Transcript Poisons and Drugs

Poisons and Drugs
Prof. Monzir S. Abdel-Latif
Chemistry Department
Islamic University of Gaza
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Syllabus
In this course, it is anticipated to cover the
following topics:
 Introduction to toxicology
 Toxicodynamics and Toxicokinetics
 Data interpretation
 Risk assessment and management
 Exposure and monitoring
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Methods of Analysis
Gas Chromatography
Liquid chromatography
Mass Spectrometry
Hyphenated Techniques
AAS and AES
Spectrophotometry and Fluorometry
Sample Preparation
Classes of drugs and poisons
According to site of action
Grouping of drugs
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Amphetamines
Halaucination drugs
Cannabis Sativa
Diamorphine and heroin
Cocaine
Qat
Psilocybin
Marijuana and its metabolite
Benzodiazepines
Opiates
Phenyl cyclidine
Pesticides
Prediction of Hazard
Antidotes
Diagnosis and treatment
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We will follow presentation chapters from several
textbooks including “Fundamantal Toxicology” by
John Duffus and Howard Worth, published by RSC in
2006, Poisoning and Toxicology handbook, 4th Ed., A
Guide to Practical Toxicology, 2nd Ed, Woolley,
Toxicological Chemistry and Biochemistry, 3rd Ed., as
well as others .
However, other books in Instrumental Analysis and
related research papers will be found very helpful.
I’ll try to maintain a web page for the course and
regularly post reading material for you to look at.
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Introduction to Toxicology
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Toxicology is the fundamental science of poisons.
A poison is a substance that can cause severe injury
or death as a result of interaction with living tissue.
Therefore, in principle, all chemicals can be
considered as potential poisons causing injury or
death upon excessive exposure. At the same time all
chemicals can be regarded as safe if exposure to
chemicals was kept below a tolerable limit.
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Exposure to toxins
Exposure is a function of the following factors:
 Amount or concentration of the target
chemical
 Time of interaction of the chemical with the
target organ
 Frequency of interaction of the chemical with
the target organ
For highly toxic chemicals, the tolerable
exposure is close to zero
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Determination of tolerable exposure
In fact, this constitutes a problem since we do
need reliable data relating exposure to injury
or adverse effect.
Unfortunately, what can be considered as an
injury or an adverse effect is not well defined
and debatable. We will look at this problem
later
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Adverse effects
An adverse effect can be defined as an
abnormal, undesirable, or harmful change of
people or organs following exposure to the
potentially toxic substance
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Although the ultimate adverse effect is death,
the following are definite adverse effects:
Altered food consumption
Altered body or organ weight
Altered enzyme or hormone levels, ..etc
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Harmful effects
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An effect is considered harmful if it causes a
functional damage to an organ, irreversible change in
homeostasis or increased susceptibility to chemical or
biological stress including infectious diseases.
One should consider the degree of alteration from
normality and the relation of the altered property to
the total well-being of the person
In some cases, a person can adapt to the irreversible
alteration and practice normal life
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In some cases of immune reactions
leading to allergy:
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The first exposure may not cause an adverse
effect of allergy, however, it may sensitize the
organism to respond adversely to future
exposures even at low levels
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Amount of exposure
The amount of exposure to a chemical that
causes injury varies over a very wide range
depending on the type of chemical and its form
(liquid, solid, or gas)
 For example:
Ethanol>>NaCl>>DDT>Nicotine>>dioxin
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This can be quantified using the median lethal
dose (LD50) concept
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Median Lethal Dose (LD50), mg
toxin/kg body weight
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LD50 is a statistically derived single dose of a
chemical that can be expected to cause the
death of 50% of organisms of a given
population, under a defined set of experimental
conditions.
LD50 when reported for human beings are
obtained by extrapolation from studies on
mammals, or observations following
accidental or suicidal exposures.
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The LD50 is used to classify and compare toxicity of
chemicals, although it is of limited merits. For
example, the LD50 classification orally to rats are:
Very toxicless than 25 mg/kg
Toxic
from 25 -199 mg/kg
Harmful
from 200 - 2000 mg/kg
However, it is not convincing to label a substance as
toxic because its LD50 is 199, while labeling another
as harmful since its LD50 is 200. That is why the LD50
values need more refinements.
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In addition, when using LD50 values, there is
no simple relationship between lethality and
sub lethal toxic effects.
In other words also, it is not informative to
what is the minimum dose that can be lethal,
and thus no indication of what can be
considered a safe exposure level.
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Toxicity versus Risk
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With regards to chemical safety, risk
assessment can be more important than actual
toxicity of chemicals.
