A

of
for Lung
The Effects
Effects of
A Mathematical
Mathematical Model
Model for
Cancer: The
Lung Cancer:
Smoke and
Second-Hand Smoke
Second-Hand
and Education
Education
BU-1525-M
BU-1525-M

Carlos
A.
Carlos
A. Acevedo-Estefania
Acevedo-Estefania

University of
of Puerto
Rico-Cayey
Puerto
Rico-Cayey
University
Christina
Gonzalez
Christina
Gonzalez

Texas A&M
Texas
A&M

University
University

Karen R.
Karen
R. Rios-Soto
Rios-Soto

University of
of Puerto
Rico-Mayagiiez
Puerto
University
Rico-Mayagiiez
Eric
D.
Eric
D. Summerville
Summerville

St.
Mary's University
St. Mary
sUniversity
Baojun
Baoj un Song
Song

Cornell
Cornell University
University
Carlos
Castillo-Chavez
Carlos
Castillo-Chavez,

Cornell
Cornell University
University
August 2000
August 2000

Abstract
Abstract
As
In the
the United
United States, lung cancer
of
deaths.
In
is the
the leading
cause
of cancer
cancer
deaths.
As of
of
States, lung cancer is
leading cause
today, cigarette smoking causes
causes 85
85 percent of
lung
cancer
deaths.
In
this
study,
a
deaths.
In this study, a non
nontoday, cigarette smoking
percent of lung cancer
linear system of
of differential
differential equations is
linear
is used
used to
to model
model the
the dy namics of
of aa population

system

which includes
includes smokers.
smokers. The
The
Which
by cancer
cancer institutes, health
health

by

institutes,

dynamics

equations

population

parameters of the model are obtained from data published

parameters of the model are obtained from data published
and government organizations. The
average number of
and
government organizations. The average number of

individuals who
who become
become smokers
smokers and
the reduction
of
by an
individuals
and the
reduction
of this
this average
education
by an education
average
program are
are determined.
determined. The
The long-term impact of
educating
a
susceptible
class
before
of
a
class
before
program
long-term impact
educating susceptible
they enter
enter the
the population model
model and
the
effect
it
has
on
the
epidemic
is
also
studied.
and
the
effect
it
has
on
the
is
also
they
population
epidemic
studied.
Simulations using realistic
realistic parameters are
carried
our
theoretical
results.
Simulations
are
carried out
out to
to illustrate
illustrate
our
theoretical
results.

using

parameters

521
521

1
1

Introduction
Introduction

Lung cancer,
cancer, also
also referred
referred toto asas bronchogenic
bronchogenic carcinomas,
of
is a
a major
contributor
of
Lung
carcinomas, is
major contributor
cancer deaths
deaths inin the
the United
United States,
accounting for
for 28
percent of
[8]. The
cancer
28 percent
of such
such deaths
deaths
The de
deStates, accounting
velopment
of
lung
cancer
occurs
on
the
lining
glands,
which
contains
damage
cells
that
are
of
cancer
occurs
on
the
which
contains
cells
that
are
velopment
lung
lining glands,
damage
located inin our
our lungs
lungs and
and broncheal
broncheal airways
airways known
known as
the tracheobronchial
system
located
as the
tracheobronchial
This
system [3]. This
part
of
a
human
being
is
important
because
this
system
is
susceptible
to
being
contaminated
of
a
human
is
because
this
is
to
contaminated
part
being important
system
susceptible
being
inhaled air,
air, which
which isis aa major
major factor
factor in
in the
the development
of lung
Scientists
cancer.
believe
by inhaled
Scientists believe
development of
lung cancer.
by
that the
the major
major cause
cause of
of lung
lung cancer
cancer isis due
to cancer-causing
cancer-causing agents
that
due to
known as
as carcinogens,
agents known
carcinogens,
such asas asbestos
asbestos and
and-radon.
However,
research
and
statistics
show
that
the
major
such
-radon.
research
and
statistics
show
that
the
of
However,
major agent
agent of
lung cancer
cancer isis tobacco
tobacco smoke,
smoke, which
which contains
contains over
over 60
60 carcinogens.
lung
carcinogens.
Today, cigarette
cigarette smoke
smoke isis responsible
responsible for
for aa great
great proportion
proportion of
within tobacco
of deaths
deaths within
tobacco
Today,
smoke. Each
Each year
year inin the
the United
United States,
400,000 people
smoke.
die from
from cigarette
States, approximately
approximately 400,000
people die
cigarette
smoke,
which
accounts
for
one
in
every
five
deaths
in
the
United
States
[14].
The
likelihood
which
accounts
for
one
in
five
deaths
in
the
United
The
likelihood
States
smoke,
every
[14].
that aa smoker
smoker will
will develop
develop lung
lung cancer
cancer from
from cigarette
cigarette smoke
many
aspects;
that
smoke depends
on
depends on
many
aspects;
such asas the
the age
age at
at which
which smoking
smoking began,
began, how
how long
long the
person has
the
number
of
such
the person
has smoked,
the
number
of
smoked,
cigarettes
smoked
per
day,
and
how
deeply
the
smoker
inhales
[
the
Surgeon
0].
In
smoked
and
how
the
smoker
inhales
the
1988,
In
1
1988,
cigarettes
per day,
deeply
Surgeon
[10].
General established
established the
the addictive
addictive potential
potential of
of cigarette
cigarette smoking
smoking by
General
that nicotine
nicotine
by stressing
stressing that
and other
other agents
agents inin cigarettes
cigarettes were
were just
just as
as
cocaine [8]. The
of
a
smoker
and
as addictive
addictive
as cocaine
The ability
of
a
smoker
ability
to
quit
is
very
difficult
because
of
the
addiction
to
nicotine.
In
fact,
90
percent
of
smokers
to quit is very difficult
because of the addiction
to nicotine.
In fact, 90 percent of smokers
would like
like toto quit
quit but
but can
can not
not [[12].
Based onon data
of current
smokers,
would
12]. Based
34 percent
data of
current
of
smokers, only
only 34
percent of
smokers attempt
attempt toto quit,
quit, but
but only
only 2.5
2.5 percent
percent succeed
succeed every
every year
year [8]. The
of
smokers
The use
use
of cigarettes
cigarettes
and the
the toxic
toxic air
air itit creates
creates has
has been
been labeled
labeled as
single most
most preventable
of
and
as the
the single
cause
of prema
preventable cause
premature death
death inin the
the United
United States.
ture
States.
The
The

relationship between
between cigarette
cigarette smoke
smoke with
with respect
respect to
to lung
has
cancer
has been
been es
esrelationship
lung cancer
case/year).
Furthermore,
(146,000
an
(146,000case/year). Furthermore, an

tablished inin 85-90

85-90 percent
percent of
of all
all lung
lung cancer
cancer cases
cases
tablished
estimated 3,000
non-smokers per
per year
year die
from lung
lung
3,000 non-smokers
estimated
die from

cancer due
to second-hand
smoke
cancer
due to
second-hand
smoke (also
(also
as enviromnental
environmental tobacco
tobacco smoke,
smoke, ETS)
[14].
The
number
of
deaths
of
non-smokers
The
number
of
deaths
of
non-smokers
ETS) [14].
may be
be lower
lower than
than active
active smokers,
smokers, but
but according
to the
the U.S.
Protection
Environmental
Protection
U.S. Environmental
may
according to
Agency,
it
is
quite
large
when
compared
to
those
associated
with
other
indoor
and
outdoor
it
is
when
to
those
associated
with
other
indoor
and
outdoor
Agency,
quite large
compared
environmental pollutants.
pollutants. This
has had
had aa great
great impact
on
public
policies
that
protect
enviromnental
This data
data has
on
that
impact
public policies
protect
people from
from second-hand
second-hand smoke
smoke [9].
people
known
known

as

Based
Based

on the
the relationship
relationship between
between lung
lung cancer
cancer and
want
to
and cigarette
we
want
to show
show
cigarette smoke,
smoke, we
the reduction
reduction of
of contact
contact between
between non-smokers
non-smokers and
smokers, and
the
and smokers,
and how
how to
to decrease
decrease the
the rate
rate in
in
which non-smokers
non-smokers and
and smokers
smokers progress
progress towards
towards lung
lung cancer.
The
of
seven
which
cancer.
The arrangement
of
seven
arrangement
different classes
classes will
will assist
assist usus toto define
the total
total population
population we
we want
want to
different
define the
to analyze.
Howanalyze. How
ever,
the
best
way
to
detail
the
transition
of
each
class
is
to
use
a
mixture
of
parameters,
the
best
to
detail
the
transition
of
each
class
is
to
use
a
mixture
of
ever,
way
parameters,
on

522
522

of each
each class,
seven
non-linear
differential
probabilities, and
and rates.
rates. Based
Based onon the
the behavior
behavior of
non-linear
differential
probabilities,
class, seven
are
created.
of
the
main
of
the
nonlinear
is
to obtain
obtain
One
equations
are
created.
One
of
the
main
purposes
of
the
nonlinear
equations
is
to
equations
purposes
equations
the
use
to find
find the
the basic
basic reproductive
the equilibrium
equilibrium points.
points. The
The Jacobean
Jacobean Matrix
Matrix is
is use
to
reproductive number,
number,
infected.
The role
role of Ro
is to
to determine
determine
Ro, which
which represents
represents the
the rate
rate that
that people
people get
get infected.
The
ifif
R0 is
RQ,
will
die
out
or
increase.
the
model
is
to
obtain
smoking will die out or increase. Through
Through simulations,
simulations, the model is analyzed
smoking
analyzed to obtain
different
the specific
classes. Using
real
different situations
situations that
that produce
produce interesting
interesting results
results among
the
among
specific classes.
Using real
life
increase of
of the
the educated
educated
class can
can
lower
life data,
data, the
the model
model isis believed
believed toto show
show how
how the
the increase
class
lower
the probability
probability ofof being
being diagnosed
diagnosed with
with lung
lung cancer.
the
cancer.

