait'iI~XlIiSJU~i?MWi&iiJEza;:u:
!"ri'''11V. JJUI'iUJiJ) r. l)(.
NOATHSIDE MEDICAL CENTER
TOO CHILDAEN'S HOSPITAL
8EEGHLY MEDICAL PAAK$orum
HEALTH
DEPARTMENT OF LABORATORY MEDICINE
SURGICAL PATHOLOGY REPORT
PATIEN"r~
ADDRESS:
AGE/SEX: 9Y M
BIRTHDATE:05/31/1S8S
SOC SEC:. 7
ACCESS NO:
HOSP ~O:
ACCOUNT NO:
PAT LOC:
CPT CODE:
S99?13639
0272192
002721920029
T307B (TOO 3)
88305 X4/88311 X4
SURGEON: _
RESIDENT:
ATTEND PHY:
COpy TO PHY:
OATS OF OPERATZON: 10/20/98
DATE OP ACCESSION: 10/20/98
DATS OF REPORT: 10/22/98 ..
"
PRE 01' DX;
OPERATION:
POST OP DX:
HISTORY:
PANCTIOPF;NIA
BILATERAL aONE MARROW ASPIRATE AND ax,
SA11S ? -ADS
PREY Ace: F96-0476 599-13470 F98?0450 598-13175 X98?3088 594-07494
589-09860
TISSUES REMOVED: A:
B:
C:
D:
RT, ;,sIS
LT. ;,sIS
RT. PSIS
LT. PSIS
INTRA/EX'!'RA CONSULT: INTRA/EXTRA .II.(I!I~~~ ???UNIVERSITY OF NEWMEXICO SCHOOL OF MEDICINE)
FINAL DIAGNOSIS:
A. RIGHT ANTERIOR BONE MARROW BIOPSY, DYSPOI8TIC BONE MARROW SUGGESTIVE OF
MYELODYSPLASTIC SYNDROME (SEE COMMENT) .
B. LEFT ~~ERIOR BONE MARROW BIOPSY, DYSPOIETIC BONE MARROW SUGGESTIVE OF
MYELODYSPLASTIC SYNDROME (SEE CO~NT) .
C. RIGHT POSTERIOR BONE MARROW BIOPSY, DYSPOIETIC BONE MARROW SUGGESTIVE OF
MYELODYSpLASTIC SYNDROME (SEE COMMENT) .
D. LEFT POSTERIOR BONE MARROW BIOPSY, DYSPOIETIC BONE MARROW SUGGESTIVE OF
MYELOD'{S~LAS'I'IC SYNDROME (SEE COMMENT) .
COMMENT: The bone marro~ biopsies (A,a,e,D) show similar histologic features.
The biopsies are normoc@llular to mildly hyperc@llular for age (SO to 9Q~
cellularity), Megakaryocytes are present and showed dyepoietic morphology.
Micrcmegakaryocytes and uninucleate mesakaryocytes are identified. Rar@ foci
of empcripolesis is also noted. Myeloid and erythroid precursors are present
and show dyspoietic maturation. The myeloid series show near maturation
arrest with only scattered mature myeloid cells present. Blasts appear
increa~ed and comprise approximately 10 to lS~ of nucleated marrow cells.
Erythroid precursors appear somewhat decreased and show mild dyspoietic
features. On PAS stained sections, the M:E ratio is approximately 4:1.
Mildly incre~ged number of histocyte; are present in the bone marrow,
500 Gypsy Lane? Youngstown, Ohio 44501 . Phone (330) 740-3767? Fax (330) 740?3790
WESTERN RESERVE CARE SYSTEM
~,i
I
)
~I
?
HEMATOPATHOLOGYREPORTS
74
UNM Department of Pathology'Trlcore Reference Laboratories
2211 lorna, Blvd HE
IIlbuqutrque. NM 97100
iiiJl-Uj-vd IUt lU: Ib Hii
1 1-~2-1998 4:05PM
Director: c.. ??:
.. ,' ""I, ,....._'.
nh?9r1osisl
pf.RIrH?RAL BL(~o:
PANCYTOPENIA WITH VYSF0IETIC CHANGES AND R~R~ ELA~TS
p,mlE~lAT<.ROW TOUCH PRF.PM::ATION AND RIop:aE5:
U.<\LIGNMl'l' BO~lE :-L\nnow XNFIUrPA'l'1! (SEE COWlStIT)
Electronic Sign~ture(5)
Pict~t.ed by:
R1)port OatefTime: 11/02/98 1602
Continued ...
HLE:CL ;el,
Comment:
The exten~iv~ ma~~ow infiltrate of larqe ~,ll~ ii morphologically molign~nt
and i~ not comp~tibl~ with a ~~~o~ive prOCQJ~. The prQsance of dyapoietic
cnCln9't!!: in th~ peri~h~ral blood suqqests th~t l:he IltarrOV' I1tal ign",ncy likely
r~p~";'!nt9 "3 my<;:toiJ prOCQiOl: (l:uch 35 high gra<1a myelodyzpla,'3ia).
Ilowever/ WE:!
WQrQ un~bl~ to char~cteri%9 th~ ~henotYP9 of tha la.qe in~ature app~~ring
c~lls by inrn~nopero~ioae~ staininq.
TO better characteri~e this di~order a rQpeat bone m~rrow exarntn~tlon \~i~h
furthar ~aterial for ~pecial studiog would be h~lpful. If a hone marrow
3zpiratg c~n be Qb~ain0d. fresh mat~rial ~ent for flow cytometric and
cyto9gnG~ti'; Eltudi9'!) EI.~ well as morl'holoqy ..,Quld be useful. II: an
a~pi.rtl\:e
C'lnnot b~ cbtained. l'xtra touch preps should he made tor bot.h cyto-:h(.!m;c::~i
:;tlli.Tls ,m<1 ill\ll1\mohi"tochemi,try. In addition, <'In \lnrix~d. bonQ m",rro',' core
hiopsy w~uld bQ u~e(ul (fr9sh cell~ can !om~tim~s be rGcovered fram blopsiQ~
for !low/cytoqanatlc studi~~) . We sh~ll be glad to provide any further
a~slscan~c on th~ optim31 ~athod of transporting/processing the~e
specimen~.
~'his ca;?! was r~viewed and dif'C\\'33ed with Dr. Kathy Foucar 1'1))
who CQncurl2 with
thQ interpret~tion.
~~F.~rr~l Acc~ssion NUmber:
~ecpivQd: 1 ~lida l~b~led ?~~~6J?lp?, 2 slid~~ labeled "9B-63?IP",
5 slidQI
labg10d "598'13639" and 1 block labqle~ ?~lJ51~?5".
returned; B ?lid~6 and 2 block.
Clinicl.\l Pllt~;
The pati~nt 19 a ~rQViou01y he~lthy nine-year old male. He prc~ent3 with ~
two?~onth hittory of feelin1 ~undo~n. A compl~te blood count
reveale~
pancytoo~ni~. periphetal blood p~ra~eter~ on lO?26?9a T.~port~o
~! follow~ ~t
th~,~
Copy To~ Patient Name:
MedIcal Record #: (00000)004256776
RclerrallD #:
lnr:ation: REF Page: 1
,.. ,.... ',..... : ,.,.",:,;". :ti~II~~-tO./Ut!!t ..YO".',.. !": ....;.:~' .. ,...'."==zJ: ."", ,I I. ?' .. ??f1~JY'M? .r;,R '16,' uT "... ';'"r";", ...~;
..,.:?.';H.;;.~ ...;?I;; ::,"'! ! .? ,.--, .'!_"=:"'''''l-:;:Lh?},';';'.ol~i~
Olrtetnr:
Clinical Dl'Itl\'
,
'.
.;~ij.?
_ .::',.4
PcalleritNamo:' {(;.: .~:..;:;.; ....:;~c? ' c?-:~/;{
M~dica' A.eOi'd..'~:.(O)x>OO)0042S6776 ~t.:" ..." _ .'.._'
DOB: OSl31/1M9~~.4?&: 9 y~S '\Sex: M '.? ~ ;1";:'
Itccoun' Numb": 0111067435
Ordered by: .?f?????
Accuslon No.: HA?98?0011 S9
Date Collected: 10/23/98
rUKUIi NilL: t-'HIHULUGI rH;\ NU. jjUI4Uj(j:J
FROM UI'JI'1H PI\TH LAB 5125 272 0:id0
UNM DepRrtment of Pathology/
Trlcore ReferQnce Laboralorles
221 t Loms.!l Blvd NE
Albuquerque, NM 87106
tluV-Uj-~b IUt lU: 1b hI!
11-e2-1 998 d I c:lGPH
peripheral blood smear~
\'IFlCI 1.5 X lOf.3/11lm:J
P.RC, 3.1 X lOEb/mm3
I1q1>1 9. <1 g/tll
Hct: :17 %
Plt~' ~3 X lOE3/mmJ
MCVI 85 n
,wvr'Cv: 13 \
Neut:
Lrmph:
MOnO,
[;0:
Baso:
3.3 "
75 '"15 Is
o \
G '\
MI)T.'pt)Ology,
Peri~horal Blo01 Sm~~r:
'l'he blOod !'m~ar show~ p~ncycpelli~. RGod :::~119
thaw modenl \;e
ani~opoikilocyto3iA. Plate16t~
includQ larq~ ~nd hypoQr~nular formR.
N~~t~ophils a.e m~rKcdly reduc~d
but show nor~~l granvla~ion. Rare ul~~ts ~re
idG:ntil:i~d.
Don~ Matrow Aspirate/Touch prep?Clot
~nd Diopsy:
::;1:in~5 clepict t()\lch preps ann
hone. mClrrow cora: biopsy. TOllch pr~p!; are
pftucicell~l~r but show num~roU6
1arQQ, ~typical hem~t0pQletic cells with fin~
lind d'?lic~te chromatin. Ml\t\\rino ho?m<l:opo1etic
Ql~me:H.5 ,H'e also seen
Tho bon~ marrow COL'~ biopsy shOW:i variable c'!!l11ular1t.y.
oVl!rt.ll apPl:o:"':.i.mat'l!ly
80\ celhllar. M~g(\k1\ryoc:rt~tl nre e<'leily idcntifiE::~'
hut. in !':1(\IlY C1l"e$ au:
em"ll an<i 13olT',cwhat atypical. Th'" m~rrOw itt
involv~d b:r' a. diHu!l'" intcr~ti.ti:~l
infilt~,,~e of lar'1E::, abnorm41 bematopClietit:'~pp<!arin-;;
cs;:ll.. 'l'h/2se c911s show
round to slightly irr~;ular nucleClr con~Qur$,
v~$icular chrQ~atin, occasional
nucleoli ~nd ~cant to mod6rately abundant cytopla~m.
7he erythroid lineAae l~
-iec'C<;!~ITC'd. Mult:.iple large lymphoid
<\ggriogatli~ arQ id~nc.irJ",d.
I/Ml\lnopbenotytll? :
ll'l'Jl\unohi~to-::h9mical ot3in.':I perfcrm'!!d
Oll pllraffin?Qmbr?uded t.iE=s\JQ at.
ttle
Univer~lty of New Mexico rg~.~l
th2 following! myeloperoxida,e at3in~
OCC1'.!>ion~l HIOnlJn'lClear c;;~11$, ll\ai:lly
with morphology 9ugg~!tive of
promyp.locytes or myeloc;;yt~s. Therg i~ rare,
equi~ocal staining of the
<lbtlOIlllal cellf'. CD)11 stains b100(\
V'l?SIlls anti a llm~ll minori ty of.
the
abnormal c~119. CD) and CD20 ~tain l~phocyt~;.
H~moqlobln A Stain, rare,
gc~tter~d islQnd~ of erythEoid
ptecursors.
R_vj"WEld by:fttlSn....,....'?????S II
Copy To:
A~por1 l)a'efTime: 11/02198 1602
Conllnued , ..
Patient Name= 
M&dical Record II: (00000)004256776
RefflfTallO It:
Location; REF Pago; 2
i,UIJ-Uj-::Jb lUt lU?!1 Hil ivKUn f'illv rHIHULUur
\ 1-02-1998 d: \a6P1-1 FROM U"'..~ PI\TH LAB 5iOS
UNM Department of Pathology!
Trlcore Reference Laboratories
22" lorna, Blvd NE
Albuquerqu9, NM 87106
PatIent 'Na > ,':"-~" .' ._, : __ '".
Medlca( R.tta:~ '(((iOOOO)00425G?7G '.,.
DOS: 05/:\m9~~\oAge:' 9 y,:ts '. . Sei(: M
AccoUnt Nuftibet:' 01 1tOG743G
Ord.r.d by: ":".; : ?
Acoc~Glon No.: HR-98-001169
Ontc Col\~ct~: 10/23/98
I b
FOnlm He~ 1 t.h
500 G:;p;"y !.'!IM
90:< 210
Young3t0~n. OH ~4~Ol'0210
Refer:x'1l1 MO:
~---
Phy~i~i3n RQvic~/verification:
With th~ exc~ption of "8AnKad only~ epecim~ng. thi~ diaqnoeis is ba~ed Dn th~
3t~rf patholoqi~t?~ xevi~w of tha report. all micro~cop~ slidee. and (if
perforli.ed) flow cytornctrlc I:cudies and electron microscopic iTl'a9!H\.
rage: 3
Pallenl Name:
Medical Record #: (00000)004256776
neferrl'llD #I:
End of Report
Copy To:
APPENDIX 2
BLOOD VALUES
75
1
05:00
05:00
05:00
05:00
05:00
05:00
05:00
05:00
05:00
! (PF5) DETAIL
! (PF9) SAVE
! (PF12) GRAPH
11/30/98
11/30/98
11/30/98
11/30/98
11/30/98
11/30/98
11/30/98
11/30/98
11/30/98
%
%
MILL/C
G%
%
CMU
MCGM
PF8 DOWN
BLOOD COUNT
WBC
CRITICAL VALUE
RBC
HEMOGLOBIN
HEMATOCRIT
MCV
MCH
MCHC
RDW
WBC DIFF
WBC MORPH
WBC DECREASEDj NO DIFFERENTIAL PERFORMED
----------------------- GROUP CONTINUED ON NEXT PAGE
DISPLAY RESULTS
?
?
?
?
?
?
?
?
?
?
(PF14) PATIENT MENU
(PF17) PRINT ALL SCREENS
! (PF16) DISPLAY MENU
REDRTG01
RESULTS DISPLAY 808
M 9 TOD3 T314A PDM PT NO: 2721920045
ADM DT: 11/18/98 PT STS: IA ISOL: I MR NO: 00272192
----------------------------------------------PAGE 1 DOWN, ACROSS 1 OF
?1 ?2 ?3 ?4
VALUE ABN NORMAL RANGE UNIT DATE TIME
0.4 L (5.0-14.5) TH/CMM 11/30/98 05:00
PHONED TO*MR AT 0725 BY NMB
2.43 L (4.00-5.20)
7.2 L (11.5-15.5)
20.3 L (35.0-45.0)
83.6 (77-95)
29.6 (25-33)
35.4 (31-37)
12.7 (11.5-14.5)
,
DISPLAY RE~TTT.'T'.~ RESULTS DISPLAY 808
9 TOD3 T314A PDM PT NO: 2721920045
ADM DT: 11/18/98 PT STS: IA ISOL: I MR NO: 00272192
----------------------------------------------PAGE 2 DOWN, ACROSS 1 OF 1
?l ?2 ?3 ?4
BLOOD COUNT CONT . VALUE ABN NORMAL RANGE UNIT DATE TIME
? PLT COUNT 34 L (140-440) TH/CMM 11/30/98 05:00
CHEM PROFILE VALUE ABN NORMAL RANGE UNIT DATE TIME
? CL 102 (101-111) MMOL/L 11/30/98 05:00
? K 3.4 L (3.5-5.0) MMOL/L 11/30/98 05:00
? NA 137 (136-145) MMOL/L 11/30/98 05:00
? BUN 5 L (6-19) MG/DL 11/30/98 05:00
? GLUCOSE,TM 107 (70-110) MG/DL 11/30/98 05:00
? PROTEIN,TOT. 5.1 L (6.0-8.5) GM/DL 11/30/98 05:00
? ALBUMIN 2.8 L (3.9-4.8) GM/DL 11/30/98 05:00
? CA 8.3 L (8.5-10.5) MG/DL 11/30/98 05:00
? CREATININE 0.3 L (0.5-1.1) MG/DL 11/30/98 05:00
----------------------- GROUP CONTINUED ON NEXT PAGE ----------------------
(PF14) PATIENT MENU PF6 MAX UP ! (PF5) DETAIL
PF7 UP l (PF9) SAVE
(PF17) PRINT ALL SCREENS PF8 DOWN ! (PF12) GRAPH
! (PF16) DISPLAY MENU
REDRTG01
1
CONT
BILI,TOTAL
ALK PHOS
SGOT
TRIGLYCERIDE
C02
?
?
?
?
?
RESULTS DISPLAY 809
M 9 TOD3 T314A PDM PT NO: 2721920045
ADM DT: 11/18/98 PT STS: IA ISOL: I MR NO: 00272192
----------------------------------------------PAGE 3 DOWN, ACROSS 1 OF
?1 ?2 ?3 ?4
VALUE ABN NORMAL RANGE UNIT DATE TIME
0.6 (0.1-1.5) MG/DL 11/30/9805:00
116 L (117-390) U/L 11/30/98 05: 00
17 (0-37) U/L 11/30/98 05:00
119 ?200) MG/DL 11/30/98 05:00
26 (23-29) MMOL/L 11/30/98 05:00
~ISPLAY RF.~TTT.'T'~
CHEMISTRIES
? MAGNESIUM
VALUE
1.6
ABN NORMAL RANGE UNIT DATE TIME
L (1.7-2.2) MG/DL 11/30/9805:00
------------------------------- END OF DISPLAY(PF14) PATIENT MENU PF6 MAX UP
! PF7 UP
(PF17) PRINT ALL SCREENS
! (PF16) DISPLAY MENU
REDRTG01
! (PF5) DETAIL
! (PF9) SAVE
! (PF12) GRAPH
:.::i?I;::.1"'1
Ci...
C::Ui:.:,i
F' F: OF? I L. ,I::
.. ;: :...
"} .....)~,::;
.:::.E;:.:,? ,,'.i i::;<T
.,
'. .... . .. ;..:;~. ;:;; .: ~ .: .
/ ~.:)(; /.' ...
() :.5 ;; /;;?;
.?.i?j(?
i. ().)
; J...I;.~ j' . i: i I I.' ,: . ::'.:..;" '::.;.:;; :;::;: .., .... ::.:::.:
::.:;::- .;.";;'.....
,::; ..
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~ .: :.' .'.,.' :.) i." ',' .~:', ,." .? :)?.. i ..'
:.)
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<> ., ::} .:,.:
,:.!:
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,0r,-~
:::'
:f;';
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, ";. :
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,",', .'y' ,. ..
"'.!
!. ;".'.~ .... /~i
-::.1 i" l:::L..Li?!!.?.?.?,;,?..i????? .'
.:::;""::' ...
L;"
.. ::.'. ~::. :::~ '.",?,i... ; iLi :,.J ... ,~ .: ".:
:. ~ ...; :?;?:.. (:.i;-??'
'".-,i. " i??,j .1 ... ';"1' \".J
',;: :.:
, .- ....
i ~,
C0?'.