Risk can be regarded as the probability that a
substance would impart unacceptable harm or
unacceptable effects to an organ or to
ecosystems upon exposure.
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Safety
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It is possible to define safety as the practical certainty
that injury will not (high probability) result from
exposure to a hazard under defined conditions.
Practical certainty is a numerically specified low risk
(or socially acceptable risk).
Assessment of risk depends on scientific data, but
acceptability is influenced by social, economic,
political and benefits arising from a chemical or a
process.
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Uncertainty (safety) factors
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A threshold of exposure above which an adverse
effect can occur and below which no such effect is
observed, is obtained from available data.
The threshold of exposure is then divided by a factor
(uncertainty or safety factor) to lower it to a new
value that toxicologists can regard as safe beyond
doubt.
US National Academy of Sciences safe drinking
water committee proposed the following guidelines
for selecting the safety factors, to be used with no
observed effect level (NOEL) data.
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Safety Factor Selection:
An uncertainty (safety) factor of 10 is used
when valid human data based on chronic
exposure is available
An uncertainty (safety) factor of 100 is used
when human data is inconclusive or limited
to acute exposure, but reliable data on
animals is available
An uncertainty (safety) factor of 1000 is used
when no human data is available and
experimental animal data is limited
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Exposure to potentially toxic
substances
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Toxins can cause injury when they reach
sensitive parts of an organism at a
sufficiently high concentration.
Exposure can occur through:
Skin (dermal or percutaneous) Absorption
Inhalation
Ingestion
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Skin absorption
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Among the chemicals that are absorbed through the
skin are aniline, hydrogen cyanide, some steroid
hormones, organic mercury compounds,
nitrobenzene, organophosphate compounds and
phenol. Some chemicals, such as phenol or
methylmercury chloride, can be lethal if absorbed
from a fairly small area (a few square centimeters) of
skin. If protective clothing is being worn, it must be
remembered that absorption through the skin of any
chemical that gets inside the clothing will be even
faster than through unprotected skin because the
chemical cannot escape and contact is maintained
over a longer time.
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Inhalation
Gases and vapors are easily inhaled but inhalation of
particles depends upon their size and shape. The
smaller the particle, the further into the respiratory
tract it can go. Dusts with an effective aerodynamic
diameter of between 0.5 and 7 µm can persist in the
alveoli and respiratory bronchioles after deposition.
Peak retention depends upon the aerodynamic shape
but is mainly of those particles with an effective
aerodynamic diameter of between 1 and 2 µm.
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Physical irritation by dust particles or fibers can cause
very serious adverse health effects but most effects
depend upon the solids being dissolved. Special
consideration should be given to asbestos fibers
which may lodge in the lung and cause fibrosis and
cancer even though they are mostly insoluble and
therefore do not act like classical toxicants: care
should also be taken in assessing possible harm from
manmade mineral fibers that have similar properties.
Some insoluble particles such as asbestos, coal dust and
silica dust will readily cause fibrosis of the lung
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Ingestion
A chemical may accumulate if absorption
exceeds excretion; this is particularly likely
with substances that combine a fairly high
degree of lipid solubility with chemical
stability. Such chemicals are found in the
group of persistent organic pollutants (POPS),
including several organochlorine pesticides,
which are now largely, but not entirely, banned
from use
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Divalent lead ions accumulate in bone where
they replace the chemically similar calcium
ions. While in the bone, they cause little harm
but when bone breaks down, or during
pregnancy or illness, the lead ions enter the
blood and may poison the person who has
accumulated them or, in the case of pregnancy,
the unborn child.
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Local versus systemic effects
Adverse effects may be local or systemic. Local
effects occur at the site of exposure of the
organism to the potentially toxic substance.
Corrosives always act locally. Irritants
frequently act locally. Most substances that are
not highly reactive are absorbed and
distributed around the affected organism
causing general injury at a target organ or
tissue distinct from the absorption site.
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The target organ is not necessarily the organ of
greatest accumulation. For example, adipose
(fatty) tissue accumulates organochlorine
pesticides to very high levels but does not
appear to be affected by them. Some
substances produce both local and systemic
effects. For example, tetraethyl lead damages
the skin on contact, and is then absorbed and
transported to the central nervous system
where it causes further damage.
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Effects of a chemical can accumulate even if the
chemical itself does not. There is some
evidence that this is true of the effects of
organophosphate pesticides and other
neurotoxins on the nervous system. This may
lead to poor functioning of the nervous system
in humans in old age. Because of the time
difference between exposure and effect,
establishing the relationship between such
delayed effects and the possible cause, no
longer present in the body, is often difficult.