Our nonlinear
nonlinear diferential
diferential equation
equation model
model that
that focuses
the
focuses on
on
the impact
of peer
Our
impact of
peer pressure
pressure
on non-smokers
non-smokers and
and the
the progression
progression toto lung
lung cancer
via
smoke.
cancer
via first
first and
and second-hand
second-hand
smoke. The
The
dynamics
of
addiction
are
shown
to
be
governed
by
a
single
non-dimensional
parameter,
of
addiction
are
shown
to
be
a
non-dimensional
dynamics
governed by
single
parameter,
Ro. R0
Ro denotes
denotes the
the number
number of
of secondary
secondary addictions
generated
small) class
addictions
the first
first ((small)
class of
of
RQ.
generated by
by the
as
the
smokers inin aa population
population of
of (mostly)
non-smokers. Obviously,
Ro
1
shows
how
the
1
as
the
>
smokers
shows
how
the
(mostly) non-smokers.
>
Obviously, R0
prevalence ofof addicts
addicts toto nicotine
nicotine isis high.
high. Our
the
then focus
focus on
on
the role
role of
of education
education
Our analysis
prevalence
analysis then
at various
various levels
levels ofof the
the progression
progression chain
chain ((to
to lung
lung cancer
)
in
the
long-term
reduction
of
at
in
the
reduction
of lung
long-term
lung
cancer)
cancer.
Our
results
show
that
the
most
important
factor
in
preventing
individuals
from
cancer.
from
Our results show that the most important factor in preventing individuals
becoming smokers
smokers osos education;
education; while
while the
the second
second most
isis to
most important
measure
to convincing
becoming
important measure
convincing
heavy
smokers
to
quit.
Our
results
partially
agree
with
those
recently
published
smokers
to
results
with
those
Ithaca
Our
heavy
quit.
partially agree
recently published by
by Ithaca
Journal.
However,
we
disagree
on
the
recommendation
of
focusing
education
on
smokers.
Journal.
of focusing education
on
smokers.
However, we disagree on the recommendation
The prevention
prevention ofof smoking
smoking isis most
most effective
effective in
in the
the long
run,
if
it
is
focused
on
non-smokers.
The
if
it
is
focused
on
non-smokers.
long run,
on

Our paper
paper isis organized
organized asas follows:
follows: section
section 22,, explains
the population
while sec
secOur
explains the
population model,
model, while
tion
explains
the
analysis
of
the
smoke-free
equilibrium,
the
basic
reproductive
number,
3,
tion 3, explains the analysis of the smoke-free
equilibrium, the basic reproductive number,
and endemic
endemic equilbrium.
equilbrium. In
In section
section 4,
we have
have an
estimation
of
4, we
and
an
estimation
of parameters
and numerical
numerical
parameters and
solutions;
section
5,
the
conclusion;
and
section
the
future
work.
6,
section
the
and
section
the
f11ture
work.
solutions;
5,
conclusion;
6,

22

A Population Model
Model for
for the
the Risk
of
A
of Getting
Cancer
Risk
Population
Getting Lung
Lung Cancer

We divide
divide the
the total
total population
population into
into two
two sub-populations,
sub-populations, which
We
which consists
consists of
of individuals
individuals
who
have
never
smoked
that
respond
to
prevention
education
and
those
who
who have never
smoked that respond to prevention education
and those who did
did not.
not. The
The
educated
population
is
denoted
by
individuals
who
never
become
smokers,
The
less
E(t)
.
educated
who never
become smokers,
The lesspopulation is denoted by individuals
educated population,
population, isis made
made up
up of
of six
six classes.
classes. The
class,
N(t
)
,
includes
the
educated
The non-smoker
non-smoker
N
includes
the
class, (t),
individuals
who
do
not
smoke
but
are
susceptible
to
smoking;
the
light-smoker
class,
t),
individuals
who do not smoke but are susceptible to smoking; the light-smoker class, h(
I1 (15),
includes
those
who
smoke
15
or
less
cigarettes
per
day;
and
the
heavy
smokers
I2(t).
There
includes those who smoke 15 or less cigarettes per day; and the heavy smokers I2(t). There
exists three additional classes
classes inin the
the less-educated
less-educated population: Q(t), the
quitter class, con
exists three additional
population: Q(t), the quitter class, conused to smoke and
sists of individuals who
who used
used toto smoke
smoke but
but stop permanently; S(t), who
sists of individuals
stop permanently; S(t), who used to smoke and
are
likely
to
smoke
again;
and
the
lung
cancer
class,
L
individuals
who
have developed
t
,
(
)
are
who have developed
likely to smoke again; and the lung cancer
class, L(t), individuals
523
523

lung cancer.
cancer. We
treat the
the people
people that
that smoke
smoke as
an
infected group,
group, in
in order
order to
to show
show the
the
We treat
as
an
infected
lung
transmission at
the infection
infection of
of smoking
smoking occurs.
occurs.
transmission
at which
which the
An
individual can
can enter
enter the
the population
population in
in two
two different
ways. One
way isis proceeding
proceeding
An individual
different
One way
ways.
class, E,
with aa probability
probability of
of q,
q, oror into
into the
the non-smoker
non-smoker class,
class, N,
with
E, with
class,
N, with
a
probability
of
(1-q).
Individuals
in
all
classes
may
develop
lung
cancer
because
of
the
of
Individuals
in
all
classes
cancer
because
of
the
pa probability
may develop lung
(1-q).
impact of
of second-hand
second-hand smoke.
smoke.
impact
Individuals
in the
the non-smoker
non-smoker class
class can
can become
become aa light
light smoker
smoker (h)
to lack
lack of
of edueduIndividuals
in
due to
(I1) due
into the
the educated
educated
into

cation and
peer pressure
pressure of
of smokers.
smokers. Once
they become
become
cation
and peer
Once they
N or
E. . Therefore,
back to
toN
or E
a
light
smoker
may
become
back
a
smoker
Therefore, light
may become

aa light
light smoker,
smoker, they
they can
can not
not move
move
aa heavy
heavy smoker
smoker ((I2),
or
they
may
or
),
J2
they may
stop smoking
smoking temporarily
temporarily (S)
permanently (Q). We
that
in order
order for
for them
them to
to
We assume
assume
that in
stop
(S) oror permanently
become aa heavy
heavy smoker,
smoker, they
they must
must start
start off
off as
aa light
light smoker.
smoker.
become
as
Once
individual becomes
becomes aa heavy
heavy smoker,
smoker, s/he
s/he may
may quit
quit temporarily
temporarily (8),
permaan
individual
Once an
(S), permanently (Q),
class, the
the individuals
individuals can
can either
either go
go back
back to
to
lung cancer.
cancer. In
the S
In the
S class,
nently
(Q), oror develop
develop lung
smoking,
in
which
we
assume
they
start
off
as
light
smokers;
or
they
can
develop
lung
can
in
which
we
assume
start
off
as
or
can
cansmoking,
they
light smokers;
they
develop lung
cer
The Q
cer (L). The
class represents
represents the
the number
number of
of individuals
individuals who
who stop
stop smoking
smoking permanently.
permanently.
Q class
However,
they
have
a
higher
probability
of
developing
lung
cancer
than
a
non-smoker.
have
a
of
cancer
than
a
non-smoker.
However, they
higher probability
developing lung
We
let the
the natural
natural death
rate (per
capita), J-t,
be the
same for
for all
the classes
classes except
except for
for
We let
death rate
the same
all the
(per capita),
p,, be
the LL
the

class, which
which isis considered
considered to
to have
have higher
higher death
rate.
death rate.
class,
Our
mathematical model
model isis given
given by
by the
the following
following non-linear
non-linear system
system of
of ordinary
ordinary differ
differOur mathematical
ential equations.
equations.
ential

N(I,L+
- J-LN,
HN,
-; ((1 - Pn)f3N+(1 - Ps)f3S)(h
h)
+
+I
S)f S) f1
--cr1 +1'1 +81 +J-t)I
T
'P")f3N+
1,.' - ((01+/1+51+/011,
gg
1' 1 h - ((72
J-t)h,
1' 2+82+
+/A)-72,
gif 7111
2J 2 +
PW1h - (8
q+J-t
)Q,
P27212
+P10'1I1
MQ,
(5q
gig* P21'
(3S(h+h) J-LS,
- u-S,
(1
P2h 2I2 P1)cr 1 h+(1
-P2)'v2I2
(1
(1
-P1)f'1I1
T
-giggig
555
h)
(Pnf3N+Psf3S+f3eE)(h +
+I2>
861,1
862,2
I
+11+
2I 2+8,QQ
qQ
T
9% <P.@N+P.@S1-@.E><I1
dN
dt
dJ1
dt
dJ 2
dt
dQ
dt
dS
dt
dL
dt

(1
)A <1- qq>A
-

(3N(I +h)
12)

+52

L,
- ((H+
J-t+d)
d)L,

dE
dt

t
h

f3e E(h+h)
E
-J-t
qA __pE,
T
'

fig? qA_5eE( 1+-72)

:

where T
where
T:
the parameters
the
parameters and
their
and their

(2)
<2>
(3)
(3)
(4)
(4)
(5)
(5)

(1)
<1>

(6)
(6)
(7)
(7)

! 2 + Q+S+L,
E
+N + h +
E-|-N-l-I1
+I2+Q-I-S-I-L,

1 and
expected values
values are
listed in
in Table
respectively.
are
listed
Table 1
and Table
Table 2,
expected
2, respectively.