~
~ ,. ',.,,?1
~ . ..,. ...i'.,:'-..,;.; ........,t-
I.l'"li
No?bIFFEREN1?IAI... PERFORMED23
I... (140-440)PHONED TO*CF AT 080') BY VR
D(~ TETJ IVi E
:UJ../O~.;j/9B O:':J ::0'
12/0::il98 O~'i :O(
H~/O~jI98 O~j :()(
:I.i.UO~:jI9B O~.'j :O(
If.UO~.;j/9B 05:0(
H?/O~'jj'18 05 :O(
li.UO~:jl?8 O::'j :O(
li.:~/0:;.:j/98 O~'j :O(
1r..~/O:::il98 O~j :()(
:I.c~ /O~i /9B O~i: (h
UNITTH/CMn
MILL/CC:i%
%CMU
MCG/"l%
%
NCJI:~MAL. 1:;:ANLjt:.
( ~:j ? 0 .... 1ri? .. ~:j )
BY vt:~
(I.~. OO???~.). PO)
( 11 .. ~J????:I.~j .. ~:J)(
~3~j .. 0-45 .. 0 )
('J'J'-?~i )(i.?5<l:3 )
(~l :1.--3'/)( :L1.
~:; ... :l.1.~ .. ~.;j )
ABN
I...
(.~r OBO'/I...
I...L
PHONED
.HL.CIOD COUN'1WBC
CF~ If lC(11... I"" t-I LUF.:.
F~BC HEMOCiLOIlIN
HEM(~'1 OCR 1'1MCV
MCH
t1CHCF\DW
WBC 1> IF: F1I.JBC
MOF~PHWile
DE::CF~r::.A~:iEI);Pl."l
ccJu~n .CF;:
I'r lCtl!.. Vt-.I...LJE
NORMAL. RANGE:. UNIT DATE TIME
(101????111) /"lNCJI... /L. H~/O~.'.i/98 O::=j:O(
(E~::l????i.:.~?) tit'l0 I II... 1P /0:::; 1'18 O~j: o(
(3.~j?-~i .. O) t?it'iDI.../1... H.~/O~:iI?8 05:0(( 1;36????
:1.tt~:!) Mt?jOl... /1... 1;::.~ /O~:=j /9(;) O~:j:: 0'( 10????20) 1i.:.
i ../O'.:'j/(jl8 O~j :0'
(6-19) MO/DI... 12/05/98 05:0'CON1INUED=============================
(:~BNCL
C02
I(
NA
PIN lUN G(~F-'
VAL.UE106
2t>4.
E~
1t~0:L ..
~)
I.?BUN 10
==============================GROUP.3:22
:L2/0~/98 FROM WKH5,REPRTGFl
JAX~j50:l. 'I
F~ESUL lS LIST INf;
P72l9E~004~J T:~O~jB PDM
UNIT DATE TIMEM(3/I)L. 12/05/98 05:0
CHEM PFWF? IL.E CONlGLUCCl:::iE, T/"l
CI:':F.:.(.~?1 Ii'?IINELA
CHE:.t1ISTF?: IE:.~i
MA(-jNL~:; IUi''-j 1.... (..~I...UE ? 1
ABN NORMAl... RANGE(')0????110)
I... (0 .. ~)????:!. .. 1)
( B ? ~r??10 .. ~5 )
ABN NORMAL. RANGE( :I. .. '/....
i.:.~ .. i:.~ )
UNIT
(?'iG/DL.
hC, /DI...
tiG/OI.-
DATE TItiiE
1i::.'/O~'j/';)B o~;;:o
:I. ;::.~ /O~::; /('.) ~~l O~:; ~ ()
:l.i.:.~/0~.'jl?}8 O~:j ::0
UF?: INA!... Y~:; Ib
U PH
U SI:?' C-j F~ A( I T
VAI...UE
::=.... 01.010
ABN NORnA I... RANGE(
~:; ? 0 _ 8 .. 0 )?:1. .. 0::10) UNIT
BLOOD BANK SPLCIMEN NO~ 206-:1.-1 DAll/TIME: 12/05/98 05:00ABO/RH :1.2/05/98 05:00
k3 .l* F?' CJ ~:;AN1IBDY SC
:1.2/05/98 05~00NEG
COMPCJNLNl 12/0~/98 05~OOF;:BC"-f;
IF;:I~,DUNIT NUMBLR 12/05/98 05:00
,(i?;~::F' X'/6 '/87=========BI...OOD BANK/MICRO RESUL1S CON1INUED ON NEil' PAGE==================
1.3:22 :l.2/0~/98 F'ROM WKH5,REPR1CiF'1
J(-,::<::!~)O:l. '/
TOD3
BLOOD BANK CONIINUED SPLCIMEN NO: 206-:1.-1l.JNJ.'[
~;?IA?f-l.JS :1.2/()~/9~$ ()5:()O
ti1._ i... CJ Ctil I::. DlRNSF' .. SlA1U 12/05/98 05:00
CJ 1< TU TF;: AN ~:;F' U~::; E:.CROSSMATCH :1.2/05/98 05:00
C(jivi F?' f;T I I-J L. E:.
DArE/TIME: 12/05/98 05:00
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F;[:~;UL. T':::; L. T~:;T TNCJ;:_:: ? E: 1(,)"' ;:.:.: () ()
i;i? ~;.:j ?r003
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(r;.I() .... :i. 1(?
(O.:':i?.. jn :I.)
(B n ~:;?_?:LO. ::'j)
Lii'" l-r
dC! /DL
(iEi /DL
i"\f3/DL
1)t',TI::: T}
1;:.:_:~ /0Z:i ./(/ E\ () :.:.~;
:I. E: / (i (,' /. ':;:: E; () ~-.:.
12/ () ':;:0 ,/9 ~:j () :.:.~;
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C: iJ /?1 F' Uj,! i::: j\i'i
(r'iL:'.. ;::::::' i~L.(,i L E:GET'iiN IT
i"/1..iI"iC:::? ii
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(~l?r ::~ ?'f ('.; '?i? t,J ~::~
i:.... i... i... CiC:(; T F D
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.::;ecc TheN NC):: ;.:::(/,:', ? ?1.. ?:1.
.1. ~~:: /'() ::? ./':/ ;:;; (j (; ;: :t I:)
j. !'.:-~ ./ I,) '7? " ?.i? ;:j (j (> :: :l. ()
PDNT30~:.:;B')'0:03
.~ . '. ? ... ',', . .' ~, ? I ?
.iF,\;j:'~?3'i;7!~i:{~:;~i~2:.;); ,~,;~::i~f\f~j;;\~;;(?~\'~2l~y~t.j\~i.':'00ib:;~~;i,~;~\~4~'2~i~i~t~~~~~
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ABN NORMAL. R~NGE
(10:L?..?l11)
(2~-29)(3.5-5,,0)
': :l.3(1)_.:to!; :.':j.l
( -; O????E:(i)
~: 1~'::1 .... .1 i.Y ) ('j Ci /DI
UNIT
NMOL/L
MMOL/LNMOL./L
(1;'101.. /1..
f1 11...1... /e
C:~ ;~
Y.ChU
hCCi(vj
UN IT fl(iTE. 'j .i:,lH./CMM 12/:1.1/98 05(iC,I?h{IL. F~{;NGE( ::; ? 0 .... :U; ":':.i )
BY ,JrYi.:~
(to .. oo?.. ::j.('?'(?)
( :l:l .. ;'::;"':L~::i .. ~-:j)
(3~.'j" ()"??{I?~:i" 0)
~ ') '/ .. .; ~~ )
(E::'.;????33 )
(::$:1. .... 37).; :L
:I. " :::; ... 1<; ? :.=.i )
( .I.?:i 0 .... ,:; ,:;0 J
BY ,)r.I?{
("jBN
I...
06110
L
LL.
'.;...13
"'f";L.UE
. " ?:lOS.':?::f'l26.. "?..?
t;.o.La
'7'
BLOOD .COUNTtime
U;; IT let,L Vf'1LUE
RE:CHEPlOGI...CJBIN
HEMATOCRIT11<:;\)
i1CH
NCHC;
t~Dv!
PL. T COI...lNTCR IT
IC(IL \.)t~iLLJE
i.~1 i... L~ c~ iJ ::::; L. 'j , :
CRE~TININE 0.3
CA d.,
~~==~~===~=========~===REPOR?r
?:,E: ;: r:;:;-:.i I.E:./:I. J /':;'f; F F.: Ui"j VI I< ,.f 3 'I F:EPF:TCiF' .i.
:3 E': l)} :t: ~::; ~:~ ~7j (~
'. .' ".~ .!?.i. "'0" .'
L (O,,~I"":l ? .I.)
" : ??f ?.,' ." ?????MG/DL. 12/:I.:L/98 05
.i. ~:.: /" t :i. ./.;:, ~:j ;".J ::..1
rOD:::; ,
c: 1-1 [(\ ISTF~ IE:::;
i"j ('; 13 i'l E.:;:;, TUjot
l.,.i {;L. UE:.
~:.:~ n ()
:..ili IT
t'l(:-:t /".01..
Dt;ff.:. ! I1
f.:~ /~ 1 .i. / .. :.;: (::. () ~5
i':. l"~ .!." ,.. I (. !'., ;'.. i" ;. ,! t'. ! .. :....: ..' ,.' ..
:.1
::":.: :.;: i',-, ,", ::' ..'; .-::' I
MRt 00272192
.. ? ? ? .- ; ?~; .'.':.:.;;:' " ',j
;~l;{i'J!~~~~;f;,2~$~~:~~r.~ ~,~<~j;lf;W"Ji;~'~:iii;!.;~~~1~i~r~{~il,:;i~~;~;i~~~~~ ~~,(\,}~y~=f;;0;r~~
RESULTS LISTIW'.1,?'?' '
2721920045 TOD3 T305B
" , ...,:,
------------------------------------------------~---------------~~~-------~.
llLOOD COUNl "~ ABN NORMAL RANGE UN IT ,DATE ,ci:;"tr'k
WBC ' ~:: L(5.0~14.5) TH!CMM 12/12/98,05:0
CR ~~ECAL VALUE PHONED 1~.'/ AT 06 :l,~ .Bt(41A'l~g."g'_-, 51"::'2. g? " MILL/c,;r:iZ'/is12198':?O'S: 0
'HEMOGLOBIN ~ L ........ .... . Gr."i?!.c12/12/,9J3j*,051,~0HEMATOCR n' 21.9 L (35.0"':45.0)
"~ "12/12/9a?!b~t:()MCV. 83.7 \ (77-95) , CMU .:
12/12/~8jbQ5:0MCH 29.4
(2ej-33) MCGM ,12/12/98"0~r:'o
MCHC 35. 1 (31-37) ~ 12/12/9805:0RDW 12.4 (11.5-14.5)
~ 12/12/98+05:0
WBC DIFF 12/12/98'05':0
WBC MORPH 12/12/98;05~0WBC DECREASED; NO DIFFERENT IAL PERFORMED,',' ,.;:?tt'1",
. RBC MORPH ' NORMAL ',12/12798()5":O
==~;~=~~~~r===========~~~======;~=~l~~~~~~~=====~~=~~~~~~~~l;~~~}~i~?
K 4.4 (3.5-5.0) MMOL/L '12/12/98~05:0
NA 136 (136-145) MMOL/L 12/12/98 05:0
AN ION GAP 14 ( 10-20) 12/12/98 05:0BUN 14 (6-19) MG/DL 12/12/98 05:0
==============================GROUP CONTINUED=============================09 :55 12/12/98 FROM WKH5 F<EPRTGF 1 " .
WAX36212 '
RESUC1's--L-fifT tr:1h
2721920045 ,_, ,,' "" '" __ , ' T305B PDM
MRt 00272192
------------------------------~----------------------- -------------------------
CHEM PROF ILE CONT VALUE:: ABN NORMAL RANGE UN n DATE TIME
GCLRUECA'OTSIENlNTME' 104 (70-110) MG/DL 12/12/98 05:C! 0.3 L (0.5-1.1) MG/DL 12/12/98 05:C
CA 8.9 (8.5-10.5) MG/DL 12/12/98 05:C==========================================================================
CHEMISTRIES VALUE ABN NORMAL RANGE UNIT DATE TIMEMAGNESIUM 1.9 (1.7-2.2) MG/DL 12/12/98 05:(
===============================END OF REPORT===========================:::
09:5~ 12/12/98 FROM WKH5 REPRTGFlWAX36212 '
-~--------~-----------~----------------------------_.-~------------~----~~---~--
DATE TIME12/15/98,05::,..~BLOOD~COUNl VALUE ABN NORMAL RANGE UNIT,"WB,C TOO,*?,3
JE",.; 'AT r70Lo BY(5B?0R-M" 14.5) TH /CMM
~~~dGL;bBIN ?:~O,\ t. ~ii~g=15:g~ ~9.LL/C 1~~1~~;~~8~';~HEMATOCRIT 24.6 L (35.0-'45.0)
% 12/15(98:05::Mev, 84.7 (77-95) CMU 12/15
/98'~'05'::MCH 30.2 (25-33) MCGM
12/15/9.8~05?: ~MCHC 35.6 (31-37) % 12/15/98 05:"
RDW 11.8 (11.5-14.5) % 12/15/9805:~wac DIFF 12/15/98 ;05::
. ", wac MORPH 12/15/98/05::wac DECREASED? NO DIFFERENT IAL PERFORMED ,.;
~""~'t'0' L '(140-440) 8 ...-::
F~ESUL TS LIST r .-.2721920045
n~ .. ...MRt 002,,2192 TOD3 T305B PDM
TIMl05 :(
05 :<
DATE12/1
tt/9812/14/98
12/14/98
UNIT
TH/CMM
NORMAL FMNGEwac I>IFF
wac MORPHwac DECREASED; NO DIFFERENTIAL PERFORMED
PLT COUNT . 12 L (140-440)CRITICAL VALUE PHONED TO*CS AT 0745 BY JK
======================================================:==:===:============:CHEM PROFILE VALUE ABN NORMAL RANGE UNIT I>ATE TIMI
CL 104 (101-111) MMOL/L 12/15/98 05:C02 24 (23-29) MMOL/L 12/15/98 05
K 4.0 (3.5-5.0) MMOL/L 12/15/98 05NA 138 (136-145) MMOL/L 12/15/98 05
AN ION GAP 14 ( 10-20) 12/15/98 05BUN 15,' (6-19) MG/I>L 1,2/15/98 05
g~~~~?~i~~ 5~g L ~6~5~I~i) ~~~Et t~~l~~~~ g~CA 8.8 (8.5-10.5) MG/I>L 12/15/98 05
ALaUMIN 3.4 L (3.9-4.8) GM/DL 12/15/98 05BILI,TOTAL 3.'l H (0.1-1.5) MG/I>L 12/15/98 05
BILl DIRECT 2.6 H (0-0.4) MG/DL 12/15/98 05ALK ~HOS 169 (117-390) U/L 1,2/15/98 05
SGPT 860 H (0-45) U/L 12/15/98 05SG01' 352 H (0-37) U/L 12/15/98 05
==============================GROUP CONTINUED============================:14:18 12/1S/98 FROM WKHS REPRTGFl
WAX3670S '
._-----------_.. ------------------------_..._._----------------------_....._-----._---._._--------------_.-
CHE(~ML PROFILE CONT V1AO~UE ABN NORMAL RANGE UNIT DATE TIME
K? ~ (101-111> MMOL/L 12/14/98 05:0NA 4,3 (3,5-5,0) MMOL/L 12/14/98 05'0136 ( 136-145) MMOL
/L. 12/14/98 0 '0(;I~ULUN(:(}SE
TM 12 (6-19) MG/DL 12/1.4/98 O~:OPR01EIN'TOT 111. H (70-110) MG/DL 12/14/98"05:0
ALBUMIN' ?'~ t ~~,0-8,~) GM/DL 12/14/9805:0
CA 8:8 (?:~=io.Jj) ~~~gt t~~t4~~~ 'g?~g
~~E~Tf~f~t O,~i L (0.5--1.1) MG/DL 12/14/98 05:0
ALK F ~HOS 118'8? H (0,1-1.5) MG/DL 12/14/98 05:0SGC}l" -': (11?--390) U/L 1.2/14/98 05:028:'.'j H
(0-:~7) U/L.. 12/1.4/98 O~,:OC02 25
(2~3-29) MMOL/L 12/14/98 O:7i:O
CH[MISTRIES=========:===VALUE=====ABN==NORMAL=RANGE=====UNIT===DATE====TIME
MAGNE::SIUM 1.9 (1.7-2,2) MG/DL 12/15/98 05:1MAGNES IUM 1. ?
<I ( 1" /--?2 ? 2 ) MG /DL 12/14/98 05:0================================================:==========================;
PDM
IMMUNOLOGY VALUE ABN NORMAL RANGE UNIT DATE TIMETOXO lOG N (NEG) IU/ML.. 12/14/98 05:0
EQUIVOCALA TWO FOLD CHANGE
,l~ I~/ML BETWEEN ACUTE AND========================TEXT CONTINUED ON NEXT
PAGE======================~L4:18 12/15/98 FROM WKH5,REPRTGF1
JAX36~J05
, RESULTS LISTI~n2721920045
MRt 002'/2192
IMMUNOLOGYTOXO IGG
TOXO HiM
CONT VALUE ABN NORMAL RANGE UNIT DATE TIMEN (NEG) IU/ML 12/14/98 05:C
CONVALESCENT PAIRED SERA SHOULD BECONSIDERED EVIDENCE OF RECENT
SEROCONVERSION. SEND ANOTHER SPECIMEN IN 2TO 4 WEEKS IF CLINICALLY INDICATED.
NEGAT IVE N (NEG) 1.2/14/98 05:C====:======================::=====================:::============================
BLOOD BANK SPECIMEN NO: 370-1-1 DATE/TIME: 12/14/98 08:00COMPONENl 12/14/98 08:00
PHER PLT LEDP IRADUNIT NUMBER 12/14/98 08:00
1.1?2FR?4E~38PHPK UNIT STATUS 12/14/98 08:00
'1 RANSFUSEDTRNSF.STATU 12/14/98 08:00
OK TO TI=i:ANSFU~;E=====================END OF MICRO/BLOOD BANK REPOR1'=======================
BLOOD BANK SPECIMEN NO: 371-1-1 DATE/TIME: 12/14/98 08:00COMPONEN1' 12/14/98 08:00
PHER PLT LEDP IRAD=========BLOOD BANK/MICRO RESULTS CONTINUED ON NEXT PAGE================::
,4:18 12/15/98 fROM WKH5,REPRTGFIJAX36?05
F~ESLJLTS l.. r81 ING
2?c~ 1<lc,~()04~5 TOD] T30~:;B PDM
BLOOD BANK CONliNUED SPECIMEN NO: 371-1-1UNIT NUMBER 12/14/98 08:00
':j. 2FI:?: ,'.J 7 1. '/ 1PHj=:' 1<UNll STA1US 12/14/98 08:00
(tl_LUCATI:::DTRNSF.STA1U 12/14/98 08:00
UK TO Tj=-:AN~;FLJ~:;E:.
DATE/TIME: 12/1.4/98 08:00
:: \ i.. ! L. i ~:.l I. l. '::\ t
,i)ti'iF
.i. j:,::': ./ J b /,.- ci (.i :~j
L;:,::: ,/ :I. b .... :.;: ;::.~ () :le::./
j.H ,/'(?d I J
i. f::. ,t.:;:'; / 'x ;::3 <':i
,1. \.~', /' .J. ;;::; ......::.... r; (;
1...\ r-'~ .i. I
iii,\.il,'I
i .\ "i~ ;. !.. ,,... i'-::
t:'-.i .>~
)' ..
J1 ???? "I'
,.; .I.