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Adverse effects related to allergies appear to be
increasing. Allergy (hypersensitivity) is the
name given to disease symptoms following
exposure to a previously encountered
substance (allergen) that would otherwise be
classified as harmless. Essentially, an allergy is
an adverse reaction of the altered immune
system. The process, which leads to the
disease response on subsequent exposure to
the allergen, is called sensitization.
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Another important aspect of adverse effects to be
considered is whether they are reversible or
irreversible. For the liver, which has a great capacity
for regeneration, many adverse effects are reversible,
and complete recovery can occur. For the central
nervous system, in which regeneration of tissue is
severely limited, most adverse effects leading to
morphological changes are irreversible and recovery
is, at best, limited. Carcinogenic effects are also
irreversible, but suitable treatment may reduce the
severity of such effects
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Chemical Interactions
Additive effect
The simplest interaction is an additive effect: this
is an effect, which is the result of two or
more chemicals acting together and is the
simple sum of their effects when acting
independently. In mathematical terms,
1 + 1 = 2, 1 + 5 = 6, etc.
The effects of organochlorine pesticides are
usually additive.
1.
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2. Synergistic (multiplicative) effect
this is an effect of two chemicals acting together, which
is greater than the simple sum of their effects when
acting alone; it is called synergism. In mathematical
terms,
1 + 1 = 4, 1 + 5 = 10, etc.
Asbestos fibers and cigarette smoking act together to
increase the risk of lung cancer by a factor of 40,
taking it well beyond the risk associated with
independent exposure to either of these agents.
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3. Potentiation
In potentiation, a substance that on its own causes no
harm makes the effects of another chemical much
worse. This may be considered to be a form of
synergism. In mathematical terms,
0 + 1 = 5, 0 + 5 = 20, etc.
For example, isopropanol, at concentrations that are not
harmful to the liver, increases (potentiates) the liver
damage caused by a given concentration of carbon
tetrachloride.
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4. Antagonism
The opposite of synergism is antagonism: an
antagonistic effect is the result of a chemical
counteracting the adverse effect of another; in other
words, the situation where exposure to two chemicals
together has less effect than the simple sum of their
independent effects. Such chemicals are said to show
antagonism. In mathematical terms:
1 + 1 = 0, 1 + 5 = 2, etc.
For example, histamine lowers arterial pressure, while
adrenaline raises arterial pressure
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Toxicity testing
Dose response and Concentration response
A dose–response (concentration–response)
relationship is defined as the association
between dose (concentration) and the
incidence of a defined biological effect in an
exposed population, usually expressed as
percentage. Historically the defined effect was
death.
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The classic dose–response or concentration–response
relationship is shown in the figure below. This is a
theoretical curve and in practice such a curve is rarely
found. Curves of this kind form the basis for the
determination of the LD50 or the LC50 (the median
lethal concentration). The LD50 and LC50 are specific
cases of the generalized values LDn and LCn. The
LDn is the dose of a toxicant lethal to n% of a test
population. The LCn is the exposure concentration of
a toxicant lethal to n% of a test population.
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the LD50 is the statistically derived single dose of
a chemical that can be expected to cause death
in 50% of a given population of organisms
under a defined set of experimental conditions.
Similarly, the LC50 is the statistically derived
exposure concentration of a chemical that can
be expected to cause death in 50% of a given
population of organisms under a defined set of
experimental conditions.
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Another important value that may be derived
from the relationship shown is the threshold
dose or concentration, the minimum dose or
concentration required to produce a detectable
response in the test population. The threshold
value can never be derived with absolute
certainty and therefore the lowest observed
effect level (LOEL) or the NOEL have
normally been used instead of the threshold
value in deriving regulatory standards.
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There is a move to replace these values by the
benchmark dose (BMD). This is defined as the
statistical lower confidence limit of the dose that
produces a defined response (called the benchmark
response or BMR, usually 5 or 10%) in a given
population under defined conditions compared to
background, defined as 0%. It involves fitting a
mathematical model to the entire dose-response
dataset, and allowing the model to estimate the
threshold dose corresponding to a level of benchmark
response (BMR).
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The use of the LD50 in the classification of
potentially toxic chemicals has been described;
it must be emphasized that such a
classification is only a very rough guide to
relative toxicity. The LD50 tells us nothing
about sub lethal toxicity. Any classification
based on the LD50 is strictly valid only for the
test population and conditions on which it is
based and on the related route of exposure.
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The LD50 tells us nothing about the shape of the
dose–response curve on which it is based.