524
524

; qA
__,, ...

B.-=EfI1+I2} 2' T

}.|E
-|

N
N

____|,u

iii

(1-q)A
(1
-<1)A

..

+ I:i>
Pn!3N(h
f T
12) IT
PnN<I1 +

+ !2)
(l-P..)j3N(h +
f T
12) IT

|<1-P,,>;sN<x1
II

(l-p1)0"1!1
(1-p1)G1I1
(1-Ps)f>S(I1 +12)
+12) f'1'
fT
Q1-Ps)|aS(11

---->

6
1!1
8111

'

'

(l-p2)'Y:&l2
(1
2) 212

...

"'

6.2!2

;|~

-+

JJ.l2
LLI2

12

U13
J.I.

P2'Y:&l2

P101!1
P16111

,...
--|

,.

(u.+d)L

'Y1
'VIII!1

__

J.l.!1
PLI1

6
qQ
5qQ
-_

--_r

uQ
u.Q

Ps SSCI1
I3S(I1 +
!2) IT
+ 12)
fT
Ps

Figure 1:
1: Diagram
Diagram of
of the
the effects
effects of
on a population.
of smoking
smoking on a, population.

Figure

525
525

..,.

Analysis
Analysis

3
3

3.1
3.1

Smoke-Free
Equilibrium
and
Reproductive
Smoke-Free
and the
the Basic
Basic
Number
Equilibrium
Reproductive Number

In
this section
section we
we analyze
the non-linear
non-linear differential
equation model.
model. We
solve the
the system
system
In this
differential
We solve
analyze the
equation
equations
to
find
the
equilibrium
points,
with
the
assistance
of the
the
to
find
the
with
the
assistance
of
equations
equilibrium points,
mathematical
program
Maple
6.
First,
we
solve
for
the
smoke-free
equilibrium,
which
is:
mathematical
program
Maple 6. First, we solve for the smoke-free equilibrium, which is:
of non-linear
non-linear differential
of
differential

(A(l-q) 00000Hi).
Throughout
consistantly use I:1 an I:2 which are:
Throughout of this paper we consistantly
'7

-W

J.t
pl

of this

0 '7 0 '7 0 '7 0 '7 0 '7

we

paper

E1

-=

use

21

J.t
pl

'

22 which

an

Y1+U1+51+Ma11d22

are:

'Y2-I-52+#

The
Matrix at
the smoke-free
smoke-free equilibrium
equilibrium is:
is:
The Jacobian
at the
Jacobian Matrix
00
00
00
00
,6(1- q)
-,6(1-u p
_B(1 q)
q)
~B(1
q)
00
00 (1
00
00
00
(1
)f3(1- q)
(1- Pn)f3(1
(1- Pn
P,,,)B(1- q)
q) 21
P,,,)B(1
q)
0
00
00
0
0
0
0
0
-22
W1
00
00
00
+ p)
P101
P272
H) 00
-(6.1+
00
00
0
0
(1(10
0
p
(1 P1)U1
_H
(1 P2)')'2
00 Pnf3(1
0
0
+Bef]
f3eq +
+
f3eq+
0
0
+ 51 Pnf3(1
+ Beq
+ 52
+ d)
(p+d)
Pn5(1- q)
f1)+
Pn5(1- q)
11)
511
_(H
00
00
00
00
-f3eq
-f3eq
p
_Beg
"Beg
_/1'
-

'Yl
PWl
PI)TI
_

'

- I:1
-

81

-I:2
P2'Y2
P2h2
-

'

-(8q
82 8q

This
matrix has
has 55 negative
negative eigenvalues,
eigenvalues, which
which are:
This matrix
are:

-(8q

+ p),
+ d
p, _(5q+
_u
H), -J.L,
fi))
_M -(J.L
_(M+

J.L.
-M-

The
rest of
of the
the eigenvalues
eigenvalues are
from the
the sub-matrix:
sub-matrix:
The rest
are
from

( (1- Pn)f3(1- q) -I:1

(1

PH-)5(1 fl)
_

l
'Y
'Y1

1 - q)
(1- Pn)f3(
21. (1
P -)5(1
fl)
_

-I:2
-22

526
526

Table
Table
of
Parameters
Table 1:
1: Table
of Parameters

Parameter
A

Recruitment rate.
Recruitment
rate.

IJ.
i3

Transmission
Transmission rate.
rate.

Dermition
Mortality
rate (per-capita).
Mortality rate
(per-capita
_

Rate in
Rate
in which
which the
the educated
educated class
class develops
develops

i3e

lung
due
cancer
due to
to second-hand
second-hand smoke.
smoke.
lun cancer

BI
5,

Ir.Rate
for developing
cancer.
I1 .Rate for
developinglung
lung cancer.
hRate for
lung
.
for developing
cancer.
I2- Rate
developinglung cancer

fu
a

Cq
51

_
_

'YI

Q
-Rate for
for developing
cancer.
Q -Rate
developinglung
lung cancer.

Rate in
Rate
in which
which light
smokers become
become heavy
light smokers
heavy
smokers.
smokers.

'Y2
0).
`

"d

Rate in
heavy smoker
Rate
in which
which aaheavy
smoker. quits
quits
smokin,g.
sm oking.
Rate in
light smoker
Rate
in which
which aalight
smoker stops
stops
smokin,g.
sm okin

Mortality rate in which a person dies of

lung
cancer.
lun cancer.
Probability that an incoming individual

enters
nto the
enters iinto
the educated
educated class.
class.
Probability that a non-educated individual

(1-q)

'

enters
enters the
the non-smoker
non-sm
oker class.
class.
Probability that a non-smoker develops

Pn
P"

lung
cancer.
lun cancer.

Probability that a non-smoker becomes a

(1-P,V

'

light smoker.
light sm oker.
Probability of getting lung cancer via

Ps
P

inS.
secondary
ou go
seconclar smoke,
if you
o in S.
smoke, if
Probability in which a person who stopped

(1-Ps)

smoking
temporarily becomes aa light
sm oking temporarily becomes
light
smoker.
sm oker.

PI

Probability that a light smoker quits

smoking permanently.
ermanentl
smokin
Probability that
quits
sm oker quits
light smoker
Probability that aa light
smoking temporarily.
l

(1-pr)

(1-p1)

Probability that a heavy smoker quits

p2

smoking
permanently.
sm

oking permanently.

Probability that a heavy smoker quits

(1-p2)

smoking
temporarily.
sm

oking temp orarily.

527

Local
stability isis guaranteed
guaranteed provided
provided that
that the
the determinant
is greater
greater than
Local asymptotical
determinant
is
than
asymptotical stability
zero,
that
is,
if
that
if
zero,
is,
(((1
)f3(1 - q1))v1
)- l:1)(
-1:2)- ((1
(1 - Pn)f3(1
))/'1 >> 00,,
Pn)5(1 - q11)
21)(-22)
((1 - Pn
Pn)5(1
-

which isis
which

8)
((8)

equivalent to
to
equivalent
) f3('y1 +
(1
l:2)
(1 - q)(1
)(1 - Pn
PMB(
+2)
>
11 >
-

9)
(

(1:2)(1:1)

Hence,
we define:
define:
Hence, we
R
R0

_
_

(1
Pn) f3('y1+
l:2)
(1-- q)(1
+2)
)(1 -PMB(

(1:2)(1:1)

(10)
(10)

'

and
conclude that
that ifif Ro
then the
the smoke-free
smoke-free equilibrium
equilibrium point
point isis locally
locally asymptotically
and conclude
< 1,
R0 <
1, then
asymptotically
Ro
implies aa smoke-free
smoke-free population.
population. Note
Note that
that Ro
can be
be rewritten
rewritten as:
as:
R0 implies
R0 can

stable.
stable.

