TECHNIQUES FOR MODELING REAL LIFE

PROBLEMS
By

Professor M. O. Ibrahim
Department of Mathematics
University of Ilorin
P.M.B. 1515, Ilorin, Kwara State.
NIGERIA.
Email: [email protected]
[email protected]
Phone Number: 07038003294, 08053633541, 09090888863
 Introduction to Mathematical Modelling

Mathematical modeling essentially consists of translating real world problem

into mathematical problems, solving mathematical problems and interpreting
these solution in the language of the real world.

Real Mathematical Mathematica

Problem Problem l Solution

Interpretation
 FLOW DIAGRAM

(a) (b)
 a
S I S I
SI model b
SIS model
dS dI
  SI ,  SI . dS dI
dt dt bI  aSI , aSI  bI
dt dt
(c) a b
S I R
SIR model
dS dI dR
 aSI , aSI  bI , bI .
dt dt dt

c
(d)
a b
S I R
SIR model

dS dI dR
 aSI  c, aSI  bI , bI  c .
dt dt dt
(e) e
a b
S I R
SIRS model
dS dI dR
 aS t  I t   eR t  T , aS t  I t   bI t , bI t   eR t  T  .
dt dt dt

b M
(f)
k r
S I D
SIDM model

dS dI dM dD
 kSI , kSI  rI  bI , bI , rI .
dt dt dt dt
(a) EXISTENCE AND UNIQUENESS THEOREM
dS dI
  SI ,  SI .
dt dt
f1   SI , f 2  SI .
f1 f1
   I   ,    S   
S I
f 2 f 2
  I  , S  
S I
As shown above, it is clear that all the partial derivatives of
the whole system of equations exist, they are finite and
bounded. Hence it has a unique solution.
(b)
dS dI
bI  aSI , aSI  bI
dt dt
f1 bI  aSI , f 2 aSI  bI
f1 f1
  aI  ,  b  aS  
S I
f 2 f 2
 aI  ,  aS  b  
S I

As shown above, it is clear that all the partial derivatives of

the whole system of equations exist, they are finite and
bounded. Hence it has a unique solution.
(C)
dS dI dR
 aSI ....... 1, aSI  bI ...... 2 , bI ..... 3 
dt dt dt
f1  aSI , f 2 aSI  bI , f 3 bI
f1 f1 f1
  aI  ,   aS  , 0  
S I R
f 2 f 2 f 2
 aI  ,  aS  b  , 0  
S I R
f 3 f 3 f 3
0  ,  b  , 0  
S I R
As shown above, it is clear that all the partial derivatives of the
whole system of equations exist, they are finite and bounded. Hence
it has a unique solution.
 dS dI dR
aSI  c ....... 1, aSI  bI ...... 2 , bI  c ..... 3 
(d) dt dt dt
f1 aSI  c, f 2 aSI  bI , f 3 bI  c
f1 f1 f1
 aI  ,  aS  , 0  
S I R
f 2 f 2 f 2
 aI  ,  aS  b  , 0  
S I R
f 3 f 3 f 3
0  ,  b  , 0  
S I R
As shown above, it is clear that all the partial derivatives of the
whole system of equations exist, they are finite and bounded. Hence
it has a unique solution.
(a)
POSITIVITY
dS dI
  SI ..... 1,  SI ..... 2 
dt dt
From 1 From 2

dS dI
  Idt ,  Sdt ,
S I
dS dI
S   Idt  ln S   It  c I  Sdt  ln I  St  c
  It c   It c  St c  St c
S e e e I e e e
S t  e   It S0 I t  e I 0
 St