1. ... : "
~,I DC
1~.: I'i" I C. ("j L ;) I;"'; i .'...'
1.),'-,
; -'. :./ ~." : Plf !. .1. 11 .....i .
:; : ::~: :;:: :::: :::: ;:.: :.: :;; :;.: :::: ::7": :;.: ::.: ::. ...,. ,. .. ::";::';::':;.':::':;.:::"
t .~
0:.:..
:l. E: / :L ;:::: /,?::;
J. r:~ /' J ;::; ./'9E~
l;'.:.~ /' lr~ /'18
.I.;'.:,:: .t'" J ;::) .,.-";.;-;;;
i.i?:.:.'" .!. C) .... T D
'Ji'-.,i I','
I'ide,!.. ./1...
j') Ivi UI... /L.
j?ii'llli. /'i.
hi"iC.!!.. / '...
". i,"
pi C)F;,i"\(,L i-.. i?;!?!!.i!::.
( JO :t ' :,. :i. :1. 'J
( (.::~ ~j .... E~ (? )
( ~:) u ~:.~i "<.~.~ " <> )
L.
L.
1, .t.
'?Of?' ('; t... L,i (.
10.l
i:::: 1
3 1I;~.i
3,~';
p"
i.o.rL t.iL.!...; :)C 'J Ii'!.
, "".:
(..; j::'f
I"ii\ ,Li::.ij,.! i,',ii'!'
.i"iL:: ri ,: i::'- I..IF: .I. L. r::.
CLl>:1i7.::
.::' .. .'. ~',:'. "" I.?:", './
i !:. '?. f
; !' ,?..i!
PDM
", . .".:'::. '::-:-.~,.:,~ ..
??~ . ."'.... ? '.' ;'. .' .-.,I,??;
itl.~~~~;:K:':~~~~~~'~";;':':;"":"W';);;':i;i':~Z(~. :t;~'~~40:i;r:i,c;:~E]:;~;i%\~~~~i'J;i'~
- ~~2192bo45, , TOD~=J T305B '/, P'DM' . . ~~,;.. ._.
~~ !_.. ~~~ Z~~ ~ ~ __. ._ .__,__.. ._. __,_,_, _. _. ..._. .__._.__.... ._~.. .'.
. .' ~BLOOD COUNT
,,~ VAL.UE ABN NOI=<MAL RANGE UN IT DATE T: I
WBC 2.5 L (::=;. 0-ltt.5 ) TH /CMM 12/i.~3 /98 05'~ i
r';:BC 2.69 L (4.00-'5.. 20) MILL/C 12/23/98 05:t
HEMOGLOB IN 8.1 L ( 11.?5-15.t;) G% . 12/23/.9805:<
HEMATOCRIT 22.8 L (35.0-45.0) .. %,>.;?.'12/23/98 05'::'(MCV 84.8 (7"}-95) CMU 12/23/98 05::(
MCH 30.0 (25--33) MCGM 12/23/9805:(
MCHC 3::=j .. 4? (31-'37) %:1.2/23/98"05:<.
RDW 12.6 (lL::=j-14.~j) % :1.2/23/9805':<
WBC DIFF :1.2/23/98 05~(
POLY % 16 L (~'j0-70) % 12/23/98 05:(STAB % 46 H (2--6) % 12/23/98 05:<.
LYMPHOCYTE 27 (20-44) % 12/23/98 05:(
MONOCYTES % 5 (2-9) % 12/23/98 05:(
METAMYELOC. 3 % 12/23/98 .05:(
MYELOCYTE. % 3 . .X .. " .,..,12/23/9805:(WBC'MORPH .." .' "
,.",,,i1f1;{',,",,~j'~~(;::;'.,::,1CV23/,.98,j.05:(TOX Ie .GRAN*MOD*DOHL.E BODY . '" .~S:,~
...,/.....; . "" ,.y,,?t-t,,":,"k
RBC MOF<PH SL. T*POLY 12/23/98 05:(PLT COUNT 3:1. L (:1.40-440) TH/CMM 12/23/98 05:(
===================================:========================================
CHEM PROFIL.E VALUE ABN NORMAL RANGE UNIT DATE TIME
CL 105 (101-11.U MMOL/L. 12/23/9805:(==============================GROUP CONTINUED=============================
ll:21 12/23/98 FROM WKH5 REPRTGFlJAX38023 '
RE8UL.T8 L. 1ST Il\Ir~
c::.':17219rc:.l()04~J? - MR:J: 00272 19Et"'<
I
CHEM PI:~OF ILE CaNT VALUE ABN NORMAL r~ANGE UNIT DATE TIME
CO2 30 H (23-29) MMOL/L 1.2/i.~3/98 05:<.1<
2.7 L (~l. ~;-?5. 0) NMOL/L. 1C.~ /23/98 05 :(
CRITICAL VALUE PHONED TO'lE-MS AT 0'700 BY TI<
NA 14t~ ( 136-??14~j) MMOL/L. 12/23/98 05 :(
ANION GAP 12 ( 10--20) 12/2~3/98 05 :(BUN f!6 H (6-19)
MG/DL 12/23/98 05 :(
GLUCOSE TM 113 H ( 70.... 1.10 ) MG/DL. 12/2~:!/98 05 :(
CREATINiNE o.Li? I... (o.~:j_.1. 1) MG/DL. 12/23/98 05 :(CA 8
n S) (B.5-10 ? ::=j ) MG/DL 12/23/90 05 :(
ALBUMIN 3.1. I... (~1.9-??Li?.B) GM/DL. 12/C!3/98 05 :(BIL.I,TOTAL 1.6 H (0. 1-,1.
~j) MG/DL. H!/23/98 05 :(
BIL.I DIRECT 0.6 H (0'-0.4) MG/DL. 1.;.~ /i.~3 /98 05 ::(ALK ~~'HOS 39<)'
H ( 1. 17-<=J90 ) U/I... 12/23/98 05 :(
SGPT 590 H ( 0--45) U/L 12/23/98 05 :(
SGOT 60 H (0?-:1'7 ) LJ/L 12/23/98 0::=; :(
==========================~=========================================~=====~CHEM
ISTF~ IES VALUE ABN NORMAL F~ANGE UNIT DATE TnH
MAGNESIUM 2.0 ( 1.7'-2.2) MG/DL. 1f!/E~~:l /98 O~5 :(.
===============================END OF REPORT============================='\:21 12/23/98 FROM WKH5,REPRTGFl
'.(3802~-J
TOD::) HEM
ril',:8: 0 0 i;:~ ./i.: :I. "I ;.:~ lIME
O~5 :00
()~5 : 00
O~.:i : 00
05:00
0~.:j : 00
Oci :00
()~.'i:OO
()~:'j :00
O~:'i : 00
O~j:OO
O~5:()O
O~:5 : 00
05:00
DATE01/0::!/(??
01/0J/9(?
01/03/99o1/03
/?'~/
01/0J/(j'))o
1/0J/(?9
01/03/(/(1
01/03/S)9
01/03/':';>9
01/0319'1)
01./03/9901/0]/99
() 110::1 /99
LJi'?! IT
TH /Ci'1ri
i'111..1.../CC,;{
?>1'
t>eMU
t'lCUi"l
.//>.,'
I>
.,',...
,A
./,.
(~iO"",}O) (,!.... 6)
( i::.~ 0 .... 'I' r.j. )
NClF:riAL f<ttNGE(:i . 0.... :lA? .. :'5 )
(f.~. OO"-:i. i:!0)
( 11.~j""15.~::j)
(3ti .. O--i\?:i .. 0)
( 'J7'-'9~j)
(25-<33 )
(31?..?3'7)( 11 ..
~i .... 1l~ .. ~:j)
H
H
L
f;BN
L
l..
l...
L
79
:::.~ 0
1
{L.OOD CUUNT
WBC
RBC
HEMUGLOBIN
HEM{-~T(JCF< ITMCV
i"iCHMCHC
FWW
WBC D 1FT
POL.Y %
STAB %
LYMPHOCYTEWElL.: t'iUF:PH
'1 OX Ie GF<f;NRBe MURPH NORMAL
01/03/99 05:00
PLT COUNT :l.J':/
L ( 1I.rO"?440) TH ICI"it1
0 1/03/(rl 0~5 :00
:====================:=:==:=====:~::==:======:===::===:=====:=:::====:=:==:==~:===:==========:=:=====CHEM PROFILE VALUE ABN
NORMAL RANGE UNIT
DAlE TIME
CL 9~l
L (10:1.????111) Mt'iOL/1...
01/03/(/9 O~.:i:OO
C02 26
(23-,29) MMOL./L
Ol/03/'.;)(/ 05 :00
I( 4?
.. :I. C].5 ..??5.0)
MMOl. /L. 01/03/9(/ O~:i: 00
NA 13l~
L (136-?1.t.~~.:j) MMOI...IL
01/03/99 05 :00
==============================GROUP CONTINUED==============================:22 01/03/99 ~ROM WKH1,REPRTGFl
(394~jO
<ESULT~> LIST ING2721920086 F
MI.. g. (') (., .:J '''''','';) .. n .::>,:u= ,. J ..... C.. .I. T._
TOD3 TJO~iB HEM
CHEM F'!:,UF ILE
(1N IUN GAF'BUN
CJLUCCJ~:;E li'i
CREATINiNE::
CUNf I.)AL.UF14?
B?4
0 .. lj. I...
Nur<r-iAL r;~t~N(3E
( 10--20)
(6?..?1.?)
(')0.... 11.0)
(0.5?..?1.. 1.)
UNIT
I"iU/DI...he; IDL.
t'i C) /I> L.
DATE
Ol/O]/(??
01/03/(/'7'
01/03/'/901/0:J
/(~'9
rIriE
()~:}=oo
0~~i :00
O~:; :O()o:.;:oc
F~E?U/:;ISr I. IC'T lW'
i... 'lL:. .. 92()O?6 ;, 02'"'J~ 1<';'2 -0 _.MIdi: 0 _,._ 7 ...
TDD::~ T30~.:jB HEM
... _-_ ..__ .__.----- -_.. _--_ __.. __ __.._--_._.--_.._.?. __ _-_ .._--_.. _._--_._------_ _-_ .._--_ _--_ _-_._---._---_ _---_ ..
HLDOD COUNT VAL.UE: ABN N(mMAL. FU~NGE UNIT DATE TIME
WBC 1.6 l.. (5.0-"14 .. :71) TH/CMM 01/02/9<") 05 :~
CRITICAl... VAL.LJI~~ PHClNED TO~' ,JV AT 071.0 BY JABr;:BC
~i. i.t1. I... (i.t ? 00-:5. f.:~0 ) MIL.l... /C 01/0;3:. /9':Y 0~"5 :~:
HEMOGUJB IN 10.2 1... ( U .? 5?_?1:7j .. ::) ) C" o1/02/lj.)(") O~:j :~:
HEMATOCRIT 29. ,~) I... (3:7J. 0-45 .. 0) % o1/OC~/99 05 :~
tlCV 86. 'j (TJ-?95 ) eMU 01/02/99 0"" ? '""J ? ~
MCH 30 .. 0 (i:!.~j?-33 ) MCGM o1 /OZ~ /99 0"" .,::;;,:) .,..
MCHC ::lit. :':j (3 :1. ?-.<l'7) Y- 01/02/9<1 0"" ? c:~ .....-
FWW H~. 'j ( 11.:7j--:1A .. ~.:j) ./ 01/02/99 0"" ? '""J ? ~
WBC DJYF o1 /O;~~ ./l?9 05 :~.:
. F"CJL Y X ~jrJ (:'::iO????'70 ) ./ o1/0E.~/9<") O~j :~.:
~:;TAB % ~i~j H ( 2 ????6 ) ./ oJ. /OE.~ /')9 0'::' ? c:~J .....
EGS INfJPH IL.. 3 ( 0 .-..~. ) \"/" o1/0::=~/99 01:.- .'"
BASClPHIL X 1 ( O.... ;.:~ ) ./ o1/0E~/9l") 0?:' ?c:
l..YMPHCJCYlE:. 3 I... (20-it4 ) % 01/02/99 05:~
ME1AMYELOC. 1 Y- 01/02/9'1 05:~
F<BC MORPH 01/02/(/9 0"" ? '"
~;L T')('TEAF~ Dr,OP*SLnWOLY
PLT CCJUNT 12::'> L ( :J.itO-440) TH/CMi"1 01/02/</<1 01::"?'"===============================================================================
NClRMAL. RANGE UNll DATE TIME
<:1.0:1.-"111.> f'lMCJL./L 0:1./o;,:~/99 05:5CCJNTINUED=============================
CHE:.M PROFILE VALUE ABN
CL 99 I...==============================GROLJP
)9:08 01/02/99 FRClM WKH1,REPRTGFl
'JAX~~9298
F~ ESLJLTS 1...:1. ST ll'-,r 
E.~ "J 2 :1. 9 2 0 0 fj.':J
hR:J: 002':J;:.!.19E~
TOD3 rJO~;.jB HEM
\
CHU'l f?'F;:OF II... E:. CCJNT IJAL.UE ABN 1'1 UfmAL. 1:~PINc-;r::. UNIT DATE lIME:co;:,>
;:~ ~5 (i~~3?-?P.'-:Y ) MhOL/!... o1/02/9<j 05 .1;;
1< 3 .. ':") (~3. ~:j_ .. ~;j .. 0) tlt'l0 1._ /1... 01 /O;:!. /99 05 .. 1;:.
NA :l.3~:j I... ( 1:36??-lit~.:.i ) i'if'lOL. /1... o1/O;~~ /9<) 05 .1;;." ....1
M~ ION GAF' :1.~) ( :1.0 .... ;.:.~O ) 0:1. /OE! /99 0:'5 .. I:;?
HUN '7 (6????19) rle;/DI... 0 1 /O;:'~ /l)l9 05 til:.:J
GLUCOSE TM :1.'79 H (70--1.10) MG/DL 0:1. /O;::.~ /')lS) 05 .. c;?
Cf"E AT TN 11'11" 0 .. i:~ L. (0 ,,::i??-:1.. :1. ) hG/DI... 0:1. /Oi':'> /?9 05 .. c:?" ....'
===============================END OF REPORT==============================)9:08 01/02/99
~ROh WKH1,RE:.PRTGF1.J
(.~ X~:). <;I .-, '"
JI... T8 I... I~:lT ... "I....~
7~~ 1?20 102 rm:fl: 002?219'd IODJ T3 :1.i.:~B PDi'l
.. _-_._-_._._._-_._._._ __ _._----_._-_._ -._._.?.._. __._ _--_.-.. _-----_._-_...?.... -_.?.. _._.........?... _.__.. _.. _ _.._ _ -._ _............?...-
NO DIFFEREN'fIAL. PERFORMED43 I... (140-440)
_ODD CUUNT
vJElC
~ IT lCAI... VALUE
F~BCHEMOGL.OBIN
HEMATOCF;: IT
MCVhCH
MCHC
I~Dvl
vlElC DIFF
vJBC MOFWH
:lC DECF~EA~1ED;PlI
COUNT .
PHONED
Vf~L.UE: 0.1
TU,)("JV AT
J" 4?910.6
30.0fJ5.9
30 .. ~'j3:7j .. :')
13.3
ABNI...
0'/00
I...
LI...
NO F: t"iPt L. I:~ (.~ N(:.IE
(~'j .. 0-,14 .. :::.i)
BY GI<L.J(4 .. 00.... ::j ..
E~0)( 11.5-1::'j.:'j)
(3:::j .. O.... (~~'j .. (),)
(7';.... 9~J )
(2~j""33 )
(]1?..?3'?
( 11.::'j--1.i.~ .. :')
UNIT DI~ITE T It'lE
lH/Ct"iI'-l 01/11/9? ()~j ::00
MIl.l... /C 01/1 :1. /'19 O~j : 00
OX 01/11/'19 O~j:OOvi 01/11/99 O:::j : 00
/.
CMU 01/11/9? O~):OO
t'lCGi"l 01/11/99 o::'j :: 00
v' 01/11/99 O:::j : 00 ,..'i'>
v/' o1/1:1. /9':"J O::-j : 00
I> 01/11/99
O~j :0001/11/9?
O~'j:OO
'1 H/Ct-1M 01/11/?9 O::;j:OO=======:==============================:===========::===========================
JE'M PI:WF ILL VALUE ABN
PILBUM IN 3.6 L.
.~.~ :;: :.. :~~ ') TDT;:\ ~.. 1. 11 :J
B IL I 2 D H-:E.CT O. ti?
(:! L I< I?' 1?1 CJ S 1")'?S8PT ]?
SGOT 18
CL 103=============================GROUP
01/11/99 FROM WKHl REPRfGF1
i::'j7 '
NORMAl... RANGE UNIT DATE lIME(3.9-4.8) GM/Dl. 01/11/9? 10:30
(0 .. 1-1.5) MG/DI... 01/11/?? 10:30
(0-0 .. 4) MG/DL. 01/11/?? 10:30(117-390) U/I... 01/11/?? 10:30
(0-45) U/I... 01/11/?? 10:30(0-]')
U/I... 01/11/9? 10:30(101-111)
MMOL/1... 01/11/9? 05:00CONTINUED==============================
(
IOD3
IEi"l F'h: UF:' II.. FC02
I(NA
(~N IUN GAF'
BUN
Gl.UCU~;E TMCI~E(.~, TIN lNE
CUi'll l.)(-'tI...UF2 r
.j.
3 .. 11JH
1"i?.",
/
L
l..
UN 11
hhOL /L.
r'lMUL /L
hMC.lI_/L
hO/D!...
t"iG/DI...hCi /.01...
D()ITE
01/11/'19() 1/11,/99
01/11/99() 1/11/':;>.;";
01/11/'/901/11/9'/
01/11/':y,)
1 It'lE0:'5 :: O()
()~:j :00
()~'j:OOo:::!
:00O::'j : ()
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UN 1'1 Dp, TE lIhEuG/hL. 01/11/?9 10:30
MG/DI... 01/11/'19 10:JOMCG/MI... 01/11/?? 07:52
.
==============================END OF" REPORT===============================o
1 / 1 1. ./99 F:' F~ Ut"i W1< Hi,! F~ L: F' F~ T () F 1
;j~:.i?
ILlS I I ~i TIl" r?~
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???? ..__????_???????????.?? ?????????M?? ??_ _.. _ _ _ _ ..__._ __ .. _ ....?... .. __ _ _ _ _-_._._.. _ _ __ .. _....??. _ _..
OOD COUNT l,.'f-1LUC ABN NmmAL F;:(-~NU[ UNIT D(.~TE TH1E ., .vJBC o.
1 L. (~j. 0-- 14?" ::,:j) TH/U'lM 01/1U/()? O~:j:OO '.IT rc
(-I L. l,.11~LUE PHONED TClxDW AT 060~j BY CM
F~BC o'J ~ ,:: L ( 4 ? 0 0 --:=:j .. c.~ () ) MIL.L./C () 1/lB /'F? () ~j : 00HEMOGLOBIN 'loon
L ( 11.5"-1~j" ~,:j ) Gy. 01/1~:l/99 () ::.:j : () 0HEMATOCI=<: IT
c~ E.~ II '/ L. (3:::joo O-??!.,?::'j" 0)
+/ o1/1BI9() O~:j :00,.
Mev B~.:j II il' (T7-95 ) CI-1U ol/Hl/")9 O::.'j :00MCH
(~")" 3 ?(~:'.'j????33 ) t1CGM ol/lB/?"? O::.:j : 00MCHC
31.,?" ::l ( 31?<l7) vI"" o1/1U/?9 O:~j : 00,.FWW
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O~.:j :00WBC
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DECF~EM;ED ~ NO DHFERENl IAL PERFOI:~MEDF'Lr COUNT .