Ro:

Poo

Pun)()(<1-q>2(1-q)g1,F

(11)
(11)

Hence,
the basic
basic reproductive
reproductive number,
number, Ro,
gives the
the number
number of
of the
the secondary
secondary smokers
smokers
Hence, the
Rg, gives
produced
by
a
typical
smoker
during
his
life
as
a
smoker.
a
smoker
his
life
as
a
smoker.
produced by typical
during
Observe
that iJ1 isis the
the average
amount
of time
time aa person
person stays
stays in
in the
the light
light smoker
smoker class
class
Observe that
amount
of
average
the average
amount
of time
time that
that aa person
person stays
stays in
in the
the heavy
heavy smoker
class ((I2);
J2);
amount
of
smoker class
(h);
average
(I1); J2
5 isis the
is
the
rate
in
which
a
nonsmoker
become
a
light
smoker
per
unit
of
time;
and,
is
the
rate
in
which
a
nonsmoker
become
a
smoker
unit
of
)
(1
f3
Pn
time; and,
light
per
(1 P,,_),B
represent the
the probability
probability of
of aa non-educated
non-educated person
person entering
entering the
the non-smoker
non-smoker class.
class.
(1
(1- qq)) represent
(1
)
)
-q ;Pn .B represents
represents the
the new
new smokers
smokers from
from light
light smokers;
smokers;
is the
the proportion
proportion of
of
Hence,
is
Hence, Q-'llxzgm
35%
1
)
)
represents new
new
aa light
light smokers
smokers who
who become
become from
from heavy
heavy smokers;
smokers; while
while ( ) ((( )-q ;Pn .B) represents
smokers from
from heavy
heavy smokers.
smokers. Ro
implies aa non-smoker
non-smoker society.
society.
smokers
1 implies
< 1
R0 <
-

Looking
the Ro,
we can
can analyze
the sensitivity
sensitivity of
of the
the system
system by
by observing
observing thethe parapara
at the
Rg, we
Looking at
analyze the
can drastically
change
the
value
of
Ro.
The
value
of
,
which
is
the
probability
can
the
value
of
The
value
of
which
is
the
q
Rg.
drastically change
q,
probability
of getting
getting into
into the
educated class,
class, would
would have
have an
important effect,
effect, particularly
particularly ifif itit isis closer
closer
of
the educated
an
important
to one.
one. If
we make
make itit approximately
equal to
to one
one oror close
close enough,
enough, we
we get
get the
the Ro
to be
be less
less
to
If we
R0 to
approximately equal
than one,
one, that
that is,
is, our
our population
population becomes
becomes smoke-free.
smoke-free. If
is
close
to
zero,
then
most
of
the
than
If q
is
close
to
then
most
of
the
q
zero,
N class.
population will
will go
go to
to the
the N
class.
population
meters that
that
meters

Other
parameter that
that greatly
greatly affect
is (3,
since this
this isis the
transmission rate
rate between
between
affect Ro
the transmission
Other parameter
R0 is
,3, since
classes. It
is obvious
obvious by
by looking
looking of
of Ro
we increase
increase the
the amount
of (3,
will increase,
increase,
classes.
It is
that ifif we
amount
of
R0 that
R0 will
,B, Ro
528
528

reducing the
the contact
contact with
with smokers.
smokers.
reducing
The
however P
is very
small. In
In the
the case
case
The other
other parameter
parameter that
that seems
seems important
important isis P
n, is
n; however
Pn;
Pn,
very small.
of
cancer.
As tt gets
of R0 << 1,
increasing Pn
leads toto the
the increase
increase of
of people
people developing
As
1, increasing
Pn leads
developing lung
lung cancer.
gets
the
number
of
cancer
cases
to
zero.
larger,
the
number
of
lung
cancer
cases
goes
to
zero.
larger,
lung
goes

Ro

3.2
3.2

Endemic Equilibria
Equilibria
Endemic

The previous
previous subsection
subsection shows
shows that
that ifif R0 <
The
<

Ro

then the
the smoker-free
equilibrium
smoker-free
is locally
1,
1, then
equilibrium is
locally
asymptotically stable,
stable, meaning
meaning eventually
eventually that
that there
there will
will be
To
be non-smokers.
non-smokers.
To look
look at
at the
the
asymptotically
case R0
Ro >> 1,
solve the
the following
following algebraic
algebraic equations
equations in
or
case
in order
order to
to find
find out
out whether
whether
or not
not
1, wewe solve
positive equilibrium
equilibrium isis possible.
possible.
aa positive

00
00
00
00
00
00

-MN,
- J.lN,
(1-q)A((1- Pn)f3N +(1 Ps)f3S)(I
(1 - q) A-

==

2)
(1
(12)

2)
+ II
- P )( S)1 +
/'1 +
)I1 ,
+ J.l
- (<01
0"1 +
+ 81
61+
+11
mf.,
T
'Y1h - ((/2
1' 2+
+6282+
J.t)I2 ,
7111
+/012,
)Q,
P2'Y
2I2+
PW1h - (8q
+ J.t
P27212
+P1U1I1
/UQ,
(54+
{3S(h+I2)
S,
+ <1
- P2h 2h (1 - P1)0"1 h+
(1 -p2>v212
- j.t
MS,
<1-P1)01I1
T
(Pnf3N+Psf3S +f3e E)(h +I2)
8 I1+82J.2+8qQ
+1
+61I1+62I2+6qQ
T
( J.t+
d)L,
- (IL
+ d)L1
f3e E(h+I2)
qA - J.tE
T
'
PMN I
-------`

{3N(I +h)
+

QT

"

-(519-%.@
-

_'

o0

qA- -pE,

where T E+N + h + I2+Q+S+L.

whereT=E-|-N-|-I1+I2+Q+S+L.
=

529
529

(13)
(13)
(14)
(14)
5)
(1
(15)
(16)
<16>

(17)
18 )
((18)

If
we let:
let:
If We
A

@(I1)

(1

Pn)(1

<1-pn><f1+(1 -pn

<1)A+ (1

(WA)

Ps)-71(1 p1)0'1+ (1 'P2) (7214)-

Then
using (14)
we can
can represent
represent I2
J2 and
in terms
terms of
of I1,
respectivly,
Then using
and (15),
and Q
h, respectivly,
Q in
(14) and
(15), We
12

AI1and

BI1.

)
(19
(19)
20)
((20)

Multiplying equation
equation (12)
find aa linear
linear relationship
relationship
by S
equation (16)
by N,
S and
and equation
We find
N, we
Multiplying
(12) by
(16) by
between S
namely
between
S and
and N,
N, namely
N
Ofi
QI1N
SS.
q
(1)A
(1 q)A
=

(21)
(21 )

-i.

Using
equations (13)
we can
can solve
solve for
for
and (21),
Using equations
(13) and
(21), we

N
N
T
T

=
=

!j.,
,

( 1
) ( (1)A)
21
(1 q(1)-A
.
<P(J1)
,6(1+ A)
sul) )
(p(1+A>)(

22 >
(<22)

'

_-__

_--_

Using
equations (12)
we can
can solve
solve for
for N
and (22),
Using equations
N,,
(12) and
(22), we

( ) ( I1(1
h(1- qq)A
)A)
.
<P(h)
(,,)(<11))

(1)A _ 1
21
(1 qq)A
N =
N
-

--i

_-_

,,

23
(23)
<>

By
using equation
equation 22,
we solve
solve for
for T
explicity in
in terms
terms of
of I1,
J1,
T explicity
22, We
By using
,3(1+ A)

I (I1) 2111
'

T<T><T->_

To
solve for
forE
To solve
E and
and

(24)
<22

we use equation
equation (18),
(18),
-g,
'
We

use

E
E
E
E
T
T
_

qAT
qAT
, an
an d
d
f3ei1
1
(
+ A) +T
6I1<1+A>+/Lf
A
qqA

1----,

ll

BeI1(1-1-A)-I-/,LT
530
530

25 )
((25)

(26)
(26 )

And
And using
using equations
equations

for
(21)
and ((22),
22) , we
we solve
solve for
(21) and
S
S
T
T
-_

,
g,

1hO
I:21119
,8(1+
A)<P(I1)
+ A>><11>
nu

27 )
(27)

-_-_-

through (18),
allows usus to
to solve
ofT,
solve for
for L
L in
in terms
terms
of T,
Adding equations
equations (12)
(12) through
Adding
(18), allows

A- J-LT .
=
L 9%-11.
d
L

(28)
(28)

Substituting equations
equations (19)
through ((28)
into (17),
we have
equilibrium
28) into
have an
an
for J1:
I1:
Substituting
equilibrium equation
equation for
(19) through
(17), we
6

FU1)

P,,211-q)AI1 + PS21zgI1)2
1'
<r>(I1)

61 + 62,4 + 6qB+

<I>(I1)

+ A)
fij,il6<1

F(O)

AI1

E1<1_P,,)(1-q)A+[/fe-H+;(1-P_.,)o]11

I1 + f% A(R6
1)
<#)(i42)(11399)

( ) we obtain:
obtain:

Once wewe solve

solve for
for F(0) and
and F(oo),
F oo ,
Once

we

F(O) = (tt!d)A(Ro-ilA(R,,
1)
(oo ) = -oo
and F
1) and
F(oo)
F(0)=5%
=

Using the
the Intermediate
Intermediate Value
Value Theorem
Theorem (IVT),
Using
(IVT),

-60

we
we obtain

obtain that
that if
if Ro
then
> 1,
R0 >
1, then

if:
if:

81+82A+82B + (tt!d) ,8(1+ A)+ (f_:) y!d ,B(A) (1 P8)0 and

and
%4%2(1-P.)n
61+62A+62B+%ilB(1+A)+Z%J;-5
<
<

,Be - ,8+ g1 (1 - P8)0 > 0

B.-5+;(1-P,,)Q>0
or
OI'

61 + 62,4 +623

>
+ A) +
lHflp(1
f?-f -P.)ol(1and
Z;2_-,5
pe-5+-,(1-PS)Q<0.
_

This shows
shows that
that there
there exists
exists at
at least
least
This

an endemic
endemic equilibrium
solution.
equilibrium solution.

an

We have
have shown
shown the
the existence
existence of
of an
an enden1ic.
endemic. Which
that
popu
We
VVhich means
means
that the
the smoking
smoking populations
are
present.
It
is
hard
to
determine
its
stability
since
we
do
not
have
the
explicit
lations
are
its stability since we do not have the explicit
present. It is hard to determine
formula for
for the
the endemic.
endemic. Our
Our numerical
numerical simulations
simulations support
our conjecture that this en
formula
support our conjecture that this endemic
is
locally
asymptotically
stable.
demic is locally asymptotically stable.
531
531

Estimation
of Parameters
and Numerical
Solutions
Estimation
of
Parameters
and
Numerical
Solutions

4
4
4.1
4.1

Estimated
Parameters
Estimated
Parameters

We
first estimated
estimated the
the parameters
parameters by
by available
data,
then used
used Matlab
Matlab to
numerically solve
solve
We first
available
to numerically
data, then
the
the system
system of
of ordinary
ordinary differential
equations
(1)-(7).
differential
equations (1)-(7).
Estimated
Values
Data
Estimated
Values By
By Data

J-Lmortality rate,
rate, isis estimated
estimated by
by the
the average
life span
span
life
p.
mortality
average
1
5%
of
smokers
quit permanently[8].
permanently[8].
&
of
smokers
2probability
given
by
data
that
2
&
data
that
2.5%
P
P
.
P2
P1
quit
probability given by
probability given
given by
by the
the data
of smokers
smokers are
in the
the 12
class [17].
data that
that 60%
are
in
/'1
60% of
I2 class
71 - probability
[17].
-

o-1
01

-given
by the
the data
that individuals
individuals in
in the
theIr
class quit
quit at
higher rate
rate [18].
data that
at a
a higher
I1 class
given by
[18].
class
quit
at
a
lower
rate
[18].
given
by
data
that
individuals
in
the
data
that
individuals
in
the
class
at
a
lower
rate
/'2
h
I2
72
given by
quit
[18].
mortality rate,
rate, given
given by
by data
that people
people who
who develop
lung cancer
cancer have
have aa mortality
mortality rate
rate
data that
dci - mortality
develop lung
of 77 years
years less
less than
than J-L
[11].
of
p, [11].
-

Assumed
Assumed Values
Values

81
that 15
out of
of 1000
individuals develop
lung cancer.
cancer.
15 out
1000 Ir
61 - assuming
I1 individuals
assuming that
develop lung
82
that
30
out
of
1000
12
individuals
develop
lung
that
out
of
individuals
cancer.
30
1000
62 - assuming
I2
assuming
develop lung cancer.
8q
assuming
that
5
out
of
1000
Q
individuals
develp
lung cancer.
cancer.
develp lung
6,1 assuming that 5 out of 1000 Q individuals
that the
the probability
probability of
of developing
lung cancer
cancer due
to previous
previous smoking
smoking oror
due to
P8
Ps- assuming
assuming that
developing lung
secondary
smoking
is
low.
is
low.
secondary smoking
that the
the probability
probability of
of developing
lung cancer
cancer due
secondary smoke
smoke isis
due to
to secondary
Pn
Pn - assuming
assuming that
developing lung
very
low.
low.
very
that the
the transmission
transmission rate
rate between
between the
the E
population and
is very
very
E population
and Ir
and 12
f3e - assuming
I2 is
I1 and
,Be
assuming that
low.
low.
A- assuming
A
that there
there isis aa constant
constant population
population that
that enters
enters our
our model;
model; itit has
has to
to be
be greater
greater
assuming that
than 1.
than
1.
-

532
532

1%

Table
of Parameters
Parameters
Table 2:
2: Estimation
Estimation of

Parameters
Parameters

I
I
I
I

A
fl.

I
I

Pn
Pu

I
I
I

1.1.

pI

I
I

(1-Pn)
g1-1=Q
o1
51

I
I

I
I 1I
I

1
p1
pl
(1-pl1)
p2
E2
(1l-p22)
cr1
U1
l'_25
Ps
Ps
(1-Ps)
Q1-Psg

I
I

I
I

I
I
I
I

I
I
I
I

I
I

I
I

ag
o2
52
ad

I
I

I
I

qq

(1-q)
(1-q)

Pe

I @,

Values
Values

14+
14+
0.014
0.014 **
.:.:
2"'2
0.00001+
0_00001+
0.99999+
0_99999+
0.015*
0_015*
0.60*
0150*
0.025*
0.025*
0.975*
0925*
0.025*
0025*
0.975*
0925*
0.50*
0.50*
0.25*
025*
0.0001
00001++
0.9999+
0_9999+
0.005*
0005*
0.03*
003*
0.016*
0016*
"
25
0 .25
U "
"
0 .735
Uy
0.00001+
000001+

I
I

I
I

I
I

I
I
I
I

I
~

The data
data
The

was obtained
obtained from
from different
different organizations
organizations such
for Disease
was
such at
at the
the CDC
CDC (Center
(Center for Disease
Control), American
American Lung
Lung Cancer
Cancer Society,
Society, National
National Cancer
Institute
(NCI),
and
other non
Cancer Institute
Control),
(NCI), and other nonprofit
and
government
agencies.
profit and government agencies.
Estimated by the use of data, + Free Parameters
values assumed in order to try to make the model
values assumed in order to try to make the model
Estimated
by the use of data, + Hee Parameters
realistic,
"-"
Values
that
will
be
randomly
changed
to
see
the behavior of our model.
- Values
that will be randomly changed to see the behavior
of our model.
realistic,
**

=
=

533
533

4.2
4.2

Numerical
Solutions
Numerical
Solutions

1 and
We
simulated our
our model
model in
in order
order to
to obtain
obtain the
the cases
cases when
when Ro
We simulated
and Ro
1. Results
Results
< 1
> 1.
R0 <
R0 >
show that
that when
when Ro
the
population
of
susceptibles
to
the
infection
would
eventually
show
the
of
to
the
infection
would
die
< 1,
R0 <
1,
population
susceptibles
eventually die
out. This
with
our
anaylsis
in
section
3.
The
results
of
our
simulations
show
that
out.
This agrees
with
our
in
section
3.
The
results
of
our
simulations
show
that
agrees
anaylsis
when Ro
endemic stable
stable state
state isis established.
established. The
two simulations
simulations shown
shown describe
when
an
endemic
The two
describe
> 1,
R0 >
1, an
graphically
what
we
have
explained
on
the
behavior
of
Ro.
what
we
have
on
the
behavior
of
RO.
explained
graphically
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2: Graph
Figure
shows the
the simulation
simulation for
for Ro
smoke-free equilibrium
equilibrium isis stab
stable.
1. The
The smoke-free
le
< 1.
R0 <
Graph shows
Figure 2:

534
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Figure 3:
3: Graph
Graph shows
shows the
the simulation
simulation for
for Ro
R0
Figure

535

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1. The endemic
equilibrium
endemic
is stable.
stable.
equilibrium is

5
5

Results
of our
Deterministic
Model
of
our
Deterministic
Model
Results

To
obtain aa realistic
realistic representation
representation on
on the
the effects
effects of
of smoking
smoking on
on aa given
given population,
population, we
we
To obtain
aa deterministic
model. Simulations
of
our
model
were
conducted
using
parame
deterministic
model.
of
our
model
were
conducted
Simulations
using parameters and
estimations from
from real
real life
life studies.
studies. We
mainly varied
varied two
two parameters
parameters to
to study
study the
the
ters
and estimations
We mainly
sensitivity
of
our
results
due
to
smoking
within
a
population;
these
were
q,
the
probability
of
our
results
due
to
within
a
these
were
the
sensitivity
smoking
population;
q,
probability
that incoming
incoming individuals
individuals would
would enter
enter our
our educated
educated class(E);
class(E); and
the transmission
rate.
that
and {3,
transmission
rate.
H, the
formulated
formulated