Thus, two chemicals may appear to be equally
toxic since they have the same LD50, but one
may have a much lower lethal threshold and
kills members of an exposed population at
concentrations where the other has no effect
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The determination and use of the LD50 are likely
to decline in future as fixed dose testing
becomes more widely used. In fixed dose
testing, the test substance may be administered
to rats or other test species at no more than
three dose levels: the possible dose levels are
preset legally to equate with a regulatory
classification or ranking system. Dosing is
followed by an observation period of 14 days.
The dose at which toxic signs are detected is
used to rank or classify the test materials.
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Fixed dose testing (no mortality)
The initial test dose level is selected with a view
to identifying toxicity without mortality
occurring. Thus, if a group of five male and
five female rats is tested with an oral dose of
500 mg/ kg body weight and no clear signs of
toxicity appear, the substance should not be
classified in any of the defined categories of
toxicity. If toxicity is seen but no mortality, the
substance can be classed as ‘harmful’.
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If mortality occurs, retesting with a dose of 50
mg/ kg body weight is required. If no
mortality occurs at the lower dose but signs of
toxicity are detected, the substance would be
classified as ‘toxic’. If mortality occurs at the
lower dose, retesting at 5 mg/ kg body weight
would be carried out and if signs of toxicity
were detected and mortality occurred, the
substance would be classified as ‘very toxic’.
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Body weight versus area
On a body weight basis, it is assumed for toxicity data
extrapolation that humans are usually about 10 times
more sensitive than rodents. On a body surface–area
basis, humans usually show about the same
sensitivity as test mammals, i.e. the same dose per
unit of body surface area will give the same given
defined effect, in about the same percentage of the
population. Knowing the above relationships, it is
possible to estimate the exposure to a chemical that
humans should be able to tolerate.
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Epidemiology and human toxicology
Epidemiology is the analysis of the distribution
and determinants of health-related states or
events in human populations and the
application of this study to the control of
health problems. It is the only ethical way to
obtain data about the effects of chemicals on
human beings and hence to establish beyond
doubt that toxicity to humans exists. The
following are the main approaches that have
been used in epidemiology.
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1. Cohort study
A cohort is a component of the population born during a
particular period and identified by the period of birth
so that its characteristics (such as causes of death and
numbers still living) can be ascertained as it enters
successive time and age periods. The term ‘cohort’
has broadened to describe any designated group of
persons followed or traced over a period of time.
Therefore, the group is selected before the study is
done.
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In a cohort study, one identifies cohorts of
people who are, have been, or in the future
may be exposed or not exposed, or exposed in
different degrees, to a factor or factors
hypothesized to influence the probability of
occurrence of a given disease or other
outcome. An essential feature of the method is
the observation of a large population for a
sufficient (long) period, to generate reliable
incidence or mortality rates in the population
subsets.
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Cohort study of lung cancer and
smoking
Lung cancer
cases
No lung cancer
control
Smokers
127 (a)
35 (b)
Nonsmokers
73 (c)
165 (d)
400 persons were selected and followed for a long period of time, with regards
to smoking and development of lung cancer.
These were classified according to being smoking or nonsmoking, developed
cancer or not
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No. of smokers with lung cancer
a
127
No. of smokers without cancer
b
35
a+b
162
No of non smokers with cancer
c
73
No of non smokers without
cancer
Total No. of non smokers
d
165
c+d
238
a/(a+b)
0.784
c/(c+d)
0.307
Total number of smokers
Proportion of smokers who
develop cancer
Proportion of non smokers who
develop cancer
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Relative risk
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Relative risk (RR) is defined as:
RR = {(a/a+b)}/{c/(c+d)}
RR = {127/(127+35)}/{73/(73+165)}
RR = 2.6
This means that the probability of developing
cancer is 2.6 times as high in smokers as in
nonsmokers. This is an evidence of association
of cancer with smoking.
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2. Case-control study
A case-control study starts with the identification of persons with
the disease (or other outcome variable) of interest, and a
suitable control (comparison and reference) group of persons
without the disease. The relationship of an attribute to the
disease is examined by comparing the diseased and nondiseased with regard to how frequently the attribute is present
or, if quantitative, the levels of the attribute, in the two groups.
Example: cancer suspected due to nuclear material exposure
To examine the effect of exposure of pregnant women to
pesticides on the birth weight of the infants
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Case control study of lung cancer
and smoking
Lung cancer
cases
No lung cancer
control
Smokers
127 (a)
35 (b)
Nonsmokers
73 (c)
165 (d)
200
200
Total
200 persons with lung cancer (cases) and 200 persons without lung cancer
(control) were selected and categorized to whether they are smokers or
nonsmokers
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Odds ratio
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OR is a measure of association between exposure and
outcome.