Therefore, for all t > 0, all the solution set { S(t), I(t)} of the system of equations 1
to 2 are all positive
(b)

dS dI
bI  aSI ..... 1, aSI  bI ..... 2 
dt dt
From 1 From 2

dS dI
 aIdt , aSdt ,
S I
dS dI
S  aIdt  ln S  aIt  c I aSdt  ln I aSt  c
aSt c aSt c
S e  aIt c  aIt
e e c
I e e e
S t  e  aIt
S0 I t  e aSt I 0
Therefore, for all t > 0, all the solution set { S(t), I(t)} of the system of equations 1
to 2 are all positive
(c)
dS dI dR
 aSI ....... 1, aSI  bI ...... 2 , bI ..... 3 
dt dt dt
From 1 From 2
dS dI
 aSI , aSI
dt dt
dS dI
 aIdt , aSdt ,
S I
dS dI
S  aIdt  ln S  aIt  c  I aSdt  ln I aSt  c
 aIt c  aIt c aSt c aSt c
S e e e I e e e
S t  e  aIt
S0 0 I t  e aSt I 0 0
Therefore, for all t > 0, all the solution set { S(t), I(t)} of the system of equations 1
to 2 are all positive
dS dI dR
 aSI  c ....... 1, aSI  bI ...... 2 , bI  c ..... 3
dt dt dt
From 1 From 2
dS dI
 aSI , aSI
dt dt
dS dI
 aIdt , aSdt ,
S I
dS dI
S  aIdt  ln S  aIt  c  I aSdt  ln I aSt  c
 aIt c  aIt c aSt c aSt c
S e e e I e e e
S t  e  aIt
S0 0 I t  e aSt I 0 0
Therefore, for all t > 0, all the solution set { S(t), I(t)} of the system of equations 1
to 2 are all positive
STABILITY ANALYSIS (DFE & EE)
dN
      N ... 1
dt
dP
 N   PC      1  P ... 2 
dt
dC
 PC   RC        2 C ... 3
dt
dJ
 C       3  J ... 4 
dt
dR
 P   J   RC   R ... 5 
dt
Crime Free Equilibrium CFE points.

Here, we are interested in a population dynamics of the system

where there is a crime free equilibrium. We assume the absence of
crime and criminality in the society i.e. C = 0 implies J = 0. Thus, the
Crime- free equilibrium
 is
0  N 0 , P0 , C0 , J 0 , R0

0  N 0 , P0 , C0 , J 0 , R0 
By equating the system of equations to zero, we have
dN dP dC dJ dR
    0.
dt dt dt dt dt
      N 0 ... 1
 N   PC      1  P 0 ... 2 
 PC   RC        2 C 0 ... 3
 C       3  J 0 ... 4 
 P   J   RC   R 0 ... 5 
Solving (1) by taking N=N0 , we have
    N 0 

N0 
 
Solving (2) by taking P = P0, we have


P0 
       1 
Solving (4) we let J = J0,
C
J0 
    1  since c = 0, then J = 0
Solving for R in (5) by letting R = R0,

We have          to = or  R0
1


R0 
        1 
The Crime free Equilibrium is given as, 0  N 0 , P0 , C0 , J 0 , R0 
    
0  , , 0, 0, 
           1          1  
Endemic Equilibrium
For the endemic equilibrium, there exist Crime and Criminality in the
Society, hence C  J 0
.

Solving the system of equation 1 – 5 .We let 

 N 
, P 
, C 
, J 
, R 

Here, C   0 , which implies existence of the crime equilibrium. Therefore we
 
express
. all the component of  in terms of x, where we assume x
C
     N  from equation (1)
 
N 
   

From (2)   C       1  P 0
 
 
P 
    x      1 
From (4)  C      3  J 

 C x
J  
     3       3 
 From (5)  P   J  C    R
   

Substituting for P , J  and C  , we have

  x
  x    R 
    x      1       3
 1    x 
R    
 x         x      1       3 
Hence, the endemic equilibrium express in terms of x is given as
  N , P , C , J , R
     
 where
  
N 
 

 
P 
    x      1 

C  x
 x
J 
     3 
 1    x 
R    
 x         x      1       3 

We need to find the real expression for the value of the assume x C
. From equation 1- 5.
  