C;" rJ L ( 140-44?0 ) TH/U1M 01.1 lB /99 O:::j :00..JI====::=========================================:=======:::::===::::::====:===::=======
EM PROFILE VALUE ABN
CL 10:lC02
28
K 3"?NA
136
(-IN IUN GAP 1.1BUN 7
GLUCOSE,TM 97============================GROUP
01/1B/99 FRClM WKH1,REF'R1GFl:'.'j4
NORMAL RANGE UNIT DATE TIME
(101-111) MMOL/L 01/18/?9 05:00
(23-29) MMClL./L 01/18/?? 05:00
(3.5-5.0) MMClL./L. 01/1B/9? 05:00
(136-145) MMClL./L. 01/1B/"?? 05:00
(10-20) 01/18/99 05:00
(6-19) MU/DL. 01./1U/?9 05:00
(70-110) MG/DL. 01/18/99 05:00CONTINUED==============================
Ll ~:; L. HiT :U' ....
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TH ICr'jM
BLOOD COUNT V~LUE ~BN NORM~L RANGE
(JIBC 0 .. :1 L. (!"j .. 0?_?/.':,? .. I=i)CRITICAL VALUE PHONED TO*KC AT
0635 BY JABF<I<C ::1 ..
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:1.0 .. 9 L. (:1.1 .. 5-/.5 .. 5) GX 0:1./20/99 05:00'HEMATOCRIT
3:1. .. 2 L. (35 .. 0-45 .. 0) X O:l./20/?9 05:00
MCV 86.0 (77-95) CMU 0/./20/99 05:00
l'jf::H 30.:1 (e~:j-<l3) l'jCGi"i ()/.li.;;:O/?;r":;? O:~j ::00-
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DIFF 0/./20/99 05:00
ul8C r'iOF.:F'H ~ 01/,:)(') I';?':;' ()::.~:: 00
1t.IBe DECF:Er-'iSF'::O:; NO D IFF .. RE .T I(.~L. F?FF:FC)f..:j"j[l) I
~=~~!~~~~~~==========~=~~j~~=====~~~=~~~~~~~2;~~~~==== !~:S~~=2~:~~:~~=g~~~2LHI:.M F ROF ILE . _UF.:.
Hr.-{I~ N.J 1',1'10'1 1... F.,~?lt .',1:. \.. NJ !'JA11:. I [ME. ...
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C:CJ;:::: 30 H (' i::::3-";~(I') i1MOl... /t. ():I. /eo /('/'j:' 0:::; ::00
l< If''';:~ ';3 .. ::~ ..??:=.i .. O) i'iNUI.../1... 01/;;:::0/(1'(;' O:."j::OO
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UNIT DATETH/CMM 01/i.:!:t./9'?BLOOD COUNTWBCCR 1'1'
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BUN 10==============================GROUF
L1::I.':t 01/21/':t? FROM WKH5~REPRTGF:I.'JAX:i20 1tl
NOR hAl... RANGE UNIT DATE TTMF(101-??U.:I.)
t'jMDI.../I... 01/i.~1/i-?9 00;:(':(23-29) MMOI.../1...
01/21/99 05:0(3.5-5.. 0) MMOI.../I... 01/21/9? 05:0
(136-145) MMOI.../I... 01./21/99 05:0(10-20)
01/21/9? 05:0(6-19) MG/DI... 01/21/99 05:0
CONTINUED=============================
F<E~:;ULT ~j I... n3T ll-Jf.;
i:!.71? 1920 :to;;!. TOD3 f:3 :1.;::1.0
CHEM F:'F<CJF II...E
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CONT 1.)(?)I..UE106
0 .. 3
ABI'I
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( 0 n ~.:i ._. :1. .. 1 )
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01 Ie)1. , 199o
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UNIT DAlE TIMETH/CMM 01/d4/99 05:00NClF:MAL. fU~NGE
( ~j ? 0 -- lt~ . ~j )BY NMB
(tj.? 00-??5 .. i.:~O )( 11 ..
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(3~) .. o--tj?~j .. 0 )( '/'/.... 'I
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CHE::M F'F::ClF II...L VAL.UF: AHNCL 104
COd 26
I< '1".1NA 140
ANION GAP 14BUN 13
GLUCClSE,TM 90==============================GROUP
1:33 01/24/99 FRClM WKH1,REPRTGF1
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NORMAL RANGE UNll DAlE TIME(101--111) t'jt'jOI../1... Ol/Pr.i?/()l')l ()~5:0
?(~3?-?r.:.~(?) t1t1Cll.../L 01/dl.j?/'?)lS' O:::j:O(3 .. 5-5 .. 0) MMClL./L 01/24/99 05:0
(136-145) MMlJL./1.. 01/24/9S' 05:0
(lO-PO) 01/24/9'? 05:0(6-19) MG/DL 01/24/99 05:0
(70-110) MG/DL Ol/d4/9S' 05:0CON1'INUED=============================
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===============================END OF? REPClRl'=============================:11:33 01/24/99 FROM WKH1,REPRTGF:L
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2?2192009~ ORDER/OCCt: :3 /00:l. .tl~:;T UF'O(.YTC:: 01 /E<:i/(?9 :u.? ::;:.:?
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CRITICAL VALUE PHONED TO*CVRBC 2.60
HEMOGLOBIN 7.71,1ABNORMAL RESUL.. T PHONED TO*CV
HEMATOCRIT 21.7ABNORMAL RESULT PHONED l'O*CV
MCV 83.5MCH 29.8
MCHC 35.7ROW 11.7
r'Ll COUNT G 6tl
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TH /Ci'1i'1
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COLLECTION DATE/TIME:
NDI:;':MAL RANGE
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TEST NAME
2?f?1920094 ORDER/oce.: ;:::/00:1. 1...(::l~:;T I.lF?J)t,TE: 01./;::'~.'i/9?:;> l::::::e
.... F'~~FiFCOLLECTION DATE/TIME:
01/25/99 11:0
CLC:(J
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2721920094 ORDER/CiCCI:
~:;F'E(; IMFN TYPE::
2/001 LAhl UPDATE: 01./25/99 1.2:E
..??r?t,f3ECOLLECTION DATE/TIME:
01/25/99 11:0
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TEST NAME:
CL
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f1 i"1 en.. /1...
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10:53 02/08/99 FROM ;+-,REERPRF6
321;./B55~50
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2721920094 ORDER/OCCI: :I. /00 :I. Lt,:~)T UPDf'tTE::
COLLECTION D~TE/'rIME:
() E ,/() 8 /'<:;:' ':/ 1() :: ~.:.:.i
??..) ,':;'. .,i':-.) \O:~ .." .,," '.y" :;.>:~ F{I['E :: <:j
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TEST NAt'iE
LDH
I)flL l...1 [
1?0 ( :I. :l.8?..?;.J.?:~~)
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U/L F
10:53 02/08/99 FROM ;+-,REERPRF6J ?
III Ij~::.i ~::j ~:i 1
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5/00J I...M?n I.WnATE: Oc.~/09l'"i9 to:::I:::;
---'--~~6GE 1.COLLEC'flON DATE/TIME' 02/09/99 9:31
L.TS FOE::
721920094 ORDER/DCCI:
CIMEN TYPE:
~, TAT OF<DEF< *.~
THi'10NC
F
F
F
FF
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TH/CM/1
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UNITS
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L. (', .00-:::;.20)L (
:I. 1.5-,15. ~.7j)
ABNORMAL RESUL.T PHONEDTE ;)T 103/>
ABNORMAL RESULT PHONED TO
TE AT to::}/) BY IH<
I... (3~). 0????',?:7;.0)TO*TE AT 1036
BY VR( '7'7 -'
(T'~; )
?(.?5-33 )(31-,37)
( 1 1. ? ~7; .... :I. 'I' .. :::; )
( :I.'I?O????L~';.(?
VALUE
c!5';>"). '-:..-:it>COUNT
OGLOBIN
ATDeR IT eli:! .. '/
NORMAL RESULT PHONED80.6
27.6
C 3~?"2
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72:1.920094 ORDER/OCCI:
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~."j/OO:l I.rd:"'" UPDtYfE:: 01.:' /0(1/99 10 :: 36
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2721920094 ORDER/OCCI:
THi"10NC
2/001 LAST UPDATE: 02/09/99 10:34
'-PfiGE :LCOLLECTION DATE/TINE: 02/09/99 09:31
'ULTS FOr;: ~
ECIMEN TYPE:
TE!3T NArlE
'ION GAF'IN
l.lCOSE,TM(HE IN,
TOT ..BUNIN
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(8.. 5-:L(}.~':j)
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( :I. :1.7-<390)(0.... 37 )
UNITS
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34 02/09/99 FROM ;+-,REERPRF6
B~"j(yB2
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i?'}219i?OO'tl l?
EC Ii"iEN TYPE:
TEST NMIE
Oh:DEF.: loee;H: ::
~)AI, .. UE
:I. 1001
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2721920094 ORDER/OCCI: 3/001 LAST UPDATE: 02/09/99 10:35-"PAGE 1
COLLECTION DATE/TIME: 02/09/99 6ij:31
TEST NAME VAl.UE ABN N()F~MAl. I~ANGE
,
UNITS
U /1..
BTS
. F
) : a~) O;-? /09/99 F I~: ON ;: ... -- " F:I::EI~PI~:F II
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2721920094 ORDER/OCCt:
,PEe Ii"IEN TYPE::
if /00:1. L.?lST UPDATE:: Of:!. /09/99 10 :: ::l~::j
????PAGE 'I..COL.l.ECTION
DATE/TIME~ 02/09/99 09:31
TEST NAME
IRIC ACID
Vf~LUF Nor?mAL F:ANGE
(::1. i"'-7 .. 0 )
I...IN ITS
MG/DL
STS
/
_..
) :: J ~:;.i 0;::' /()c;- /"9 q F F'Oi"j :; ....... 'I r:.'[r::F'F;'I~:F "I
!.i ,"
-----------------------------_.._._-----_._-----------------_._-----_.__ ._---------
BLOOD COUNT VALUE ABN NORMAL RANGE UNIT DATE T1WBC 2.0 L (5.0-14.5) TH/CMM 03/03/99
O~RBC 3.20 L (4.00-5.20) MILL/C 03/03/99
O~HEMOGLOBIN 10.3 L (11.5-15.5) GX 03/03/99
O~HEMATOCRIT 30.3 L (35.0-45.0) X 03/03/99
O~MCV 94.5 (77-95) CMU 03/03/99
O~MCH 82.2 (25-33) MCGM 03/03/99
o~l1CHC 34.1,31-37) X 03/03/99
o~ROW 25.6 H (11.5-14.5) X 03/03/99
O~WBC DIFF 03/03/99
o~POLY X 28 L (50-70) X 03/03/99
o~STAB
X 10 H (2-6) X 03/03/99 o~EOSINOPHIL 9 H (0-4) X 03/03/99
o~BASOPHIL X 1 ,0-2) X 03/03/99
o~LYMPHOCYTE 32 (20-44) X 03/03/99
o~MONOCYTES X 20 H (2-9) X 03/03/99
O~RBC MORPH 03/03/99
o~SEV*ANISO*SLT*POLY*SLT*TEAR DROP*SLT*ELLIPT*SLT*SPHERO
PLT COUNT 210 (140-440) TH/CMM 03/03/99 O~
======================================================:================~~CHEM PROFILE VALUE ABN NORMAL RANGE UNIT DATE T]
CL 105 (101-111) MMOL/L 03/03/99 O~C02 25 (23-29) MMOL/L 03/03/99
O~==============================GROUP CONTINUED===========================
08:45 ~3/03/99 FROM WAS1,REPRTGFl32WB9549
RESUL.TS LIST!l\Jn2721920151
11R:t 002'/2192 TOD2 T207B HEM _
CHEi"! PFWF IL.E CDNT ,)r:-'tLUE ABN NORMAL I~ANGE I..lN IT DATE T .~.,
I< ::3 ? () \:3.5--5.0) MhO!.. ,.'1... 03/03/r O~.'NA 1'1?1
( 136-lLi-5 ) i'ji'~OI....'" ;', .-., ........... ,'.''::', .~! 0~:
ANION GAP 1'=- ( lO--20) 03/0~i/C?9 0':BUN
1'7 ?;)-??19) i'1G /DL (i~3 /'i~) ~3 /'1= ry 0::GL.UCOSE1TM
83 (70?- 110) ;?113 IDL. 0:3/0:3/99 O~CPEAT IN" NE: () ? ri-
L. ?) . ::; -- 1- 1) 11G/DI... 03/0;3/r;'9 O~:
,
OF REPORT~~~~:======================'
'-)
-----_.. _-_.__ ._-_._--_._----------_._--------_.__.....-.._ _--.-..__._.._--_.....-._-_._-_._----_. __ .?. --_._---_.-----_..
J:/I... OOO COUNT 1?.I;\L?lIE
II.' F3 c:: '-!., '1?.:;.:.;/?_."":. :,?.:.:.:;::.oO""".I::.i?:> ".... i ../'.eF~' I TIC{': 1._ I){iI.. IJF: F' HDNF :0 ' . ,.
RBC ~ _.
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~r ,::::g~~; .
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( (.:;: ~.:S .... ~:~ :::.' )
( ;J :I. ._. J ''? )
H .; 1 1 .. ::;i ._. l,:i? .. ::.i )
UNIT
?fl?I/Ci"li'l
~"'f Tt.L ,/t::
0"'?.\,'i,J
/+
'~I
(.
Chlj
i-lCGh
~ .',.
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(J :3 ,/;:.:.:: ~~\ / 0:.;' .:.;:' ()
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O .. ~.::i?-?l" 1)
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UNIT
'?ii'?ji"?li .. ?i
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i?if:; /DI.
hG/OL.
i1C:i /DL
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(j:3 ./~.~ ~3 /,;.. ~;J {){) ::i ,/
i.? ~3 / '7' .;.. (I
{)::3 {"(? ::~~ /99 (j
::;:~ .::::~~~ ::~:~:~ g
():'~{ /'E;: ~:~ ./9 r1' ()
(i3 ,.' ;.::: :3/':;:. '? n
=~~~=~~=~=======~==============ENO OF REPGRT==,"=====================~==
(J :},::, :: :}.... ():3 ,/;:::0:; /:y' .:/ F: F:: IJi"i Itli<:,J 3 .? F: F j:: h: ?1? c-:i F:i.
HEM
BLOOD COUNT %,ue: ABN NORMAL RANGE UN IT DATE TIMEWBC 3.7_} L (5.0-14.5) 5'" fH/CMM 03/04/99 05:01
RBe ? .1 L (4.00-5.20) 4.ilr MILL/C 03/04/99 05:01
HEMOGLOBIN ~-:-p L (11.5-15.5) IJs GX 03/04/99 05:0~HEMATOCRIT L (35.0-45.0) X 03/04/99
05:0~
MCV 94.0 (77-95) CMU 03/04/99 05:0~
MCH 32.3 (25-33) MCGM 03/04/99 05:0~MCHC 34.
(~ (31-37) X 03/04/99 05 :O(
ROW 25.0 H (11.5-14.5) X 03/04/9905:0(
WBC 1) IFF 03/04/99 05 :O(
POLY X GD75-- H (50-70) X 03/04/99 05:0'STAB X 13 H (2--6) X 03/04/99 05:0'
EOS INOPH IL (0-4) X 03/04/99 05 :0\LYMPHOCYTE 3 L (20-44) X 03/04/99 05:0(
MONOCYTES X 7 (2-,9) X 03/04/99 05:0;
RBC MORPH 03/04/99 05 :0>SEV*AN
ISO*SLT*HYPO?)fMOD~SL T*SF'HERO*SLT*'TEAF~ DROP
=-"=~~~=~~~~l===========~==:========~;':~:::~~~===~~'J-== ~~;~~~=:~~;~:;;;=~~~~:
CHEM PROFILE VALUE ABN NORMAL RANGE UNIT DATE TIME
CL :1.04 (101-111) MMOL/L 03/04/99 05:0'C02 23 (23-29) MMOL/L 03/04/99 05 :0,
I< 3.8 (3.5-5.0) MMOL/L 03/0{~/99 05:0'==============================GROUP CONTINUED=============================:
'9 :25 03/04? /99 FROM WI<H5 I=<EPRTGF 1iAX39842 '
F~ESUL TS L 1ST Hit?,
E!721920151
MRt 002'Ie192
-----~--------------~-_._-------"-------------._._--------~---_._._--------------_._---
rIME05:0
05:0
05:005:0
05:0
DATE:03/04/99
03/04/9903/04/99
()3/0(~/99
03/04/99
UNIT
MMOL/L
MG/DL
MG/DL
MG/DL
NOF~MAL RANGE(
136-1(~:':j)( 10-,20)
(6-,19)
(')0-110)
(0.5-1.1>
ABN
139
16:1.0
96
0.3
CONTNA
ANION GAP.BUN
GLUCOSE TMCREATINiNE
===============================END OF REPORT==============================9:25 03/04/99 FROM WI<H5 REPRTGFl
AX39842 '
~~~============================END OF REPORT~=~======~====~===~========?08:34 03/05/99 FROM WKJ3,REPRTGFl
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APPENDIX 3
Environmental Data: Map of Berlin Lake, EPA documentation of spills into
Berlin Lake Reservoir
76
MAP OF BERLI N LAKE
77
BERLIN
LAKE
RECREATION
AREAS
II
u
1I
C>
I
Mock
Rd.I
I
~
MAHONING!
CO.OHIO
Helser
COMMERCIAL
(s)
Dutch
H<rt>or
Morlna
Q"ld
Conceaalonalr
(t,)
L_'a
Bait
Shop
OTHER
AGENCY
(j)
Deer
Creek
Reo.
Area
(H)
IIIow
Creek
Reo.
Area
?
Bomer
Road
Boat
LCUlOtlIno
RCJIIIP
"D
a:
10
q)
C
o
J
-----..
"
"
/
\
"\
.J
~
CORPS
OF
ENQNEERS
Dam
PIcnicArea
lolll
Creek
Rec
AreaResolTce
lolCI"lagerll
OffIce
CerIll<ll'1
ChlTchCampQrol6ld
j
~
ai
+-
a:
0
"Ci
a:
Yole
Rd.
:c
01
a
L
0
I.E
PORTAGE
CO.
f-
lO
OHIO
..l?
0
~I
0
+-
~
-
c
u
0
:2
I
Mottown
Rd.
"D
a:
C
o
E
+ 
o
z
"D
a:
q)
o
c
o
:;(
-N-
SCALE
IN
htILES
US
Army
Corps
of
Engineers
PIttsburgh
DIstrIct
1/20
NOTE
II
o
SCAlE
IN
Wl..ES
VICINITYMAP
25
No
IIlOtors
permItted
wIthin
2000
feet
of
the
dam.
No
boats
permItted
wIthIn
500
feet
of
the
Int~e
tower
Q"ld
crest
gate,lt
111
lriawfu
to
caullea
w~e
wIthin
ISO
feet
of
exlstlnQwaterlIne
or
bridge.
RevIsed:
1993
AreoB-
from
U.S.
224
brIdge
to
Corv-oIl
brldoe.AreoC-
from
Corv-oll
brl~
to
route
14
brl~.
Areo0-
from
Route
14
brIdge
to
Route
225
brldQe.AreoE-
from
Route
225
brIdge
to
end
of
I~
..
,r.
{')
....
To
LJmo~
LEGEND
u.s.