We
produce several
several simulations
simulations showing
showing the
the effects
effects of
of smoking.
smoking. Based
on the
the analysis
We produce
Based on
analysis
of Ro
in the
the previous
previous section
section and
our endemic-equilibrium
endemic-equilibrium point,
point, we
we established
established that
that the
the
of
and our
R0 in
of
will
establish
that
1.
will
epidemic
of
smoking
will
establish
itself,
provided
that
Ro
>
1.
Otherwise,
smoking
will
>
R0
epidemic
smoking
itself, provided
Otherwise, smoking
die
out in
in our
our population.
population. When
we got
got qq 0.25
which allowed
us to
to
die out
VVhen Ro
and j3
allowed us
0.25 and
> 1,
R0 >
1, we
,3 2,
2, wl1ich
obtain Ro
4.04(Figure 3). By
looking
at
the
seven
classes,
we
can
see
that
when
Ro
>
1,
obtain
at
the
seven
we
can
see
that
when
>
R5 4.04(Figure3).
R0
By looking
classes,
1,
then all
then
seven classes
classes will
will establish
establish themselves.
themselves. If
we make
make qq 0.85
2,
then
Ro
all seven
If we
and j3
then
0.85 and
R0
,3 2,
In this
and ex-smokers
0.808(Figure
2). In
this simulation,
simulation, the
the population
population of
of smokers
smokers and
ex-smokers eventually
eventually
0.808(Figure2).
die
out . The
sum of
of the
the non-smoker
non-smoker class,
class, N,
and
the
educated
class,
E,
reaches
the ap
die out
The sum
and
the
educated
reaches
the
N,
class, E,
approximate q-dependent
equilibrium values.
values. This
simulation shows
shows that
that for
for the
the given
given values,
values,
This simulation
proximate
q-dependent equilibrirun
there will
will be
be no
no smoke-induced
smoke-induced population.
population.
there
=
=

=
=

=
=

=
=

=
=

=
=

When
o-1
consists of
of l1igh
high values,
values, that
that is
is when
when light
light and
heavy smokers
smokers quit
quit
When
and 'Y2
and heavy
01 and
72 consists
permanently
and
at
a
faster
rate
then
likely
smokers
becoming
smokers,
then
Ro
should
and
at
a
faster
rate
then
smokers
then
should
R0
permanently
likely
becoming smokers,
eventually be
be less
less than
than 1.
individuals from
from the
the light-smoking
light-smoking class
class quit
quit at
higher rate
rate
1. If
If individuals
at a
a higher
eventually
than individuals
individuals that
that become
become heavy
heavy smokers,
then we
we will
will be
be left
left with
with aa smaller
smaller population
population
than
smokers, then
1
of smokers
smokers in
in general.
general. If
we make
make Ro
>
1,
but
close
to
1
in
the
simulations,
then
the smoksmok
of
If we
but
close
to
in
the
then
the
>
R0
1,
simulations,
ers (J1
will have
have aa small
small population,
population, but
but still
still have
have aa very
very large
large portion
portion of
of the
the total
total
ers
and h)
(I1 and
I2) will
population
in
the
temporary
quitters
(S),
meaning
that
individuals
are
still
susceptible
to
in
the
that
individuals
are
still
population
temporary quitters (S), meaning
susceptible to
smoking
again.
If
we
make
o-1
high
enough
so
that
Ro
<
1,
then
the
total
population
will
If
we
make
so
that
then
the
total
will
01 high enough
R0 < 1,
smoking again.
population
be concentrated
concentrated in
in the
the likely-smoker
likely-smoker class
class ((N)
N) and
the educated
educated population
population (E).
be
and the
Simulations
were 'Y2
is varied
varied can
can affect
the values
values of
of Ro
significantly, ifif we
we let
let 'Y2
were
affect the
Simulations
R0 significantly,
72 is
72 ---t oo,
oo,
then the
the Ro
equation could
could be
be less
less than
than 1.
effects the
the equation
equation by
by eliminate
eliminate the
the concon
then
1. This
This effects
R0 equation
tribution of
of heavy
heavy smokers,
smokers, but,
but, since
since we
we still
still have
have the
the contribution
contribution of
of light-smokers,
light-smokers, we
we
tribution
can not
not necessarily
necessarily say
say that
that the
the equation
equation for
for Ro
will be
be lower
lower than
than 1(Figure
can
and 7)
R0 will
1(Figure66 and
7)..
->

When
VVhen we
we ran
ran simulations
simulations varying
varying j3,
we found
found out
out that
that ifif we
we made
made j3
high enough,
enough, then
then
,3, we
,3 high
the smoking
smoking populations
populations would
would establish
establish themselves
themselves and
the prevalence
prevalence of
of smokers
smokers ( hh)
the
and the
grows. Also,
when j3
is aa l1igh
high value,
value, the
the smokers
smokers will
will convert
convert faster
faster the
the likely
likely smokers;
smokers; then,
then,
grows.
Also, when
,3 is
our Ro
the risk
risk of
of lung
lung cancer
cancer increases(Figure
increases(Figure 4).
we decrease
to aa point
point where
where
our
and the
If we
decrease j3
R0 and
,3 to
4). If
it is
is close
close enough
enough to
to zero,
then
less
individuals
will
start
smoking
due
to
peer
pressure.
it
then
less
individuals
will
start
due
to
zero,
smoking
peer pressure.
Eventually,
could be
be less
less than
than 1(Figure
5).
R0 could
Eventually, Ro
1(Figure5).
536
536

The
The parameters
parameters that
that

we
to reduce
reduce the
the prevalence
of smoking
we need
need toto change
change in
in order
order to
prevalence of
smoking
cancer
are
and
one
must
concentrate
on
the
most
sensitive
lung
cancer
are
q,
{3,
O"I,
and
1'2

Ideally,
one
must
concentrate
on
the
most
sensitive
lung
q, ,U, 01,
72. Ideally,
shown by
the data
data of
of the
the parameters
parameters, wl1ich
which are
are qq and
and ,U.
{3. We
We say
say that
that because
because shown
parameters,
by the
parameters
and
it
is
much
harder
to
affect
individuals
since
there
is
a
of smokers
smokers
O"
,
and
'/'2
,
it
is
much
harder
to
affect
individuals
since
there
is
a
high
percentage
l
01,
72,
high percentage of
tht would
would like
like toto quit,
quit, however,
however, only
only 2.5
2.5 percent
percent of
of those
those do
tht
do it.
it.

and
and

does not
not have
have a
a big
effect at
at the
the
our simulations,
simulations, we
we observed
observed that
that Pn
Pn (0.00001)
big effect
(0.00001)does
in Ro,
the value
value would
would
population level
level of
of lung
lung cancer.
cancer. For
For Pn
Pn toto have
have aa significant
RO, the
population
significant change
change in
have toto change
change dramatically;
dramatically; however,
however, the
the data
indicates the
have
data indicates
the opposite.
opposite.
From
From

66

our

Conclusion
Conclusion

In our
our model
model the
the use
use of
of non-linear
non-linear differential
In
differential

equation was
was crucial
crucial to
to study
the dynam
equation
study the
dynamics of
of lung
lung cancer
cancer atat the
the population
population level
level caused
caused by
by smoking
smoking and
smoke.
ics
and second-hand
second~hand
smoke. By
By
building
this
population,
we
found
an
important
aspect
of
mathematical
biology,
Ro,
which
tl1is
we
found
an
of
mathematical
wl1ich
building
population,
important aspect
biology, RQ,
controls the
the dynamics
dynamics of
of our
our model.
model.
controls
On
On

August 5,
5, 2000,
2000, anan article
article based
based on
on lung
lung cancer
cancer was
was pulished
in the
the Ithaca
Ithaca Journal,
Journal,
August
pulished in
which came
came from
from aa British
British Journal
Journal of
of Medicine.
This
article stated
decrease
wl1ich
Medicine.
Thisarticle
stated that
that if
if we
we
decrease the
the
education
education

on non-smokers
non-smokers and
and concentrate
concentrate on
on smokers,
smokers, than
on
than the
the prevalence
of a
a smoker
smoker
prevalence of
developing
lung
cancer
is
low.
However,
using
our
model
along
with
our
simulations,
is low.
we
developing lung cancer
However,using our model along with our simulations, we
argue
that
when
there
is
an
increase
of
the
number
individuals
that
are
educated,
than
that
when
there
is
an
increase
of
the
number
individuals
that
are
than
argue
educated,
their probability
probability of
of becoming
becoming smokers
smokers decreases
will
their
decreases and
and eventually
we
will have
have a
a smoke-free
smoke-free
eventually we
population
(Ro
<
1).
However,
if
Ro
>
1,
then
our
population
of
light
and
heavy
smokers
population (RO< 1). However, if R0 > 1, then our population of light and heavy smokers
will establish
establish themselves.
themselves. By
By changing
changing {3,
we
found
that
it
had
a
significant
effect
on
the
will
we
found
that
it
had
a
effect
on
the
,3,
significant
number
of
individuals
that
were
infected.
However,
the
greatest
difference
ocurred
where
number
of individuals
that were
infected.
However, the greatest difference ocurred where
the value
value of
of qq changed
changed and
and when
when we
we educated
educated aa l1igh
high number
in
population.
the
number of
of individuals
individuals
in our
our
population.
In conclusion,
conclusion, the
the best
best way
way toto lower
lower the
the number
number of
who
In
of smokers
smokers and
and individuals
individuals
who

develop
develop
lung
cancer
is
by
increasing
the
number
of
individuals
that
are
well-educated
on
the
effect
cancer
is
the
number
of
individuals
that
are
well-educated
on
the
effect
lung
by increasing
of
smoking.
of smoking.
7
7