N   ......(6)
  k1
 
P  ......(7)
     x      1  k1  C  k 2 
 P   R      2 from 3 
k3  P   R ......(8)
C C
J   ......(9)
     3  k4
 P   J  C    R From 5 
P   J    C
R  ......(10)
 C   k1k 4   C  k 2  C   
     C 
k 3     
k1   C  k 2   1 4
k k  C  k 2  C   
     C 
k3   
k1   C  k 2   k1k 4   C  k 2  C    
 Basic reproductive number, R0

Expected number of cases caused by a typical infectious individual

in a susceptible population.

R0  1 R0 > 1

disease dies out disease can invade

Outbreak dynamics Disease control

• probability of fade-out • threshold targets
• epidemic growth rate • vaccination levels
Calculating R0 – Intuitive approach

R0 = Per capita rate × Duration of

of infecting others infectiousness
… in a completely susceptible population.

Under frequency-dependent transmission:

Rate of infecting others = b S/N

= b in wholly susceptible pop’n

Duration of infectiousness = 1/recovery rate

= 1/g

 R0 = b / g
Effective reproductive number
Expected number of cases caused by a typical infectious individual
in a population that is not wholly susceptible.
Reffective = R0 × S/N

Endemic disease: At equilibrium Reff = 1, so that S*/N = 1/R0

Epidemic disease: Reff changes as epidemic progresses, as

susceptible pool is depleted.
No. new cases

Note: Sometimes “effective

Reff > 1 Reff < 1 reproductive number” is
used to describe
Time
transmission in the
presence of disease
Time control measures.
This is also called Rcontrol.
Reffective and herd immunity

Reffective = R0 × S/N

If a sufficiently high proportion of the population is immune, then

Reffective will be below 1 and the disease cannot circulate.

The remaining susceptibles are protected by herd immunity.

The critical proportion of the population that needs to be immune is

determined by a simple calculation:
• For Reff < 1, we need S/N < 1/R0

• Therefore we need a proportion 1-1/R0 to be immune.

 What does R0 tell you?
• Epidemic threshold
NOTE: not every epidemic threshold parameter is R0!
• Probability of successful invasion
• Initial rate of epidemic growth
• Prevalence at peak of epidemic
• Final size of epidemic (or the proportion of susceptibles
remaining after a simple epidemic)
• Mean age of infection for endemic infection
• Critical vaccination threshold for eradication
• Threshold values for other control measures
The basic framework for macroparasite dynamics

For macroparasites the intensity of infection matters!

Basic model for a directly-transmitted macroparasite:

M L

death death

State variables
N(t) = Size of host population
M(t) = Mean number of sexually mature worms in host population
L(t) = Number of infective larvae in the habitat
The basic framework for macroparasite dynamics
dM
d1 L( t   1 )  (   1 ) M
dt
dL
 s d2 NM ( t   2 )  2 L  NL
dt
b infection rate
m death rate of hosts
m1 death rate of adult worms within hosts
m2 death rate of larvae in environment
d1 proportion of ingested larvae that survive to adulthood
d2 proportion of eggs shed that survive to become infective larvae
t1 time delay for maturation to reproductive maturity
t2 time delay for maturation from egg to infective larva
s proportion of offspring that are female

Further complexities: parasite aggregation within hosts and

R0 for macroparasites

For macroparasites,
R0 is the average number of
female offspring (or just offspring
in the case of hermaphroditic
species) produced throughout
the lifetime of a mature female
parasite, which themselves
achieve reproductive maturity in
the absence of density-
dependent constraints on the
parasite establishment, survival
or reproduction.
Effective R0 for macroparasites

For macroparasites, Reff is the average number of female offspring

produced in a host population within which density dependent
constraints limit parasite population growth.

For microparasites, Reff is the reproductive number in the presence of

competition for hosts at the population scale.