GoVenNnt
Property
Line
EPA DOCUMENTATION
OF SPI LLS INTO BERLI N LAKE RESERVOI R
78
EWTTTY COUNTY
A Y S MEDICAL EQUIPMEWT IN MAHONING
"'-I AUTO BODY PORTAGE
AEROUKE EXTRUSION CO MAHONING
AEROLITE EXTRUSION CO MAHONING
ALL AMERJC4N TRACK CO MAHONING
ALL AMERJCAN TRACK CO MAHONING
ALLJA.NCE BOARD OF ED. STARK
ALLJA.NCE STP STARK
ALLJA.NCE STP STARK
ALLJA.NCE TUBULAR STARK
ALLJA.NCE WATER DEPT STARK
ALSiD OIL '" GAS CO MAHONING
ALUMINUM COLOR INOUSTRIE MAHONING
AMERJC4NPAPER PRODUCTS MAHONING
AMERISOURCE MAHONING
AAIOCO OIL CO PORTAGE
ANDEL RESIDENCE PORTAGE
AReO PIPELINE MAHONING
ASHLAND BRANDED MARKET! STARK
ASHLAND OIL CO. TRUMBULL
AUTUMN /ND TRUMBULL
AVILA CONTRACTING TRUMBULL
BFI PORTAGE
BFI PORTAGE
BFI PORTAGE
BFI PORTAGE
BFI PORTAGE
B FI STARK
B F I MAHONING
BFI PORTAGE
B P OIL CO I PlPEUNE ON TRUMBULL
B-RlGffr TRUCKiNG CO MAHONING
BABCOCK LUMBER TRUMBULL
BABCOCKS & WILCOXI TUBUL STARK
BAGETTA TOWNSHIP GARAGE TRUMBULL
BAZETTA TWP TRUMBULL
BEAZER EAST INC MAHONING
BEAZER EASTINC MAHONING
BEAlER EAST INC MAHONING
BEAlER EAST INC MAHONING
BEAZER EAST INC MAHONING
BELDON & BLAKE MAHONING
BELOrrSTP MAHONING
BELOIT STP AIAHONiNG
BELOIT STP MAHONING
BELorr STP MAHONING
BELOIT STP MAHONING
BELorr STP MAHONING
BELOIT STP MAHONING
BELOIT STP MAHONING
BELOIT STP MAHONING
BELOIT STP MAHONING
BELOIT STP MAHONING
BELOIT STP MAHONING
BELOIT STP MAHONING
TWP_CfTY WA TERWA Y MATERlAL_'
YOUNGSTOWN STORM SEWER RED DYE
FREEDOM TWP UNKNOWN CREEK OIL
BOARDMAN TWP MAHONING RIVER SOOIUM HYDROXIDE SOLU
BOARDMAN UNKNOWN CAUSTIC SODA
BCAR[)MAN MILL CREEK SUBSTANCE 41 70
BOARDMAN SAWMILL RUN CREEK LATexPAlWT
ALLlANCE AIAHONING RIVER STYRENE BUTADIENE POL Y
ALLlANCE MAHONING RIVER TRiB OIL
ALLlANCE BEECH CREEK TRlB DIESEL FUEL
AL1.JANCE MAHONING RIVER MILKY WHITE STUFF
ALLlANCE DEER CREEK HYDRAULIC OIL
SMfTH TWP BELOIT OITCH CRUDE OiL
LOWELLVILLE MAHONING RIVER TRlB WASTE ACID
YOUNGSTOWN SEWER cousnc SODA
YOUNGSTOWN UNKNOWN TRANSFORMER OiL
GANETESV/LLE SILVER CREEK MOTOR OIL
GARRETTSVILLE "'AHONING RIVER TRiB SEPTIC TANK SOLIDS
N.JACKSON UNKNOWN FUEL OIL '2
ALLlANCE STOR'" SEWER KEROSINE
wARREN STORM SEWER .2 FUEL OIL
WARREN SWAMP HAL4RDOIJS WASTE RESID
I.J8ERTY TWP UNKNOWN CREEK POND SLUDGE
A TWATER BERUN RESERVOiR GARBAGE
ATWATER BERUNRESERVOIR GARBAGE
ATWATER BERlJN RESERVOIR LEACHATE
A TWATER MILL CREEK ODORS
ATTWATER WILLOW CREEK ODOR
LEXlNGTON TWP UNKNOWN HYDRAULIC OIL
BERLIN CENTER UNKNOWN HYDRAULIC OIL
A TWATER BERUN RESERVIOR SULFUR DIOXIDE
LORDSTOWN TW STORM SEWER DIESEL FUEL
YOUNGSTOWN STORM SEWER DIESEL FUEL
'"*JBBARD UNKNOWN DIESEL FUEL
ALLlANCE RYANS RUN WASTE SULFURIC ACID
CORTLAND GROUNDWATERIMOSQU/TO RE SALT
SAZETTA TWP POND SEPTIC WASTE
YOUNGSTOWN CRAB CREEK TOC 73.5
YOUNGSTOWN CRAB CREEK WASTE WATER
YOUNGSTOWN CRAB CREEK WASTE WATER
YOUNGSTOWN GLADE CREEK WASTE WATER
YOUNGSTOWN CRAB CREEK WASTE WATER
SMfTH TWP UNKNOWN CRUDE OIL
BELOIT MAHONING RIVER WASTE WATER
BELOIT BERUN LAKE TRlB WASTE WATER
BELOIT "'AHONING RIVER WASTE WATER
BELOIT "'AHONING RIVER WASTE WATER
BELOIT MAHONING RIVER SEWAGE
BELOIT MAHONING RIVER WASTE WA TER
BELOIT MAHONING RIVER SEWAGE
BELOIT MAHONING RIVER WASTE WATER
BELOIT MAHONING RIVER SEWAGE
BELOrr MAHONING RIVER WASTE WATER
BELOIT "'AHONING RIVER WASTE WA TER
BELOIT MAHONING RIVER WASTE WATER
BELOIT MAHONING RIVER WASTE WATER
A"'OUNT_' UNlTS_' RECOVER_I
o UNK 0
o UNK 0
50 GAL 0
o UNK 0
400 GAL 0
JO() GAL 0
5 GAL 0
20 GAL 0
120 GAL 120
o UNK 0
100 Glol 0
2 GAL 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
1252 GAL 0
GAL 0
5 GAL 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
7550 GAL 0
40 GAL 0
o UNK 0
8400 GAL 0
50 GAL 50
o UNK 0
100 GAL 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
7= GAL 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
- en ?"
AMOUNT_' UNTTS_, RECOVER_'
'" GAL 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
480:) GAL 4000
o UNK 0
o UNK 0
o UNK 0
o UNK 0
'" GAL 40
YR EWTTTY COUNTY TWP_CfTY WATERWAY
P2 DA YCO I DIETRICH IND TRUMBULL WARREN STORM SEWER
go DA YTON POWER & UGHT TRUMBULL NILES WETLAND
8P DEFTINC STARK ALLWoICE UNKNOWN
QJ DENMAN TIRE & RUBBER TRUMBULL BRACEYItiE TW MAHONING RNER
8P DENMAN TIRE & RUBBER TRUMBULL LEVfTS8URG MAHONING RIVER
8P DIAMOND HEAD EXTENDED C MAHONING /oIORTH UMA UNKNoWN
P' DON FOSTER & SONCARPET STARK ALLWoICE STORM DRAIN
QJ DONFOSTOR & SON CARPET STARK ALLWoICE UNKNOWN CREEK
P2 DORFMAN PRODUCTION MAHONING DAMASCUS UNKNOWN
QJ DOUG'S TRUCK & TRAiLER MAHONING YOUNGSTOWN UNKNOWN CREEK
P' DOWELL SCHLUMBERGER INC MAHONING AUSTINTOWN SEWER
P' DUFF'S CARPET CLEANING MAHONING AUSTINTOWN UNKNOWN
P' EAGLE CHEVY OLDS TRUMBULL HUBB.4RD UNKNOWN
QJ EARL COREY CO COLUMBIAN COLUMBIANA E BR MILL CREEK
QJ EARL COREY CO COLUMBIAN COLUMBIANA UNKNOWN CREEK
8P EAST OHIO GAS MAHONING DEERFIELD POND
go EAST OHIO GAS MAHONING BERUN CENTER BERLIN RESERVOIR
P2 EAST OHIO GAS MAHONING AUSTINTOWN TW MEANDER CK RESV.
P2 EAST OHIO GAS MAHONING YOUNGSTOWN STORM SEWER
Q2 EASTERN EVERFLO MAHONING ELLSWORTH TW MEANDER CREEK
P' EASTERN PETROLEUM TRUMBULL WEA THERSRELD UNKNOWN
8P EASTERN PETROLEUM MAHONING TRUMBULL CO UNKNOWN
go EMRO MARKETING I GAS TOW MAHONING /oIORTH UMA UNKNOWN
P' EMRO MARKETING I SPEEDW MAHONING AUSTINTOWN SULFUR RUN TRiB
P' EYERFLOW EASTERN MAHONING ALLWoICE MAHONING RIVER TRJB
P2 FAUL & SONS TOOL & DIE CO TRUMBULL NILES UNKNOWN
P2 FFE TRANSPORTA TION SERVI TRUMBULL WEA THERSFIELD MAHONING RIVER
8Q FISHBURN WELL SERVICE MAHONING MINERAL RJDGE MEANDER CREEK
8P FfTNESS CENTER TRUMBULL BAZETTA STORM SEWER
P' FORMER OPEN PIT MINING/NA MAHONING GOSHEN TWP MEANDER CREEK TRiB
P' FORT INDUSTRIES MAHONING YOUNGSTOWN UNNAMED CREEK
8lI FRANK MARTUCCIO ENTERPRJ MAHONING J.l1L TON TWP LAKE MIL TON
QJ GASTOWN GAS STATION MAHONING NEW MIDDLETON STORM SEWER
go GENERAL AGGREGATES TRUMBULL KJNGSJ.lAN OLD ROCK OUARRY
go GENERAL ELECTRIC TRUMBULL NILES MOSOUfTO CREEK
Q2 GENERAL ELECTRIC TRUMBULL NILES MOSOUfTO CREEK
QJ GENERAL ELECTRIC PORTAGE RAVENNA UNKNOWN CREEK
QJ GENERAL ELECTRIC TRUMBULL NILES MOSOUfTO CREEK
QJ GENERAL ELECTRIC TRUMBULL NILES J.lOSOUfTO CREEK
QJ GENERAL ELECTRIC TRUMBULL NILES J.lOSOUfTO CREEK
QJ GENERAL ELECTRIC TRUMBULL NILES MOSOUfTO CREEK
QJ GENERAL ELECTRIC TRUMBULL NILES MOSOUfTO CREEK
~ GENERAL ELECTRIC TRUJ.lBULL NILES MOSOUfTO CREEK
P2 GENERAL ELECTRIC TRUMBULL NILES MOSOUfTO CREEK
QJ GENERAL ELECTRIC TRUMBULL NILES MOSOUfTO CREEK
go GENERAL MOTORS ILORDSTO TRUMBULL LORDSTOWN MEANDER CR RESV.
go GENERAL MOTORSILORDSTO TRUMBULL LORDSTOWN STORM SEWER
P' GENERAL MOTORSI LORDSTO TRUMBULL LORDSTOWN MUD CREEK TRiB
P' GENERAL MOTORSILORDSTO TRUMBULL LORDSTOWN STORM DRAIN
QJ GENERAL MOTORSI PACKAR TRUMBULL WARREN MAHONING RJVER
go GENERAL MOTORS I PACKAR TRUMBULL WARREN RED RUN CREEK
QJ GIRARD STP TRUMBULL GIRARD UTTLE SOUAWCREEK
go GRANT STREET SCRAP OIL TRUMBULL NILES MAHONING RNER
P' GREENWOOD ACCURA MAHONING BOARDMAN STORM DRAIN
QJ GWIN CONTRACTING COLUMBIAN COLUMBIANA UNKNOWN CREEK
MATERIAL_'
WASTE CHEMICALS
CRUDE OIL
STAIN
DIESEL FUEL
CARBON BLACK
SEWAGE
GREY GREENISH STUFF
CLEANING CHEMICALS
CRUDE OIL
OIL
ACIDS
WASTEWATER
ANTIFREEZE
OIL
MOTOR OIL
CRUDE OIL
.2FUEL OIL
NA TURAL GAS CONDENSAT
GASOLINE
NATURAL GAS
CRUDE OIL
UNK
DIESEL FUEL
DIESEL FUEL
DIESEL FUEL
WASTE OIL
DIESEL FUEL
RUSTY RED MA TERJAL
SWIMMING POOL CHEMICA
IRONOXIOE
ASBESTOS
DIESEL FUEL
GASOUNE
UNK
LUBRICA TlNG OIL
HYDRAULIC DlL
DIESEL FUEL
WASTEWATER
WASTEWATER
WASTEWATER
WASTEWATER
WASTEWATER
WASTEWATER
WASTEWATER
WASTE HYDRAULIC OIL
DIESEL FUEL
WA TER BASED PAiNT
ANTIFREEZE
RJNSEWATER
WASTEWATER
AMMAL FAT & LUBRICATIN
SEWAGE
MOTOR OIL
MOTORDIL
FUEL OIL
o UNK
,(X] GAL
o UNK
, GAL
4 GAL
o UNK
o UNK
o UNK
~ GAL
o UNK
'" GAL
o UNK
,~ GAL
o UNK
o UNK
o UNK
o UNK
200 GAL
o UNK
o UNK
8 GAL
, GAL
~ GAL
o UNK
o UNK
o UNK
o UNK
o UNK
o UNK
o UNK
20 GAL
o UNK
1100 GAL
o UNK
200 GAL
o UNK
" GAL
o UNK
o UNK
o UNKl'
GAL
o
o
o
o
o
o
o
o
o
o
2'
o
2'
o
o
o
o
100
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
YR
go
go
go
all
go
llJ
go
go
SlI
III
go
all
111
all
go
go
SlI
all
all
go
go
go
go
go
go
III
III
III
III
III
III
112
llJ
llJ
llJ
llJ
llJ
114
all
llJ
III
III
112
go
112
III
all
111
all
llJ
all
112
go
112
114
E/oITTTY COUIVTY TWP_CITY WATERWAY MATERJAL_l
HARE EXPRESSIRUAN LEASIN MAHONING YOUNGSTOWN STORM SEWER DiESEL FUEL
HILL TOP LANDFILL MAHONING ELLSWORTH TW PALMYRA LAJ<E?MEANCE RES. VARJO()S lAORGANIC
HOWELL INOUSTRJES TRUMBULL MASURY SHENANGO RJVER UNK WHITC STUFF
HUBBARD ELECTRJC DEPT TRUMBULL HUBBARD UNKNWON TRANSFORMER OIL
INOUSTRJAL CLEANING SERVI TRUMBULL GERRALD CfTY SEWER ~/NS BLACK LJQUID
J&/ITRUCKJNG PORTAGE ATWATERTWP UNKNOWN CREEK BRINE
J J COAS TRUCKJNG TRUMBULL WARREN /lAHONING RIVER UNK
J L COATS DPJLUNG IAAHONING AUSTCNTOWN S/IALL CREEK BRINE
J L COATS WELL SERVICE /lAHONING ELLSWORTH TW /lEANDER CREEK WATER PICKUP
JA/IES DRJLUNG CORP ASHTABULA DORSETT TWP weTLAND CRUDE
OIL
JEFFERY F. SATES PORTAGE GARRETTSV1U.E SILVER CREEK WASTE
OIL
JOHN KETTtER TRUMBULL SROCKRELD SPRiNGFED CREEK CONSTRUCTION
WASTE
JOHN PrTTMAN MAHONING PQU.N() TWP STORM DfTCH RED STUFF
KAUFMAN DEPT STORE MAHONING SQAFIDI.AAN UNKNOWN ASBESTOS
KUNTZIAAN TRUCKJNG MAHONING GOSHEN TWP MILL CREEK DiESEL FUEL
LTVSTEEL. CAMPBELL MAHONING CAMP8ELL MAHONING RIVER HYDROCARBON
LTVSTEEL.. WARREN COKE TRUMBULL WARREN MAHONING RIVER WASTE
WA TER
LTVSTEEL.. WARREN COKE TRUMBULL WARREN STORM sewER WASTE WATER
LTVSTEEL.. WARREN COKE TRUMBULL WARREN STORM SEWER WASTE WATER
LTVSTEEL.WARREN COKE TRUMBULL WARREN MAHONING RIVER WASTE
WATER
LTVSTEEL.. WARREN COKE TRUMBULL WARREN MAHONING RJVER WASTE
WA TER
LTV STEEL. WARREN COKE TRUMBULL WARREN MAHONfNG RJVER ABSORBENT OIL
LTVSTEEL.WARREN COKE TRUMBULL WARREN MAHONING RIVER DiRECT COOLiNG WATER
LTVSTEEL.. WARREN COKE TRUMBULL WARREN MAHONfNG RJVER WASTE
WATER
LTVSTEEL. WARREN COKE TRUMBULL WARREN MAHONfNG RIVER TRlB UNK HYDROCARBON
LTV STEEL.. WARREN COKE TRUMBULL WARREN MAHONfNG RJVER OIL
LTVSTEEL.. WARREN COKE TRUMBULL WARREN MAHONfNG RJVER SULFURIC ACID
LTV STEEL.WARREN COKE TRUMBULL WARREN MAHONING RIVER SULFURJC
ACID
LTVSTEEL.. WARREN COKE TRUMBULL WARREN MAHONfNG RIVER TRIB ACID WASTEWATER
LTV STEEL.WARREN COKE TRUMBULL WARREN STORM SEWER TAR
LTV STEEL.. WARREN COKE TRUMBULL WARREN UNKNOWN CRUDE COAL TAR
LTVSTEEL..WARREN COKE TRUMBULL WARREN IAAHONING RIVER WASTE
WA TER
LTV STEEL.WARREN COKE TRUMBULL WARREN MAHOMNG RIVER WASTE
WA TER
LTV STEEL.WARREN COKE TRUMBULL WARREN MAHONING RIVER WASTE OIL
LTV STEEL.. WARREN COKE TRUMBULL WARREN MAHONING RIVER CONTAMINATED WASTEWA
LTVSTEEL.WARREN COKE TRUMBULL WARREN MAHONING RJVER OIL
LTV STEEL.. WARREN COKE TRUMBULL WARREN MAHONING RIVER OIL
LTV STEEL.. WARREN COKE TRUMBULL WARREN UNKNOWN CREEK WASTE WATER
LAMAK PETROLEUM PORTAGE WINDOM SILVER CREEK TRlB CRUDE
OIL
LARRY MURPHY TRUCKJNG COLUMBIAN SEBRlNG DEER RUN PETROUUM
OIL
LESKO RJDE CO TRUMBULL CORTLAND STORM SEWER HYDRAULIC FLUID
LOUISIANA PACIFIC CORP Jl,AHONING BOARDMAN MAHONING RIVER TRIB . HYDRAULIC OIL
LOWELVILLE ROD & GUN MAHONING LOWELV1U.E UNKNOWN CREEK SOAPY STUFF
LYDEN OIL IAAHONING CAJI,PSEll Jl,AHONING RJVER GASLOINE
LYNN STRANG I STRANG'S,JU ASHTABULA DORSET UNKNOWN CREEK SLUDGE
JI,&BOPERATINGCO PORTAGE ROOTSTOWNTW SWAMP CRUDE
OIL
Jl,AHONING CO SANI ENG DEP Jl,AHONING AUSTINTOWN T.JNNAMED CREEK SEWAGE
Jl,AHONING PAINT CORP IAAHONING YOUNGSTOWN MAHONING RIVER PAINT
IAAHONING VALLEY SANfTARY IAAHONING MINERAL RJDGE MEANDER CREEK SEWAGE
IAAHONING VALLEY SANfTARY TRUMBULL NILES MEANDER CREEK FLUOROSILICIC ACID
Jl,CGUIRES JUNKYARD """HONING SPRiNGRELD TW UNKNOWN TRASH
MEANDER STP TRUMBULL MINERAL RJDGE MEANDER CREEK SEWAGE
MID STATE OIL FIELD PORTAGE GARRETSVILLE UNKNOWN NATURAL GAS
/l1U.ER BROTHERS ASHTABULA CHERRY VALLEY UNKNOWN CREEK FERTILIZER 211%
MIWKEN AUTOMOTIVE TRUMBULL WARREN STORM SEWER KEROSENE
AJI,OUNT_
1 UNfTS_1 RECOVER_1
70 GAL 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o NOS 0
84 GAL 84
27' GAL 0
o UNK 0
o UNK 0
o UNK 0
!!O GAL 0
o UNK 0
3(XX) GAL 0
1!JlX) GAL 100
!JlX) GAL 0
o UNK 0
2000 GAL 0
100 GAL 0
JCO GAL 0
!JlX) GAL 0
o UNK 0
, GAL 0
20 GAL 0
o UNK 0
10fICXXJ GAL 107CXXJ
110 GAL 0
200 GAL 0
2000 GAL 0
o UNK 0
20 GAL 0
!JlX) GAL 0