Future Work
Work
Future

Even though
though we
we considered
considered the
the total
total population
population of
model,
can
add
Even
of smokers
smokers in
in our
our
we
can
add
model, we
to
our
conditions
a
number
of
variations.
An
age
structure
and
ethnicity
diversification
to our
conditions
a number
of variations.
An age structure
and ethnicity diversification
can be
be added
added that
that will
will study
study and
and analyze
analyze the
the prevalence
prevalence of
This
can
of lung
cancer.
This is
is due
due to
to
lung cancer.
537
537

the fact
fact that
that
the

smoking and
its consequences
consequences are
different
if we
we take
take into
into account
age,
sex,
and its
are
different if
account
smoking
age, sex,
and
ethnicity. Also,
studying aa more
more realistic
realistic model
model that
that deals
with the
the impact
impact of
of smoking
smoking
and ethnicity.
deals with
Also, studying
and
the behavior
behavior itit has
has on
on the
the prevalence
prevalence of
of lung
lung cancer.
cancer. One
example is
is studying
studying certain
certain
and the
One example
brands of
of cigarettes.
cigarettes. Also,
we
could
build
a
model
that
would
incorporate
the
recovery
rates
brands
we
could
build
a
model
that
would
the
rates
Also,
incorporate
recovery
for lung
lung cancer,
cancer, meaning
meaning to
to add
class, aa recovery
recovery class
class (R),
were the
the population
population
for
add another
another
class,
(R), were
of the
the lung
lung cancer
cancer class
class (L)
could
go.
Looking
into
the
development
of
lung
cancers,
we
of
could
into
the
of
go. Looking
development
lung cancers, we
(L)
could take
take into
into consideration
consideration creating
creating aa model
model that
that looks
looks at
the effects
effects of
of two
two types
types of
of lung
lung
could
at the
cancers,since once
once an
individual recovers
recovers from
from lung
lung cancer
cancer the
the first
time ,Type
then they
they
an
individual
first time
cancers,since
1, then
,Type 1,
have aa chance
chance of
of getting
getting aa new
new type
type of
of lung
lung cancer,
cancer, Type
2.
Finally,
we
could
forward
have
2.
we
could
forward
Type
Finally,
our research
research by
by looking
looking at
the effects
effects of
of reducing
reducing the
the impact
impact of
of peer
peer pressure
pressure on
on likely
likely new
new
our
at the
smokers,
such
as
current
smokers
and
the
mass
media.
such
as
current
smokers
and
the
mass
media.
smokers,
8
8

Acknowledgement
Acknowledgement

This
study was
was supported
supported by
by the
the following
following institutions
institutions and
grants: National
National Science
This study
and grants:
Science
Foundation
(NSF
Grant
DMS-9977919);
National
Security
Agency
(NSA
Grants
MDA-904Foundation
Grant
National
Grants
MDA-904Security Agency (NSA
(NSF
DMS-9977919);
00-1-0006);
Faculty
DEB) and
Presidential
Award (NSF
Grant DEB)
and the
the Presidential
Presidential
Faculty Fellowship
Fellowship Award
00-1-0006);Presidential
(NSF Grant
Mentoring Award
Grant
HRD)
to
Carlos
Castillo-Chavez
and
the
office
of
the provost
provost
Award (NSF
Grant
to
and
the
office
of
the
Carlos
Castillo-Chavez
Mentoring
(NSF
HRD)
of Cornell
Intel
Technology
for
Education
2000
Equipment
Grant.
of
Intel
for
Education
Grant.
Cornell University;
2000
University;
Technology
Equipment
Thanks
to our
our advisors
for your
your help
help and
Thanks
to
advisors Baojun
and Carlos
and
Carlos Castillo-Chavez,
Castillo-Chavez, for
Baojun Song
Song and
ideas. Also
we want
want to
to thanks
thanks Carlos
Steve
Wirkus,
Brisa
Ney
Sanchez
and
ideas.
Also we
Brisa
and
Carlos Hernandez,
Steve
Sanchez
Hernandez,
Wirkus,
Ney
the MTBI
MTBI program
program for
for allowing
us to
to have
have the
the opportunity
opportunity of
of doing
this research.
research. Finally
the
allowing us
doing tl1is
Finally
thanks to
to MTBI
MTBI students
students for
for your
your moral
moral support.
support.
thanks
References
References

[1]
for an
an SI
in Age-Structured
Fred. A
A Model
Model for
SI Disease
Disease in
Brauer, Fred.
Age-Structured Population.
Population.
[1] Brauer,
[2]
Methods
and Principles
in Mathematical
Biol
Fred and
and Carlos
Methods and
Mathematical
BiolCarlos Castillo-Chavez.
Castillo-Chavez.
Brauer, Fred
Principles in
[2] Brauer,
ogy with
with Applications
to Epidemiology
and Resource
Resource Management.
ogy
Applications to
Epidemiology Population
Population Biology,
Biology, and
Management.
(2000)
pp.
271-294.
271-294.
(2000)pp.
[3]
Cancer Sourcebook.
pp. 6-10,
41-48,
Allan R.
The New
New [Cancer
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R. The
Cook, Allan
6-10, 41-48,
Onmigraphics (1996)
(1996) pp.
[3] Cook,
251-282.
251-282.
[4]
Evidence
for Age
W. and
and John
L. Morrison.
Morrison.
Evidence for
Genetic Relative
Relative Risks
Risks
James W.
John L.
Gauderman, James
Age Genetic
[4] Gauderman,
in Lung
in
Cancer.
American
Journal
of
Epidemiology.
Volume
151,
Number
1,
January
American
of
Volume
Number
Cancer.
Journal
151,
1, January
Lung
Epidemiology.
1,
pp.41-49.
2000 pp.41-49.
1, 2000
[5]
pp.3-115.
Hans. Ro.
Rg. pp.3-115.
Heesterbeek, Hans.
[5] Heesterbeek,
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& Human
Human
SEER Cancer
Statistics
ReServices. SEER
Cancer Statistics
[6] United;States
UnitedStates Department
Department of
of Health
Health &
Services.
Re
Gloeckler
M.S. pp
15-105.
view, 1973-1994.
1973-1994. Ed.
Ed. Lynn
Lynn A.
A. Gloeckler
Ries,
Ries, M.S.
view,
pp 15-105.
as
an
Thesis
[7] Zhang,
Zhang, Tongxiao.
Tongxiao. Role
Role of
of Peer
Peer Pressure
Pressure of
of Smoking:
an
Epidemic.
Smoking.' Smoking
Smoking as
Epidemic. Thesis
(1999).
(1999).

March 1998.
1998. pp.
1-5
[8] http://www.aacr.org/5000/5001/5110g.htm1.Lung
http://www.aacr.org/5000/5001/5110g.html.Lung Cancer.
Cancer. March
pp. 1-5
2000 Facts
Tobacco
[9] http://www.cancer.org/statistics/cff2000/tobacco.htm1.
http://www.cancer.org/statistics/cff2000/tobacco.html. 2000
Facts Figures:
Figures: Tobacco
Use pp.
pp. 3-4.
3-4.
Use

[10] http://cancernet_nci.nih.gov/wyntk_pubs/lung.htm#5
http://cancernet.nci.nih.gov/wyntk_pubs/lung.htm#5 Lung
Who's
Who s at
at Risk'?
Risk?
Cancer:
Lung Cancer:
pp. 1-2.
1-2.
pp.
[11] http://www.1ungcheck.com/info/stats.htm.Lung
http://www. lungcheck.com/info/stats.htm.Lung Check
-Statistical Facts.
Facts. pp.
1-3.
Check-Statistical
pp. 1-3.
[12] http://rex.nci.nig.gov/NCI_Pub_Interface/raterisk/risks70.html.
http:/ /rex.nci.nig.gov /NCLPub.lnterfacejraterisk/risks70.html. Risk
Ciga
Risk Factors:
Factors.'
Cigarette Smoking
Smoking asas aa Cause
Cause of
of Cancer
Cancer pp.1-2.
pp. 1-2.
rette
[13] http:
http:/
/www.cdc.govjtobaccojtab_3.htm.
/ /www.cdc.gov/tobacco
/tab_3.htm.
Adults. (1965-95)
pp.1-3.
Among
Among Adults.
(1965-95)pp.1-3.