For macroparasites, Reff is the reproductive number in the presence of

competition at the within-host scale.

For both, under conditions of stable endemic infection, Reff=1.

Major decisions in designing a model

Even after compartmental framework is chosen, still need to

decide:
 Deterministic vs stochastic
 Discrete vs continuous time
 Discrete vs continuous state variables
 Random mixing vs structured population
 Homogeneous vs heterogeneous
(and which heterogeneities to include?)
Deterministic vs stochastic models
Deterministic models
• Given model structure, parameter values, and initial
conditions, there is no variation in output.

Stochastic models incorporate chance.

• Stochastic effects are important when numbers are small, e.g.
during invasion of a new disease
• Demographic stochasticity: variation arising because individual
outcomes are not certain
• Environmental stochasticity: variation arising from fluctuations in
the environment (i.e. factors not explicitly included in the model)
Important classes of stochastic epidemic models
Monte Carlo simulation
- Any model can be made stochastic by using a pseudo-random number
generator to “roll the dice” on whether events occur.

Branching process
- Model of invasion in a large susceptible population
- Allows flexibility in distribution of secondary infections, but does not
account for depletion of susceptibles.
Important classes of stochastic epidemic models
Chain binomial
- Model of an epidemic in a finite population.
- For each generation of transmission, calculates new infected
individuals as a binomial random draw from the remaining
susceptibles.

Diffusion
- Model of an endemic disease in a large population.
- Number of infectious individuals does a random walk around its
equilibrium value  quasi-stationary distribution
Continuous vs discrete time
dN
Continuous-time models (ODEs, PDEs)  N
• Well suited for mathematical analysis dt
• Real events occur in continuous
• Allow arbitrary flexibility in durations and residence times

Discrete-time models N ( t  1)  N ( t )
• Data often recorded in discrete time intervals
• Can match natural timescale of system, e.g. generation
time or length of a season
• Easy to code (simple loop) and intuitive
• Note: can yield unexpected behaviour which may or may
not be biologically relevant (e.g. chaos).
Continuous vs discrete state variables

Continuous state variables arise naturally in differential equation

models.
• Mathematically tractable, but biological interpretation is
vague (sometimes called ‘density’ to avoid problem of
fractional individuals).
• Ignoring discreteness of individuals can yield artefactual
model results (e.g. the “atto-fox” problem).
• Quasi-extinction threshold: assume that population goes
extinct if continuous variable drops below a small value

Discrete state variables arise naturally in many stochastic

models, which treat individuals (and individual outcomes)
explicitly.
Models for population structure

Random mixing Multi-group Spatial mixing

Network Individual-based model

Population heterogeneities

In real populations, almost everything is heterogeneous – no two

individuals are completely alike.

Which heterogeneities are important for the question at hand?

Do they affect epidemiological rates or mixing? Can parameters be
estimated to describe their effect?
• often modelled using multi-group models, but networks, IBMs,
PDEs also useful.
SIR output: the epidemic curve

S I R

Susceptible
dS SI
 Removed
dt N

Proportion of population
dI SI
  I
dt N
dR
I Infectious
dt

Time
SIR output: the epidemic curve
1

0.8

Proportion of population
0.6

R0=10 R0=5
0.4

0.2 R0=3
R0=2
0

0 0.2222 0.4444 0.6667 0.8889 1.111 1.333 1.556 1.778 2

Time

Basic model analyses (Anderson & May 1991):

Exponential growth rate, r = (R0 − 1)/D
Peak prevalence, Imax = 1 − (1+ ln R0)/R0
Final proportion susceptible, f = exp(− R0[1−f]) ≈ exp(−R0)
SIR output: stochastic effects