GAL 0
o UNK 0
o UNKNO 0
o UNK 0
1 UNK 0
20 GAL 0
o UNK 0
o UNK 0
1~ GAL 0
o lJNK 0
2l14O GAL 0
o UNK 0
o UNK 0
o UNK 01=
GAL 0
o UNK 0
o UNK 0
o UNK 0
10 GAL 0
o UNK 0
NTlTY COONTY TWP_CITY WATERWAY MATERlAL_I
'OTHER NATURE STARK ALLJANCE DEER CREEK UNKNOWN
'OTHER NATVRE ASHTABULA ANDOVER TWP BLOCK CREEK TRIB ALGAE
IOTHER NATVRE MAHONING LAKE J./IL TON LAXE MIL TON ALGAE
fOTHER NATURE MAHONING YOONGSTOWN PUBLIC POND ALGAE
?JTHER NATVRE PORTAGE ROOTSTOWN POND OIL
?JTHER NATVRE MAHON/NG LAKE MR. TON LAXE MIL TON NO sPILL
~OTOR FREIGHT I NC. MAHONING Mil. TON TWP LAXE MIL TON
DIESEL FUEL
I./R ART TIL TON TRUMBULL LEAVTTTSBURG UNKNOWN CREEK FUEL
OIL
WR BARRY BAER TRUMBULl. NEWTON FALLS UNKNOWN OIL
WR BENOWSKJ PORTAGE HIRAM EAGLE CREEK MANURE
WR CHARLES SMITH MAHOMNG CRAJG BEACH LAKE MIL TON OIL
J./R DENZlL SNYDER TRUMBULL CORTU.ND J./OSQUITO CREEK TRIB FUEL
OIl
MR HERMIT DEAN JR PORTAGE WlNOOW TWP UNKNOWN CREEK UNK
MR JOHN GORAL TRUMBULL BRACEY1U.E 1W MAHONING RIVER TRIB PAINT
MR JOHN PrTTMAN MAHONING F"::)UND STORM DITCH RED STVFF
MR LAURA HlJTCHINS TRUMBULL C~4IP/ON TWP STORM SEWER-MAJ.;ONING RIV HEATING OIL
MR LEO SORICE MAHONING BOARD4iAN MILL CREEK DIESEL FUEL
MR LLOYD SHERIDAN MAHONING YOONGSTOWN UNKNOWN CREEK CONCRETE
MR NOVAK TRUMBULL HARTF<:!RD WETLANDS ASPHALT
MR PETERS COLUMBIAN KNOX TWP UNKNOWN CREEK BLACK OIL STVFF
MR FV.NDY SMILEY MAHONING ELL~TH UNKNOWN MOTOR
OIL
MR RANKIN PORTAGE FV.V?NNA TWP UNKNOWN CREEK TFV.SH
MR RICHARD GRUND PORTAGE FV. V~A HINKLEY CREEK FUEL OIL
MR ROBERT COOK MAHONING YOONGSTOWN SEWER WASTE
OIL
MR ROY CARSON MAHONING BEFIUN TWP MILL CREEK FUEL
OIL
MR SAM RAFIDE MAHONING YOIJNGSTOWN STORM SEWER OIL
Y STVFF
MR VANDERHOVER PORTAGE NELSON MAHONING RIVER TRiB DRUMS
MR VINCE HAROLD STARX LEXINGTON DEER CREEK DIESEL FUEL
MR ZALJD PORTAGE WlNOOW SFCREEK WASTEWATER
MR. WILBER HOPTON STARX LEXINGTON TWP UNKNOWN FUEL
OIL
MS IRENE WORK PORTAGE NaSON TWP UNKNOWN CREEK GARBAGE
MULTICLEAR SERVICE MAHONING YOONGSTOWN STORM SEWER UNKNOWN
MUNSON TRANSPORTAnON MAHONING YOIJNGSTOWN STORM SEWER DIESEL FUEL
MURPHY TRUCKING CO COLUMBIAN DAMASCUS MAHONING RIVER BLUE GREEN STVFF
NOBLE OIL PORTAGE E.DiNBURG TWP UNNAMED CREEK CRUDE
OIL
NORTH AMERJCAN VAN UNES PORTAGE PAUA/RE TWP UNKNOWN DIESEL FUEL
NORTH CANTON TRANSFER MAHONING YOIJNGSTOWN UNKNOWN DIESEL FUEL
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER WASTE WA
TER
NORTH
STAR STEEL' MAHONING YOIJNGSTOWN MAHONING RIVER OIL & GREASE
NORTH STAR STEEL MAHONING YOONGSTOWN MAHONING RIVER WASTE WATER
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER OIL & GREASE
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER WASTE WATER
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER WASTE WATER
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER WASTE WATER
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER MOI!J(;REASE
NORTH STAR STEEL M-'\HONING YOIJNGSTOWN MAHONING RIVER TS.S. WASTE WATER
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER HYDROCAREON
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER WASTEWATER
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER OIL
AND GREASE
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAJ.;ONING RIVER OIL AND GREASE
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER WASTE WA TER
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER OIL
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER OIL
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER OIL
NORTH STAR STEEL MAHONING YOIJNGSTOWN MAHONING RIVER OIl
AMOIJNT_I UNITS_I RECOVER_I
o UNK 0
o UNK 0
o UNK 0
o NOS 0
o UNK 0
o NOS 0I"
GAL 0
, GAL 0
o UNK 0
o UNK 0
o UNK 0
27' GAL 100
o UNK 0
, GAL 0
o UNK 0
20 GAL 15
o UNK 0
o UNK 0
o UNK 0
o UNK 0
70 GAL 0
o UNK 0
100 GAL 0
o UNK 0
o UNK 0
5 GAL 0
o UNK 0
5 GAL 3
o UNK 0
144 GAL 0
o UNK 0
o UNK 0
100 GAL 0
o UNK 0
JO GAL 0
100 GAL 0
1200 GAL 1200
P.Xro GAL 0
o GAL 0
13= GAL 0
o UNK 0
I64CCO GAL 0
o UNK 0
o UNK 0
300 GAL 0
18= GAL 0
o UNK 0
13= GAL 0
o UNK 0
o UNK 0
22= GAL 0
24 KGS 0
o UNK 0
41 KGS 0
18 KGM 0
YR
IJQ
IJQ
IJQ
go
Q.J
Q.J
112
IJII
go
III
Q.J
Q.J
Q.J
Q.J
Q.J
Q.J
III
IJII
112
III
go
111
IJII
112
Q.J
Q.J
go
Ql
IJlI
Q.J
Q2
Q.J
go
IJlI
go
112
112
IJII
111
112
go
Q2
Q.J
111
Q.J
114
IJQ
Q2
Q2
IJII
Q.J
111
IJII
III
Q.J
EWTfTY COUIflY TWP_CfTY WATERWAY
NOVAK AIRCRAFT MAINTENAN PORTAGE RAVENNA UNKNWON
0& P FUEL OIL CO ASHTABULA RJCHMAN UNKNOWN
ODOT MAHONING CANFIELD STORM SCWCR
ODOT TRUMBULL CORTLAND STORM SCWCR
ODOT lAAHONlNG CANFIELD MEANDER CREEK
ODOT TRUMBULL Hl.JBBAAD UNKNowN CREEK
OHIO DEPT NATURAL R?SOUR PORTAG? DE?RFlEW BERUN R?S?RVIOR
OHIO EDISON TRUj,fBULL WEATJ-IERSF,?W MAHONING RIVER
OHIO ?DlSON TRUMBULL NILES j,fAHONING RIVER
OHIO EDISON TRUMBULL NILES MAHONING RIVER
OHIO EDISON TRUj,fBULL NILES MAHONING RIVER
OHIO EDISON TRUMBULL NILES MAHONING RlV?R
OHIO EDISON TRUMBULL NILES MAHONING RIVER
OHIO EDISON TRUMBULL NILES MAHONING RIVER
OHIO EDISON TRUMBULL NILES MAHONING RIV?R
OHIO EDISON TRUMBULL NILES j,fAHONING RIVER
OHIO EDISON TRUMBULL NILES MAHONING RIVER
OHIO EDISON ELECTRIC CO TRUMBULL WARREN MAHONING RIVER
OHIO SCRAP & IRON TRUMBULL WARREN MAHONING RIVER
OHIO WATER SERVICE TRUMBULL GIRARD SQUAW CREEK TRlB
OLD SHEET & TUB MILL MAHONING STRUTHERS j,fAHONING RIVER
ORCHARD ESTATES TRAiLER PORTAGE RAVENNA PUBLiC WATER SUPPLY
ORION ENERGY PORTAGE A7WATERTWP WATER SUPPLY
ORION PETROLEUM CORP PORTAGE A7WATER TWP DEER CREEK
P N L HEAT TREA TMENT MAHONING YOUNGSTOWN STORj,f SE'WER
PACKARD ELECTRIC CO TRUMBULL VIENNA TWP SPRING RUN
PALUj,fBO CLEANERS MAHONING CANFIELD STORM SE'WER
PANDA TRUCKING CO TRUMBULL WARREN UNKNOWN CREEK
PAUL BIGELOW & SONS MAHONING j,f/LTON TWP UNKNWON
P?NTECH ENTERPRISES TRUMBULL FOWLER TWP UNKNOWN CREEK
PL y.TRIM CORP MAHONING AUSTINTOWN MAHONING RIVER TRiB
PORTAGE COUIflY ENGINEER PORTAGE RA VENNA SlLVER CREEK
PORTS PETRCLEUM MAHONING AUSTlWTOWN UNKNOWN
PROOEXINC PORTAGE RAVENNA HINKLCYCREEK
PSI< STEEL TRUMBULL HUBBARD STORM SE'WER
PUTNAM TRANSFER PORTAGE RAVENNA STORM SCWCR
QUAKER STATEOIL ICRUOE 0 PORTAGE A7WATERTWP UNKNOWN
QUAKER STATE OIL CO ASHTABULA WAYNE TWP UNKNOWN
QUAKER STATE OIL CO TRUMBULL WEATHERSFIEW UNKNOWN
R KUNZMAN INC STARK ALLJANCE STORM SCWCR
R M I TrTANIUM TRUMBULL NILES MAHONING RIVER TRlB
R 1.11 TrTANIUM TRUMBULL NILES MAHONING RIVER
R M I TrTANIUM TRUMBULL NILES MAHONING RIVER
R j,f I TrTANIUM TRUMBULL NILES HOLDING POND
R M I TrTANIUM TRUMBULL NILES MAHONING RIVER
R M I TrTANIUM TRUMBULL NILES MAHONING RIVER
RAVENNAARMYAMMUNIT10N PORTAGE WINDHAM UNKNOWN
RAVENNA ARMY AMMUNIT10N PORTAGE RA VENNA SAND CREEK TRIB
RAVENNA CfTYGARAGE PORTAGE RAVENNA SEWER
RAY PANDER TRUCKING MAHONING CANFiEW SMALL CREEK
RA YMOND ANDERSON FARM MAHONING CANFIELD INDIAN RUN
REGAL TRANSPORTATION TRUMBULL NILES UNKNOWN
REMMANT ROOM TRUMBULL BROOI<AEW 7W UNKNOWN
RIVER BEND TRANSPORTKJTR MAHONING AUSTIN UNKNOWN
RIVERSIDE AUTO CENTER MAHONING ALLJANCE MAHONING RIVER
MATERIAL_I
OIL
FUEL OIL
DIESEL FUEL
DIESEL FUEL
ASPHAL TEMULSION
WASTE OIL
FUEL OIL
SOOT
WASTE HYDROCHLORIC AC
ASH
WASTEWATER
WASTEWATER
WASTEWATER
WASTEWATER
WASTEWATER
WASTEWATER
ACID
GASOUNE
HYDRAULiC OIL
ODOR OF SULFUR
OIL
RUSTY ORANGE WATER
CRUDE OIL
CRUOEOIL
OIL
GREEN STUFF
SUDS
WATER PICKUP
SEWAGE
DIESEL FUEL
WATER BASED LA TEX PRIM
HYDRAULiC OIL
DIESEL FUEL
WASTEWATER
CUTTING OIL
GASOLiNE
OIL
CRUDE Oil
CRUDE Oil
DIESEL
PCB COWTAMINATED WAST
WASTEWATER
OIL
HYDROFlOURIC ACID
OIL
WASTEWATER
TNT WASTE WATER
WASTEWATER
GASOUNE
BRINE
PESTICIDES
DIESEL FUEL
CHEMICALS
DIESEL FUEL
JUNK
AMOUNT_I UNITS_I RECOVER_I
3 GAL 0
27~ GAL ~
1000 GAL 0
o UNK 0
!Ji)() GAL 0
o UNK 0
J9) GAL a
a UNK 0
1~ GAL 0
~ CFT a
o UNK 0
o UNK 0
a UNK 0
o UNK 0
o UNK a
o UNK a
21~ GAL a
000 GAL a
o UNK 0
o UNK 0
a UNK 0
o UNK a
J300 GAL 3200
JS70 GAL 2000
a UNK a
a UNK a
a UNK 0
a NOS a
a UNK a
1~ GAL a
~ GAL a
10 GAL a
a UNK a
a UNK a
a UNK a
~ GAL a
714 GAL ~72
~ GAL a
42 GAL a
~ GAL a
a UNK a
a UNK 0
a UNK a
I~ GAL a
2~ GAL 0
a UNK a
J9) GAL a
180000 GAL 0
2~ GAL 20
a UNK a
a UNK a
a UNK a
o UNK 0
JOO GAL a
o UNK 0
ENTTTY COUNTY
ROBERTSON HE.... TlNG & SUPP ST....RK
ROU.ND BROTHERS WAREHO MAHONING
RYDER TRUCK REIVT....L MAHONING
SAFETY KLEEN TRUMBULL
SAUNDERS CO PORT GE
SAUNDERS EXC.... v.... TlNG PORT GE
SAVAET SERVICE INC MAHONING
SAVEA T OIL CO MAHONING
SCHAEFER EOUIPMEIVT INC TRUMBULL
SCHAEFER EOUIPMEIVT INC TRUMBULL
SCHAEFER EOUIPME/oIT INC TRUMBULL
SCHAEFER EOUIPME/oIT INC TRUMBULL
SCHAEFER EOUIPME/oIT INC TRUMBULL
SCHl\EFER EOUIPMEIVT INC TRUMBULL
SCHAEFER EOUIPMEIVT INC TRUMBULL
SCHl\EFER EOUIPMEIVT INC TRUMBULL
SCHAEFER EOUIPMEIVT INC TRUMBULL
SCHAEFER EOUIPMEIVT INC TRUMBULL
SCHAEFER EOUIPMEIVT INC TRUMBULL
SCHAEFFER METAL PRODUCT PORTAGE
SEBRING CHURCH OF CHRIST MAHONING
SERVO CLEAN MAHONING
SHl\DYBROOK MOBIL HOME P MAHONING
SHAHEEN PLUMBING & HEATI STARK
SODA CONSTRUCTION STARK
SOUTHERN RAOIATOR MAHONING
SOUTrflNCST MOTOR FREIGHT MAHONING
SPARKS TUNE UP TRUMBULL
STANDARD LAFARGE MAHONING
STAR ROOFING>COVEW PRO TRUMBULL
STELL CfTY MAHONING
STRUTHERS AUTO SERVICE MAHONING
STRUTHERS CSO MAHONING
STRUTHERS STREET DEPT MAHONING
SUMMrT N....TIONAL PORT....GE
T & W FORGE INC. STARK
THER~NK PORTAGE
THERMAL TECH INC. TRUMBULL
THERMATEX MAHONING
nM WEA VER MAHONING
roM'S SEWER & DRAINS TRUMBULL
TOP UNE TRUMBULL
TRJ STATE MOTOR TRANSrT C PORT....GE
TRUCK STOPS OF AMERICA MAHONING
TRUCK STOPS OF AMERIC.... MAHONING
TRUCK STOPS OF AMERIC.... MAHONING
TRUCK WASH MAHONING
TRUE GREEN CHEMICALS MAHONING
TRUMBULL MEMORIAL HOSPfT TRUMBULL
TURKEY FARM PORTAGE
UNrTED EXCAVATING AVE M....HONING
UNIVERSAL TRUCK PLAZAlMA MAHONING
UNK MAHONING
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
?J
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
?J
o
o
o
o
o
o
o
o
o
o
o
o
o UNK
o UNK
o UNK
o UNK
o UNK
o UNK
o UNK
o UNK
26 PPM
o UNK
o UNK
o UNK
o UNK
o UNK
o UNK
o UNK
(J() rTM
o UNK
200 GAL
?J GAL
110 GAL
o UNK
1:r:J GAL
o UNK
o UNK
o UNK
o UNK
l' GAL
o UNK
o UNK
o UNK
XX) GAL
o UNK
o UNK
o UNK
o UNK
o UNK
100 GAL
:r:J GAL
o UNK
o UNK
o UNK
o UNK
1'4 GAL
~ GAL
200 ITM
o UNK
200 GAL
o UNK
o UNK
o UNK
AMOUNT_, UNrTS_l RECOVER_l
1'" GAL go
o UNK 0
:r:J GAL 0
Q GAL 0
ILLEGAL DUMPING
JUNK. TRASH
GREEN MATERIAL
NO SPILL
WASTE W....TER
MATERIAL_l
DIESEL FUEL
SMOKE
DIESEL FUEL
MINERAL SPlRfTS
DIESEL FUEL
OIL
OIL
MILL CREEK
UNKNOWN
UNKNOWN
W.... TER'WAY
STORM SEWER
BOARDII.AN
SMfTHTWP
GIRARD
YOUNGSTOWN FOURM~ERUN
NEW MIOD<..ETON UNKNOWN
I-AlBBARD STORM SEWER
RAVEMY.... UNKNOWN
RAVENNA UNKNWON
N UMA UNKNOWN CREEK
NORTH UMA UNKNOWN
WARREN RED RUN CREEK
WARREN RED RUN CREEK
WARREN RED RUN CREEK SUSPENDED SCUDS
WARREN RED RUN CREEK DlL (13 MGA)
WARREN RED RUN CREEK OIL
WARREN RED RUN CREEK OIL
WARREN RED RUN CREEK WASTE WATER
WARREN RED RUN CREEK WASTE WATER
WARREN RED RUN CREEK OIL
WARREN RED RUN CREEK WASTE WATER
WARREN RED RUN CREEK WASTE WATER
RAVEMYA STORM SEWER WASTE CHEMICALS
SEBRING PRlVATE POND FISHKILL
YOUNGSTOWN STORM SEWER UNK BLACK UO/JID & SLUD
BOARDMAN STORM SEWER-MILL CREEK FUEL OIL
ALLJANCE STORM SEWER WASTE OIL
LEXINGTON TWP BERUN RESERVOIR UNKNCWN
YOUNGSTOWN SEWER A/oITIFREEZE
AUSTINTOWN MAHONING RiVER TRIB DIESEL FUEL
WARREN STORM SEWER OIL
YOUNGSTOWN UNKNOWN GREASE
NILES MOSOUrTO CREEK TRIB TAR
....USTINTOWN TW STORM SEWER OIL
STRUTHERS MAHONING RiVER TRiB GASOUNE
STRUTHERS YELLOW CREEK SEWAGE
STRUTHERS MAHONING RiVER METAL SHAVINGS
DEERFIELD BERUN RESERVOIR WASTE WA TER
ALLJANCE UNKNOWN FUEL OIL
GARRETTSVILLE SlLVER CREEK YELLOW MATERiAL
MAHONfNG RIVER ORANGE STUFF
NEWTON FALLS MAHONING RIVER SOLUBLE OIL
POLAND EVANS LAKE TAR OIL
GERRAD MAHONING RiVER SEWAGE
LORDSTOWN UNKNOWN DIESEL FUEL
CHARLESTON TW W BRANCH RESERVOIR DIESEL FUEL
UMA UNKNOWN DIESEL FUEL
NORTH UMA UNKNOWN DIESEL FUEL
N. UMA MILL CREEK GASOLiNE
UMA UNKNOWN CREEK SOAP & DIRT
N JACKSON TWP PRIVATE POND FERTfUZER
WARREN MAHONING RIVER DIESEL FUEL
NELSON TWP COMP CREEK FISHKILL
YOUNGSTOWN STORM SEWER-MAHONING RiV OIL
YOUNGSTOWN UNNAMED CREEK DIESEL FUEL
MAHONING
MAHONING
UNK
UNK
ENTITY
UNK
UNK
UNK
UNK
UNK
UNK
UNK
UNK
UNK
UNK
UNK
UNK
UNK
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
UNKNOWN
COUNTY 7WP_CITY WATERWAY
MAHONING N JACXSON MEANDER CK RESV.