CDC'S
Smoking
TIPS- Current
Status
CDC S TIPS-Current
Smoking Status

[14] http://www.cdc.gov/tobacco/morta1i.htm.
http://www.cdc.govjtobaccojmortali.htm. CDC'S
Cigarette
TIPS
CDC S TIPSCigarette Smoking-Related
Smoking-Related
Mortality.
Mortality.
-

[15] http://wwW.cdc.goV/tobacco/initfact.htm.
http:/ /www.cdc.govjtobacco/initfact.htm. CDC'S
of
of
TIPS - Incidence
Incidence
Initiation
CDC S TIPS
of Initiation
of
Cigarette
Smoking
Among
US
Teens-Fact
Sheet.
pp.1-2.
Sheet. pp.1-2.
Cigarette Smoking Among US Teens-Fact
-

[16] http://www.cdc.goV/tobacco/adstat1.htm.
http:/jwww.cdc.govjtobaccojadstatl.htm. CDC'S
Adult
Data.
TIPS
Adult Prevalence
Prevalence
Data.
CDC S TIPS-

[17] http://www.cdc.gov/tobacco/adstat3.htm.
http://www.cdc.govjtobacco/adstat3.htm. CDC'S
Adult
Data.
TIPS
Adult Prevalence
Prevalence
Data.
CDC S TIPS-

[18] http://www.cdc.goV/tobacco/adstat4.htm.
http:/ /www.cdc.govjtobaccojadstat4.htm. CDC'S
- Adult
Former
Smoker
TIPS
Adult
Former
Smoker
CDC S TIPS
Prevalence Data.
Data.
Prevalence
-

539
539

APPENDIX
APPENDIX

99

In
In order
order toto work
work

create
m MATLAB
MATLAB
that
on the
the simulatlons,
simulations, we
we needed
needed to
to create
aa program
in
that
program
was
data we
we
and the
the plotting
of
was composed
composed basically
basically of
of the
the differentlal
differential equat1ons,
equations, the
the data
found,
found, and
plott1ng of
the
the graphs.
graphs.
In
m
order to
to run
run
the simulations.
s1mulat1ons
In MATLAB,
MATLAB, we
we needed
needed toto bu1ld
build two
two programs
programs in
order
the
Program 11
Program
tspan=[O
1000];
tspan=[0 1000];
[500 200
200 200
200 200
200 200
200 200
200 200]
200];
:1:0=
xO=[500
0=[250
100
100
100
100
100
100
100
100
100
100
100];
y
2/0= [250
100]
z0=
350 350
350 350
350 350
350 350
350 350]
350];
z0=[750
[750350
0.25;
qq = 0.25;
f-L
0.014;
=
/.L
0.014;
2
(3 - 2;
H
'
0.015;
81 = 0.015;
61
0.03;
82 = 0.03;
62
0.01;
8q = 0.01;
6q
A = 14;
14;
A
0.0001;
P 8 = 0.0001;
Ps
0.00001;
Pn = 0.00001;
P"
0.025;
=
P1 0.025;
P1
0.025;
P2 = 0025;
p2
0.6;
=
/'
1
0-6;
71
0
/'2 = 0.25;
.25;
'y2
0.016;
dd = 0.016;
f3e = .00001;
,3e
on

P Pu P1 P2 'Y1 U1 'Y2 5q d Q (3
[t,x] = ode45('lung
ode45('lung', tspan,
xo, ll#
[],p,(3,81,82,A,
5 e);
5 51 62 A Fs,Fn,PbP2,')'1,a"!,')'2,8q,d,q,
,tspa.n,r1r0,
[t,a:]
q
/'
d fl , f3e);
85q,
,p,(3,
ode45('lung', tspan, yo,[[]],y,
A F8,
[s,y] = ode45('lung',tspa,n,y0,
U1 2,
61 82,
62 A,
PP1 P2 ')'1,
Y2
P, Fn,PbP2,
'Y1 at,
,H 81,
qd,
[s,y]
q11, f3e) ;
8
6
d
[]
t
zo,
45(
a1,
')'2,
q,
d,
A
P
,
span,
'lung'
[r,
z]
=
o
e
(3,
81,
82,
A,
F8,
Fn,PbP2,
')'1,
p,
01
,
61
62

Y2
Ps
P1 P2 'Y1
d
,H
q
[fr-,z] ode45(lung,tspa,n,z0,[],y,
=
R
*
*
((((1
(1
o (1-<1)*((((1-Pm)*3)/('71+51+01+H))+
- Pn) (3)/(!'1+81+a1+p)) +
- q)
R0=
** (1 - Pn) * (3)/((/'1 +
+
82 +
p) ** (/'2
p))));
+ ((!'1
+62
+01a1 +
+u)
+u))))
((71 (1 -Pn) *ID/((v1 +6181 +
(22+
figure
figure
subplot(231)
subplot
(231)
hold onon
hold
plot(t,x(:,1),'c')
P10'v(',X(=,1),
C)
'b')
plot(s,y(
:,1
),
P10'U(SY(1) b )
plot(r,z(:,1), 'm') II1 )
P10'G(f,2(=,1),
title(['RoRo
',num2str(Ro)]);
=
,num2str(Rg)]);
title([
xlabel('time')
xlabel( time )
=

,,,

540

ylabel('# Individuals
Individuals
(N)')
yla,bel(
#
(Ny)
hold
hold Off
off
subplot(232)
subplot(232)
hold
hold onon
plot(t,x(:,2), 'r')
P10'G('v,X(=,2),
f)
plot(r,z(:,2),'g')
P10'G(1
,2(=,2), g )
plot(s,y(:,2),'b')
p10'v(S,y(=,2),
b)
tr(q)]);
',num2s
title(['q
title([ q ,num2str(q)]);
xlabel('time')
xlabel(
time )
ylabel('#
Individuals
Individuals
(I1)') )
ylabel( #
(I1)
hold
off
hold off
subplot(233)
subplot(233)
hold onon
hold
plot(t,x(:,3), 'r')
p10'v('v,X(=,3),
i )
,'b')
plot(s,y(:,3)
p10'v(S,y(=,3),
b)
plot(r,z(:,3), 'g')
P10'G(1
,2(=,3)/g )
xlabel('time')
xlabel( time )
ylabel('# Individuals
Individuals
(I2)') )
ylabel(
#
(I2)
)]);
',num2str(,B
title([',8 H

,num2stf<@>1>;
tit1e([
holdoff
off
hold
subplot(236)
subplot(236)
hold onon
hold
plot(t,x(:,4), 'g')
p10'v('v,X(=,4),
g)
plot(s,y(:,4),'m') m )
p10t(S,y(=,4),
plot(r,z(:,4), 'y')
P10'G(1 ,2(=,4), I>")
xlabel('time')
xlabel( time )
ylabel('# Individuals (Q)')
ylabel(Individuals
#
(Q) )
off
hold off
hold
subplot(235)
subplot(235)
hold on
hold on
plot(t,x(:,5),'g')
p10'v('v,X(=,5), g )
plot(s,y(:,5), 'm')
p10t(S,y(=,5),
m)
plot(r,z(:,5),'b')
P10'G(1 ,2(=,5), b )
xlabel('time')
xlabel( time )
ylabel('# Individuals
Individuals (S)')
ylabel(
#
(S) )
hold
off
hold off
subplot(234)
subplot(234)
hold on
hold on
plot(t,x(:,6),'g.')
p10'v('v,X(=,6),
g- )
plot(s,y(: ,6),'y. ')
p10t(S,y(=,6), y- )
==

'

==

541

plot(r,z( :,6),'k. ')k. )

p1ot(r,z(:,6),
plot(t,x(:, 7),'r')
P10'G('G,X(=,7),
1")
plot(s,y(
:
'm')
,
7),
1H0tG%y(a7)Hf)
plot(r,z(: ,7),,2(=,7),
'b')
P10'G(1
b)
xlabel('time')
x1abe1( time )
& .L.)
ylabel('# Individuals
(E
L)) )
Individuals
y1abe1(
#
(E &
hold off
off
hold
.

'

2
Program
Program 2

function
function

1, 8 2, A, F8, Fn,P 1,P2, 'Yl, 0" 1, 'Y2, 8q, d, q, f3e )

ddIE=l
x, flag,
j.L, /3,
x=lung(t,
/6186]-1621A1PS1PM-1p11p21'Y110'11'Y216q1d1(11166)
flag;/'51
(.l,'l'Lg(t,$,
N = x(1);I
5);L = x(6);
2);h
S = x(
3);Q = x(
4);S
E = x(7);
N
I2 = x(
a:(6);E
a:(7);
a:(1);I11 = x(
a:(2);
a:(5);L
:1:(3);Q
a:(4);
T
= N+I l +12+Q+S+L+E;
T=N+I1+I2+Q+S+L-I-E;
eq1 = (1q) * A- j3 * N * (h+h)/'IJ.L * N;
-,u,=|
eq1=
(1-q)=|-,u,=|
(1- Pn) * /3 * N * (11+12)/'I+(1- Ps) * f3 * S * (11+12)/'I- (a1+'Y1 + 8 1 +J.L) * 11;
eq2 =
eq2
=(1-Pn)*,6*N*(I1+I2)/T-l-(1-Ps)=|
3
=
eq
11- ('Y2+82+J.L) * h;
eq3 ='Y1'Y1 **I1-('Y2+52+U)*-72;
9
eq4 =
P2 * 'Y 2 * h+P 1 * a1 * 11- (8q+J.L) * Q;
eq4
=P2*'Y2*I2+P1*U1*I1-(5q+U)*Q
(1- P 1) * a1 * 11+(1- P2) * 'Y2 * 12- f3 * S * (h +h)/'I - J.L * S;
eq5 =
eq5
=(1-P1)*U1*I1+(1"'P2)*'Y2*I2-5*S*(I1+-72)/7'U*S
Pn * f3 * N * (h+h)/'I +Ps * f3 * S * (h+12)/'I +f3e * E * (11+h)/'I +8 1 * 11+82 * h+8q * Q
eq6 =P,,=|
eq6
eq7 =
q * A- f3e * E * (I l +12)/'I- J.L * E;
eq7
=q=|
=

dda:x = [e
q1;eq2; eq3; eq4; eq5; eq6;eq7];
[@q1;eq2;eq3;eq4;eq5;eq6;eq7k

542
542

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simulations
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behavior
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In this
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