Susceptible
Susceptible
Removed
Removed

Proportion of
Proportion population
of population

Infectious
Infectious

Time
SIR output: stochastic effects

6 stochastic epidemics Probability of disease

with R0=3. extinction following
introduction of 1 case.
1
Proportion of population

ofextinction
0.8

extinction
0.6

Probabilityof
0.4

Probability
0.2

0
0 1 2 3 4 5
Basic reproductive number,R0
Time R0

Stochasticity  risk of disease extinction when number of cases is

small, even if R0>1.
 SIR with host demographics: epidemic cycles

births S I R

deaths

Proportion of population
dS SI
N   S
dt N
dI SI
  (   ) I
dt N
dR
I  R
dt
Time

Cycle period T ≈ 2p (A D)1/2

where A = mean age of infection
D = disease generation interval
or can solve T in terms of SIR model parameters by linearization.
 140
12

(in thousand)
(in thousand)

Susceptible
Infected
8 125

4
110
0

Oct 53 Aug 54 Apr 55 Jan 56 Nov 56 Aug 57

The S-I phase plot

5000
1000
Infected

200
50
20
110000 120000 130000 140000

Susceptibles
Summary of simple epidemic patterns
• Absence of recovery: logistic epidemic
• No susceptible recruitment (birth or loss of immunity): simple epidemics
• Susceptible recruitment through birth (or loss of immunity): recurrent
epidemics
Herd immunity and epidemic cycling

Herd immunity prevents further outbreaks

Proportion of population
until S/N rises enough that Reff > 1.

Time

The classic example: measles in

London
Herd immunity and epidemic cycling

Measles in London Grenfell et al. (2001)

Vaccine era

Baby boom

Cycle period depends on the effective birth rate.

Persistence and fadeouts
UK ~ 60M people
Measles again…

Note that measles dies out

between major outbreaks in
Iceland, but not in the UK or
Denmark. Denmark ~ 5M people

What determines persistence

of an acute infection?

NB: Questions like this are

Iceland ~ 0.3M people
where “atto-foxes” can cause
problems.

S
I
Intrinsic vs extrinsic forcing – what determines outbreak timing?

Untangling the relative roles of

intrinsic forcing (population dynamics and herd immunity)
and
extrinsic forcing (environmental factors and exogenous inputs)
is a central problem in population ecology.

This is particularly true for ‘outbreak’ phenomena such as infectious

diseases or insect pests, where dramatic population events often
prompt a search for environmental causes.
100

80

Leptospirosis in
Number of lepto deaths

60
California sea
lions 40

20

0
84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 00 01 02 03 04 05 06
Intrinsic vs extrinsic forcing – what determines outbreak timing?

Example: leptospirosis in California sea lions

Intrinsic factors
Host population size and structure, recruitment rates and herd immunity

Extrinsic factors
Pathogen introduction: contact with reservoirs, invasive species, range shifts
Climate: ENSO events, warming temperatures
Malnutrition: from climate, fisheries or increasing N
Pollution: immunosuppressive chemicals, toxic algae blooms
Human interactions: Harvesting, protection, disturbance
Data needs I. What’s needed to build a model?

Individual “clinical” data

• Latent period: time from infection to transmissibility
• Infectious period: duration (and intensity) of shedding
infectious stages
• Immunity: how effective, and for how long?

Population data
• Population size and structure
• Birth and death rates, survival, immigration and emigration
• Rates of contact within and between population groups

Epidemiological data
• Transmissibility (R0)
- density dependence, seasonality
Data needs II. What’s needed to validate a model?
Time series
• Incidence: number of new cases
• Prevalence: proportion of population with disease

Seroprevalence / sero-incidence: shows individuals’ history of

exposure.