MAHONING YOUNGSTCYtVN STORM SEWER
MAHONING YOUNGSTCYtVN STORM SEWER
MAHONING BOARDIJAN STORM SEWER
MAHONING N. UAU. UNNAMED CREEK
PORTAGE GAl'/RETTSvll.I..E SlLVERCREEK
PORTAGE ATWATER STORM SEWER
PORTAGE PALJAIRA TWP UNKNOWN
PORTAGE GARFlETSVTLLE UNKNOWN
PORTAGE PALJAYRA TWP UNKNOWN CREEK
TRUMBULL UBERTY TWP UTTLE. SOUAW CREEK
TRUMBULL NEWTON FALLS MAHONING RIVER TRiB
TRUMBULL CHAMPION STORM SEWER
MAHONING YOUNGSTCYtVN BEAR CREEK
MAHONING AUST/NTOW1II TW BEAR CREEK
MAHONING BRQADI,lAN 7WP HUNTERS CREEK
MAHONING YOUNGSTCYtVN LAKE GLACIER
MAHONING AUSTINTCYtVN TW MEANDER CK RESV.
MAHONING EllSWORTH MEANDER CREEK
MAHONING AUTWTCYtVN UNKNOWN
MAHONING GASHEN UNKNOWN
MAHONING BEAVER TWP UNKNOWN
MAHONING BOARDIJAN UNKNOWN CREEK
MAHONING NORTH UMA YELLOW CREEK
MAHONING POt.AND YELLOW CREEK
PORTAGE PALJAYRA TWP POLE CREEK
PORTAGE RAVENNA POND
PORTAGE GARFlETSVILLE SlL VCR CREEK
PORTAGE ATWATER 7WP UNKNOWN
PORTAGE ATWATER 7WP UNKNOWN
TRUMBULL WAJlREN MAHONING RIVER
TRUMBULL WAJlREN MOSOUITO CREEK
TRUMBULL BRCX>KFIEJ.D TW UNKNOWN
TRUMBULL ~8BA.RD TWP UNKNOWN
COLUMBiAN BELOfT WESTVILLE LAKE RESERVIOR
MAHONING YOUNGSTCYtVN BEAR CREEK
MAHONING POI.EN BURGESS LAKE
MAHONING AUSTINTOWN HOLDING POND
MAHONING STROTHERS MAHONING RIVER
MAHONING C.ANFtaD MILL CREEK TRIB
MAHONING NEWTON FALLS POND
MAHOMNG YOUNGSTOWN UNKNOWN
PORTAGE DEAAFlELD UNNAMED CREEK
PORTAGE UNNAMED CREEK
STARK AWANCE UNKNOWN
STARK AWANCE UNKNOWN
STARK AWANCE UNKNOWN
TRUMBULL MlES MAHONING RIVER
TRUMBULL NEWTON FALLS MAHONING RIVER
TRUMBULL CHAMPION TWP MAHONING RIVER TRIB
TRUMBULL BAZETTA MOSOUITO CREEK
TRUMBULL WAJlREN UNKNOWN
TRUMBULL NEWTON FALLS W B MAHONING RIVER
TRUMBULL C UBERTY TWP UBERTY GERARD LAKE
ASHTABULA WAYNETWP POND
MA TERiAL_I
UNK
UNK
UNK
CUTnNGOIL
UNK
DIESEL FUEL
OILY SUBSTANCE
DIESEL FUEL
UNK
OIL
BLACK WA TER-DRIVEWA Y
OIL
UNK
CUTTING OIL
MILKY WHITE STUFF
ORANGE STUFF
SEWAGE
UNKNOWN
CRUDE OIL
WHITE STUFF.
BLACK STUFF
OIL
BRINE
HYOROCARBON
TRASH
FISHKILL
FISHKILL
DIESEL FUEL
FUEL OIL
OIL
FOAM
BRIGHT BLUE SUBSTANCE
CHEMICAL
ASBESTOS
DIESEL FUEL
UNK WHITE STUFF
RAW SEWAGE
DIESEL FUEL
OIL Y SUBSTANCE
GREEN STUFF
OIL SHEEN
BRINE
RED WATER
BRiNE
BRINE
CRUDE OIL
DIESEL FUEL
BROUN STUFF
FISHKILL
OIL
DIESEL FUEL
ABANDONED DRUMS
WHITE FOAM
FOAM
UNIDENTIFIED OIL
AMOUNT_I UNITS_I RECOVER_I
o UNK 0
10 DRill. 0
o UNK 0
o UNK 0
DRill. 0
.XlO GAL 0
o UNK 0
.XlO GAL 0
flO GAL 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
100 ITlJ 0
o UNK 0
400 GAL 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
100 GAL 0
o UNK 0
o UNK 0
160 GAL 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
2 ITlJ
o UNK 0
o UNK 0
GAL
--------~-~--------------------
YR EHTTTY COUf'ITY TWP_ClTY WATERWAY MATERIAL_I
01 UNKNOWN MAHONING YOUNGSTOWN BEAR CREEK OIL.
01 UNKNOWN MAHONING YOUNGSTOWN MIU CREEK TRiB ANTI FRECZE
01 UNKNOWN MAHONING AUSTINTOWN TW STORM SEWeR?MIU CREEK TR WHITE SOLUBLE OIL
01 UNKNOWN MAHONING BEAVER 7WP TURKEY CREEK TRiB BLUE DYE
01 UNKNOWN MAHONING POL.ANO UNKNOWN DYE
01 UNKNOWN TRUMBULL NEWTON FALLS MAHONING RIVER CONCRETE
01 UNKNOWN TRUMBUU WARREN MAHONING RIVER TRIB OIL.
01 UNKNOWN TRUMBULL ALLEN MOSQUITO CREEK TRiB SEWAGE
01 UNKNOWN TRUMBULL HOLU.NO TWP MOSQUITO CREEK TRiB GREEN STUFF
01 UNKNOWN TRUMBUU WARREN PARK POND VOL VOX AQUATIC UFE
01 UNKNOWN TRUMBULL HOWlAND TWP POND ABANDONED DRUM
01 UNKNOWN TRUMBUU BROOKFIELD STORM orrCH OIL
02 UNKNOWN ASHTABULA WlUJAMSFIELD UNKNOWN CREEK OIESEL FUEL
02 UNKNOWN MAHONING YOUNGSTOWN BEAR CREEK WNITE STUFF
02 UNKNOWN MAHONING BERLJN CENTER BERUN RESERVOIR ALGAE
02 UNKNOWN MAHONING YOUNGSTOWN LAKE NEWPORT MII.J(Y STUFF
02 UNKNOWN MAHONII/G YOUNGSTOWN LAKE NEWPORT OIL.
02 UNKNOWN MAHONING YOUI/GSTOWN MAHONII/G RIVER GREEN STUFF
02 UNKNOWN MAHONING AUSTINTOWN MEANDER CREEK DiESEL FUEL
02 UNKNOWN MAHONII/G BOARDIAEN MILL CREEK COLOR
02 UNKNOWN MAHONING BOARDMAN MILL CREEK UNKNOWN
02 UNKNOWN MAHONII/G BOARDMAN MILL CREEK IRON
02 UNKNOWN MAHONII/G CANRELD MILL CREEK HEATlI/G OIL
02 UNKNOWN MAHONII/G CANRELD MIU CREEK OIL.
02 UNKNOWN MAHONII/G CANFIELD SAWMILL RUN CREEK TRiB UNKNOWN STUFF
1/2 UNKNOWN MAHONING BOARDMAN TWP STORM SEWeR GASOLINE
02 UNKNOWN MAHONII/G BEAVER TWP STRIP MINE LAKE OUTLET UNKNOWN STUFF
02 UNKNOWN MAHONII/G COITSVI.J..E TWP UNKNOWN CRUSTY SHEEN
02 UNKNOWN MAHONING YOUNGSTOWN UNKNOWN DEAD FISH
02 UNKNOWN PORTAGE DEERFIELD TWP BERUN RESERVOIR DRUM
02 UNKNOWN PORTAGE EDINBURGH TWP UNKNOWN CREEK BRINE
02 UNKNOWN STARK LEXINGTON BERUN RESERVOIR BLACK FOAMY STUFF
02 UNKNOWN TRUMBUU NEWTON FALLS E B MAHONII/G RIVER IRON
02 UNKNOWN TRUMBULL NEWTON FALLS MAHONII/G RIVER SEWAGE
02 UNKNOWN TRUMBUU WARREN MAHONII/G RIVER OIL
02 UNKNOWN TRUMBUU WARREN RED LAKE BLUE STUFF
02 UNKNOWN TRUMBULL GIRARD UNKNOWN KEROSENE
02 UNKNOWN TRUMBUU BRACEVIUE UNKNOWN OIL
02 UNKNOWN TRUMBULL NEWTON FALLS W B MAHONING RIVER TRIB IRON
gJ UNKNOWN COLUMBIAN BUTl.ER 7WP STORM SEWER-PRIVATE POND RSH KJU
gJ UNKNOWN MAHONING YOUNGSTOWN CASCADE RA VINE SOAP
gJ UNKNOWN MAHONING STRUTHERS MAHONII/G RiVER OIL
gJ UNKNOWN MAHONING GOSHEN UNKNOWN DiESEL FUEL
gJ UNKNOWN MAHONII/G SMITH 7WP UNKNOWN CREEK OIL
gJ UNKNOWN MAHONII/G AUSTINTOWN UNKNOWN CREEK OIL
gJ UNKNOWN MAHONING POLAND YEUOWCREEK OIL.
gJ UNKNOWN STARK AL1..JANCE UNKNOWN CREEK OIL.
gJ UNKNOWN TRUMBUU CHAMPION MAHONING RIVER FLUORESCEIN DYE
gJ UNKNOWN TRUMBUU WEA THERSFIELD MAHONII/G RIVER TRiB FOAM
gJ UNKNOWN TRUMBUU UNKNOWN F'UlSTIC
110 UNKNOWN STP PORTAGE LAKE MIL TON LAKE MIL TON RAW SLUDGE
02 UNKNOW/>rSUSPECTED"NEW MAHONING AUSnNTOYoIN UNKNOWN CREEK OIL
01 UNOCAL REFINII/G & MARKETI MAHONING AUSTINTOWN TW SULFUR RUN TRiB DiESEL FUEL
110 UNOCAUYOUI/GSTOWN 78 MAHONING YOUNGSTOWN UNKNOWN DiESEL FUEL
02 VALVOLINE INSTANT OIL CHAN MAHONII/G AUSTINTOWN UNKNOWN CREEK ANT1-FRECZE
AMOUNT_l UNlTS_1 RECOVER_l
o UNK 0
o UNK 0
!lO CAL 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
20 GAL 0
o UNK 0
o UNK 0
100 ITlI 0
1 ITlI 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
2' GAL 0
o UNK 0
24 ITlI 0
o UNK 0
o UNK 0
o UNK 0
o UNK 0
4 GAL 0
o UNK 0
o UNK 0
o LINK 0
o UNK 0
o UNK 0
o UNK 0
XI GAL 0
o UNK 0
1!lO GAL 0
o UNK 0
YR ENTTTY COUNTY
gJ VAL VOl.JNE OIL CHANGE MAHONING
go VARIOUS JUNKYARDS STARK
go VERNAL PAVING MAHONING
go VERNON SAND & GRA VEL TRUMBULL
112 VERNON TWP TRUSTEES TRUMBULL
go VlKlNG RESOURCES PORTAGE
gJ VIKlNG RESOURCES CORP PORTAGE
'0 W C I STEEL TRUMBULL
'0 W C I STEEL TRUMBULL
'0 W C 1STEEL TRUMBULL
'0 W C I STEEL TRUMBULL
go W C I STEEL TRUMBULL
01 W C I STEEL TRUMBULL
02 W C I STEEL TRUMBULL
02 W C I STEEL TRUMBULL
112 W C I STEEL TRUMBULL
112 W C I STEEL TRUMBULL
02 W C I STEEL TRUMBULL
112 W C I STEEL TRUMBULL
gJ W C I STEEL TRU MBULL
02 W C I STEEL TRUMBULL
112 W C I STEEL TRUMBULL
02 W C I STEEL TRUMBULL
02 WC I STEEL TRUMBULL
02 W C I STEEL TRUMBULL
112 W C I STEEL TRUMBULL
02 W C I STEEL TRU MBULL
gJ W W OPERATION SERVICES MAHONING
'0 WARREN STP TRUMBULL
gJ WARREN STP TRUMBULL
01 WARREN WATER PLANT TRUMBl./LL
10 WEAN /NO MAHONING
go WEIMER ENTERPRlSES MAHONJNG
go WESTERN RESERVE FARM CO PORTAGE
'0 WlU.OWCREEKLANOFIU PORTAGE
~ WINDHAM MOBIL PORTAGE
gJ WINDHAM MOBIL SERVICE PORTAGE
go WINDHAM STP PORTAGE
~ WINDHAM STP PORTAGE
SO WISE OIL CO PORTAGE
go YELLOW FREIGHT TRUMBULL
01 YELLOW FREJGHT SYSTEMS MAHONING
80 YOUNGSTOWN STP MAHONING
01 YOUNGSTOWN STREITDEPT MAHONING
01 YOUNGSTOWN WELDiNG & EN MAHONING
PI YOUNGSTOWN WELDiNG & EN MAHONING
gJ YOUNGSTOWN WELDING & EN MAHONING
112 YOUNGSTOWN WELDiNG & EN MAHONING
TWP_CITY WATERWAY MATERlAL_1
BOARDMANSTORM SEWER
OIL
ALUANCE MAHONING RiVER TRASH
& JUNK
N.UMA UNKNOWN OIl.
VERNON ENTIRE WATERTABLE UNCENERATED
ASH
VERNON TWP PYMATUNING CREEK DIESEL FUEL
A TWATER TWP UNNAMED CREEK CRUDE
OIL
PALMYRA TWP I?LE CREEK CRUDE
OIL
WARREN MAHONING RIV ER WASREWA
TER
WARREN MAHONING RIVER COOUNG WATER
WARREN MAHONING RIVER WASTEWA
TER
WARREN IAAHONING RIVI:R WASTE
WATER
WARREN MAHONING RIVER OIL
WARREN MAHONING RIVER LUBE
OIL
WARREN MAHONING RIVER HYOROCHLORJC ACID
WARREN MAHONING RlVER WASTE
WATER
WARREN MAHONING RlVER WASTE WATER
WARREN IAAHONING RIVER WASTE
WATER
WARREN MAHONING RIVER OIL
WARREN IAAHONING RIVER WASTE WATER
WARREN IAAHONING RIVER OIL
WARREN MAHONING RiVER WASTE
WATER
WARREN MAHONING RIVER STORM
WATER
WARREN MAHONING RIVER WASTE WATI:R
WARREN MAHONING RIVER WASTE WATER
WARREN MAHONING RIVER WASTE WA TER
WARREN MAHONING RlVER HYDRAUUC
OIL
WARREN MAHONING RIVER UNTREATED RECYCLED W
BOYD MAHONING RIVER SUSPENDED
SOUDS
WARREN MAHONING RIVER SEWAGE
BAZETTA TWP MOSOUITO CREEK ALUM SLUDGE
WARREN MOSOUITO CREEK TRlB POTASSIUM PERMANGANA
YOUNGSTOWN BEARS DEN RUN OIl.
8ERl.JNE CENTER UNKNOWN GASOUNE
RA VANNA UNKNOWN 2,."
UQUID NITROGEN
A TWATER BERUN RESERVOIR LEACHATE
WINDHAM UNKNOWN CREEK KEROSENE
WINDHAM EAGLE CREEK GASOUNE
WINDHAM SF EAGLE CREEK SEWAGE
WINDHAM SF EAGLE CREEK SEWAGE
RAVENNA STORM SEWER GASOUNE
UBERTY UNKNOWN DIESEL FUEL
CANRELD TWP UNKNOWN DIESEL FUEL
YOUNGSTOWN MAHONING RIVER SEWAGE
YOUNGSTOWN STORM SEWER PAINT
AUSTINTOWN TW FOUR MILE RUN NITRIC ACID
AUSTINTOWN TW STORM SEWER-BEARS DEN RU HYDRAUUC OIL
YOUNGSTOWN STORM SEWER HYDROFLURIC ACID
YOUNGSTOWN FOUR MILE RUN OIL
AMOUNT_l UNfTS_l RECOVER_l
!;CO GAL 0
o UNK 0
o UNK 0
o UNK 0
2t;O GAL 2t;O
o UNK 0
21ecJ GAL 0
18tXC GAL 0
o UNK 0
o UNK 0
2000 GAL 0
o UNK 0
:yj GAL 0
1/lCO GAL 0
o UNK 0
12000 GAL 0
o UNK 0
o UNK 0
o UNK 0
DUNK 0
DUNK 0
o UNK 0
o UNK 0
100 GAL 0
2000 GAL 11000
DUNK 0
DUNK 0
DUNK 0
DUNK 0
1= GAL 0
o UNK 0
o UNK 0
I' GAL 0
11000 GAL 0
o UNK 0
100 GAL 0
o UNK 0
3IXXXJ GAL 0
o UNK 0
DUNK 0
40 GAL 0
SO GAL 0
DUNK . 0
DUNK 0=
GAL 0
SO GAL :yj
106 LBS 0
DUNK 0
APPENDIX 4
IR SPECTRA
79
First Soil Sample-taken from the patient's yard
Collected 10.22.98
Sample run 4.29.99
This sample was stored, after collection, in cleaned aluminum foil within a
labeled plastic bag at 4?C until further work-up was possible.