Age/sex/spatial structure, if present.

e.g. mean age of infection  can estimate R0

Cross-sectional data
Seroprevalence survey (or prevalence of chronic disease)
endemic disease at steady state  insight into mixing
epidemic disease  outbreak size, attack rate, and risk groups
Contact tracing
SARS transmission chain, Singapore 2003

Morbidity & Mortality Weekly Report (2003)

Household studies
Observed time intervals between two cases of measles in families of two children.
Data from Cirencester, England, 1946-1952 (Hope-Simpson 1952)
40
35
30
25

20
Cases

15
10
5
0
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21
Days
Presumed double Presumed within-family
primaries transmission
Measles:
Latent period 6-9 d, Infectious period 6-7 d, Average serial interval: 10.9 d
Other fields of disease modelling
Within-host models
• pathogen population dynamics and immune response
Community dynamics of disease
Co-infections
What happens when multiple parasites are present in the same host?
How do they interact? Resource competition? Immune-mediated indirect
competition? Facilitation via immune suppression
Multiple host species
Many pathogens infect multiple species
- when can we focus on one species?
- how can we estimate importance of multi-species effects?
Zoonotic pathogens – many infections of humans have animal
reservoirs, e.g. flu, bovine TB, yellow fever, Rift valley fever
Reservoir and spillover species
Host jumps and pathogen emergence
Example 1: TB treatment model
dS 1SI
bN  dS 
dt N
dE 1SI  2TI
   d  v  r1  E  pr2 I
dt N N
dI
vE  d  r2  I  qr2 I
dt
dT  2TI
r1 E  qr2 I  dT  .
dt N
Rearranging the equation so that we start with infectious
classes, we obtain;
dE 1SI  2TI
   d  v  r1  E  pr2 I
dt N N
dI
vE  d  r2  I  qr2 I
dt
dS 1SI
bN  dS 
dt N
dT  2TI
r1 E  qr2 I  dT  .
dt N
In the case m = 2 (two infected compartments)

 1SI  2TI 
 N  
N
 
F  0 
 0 
 
 0 
 d  v  r1  E  pr2 I 
 
 d  r2  I  qr2 I  vE 
 1SI 
V Vi   Vi   dS   bN 
 N 
  2TI 
 dT  r1 E  qr2 I  
 N 
The disease free equilibrium point of the system has coordinates
E 
, I  , S  , T   0, 0, 1, 0 
The derivative of F and V at 0, 0, 1, 0  are given by
 0  1  d  v  r1  pr2  respectively. The inverse of V is given by
F   and V  
0 0   v d  r2 

1 1  d  r2 pr2 
V   
d  v  r1 d  r2   vpr2  v d  v  r1 
1 v
R0 FV 
d  v  r1 d  r2   vpr2
Example 2: Multi-Strain Model

We consider the model

dI1
1SI1  b  v1  I1  vI1 I 2
dt
dI 2
 2 SI 2  b  v2  I 2  vI1 I 2
dt
dS
b  bS  v1 I1  v2 I 2  1 I1  1 I1  S
dt
The disease free equilibrium is 0, 0, 1 and the derivative of F and V.
 0 1   b  r1 0 
F   and V  
 0 2   0 b  r2 
 i
Ri  , i 1, 2.
b  ri
So that the reproduction number of the model is given by

R0 max Ri .
i 1, 2
OPTIMAL CONTROL
Example 1:
1
min u t  dt Subject to x t   x t   u t , x 0  1, x 1 free
2

Solution:
H u 2    x  u  The optimality condition is
H   1
0 2u   at u  u  
u 2 2 H
We see the problem of minimization as 2
2  0
u
 H
The adjoint equation is given by        t  ce  t
u
For some constant C. But, the transversality condition is
 1 0  ce 0  c 0
1


Thus,  0 so that u  0. So,

x  satisfies x  x and x 0  1
2
Hence, the optimal solutions are;
 0, u  0, x t  et .
Example 2:
1

u
1
20
 2 2

min  3 x t   u t  dt Subject to x t   x t   u t , x 0  1.