The soil was later thawed and manually mixed to promote homogeneity.
Approximately l5.27lg of soil was mixed with sodium sulfate to remove
any water. Th dried soil was spiked with 452ng PCB?l03, transferred to a
clean cellulose thimble and extracted via soxhlet with dichloromethane,
24h. The extract was then reduced via rotary evaporation, transferred into
hexanes and concentrated under nitrogen, to 2m/.
The extract was then cleaned via an alumina column composed of a glass
wool plug, on top of which was 2g AI203 and lcm Na2S04. The alumina
column was pre-prepared with 5ml of 5% dichloromethane in petroleum
ether. Th resulting eluent was then concentrated and solvent exchanged
into iso-octane under nitrogen.
oo
III
IE
u
oo
o
~
oo
III
...-t
oo
oC\I
oo
IIIC\I
?"1 :'"
(T')D1
t..N CJ
to Ctl..:
oo
of"l
oo
IIIf"l
Second Soil Sample-taken from patient's yard
Collected 10.22.98
Sample run 4.30.99
This sample was prepared in accordance with the protocol as outlined for
the first soil sample.
~ -----~;! 0-0an
TE
u
oo
o
..-t
o
~O ttl
~ ..
o_0
oN
o
"-0an
N
oo
ortl
.-- J
t.... >- 001
't.an m
-:r c1LJ
~ ..-, - J --
,0
r~
rtl
II
I\0
LojO
N -::
~ ,
o
Water sample-(filter) 3B Feed
3B Feed-area corresponds to the map of Berlin Lake, located in
Appendix 3
Collected 10.22.98
Sample run 5.3.99
The water samples were collected in cleaned 4L solvent jugs, from
locations in and around Berlin Lake. The samples were stored at 4?C until
extraction was possible.
The polyurethane foam plugs were extracted via soxhlet, in petroleum
ether, for 24h. The filters, prior to use, were refluxed in dichloromethane
for 18h.
The water samples were transferred into individual stainless steel
canisters. The water samples were pushed, via nitrogen pressure, through
a 47mm GMF water filter, in attempt to remove any particulate matter;
each sample required several filters, due to high levels of particulate
matter. The water filters were then wrapped individually in cleaned
aluminum foil and stored in plastic bags at -10?C.
The filters were soxhlet extracted with dichloromethane 24h. The extracts
were then reduced to 5-10ml and solvent exchanged into iso-octane via
rotary evaporation. The entire sample inventory was reduced individually
to 1ml under nitrogen. The samples were cleaned using a silicic
acid/alumina column; a glass column was dry-packed with a first layer of
3g silicic acid )1.7% water added), followed by a second layer of 2g
adsorption alumina (6% water added), and a third layer of 2cm anhydrous
sodium sulfate.
o-0
III
TE
u
i
!'0
Lo:0
~
10;...0
'Ill
~
'0, 0
~oi
~
i
I,
oo
oN
I!
iI
10L.o
'IllI ~
!I
,
\I
i
----??--T------??-.--------i
~o.
o
~I-_._._--.---;;-_.. ;;----;;;-;;;..... ;;;-_..;;;-~-~.--===- ... ~!!====~----- .--...---.------'-1
!o'0
rilliN
--.- _ -_.__ ,-.--.---------..--.,----------- _.- r--
Ill~
~Q ~~o
? '- III 191\ ?T
III m .~OO ~ ENC m~lllu
UJ :J ~U N
Water sample?(syringe) B Feed
B Feed?area corresponds to the map of Berlin Lake, located in
Appendix 3
Collected 10.22.98
Sample run 5.3.99
This sample was prepared in accordance with the protocol as outlined for
The first water sample.
(!>
('1.
.2300
ev..-'
-1l.A..-JJ
u.I
(
ou-
t
w\...
(2Pcj~
-------r
em-I
500
-----.-------------------
T-
15001000
IU').'f""~.
"
I
,
I
!
-;
I
,
I
I
I
I
,
O.
40-f-----?-T--------rL----------
i
--
------"1--
4000
35003000
2500
2000
I
44.98.,
Energy
I
II
\
i
t
!
~
Il
13.13
I,
~oBJ
'
I
2960.1
I
em-I
i
-1
!
I
I
I
Water sample-(filter) 4B Feed
4B Feed-area corresponds to the map of Berlin Lake, located in
Appendix 3
Collected 10.22.98
Sample run 5.2.99
This sample was prepared in accordance with the protocol as outlined for
The first water sample.
oo
In
TE
o
II
Ito
t- 0I~
i
I
iI
Ii
I
~g
lin...
I
ILg
11il
I
I
I
1 0~O
linIN
I
!
~g
1 0I l!'1
I
ii
!
I!
,0
~O,In
1l!'1
I
-- -------1'
___. .__~ .._ .. _._ 01 --_.__.... -- 0
... 0o
'<:t.
o
Water sample?(fiIter) 2B Feed
2B Feed?area corresponds to the map of Berlin Lake, located in
Appendix 3
Collected 10.22.98
Sample run 5.3.99
This sample was prepared in accordance with the protocol as outlined for
The first water sample.
oo
In
Te
u
oo
o'"
1 0
~o
I~
I
I10
r~
1I
\0'0
linI
~
I
I19
'0iN
II
Ii
j!
i
~~
oo
o
'" -.;ro.
o
'--~~-------T'--- ._--
01 1m U'J_'" 0 ? I
'1(1) U'J eo lCJ:j
N (J'"j::J CD
u m
~-------'-'-I----
-.;r""l'lCl
? t.
...... lI)Nt:
lJJ
-
Water sample-(fiIter) 1B Feed
1B Feed?area corresponds to the map of Berlin Lake, located in
Appendix 3
Collected 10.22.98
Sample run 5.2.99
This sample was prepared in accordance with the protocol as outlined for
the first water sample.
(\
I)
TE
u
oo
10N
iI
101
0rO
I~
1I
\I
!10
r~
I
~gIN
........_---------------------':~ g_ I 10
------------~
I1';>.
mel-c.
.... mlOt:
UJ
oo
of'l
oo
10f'l
------
o
---------,-------~----,---------+ g
n; ~a: ~ T ~ "=f
-enlOE -
I' rnJa:. N U 0f'l :::J m
u f'l
Water sample?(filter) C Feed
C Feed?area corresponds to the map of Berlin Lake, located in
Appendix 3
Collected 10.25.98
Sample run 4.30.99
This sample was prepared in accordance with the protocol as outlined for
the first water sample.
---'...-------------_...:..._----------------_.-...~'~
TE
(J
10.... 0
?0.....
oo
ll).....
---.-'-.~-~_.--_._-_._- ?..-_.~ .. - -~~. ~- ~ ~---
oo
ll)
N
---T? 1 -
~i[flCD~ 1601 ? T?. enl
rr'I E
~la: 0 (J..: i::il ....
L;Jj N
., ._., -..
I
I:0
L.o10
t'1
, 0.... 0
Ill)
it'1I
!
o
Water sample-(filter) 18 Feed
18 Feed-area corresponds to the map of 8erlin Lake, located in
Appendix 3
Collected 10.25.98
Sample run 5.4.99
This sample was prepared in accordance with the protocol as outlined for
the first water sample.
.o
oo
In
TE
u
,
10
'0"'0....
,
tI
0, 0
10:rrJ
I10
'010
i N
!
!I
Ii
ior O
lKl
i
!
ILg
'10I ....
I
?. _.--_.... _<'-"011
Water sample-(filter) 2B Feed
2B Feed-area corresponds to the map of Berlin Lake, located in
Appendix 3
Collected 10.25.98
Sample run 5.3.99
This sample was prepared in accordance with the protocol as outlined for
the first water sample.
---,..._ _--------.._---
N>o""01
.r..
.... CDItlc:
lJJ
o
I~
Il T
I ~
II
10
~g
I ""'
I10,g
I""'
I
~g o
N
oo
ItlN
oo
o(Il
oo
Itl(Il
o._-J- 0
oN -q-
o.
o1
Water sample-(filter) Section A/Dam Water
Section A/Dam Water-area corresponds to the map of Berlin Lake, located
in Appendix 3
Collected 10.25.98
Sample run 5.18.99
This sample was prepared in accordance with the protocol as outlined for
the first water sample.
~'-~~--
/
'/~UJ
J!JtO:u..
.
I
o
.03+---
~
....
'r-----------.,..-------
..
-------
?-----r------????-1.??
--"-'."-
._.-....
..
..
------1--
-_._
..
-_
...
--
_.-
4000
35003000
25002000
1500
1000
em-I
~
!
,
-+
i
43.76-j
Energy
N-
,I
1_
~
\
$.
f
~
.
i
I
I
~
I
,
~l
!
1
i
I
1.32
I
--
..
-
--
-;.;J
:U8S0~
1640.9
l
I
em-I
~
,
I
.....
r
?
I
t
\
:
-
r
Water sample-(filter) Dam Water
Dam Water-area corresponds to the map of Berlin Lake, located in
Appendix 3
Collected 10.25.98
Sample run 5.18.99
This sample was prepared in accordance with the protocol as outlined for
the first water sample.
oo
o""
oo
LO
~
o.... 0
'0C\l
:0:"'0
;0
C")
, 0
~o 'In
C")
1 0,-f. g
co -:fC").
o
Water sample-(filter) Beyond Dam
Beyond Dam-area corresponds to the map of Berlin Lake, located
In Appendix 3
Collected 10.25.98
Sample run 5.4.99
This sample was prepared in accordance with the protocol as outlined for
the first water sample.
~g
-' ,,' .~<"". "'----- ~.-" '"''--''-'_??- '-"--.~ ..' _...->-~---~, ~- ...?., .....---1 N
I
-J
j"e
o
i 0
~o10
I t'1
o
~o?tn
1 0Lo
lClt\l
i
'01 0
1- 0
~
Water sample-(filter) C Feed
C Feed-area corresponds to the map of Berlin Lake, located
In Appendix 3
Collected 10.25.98
Sample run 4.29.99
This sample was prepared in accordance with the protocol as outlined for
the first water sample.
oo
ll1.
Eu
oo
o
-c-i
oo
1I1
",--i
oo
o
C\J
oo
i.rJC\i
oo
o
tT1
oo
ll1rrl
0
0
0
() , c-;? -:r
t.i; cJl CD ~_C'
?.'i 0
r' (J) rrl E ;:',)-' r...:
"r 0 U
J7 -. ... 1
U (\;
Water sample-(syringe) C Feed
C Feed-area corresponds to the map of Berlin Lake, located
In Appendix 3
Collected 10.25.98
Sample run 5.3.99
This sample was prepared in accordance with the protocol as outlined for
the first water sample.
oo
10N
~ __----------~-------------?Ir glini
TI E
I U
I,
~g,0,
~I
j
I10
r~
ILg
I~
oo
oCI'l
-~-T"--?--- ----"~---"--?r--
0> COat.
" NCD
InCW
oo
oo "'if
"l;f.
o
APPENDIX 5
HUMAN SUBJECTS PROTOCOL REVI EW FORM
80
Youngstown State University lOne University Plaza I Youngstown, Ohio 44555-0001
May 31,2000
Dr. Peter J. Kasvinsky
Dean
School of Graduate Studies
Youngstown State University
CAMPUS
Dear Dean Kasvinsky:
This is to report on the results of the administrative review of human subjects activity
related to the thesis proposal of Ms. Meredith Tuttle, M.S. candidate in Chemistry,
entitled "The Convergence of Environmental Influences as Potential Precipitating Factors
of AML-M2," which was prepared under the advisement of Dr. Daryl Mincey, Chairman,
Department of Chemistry.
Although the research was not federally-funded, and consequently not materially subject
to federal regulations, as you directed, a rigorous review of the human subjects-related
aspects of Ms. Tuttle's thesis research was nonetheless conducted using expedited protocol
procedures consistent with U.S. Department of Health & Human Services, National Institutes
of Health, Office of Extramural Research, Office for Protection from Research Risks
guidelines. The reviewers consisted of: YSU Human Subjects Research Committee
(HSRC) Program Chairperson, JoLynn Carney, Ph.D., Anita Hakstedde, M.D., who served
as expert biomedical reviewer, and Eric C. Lewandowski, Certified Research Administrator,
in his capacity as HSRC Administrative Co-chair.
Each of the reviewers was provided a copy of the full committee human subjects protocol
form, prepared by Ms. Tuttle, as well as access to the full thesis under consideration. As
is customary in expedited protocol reviews, this review was conducted via correspondence.
Based on the review, the consensus findings were, and are, that: (1) the nature of the study,
being essentially a review of medical records, allowed no subject harm, and reflects activity
that normally qualifies for exemption from full committee review under DHHS Category 4
exemption; (2) the study utilized data that was voluntarily provided to the investigator by
persons authorized to release it; (3) the investigator, acting in a good faith manner, provided
background information to the purveyors of the subject data sufficient for them to form an
adequate judgment with respect to the elements of informed consent, and to allow its release
without coercion; (4) the investigator properly utilized the data collected for the purpose of
her thesis develooment and exercised mature academic consideration and discretion in its use.
urn, the reviewers commend the intuitively sensitive approach to human subject data
~tion and use employed by Ms. Tuttle in conducting her study. At the same time,
reviewers earnestly hope that thesis committee members, in future, will appreciate
weight of their responsibility to correctly inform candidates of proper IRB practice,
will adhere to the institutionally-defined IRB process.
>ectfully submitted,
2
~~r&)
fnn Carney, Ph.D.
~ram Chairperson
/ECL
Dr. Darryl Mincey
Ms. Meredith Tuttle
Eric C. Lewandowski, eRA
Administrative Co-chair
Protocol #
To be complefe4 by?--:':'H_-.-::Sub~;---::See-Rfaly-~)
YOUNGSTOWN STATE UNIVERSITY
Human Subjects Protocol Review Fonn
Meredith Tuttle,Masters Candidate Chemistry 783-3224
Typed Name & Title Department Name & Telepbooe ,
lcipal Investigator* Daryl Mincey,
student investigators, Typed Name & Tide
tdvilOr" uame first)
Investigator*
Ph.D. Chemistry-Chair 742-3663
Department Name & Telephone #
Investigator*
Typed Name & Title Department Name & Telephone /I
lSe Note: Do not list collaborators from other iDatitutioos here uolesa they bold approved joint appointment(s) at YSU
e ofStudy The Convergence of- Environmental Influences as
Potential Precipitating Pactore of AML-M2
~xternal Funding Involved?
Ie check appropriate box)
fI
NO
o
YES
'es, Type in Name ofFunding Agency/Prop'am _
tivity Start Date_ End Date Anticipated Funding Date- _
Collaborating Institutions Involved?
Ie check appropriate box)
IJ
NO
[J
YES
'es, Type in tile Following -:-~-:---:-:- _
Institution Name
Institution Name
Name Ii. Title ofCbiefCollaborator
Name & Tide ofChief Collaborator
Ilk Study Subject to Other
:itutional Human Subjects Review?
'es, Type in the Following
Iostitution Name
il
NO
[J
YES
Protocol Review Date/Detennination
itution with Primary Review Responsibility Ii 0
YSU OTHBR (please Identify)
INSTRUcnONS TO INVESTIGATORS
purpose ofan institutional /wmQn subjects review is to foster academic inquiry through the study of
zan processes and behavior, while protecting subjea rights andinterests. Thefollowing questions are
TIded to promote both ofthese ends. Please answer each question below accurately, completely and
rmguage comprehensible to an ilfformed loyperson. Attach additional pages as necessary. Requests for
"er itiformtltion or clarification ofissues orquestions related to humon subjects research or this protocol
,be directed to the c,,"ent cO<hairs ofthe YSU Humtm Subjects Committee via the OjJice ofGrants and
mored Programs (relepluJne 742-2377). PUase type all respon,e, on thUform and any ilttachnunts.
Briefly describe the nature ofthe activity you are proposing to conduct involving human subjects.
Please try to limit your "poIUIe to the space provided, aDd be sure to address the following: (A) the purpose ofthe research and the
laypotheNa to be teItoci; (B) short refereDCel to the pertiDeDt scientific literature; (C) an overview of the research design, method and
mode ofanalysis; (D) an appraisal of the anticipated value ofthe I'CllIeaJ'Ch to the investigator(s), the human subjects. YSU. the scientific
::ommunity. aDd lOciety-at-large; (E) the specific site(l) ofthe research; aDd (F) investigator access to them.
The purpose of this research is to explore the potential environ.ental
factors contributing to acute myelogenous leukemia-K2; working upon
the hypothesis that a convergence of environmental influences may
influence the development of this leukemia.
, .
I
"
'.
medical texts; scientific journals; medical journals; pharmaceutical
manufacturer product inserts; extant medica1 records
collection of soil and water samples with lab work-up and analysis;
literature search with extant medical record corroboration
to further elucidate the potential environmental influences on acute
myelogenous leukemia
I. YSU labs
graduate student at YSU
Please describe the target population in specifIC terms. Be sure to provide detaU about numbers of
subjects, age, gender, physical condition or any other information that establishes the parameters
ofthe population or your study.
Iv 10 year old cousin diagnosed with acute myelogenous leukemia-M2
(male)
Brieny describe each ofthe different conditiom ormaaipulatiom to be conducted in the study.
~eview of cousin's extant medical records
Brieny describe the nature ofthe measures or obsenatioDS that will be taken in the study.
iview of cousin's extant medical records
Ifany questionnaires, tests, or other iDstnuaeats are to be used, please provide a brief description
and either a copy or an indication ofwhen a copy will be submitted to the Committee for review.
N/A
Will tbe subjects encounter tbe possibility ofpsychological, social, physical or legal risk, that is, the
probabiHty ofharm or iDjury occurring as a result ofparticipation in tim researc:b study?
DYes 11 No Ifso, please describe.
Will the study involve any st.".., that is, any physical, chemical or emotional factors that may
cause bodily or mental tension and may be a factor in calMing disease? [J Yes II No
Ifso, please describe.
Will the subjects be deceived or misled in any way? 0 Yes 111 No
Ifso, please describe and indude a statement regarding the nature oftheir debriermg.
Will tbere be any probiDg for information that an individual might consider to be personal or
sensitive? 0 Yes f] No Ifso, please describe.
Will subjects be presented with materials that they might regard to be offensive, threatening, or
degrading? t.1 Yes iJ No Ifso, please describe.
Approximately how much time will be required ofeach subject?
No time commitment
How will subjects for this study be solicited or contacted?
My help was solicited by my family
What steps will be taken to insure that subjects' participation is voluntary? What inducements
will be offered to subjects for their participation? What is the source ofthose inducements?
Please refer to #12
Itis important that subjects be informed regarding the general nature ofthe proposed human
subject activity, especially including a description ofanything they may consider unpleasant or
risky. Please provide a statement regarding the nature ofthe information whid! will be stated
oraDy or otherwise made available to potential subjects prior to their volunteering.
N/A