Solution: From the Hamiltonian of the problem

3 2 1 2
H  x  u  x  u The optimality condition is
2 2
H
0 u   at u   u    .
u
2 H
2
1  0.
u
We use the Hamiltonian to find a differential equation of the adjoint
  H
 t    3 x   ,  1 0.
x
Substituting the derived characterization for the control variable u in the
equation for x, we arrive at
 x   1  1   x 
    
     3  1   
The eigenvalues of the coefficient matrix are 2 and -2. Finding the
eigenvectors, the equations for x and  are
 x  1  2t  1   2t
  t  c1   e  c2   e using x 0  1 and  1 0 we find
   1  3
4 1
c1 3c2e and c2 
3e  4  1
Thus, using the optimality equation, the optimal solution are;
4
 3e 2t 3  2t
u  4 e  4 e
3e  1 3e  1
4
3e 1
x t    4 e   4 e
 2t  2t

3e  1 3e  1
 LYAPUNOV ANALYSIS
Example 1: Find the Lyapunov of V  x1 , x2   x12  x22 if
x1 t   x2 t , x2 t   x1 t   x2 t 
Solution:
 V V
V  x1  x2
x1 x2
2 x1 x2  2 x2  x1  x2 
2
2 x1 x2  2 x1 x2  2 x
2
2
 2 x  0.
2
 LYAPUNOV ANALYSIS
Example 2: For the system

Define the function V  x1 , x2  1  x  x 

2 2 2
1 2

Solution:  V V
V  x1 , x2   x1  x2
x1 x2
2  2 x1 1  x12  x22  x1  2  2 x2 1  x12  x22  x2
 4 1  x  x
2
1
2
2  x x  x x 
1 1 2 2

 4  x  x 1  x  x 
2 2 2 2 2
1 2 1 2

0.
 Issue Overview Typical aspects addressed by
modeling
Air pollution Local pollution (e.g., urban Concentrations, health impact,
smog, toxic releases), acid rain, trends, impact and cost/benefit
global issues (e.g., CFCs and analysis of proposed control
related chemicals). measures.

Water Sewage, agricultural runoff, Transport and environmental fate

pollution pesticide residues, acid rain, of pollutants. Effectiveness of
chemical discharges. Relatively remedial measures.
few people in the world have
access to clean water.

Ground Availability of ground water and Safe yields from wells, direction
water the investigation or remediation and rate of movement, spread of
of contamination problems. contaminants, evaluation of
remedial measures.
Water They are many notable instances Determining the capacity of
supply where surface or ground water is supplies. Effectiveness of policy and
being used at a non-sustainable incentive programs.
rate.
 Issue Overview Typical aspects addressed by
modeling
Global Greenhouse gases, such as CO2 , Interactive effects of greenhouse
warning cause more of the sun’s energy to gases, sunlight reflection by
be retained by the Earth, leading to aerosols and increased cloud
a rise in average temperature. cover, changes in vegetation, etc.
Economic impacts (e.g., on
agriculture).

Sea level Melting of polar ice due to increase Feedback loops; e.g., larger ocean
changes in global temperature could may lead to a higher amount of
redefine coast-lines, displace evaporation, more water in cloud
populations, and affect ocean state, perhaps more reflection of
currents and climate. solar energy, etc.

Forest Injects more greenhouse gases into Role of forests as carbon

destruction atmosphere and reduces world reservoirs in world climate
photosynthetic capacity (which models. Impacts on deforestation
removes CO2 ), Also leads to of trade policies or economic
erosion, silting of waterways, and incentives.
species loss.
 Issue Overview Typical aspects addressed by
modeling
Ozone Certain chemicals (e.g., CFCs) Short and long term ozone
depletion deplete ozone in the predictions. Quantifying physical and
stratosphere, such ozone shields economic impacts on health and
the surface from ultraviolet agriculture. Effects of CFC
light, which can harm humans replacement.
and plants.
Hazardous Dangers to the public and the Concentration, transport through
materials environment from both planned the environment, population
and unplanned releases. exposure , health effects, probability
and effects of accidents.
Solid waste Management and disposal of Evaluation of both technical and
municipal solid waste, industrial cost/benefit aspects under certain
waste , and miscellaneous future scenarios regarding
wastes (e.g., mine tailings, quantities, characteristics, etc.
dredging spoils).
Hazardous Hazardous wastes are now Environmental effects of various
wastes variously incinerated, buried, disposal systems. Effectiveness of
reprocessed, or otherwise alternative regulatory or
treated for disposal or reuse. environment incentive programs.
 Issue Overview Typical aspects addressed by
modeling
Ocean Years of routine dumping of Environmental fate of materials
pollution waste material at sea by many disposed of at sea, both in the
nations make it difficult to physical environment and in the
control this practice, despite food chain.
some treaties.

Environmental Evaluation of the total Air, water, noise, traffic, thermal,

impact environmental impact of ecological and other issues.
analysis major development projects Cost/benefit analysis of alternatives.
or industrial facilities.

Population Ecological effects on plant and Retrospective or advance evaluation

dynamics animal population of natural of projects or government policies
changes or perturbations by by model simulation.
human action (e.g.,
overfishing, predator control,
dams).

Environmental Determining whether there is Exposure modeling; statistical

health impacts a connection between evaluation of suspected disease
observed disease and some anomalies.
environmental cause or
contributor.
 Issue Overview Typical aspects addressed
by modeling
Biodiversi Preservation of diverse species and Quantitative measurements of
ty gene pools for reasons ranging from diversity and how it is affected
aesthetics to ecology to development by human actions or
of medicines and other products. environmental changes.
Wetlands Wetlands are important for many Quantitative evaluation of
reasons (e.g., habitat, flood, and value, either for advance
erosion control, groundwater decisions or setting charges for
recharge). past damages.
Desert In many parts of the world, human Interactive effects of human
growth overpopulation combined with poor activities and climatic episodes.
conservation practices has led to the Viability of restoration
growth of deserts in areas of that were programs.
previously covered by vegetation.
Ionizing Radiation exposure from normal Environmental and health
radiation operations (e.g., nuclear power plants) impacts of releases. Probability
or accidents (e.g., Chernobyl). Disposal of major accidents. Suitability
of radioactive wastes. of waste disposal concepts.
 Issue Overview Typical aspects addressed
by modeling
Non-ionizing Radiation from electromagnetic Estimation of population
radiation sources, such as power lines and exposure at different levels.
electronic equipment. Statistical correlation with health
data.
Indoor air Many substances in the indoor Movements of Air pollutants
pollution environment maybe harmful (e.g., through buildings ventilation
radon gas, household materials.) systems. Correlation of health
impacts to psopulation exposure
data.
Noise An area of great importance Advance calculation of expected
pollution abutters of many projects (e.g., noise levels and evaluation of
highways, airports, rest areas, control strategies.
construction activities, windmills,
industrial plants).
Aesthetic Human aesthetic response to the Sometimes evaluated using
degradation environment is recognized as a quantitative ranking schemes to
formal element of assessing measure preferences and
environmental impact and responses.
degradation.
 Issue Overview Typical aspects addressed by
modeling
Natural hazards Natural environment Prediction, risk of damage to
occurrences can cause great engineered systems. (e.g., water
environmental damage supply, power, hazardous facilities),
(e.g., volcanoes, mud slices, cost effectiveness of investments to
forest fires earthquakes, prevent or mitigate.
floods, etc.)
Land subsidence Land subsidence caused by Prediction of such effects and
underground mining, evaluation of control measures
withdrawal of ground water, (e.g., rock mechanics modeling to
underground dissolution of change mining system).
soluble rock formations,
consolidation of sediments,
or other factor.
Salt water Incursion of salt water from Calculation of safe yields by
incursion coastal areas into nearby ground-water modeling.
aquifers due to
overpumping.
Thank you for
Listening