OR = (a/c)/(b/d)
Odds of exposure among cases = a/c =127/35 = 1.7397
Odds of exposure among control = b/d = 35/165 = 0.2121
Odds ratio = 1.7397/0.2121 = 8.2
This means that the odds of exposure to smoking among cases
of lung cancer are 8.2 times as large as the odds of smoking
among control. This indicates an important association
between lung cancer and smoking.
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Risk factors
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Risk factors are factors that increase the
probability of having the disease
Protective factors are factors that will decrease
the probability of having the disease. This is
implied by an odd ratio less than 1
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Case control study of obesity and
regularly eatig vegetable
Obese cases
No obese control
Eat vegetable
121 (a)
171 (b)
Do not eat veget
129 (c)
79 (d)
250
250
Total
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Odds ratio
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OR = (a/c)/(b/d)
Odds of exposure among cases = a/c =121/129 = 0.938
Odds of exposure among control = b/d = 171/79 = 2.1646
Odds ratio = 0.938/2.1646 = 0.43
This means that the odds of exposure to eating veget among
obese persons were 0.43 times as large as the odds among non
obese control. This indicates that eating vegets could be a
protective factor decreasing the probability of obesity
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Case-control study of depression and
regularly eatig vegetable
Depressed cases
undepressed
control
Eat vegetable
90 (a)
90 (b)
Do not eat veget
130 (c)
130 (d)
220
220
Total
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Odds ratio
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OR = (a/c)/(b/d)
Odds of exposure among cases = a/c = 90/130 = 0.6923
Odds of exposure among control = b/d = 90/130 = 0.6923
Odds ratio = 0.6923/6923 = 1.0
This means that the odds of exposure to eating veget among
depressed persons were the same as the odds among
undepressed control. This indicates that eating vegets has no
association with depression.
Conclusion: OR>1 suggests a possible risk factor, an OR<1
suggests a possible protective factor, while an OR=1 suggests
no association between exposure and outcome
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Advantages of a case-control study
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Can be easily used for studying infrequent
diseases
Relatively inexpensive as no follow-up is
necessary
Fast process, as no need to wait for the
accumlation of enough cases as in cohort
studies
Cheaper to do than cohort studies
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Limitations of case-control studies
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Unlike cohort, Cannot be used to calculate the incidence rate,
which is necessary to calculate the relative risk.
It is not possible to elucidate the chronologic order of exposure
and disease, which one occurred first
Results of a case control study is affected by selection bias if
the control group does not come from the same population as
the cases
Recall bias between cases and control may be a real limitation
as cases remembrance are usually better
Although good for rare diseases, the study is not suitable for
rare exposures, like studing the risk of asthma among workers
in a nuclear submarine.
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3. Confounding studies
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A confounding variable is a variable (say,
pollution) that can cause the disease under
study (cancer) and is also associated with the
exposure of interest (smoking). The existence
of confounding variables in smoking studies
made it difficult to establish a clear causal link
between smoking and cancer unless
appropriate methods were used to adjust for
the effect of the confounders
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An example of a confounding study
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We are studying categories which developed a disease and
did not develop a disease as a consequence of exposure.
First a table like the one below is constructed:
diseased
No disease
Total
Exposed
a
b
a+b
Not exposed
c
d
c+d
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No. of people with disease
a
No. of people without disease
b
Total number of exposed
No of unexposed but diseased
No of unexposed without disease
Total No. of unexposed
Proportion of exposed who developed
disease
Proportion of unexposed who developed
disease
a+b
c
d
c+d
a/(a+b)
c/(c+d)
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Three cases:
1.
a/(a+b) > c/(c+d)
This means that exposure and disease are positively
associated
2. a/(a+b) < c/(c+d)
This means that exposure and disease are negatively
associated. Exposure is thus a protective factor
3. a/(a+b) = c/(c+d)
This means that there is no association between
exposure and disease
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The relative risk (RR) is a measure of the
degree of association between the exposure
and development of the disease
RR = {(a/a+b)}/{c/(c+d)}
RR>1 means that exposed individuals have
higher probability of developing the disease
RR<1 means that exposure leads to less risk of
the disease, i.e. exposure is a protective factor
RR=1 suggests no association between
exposure and disease
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An Example: Bedsores and mortality
died
Did not
die
Total
Bedsore
79
745
824
No bedsore
286
8290
8576
Total
365
9035
9400
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No. of people with bedsore who died
a
79
No. of smokers with bedsore who did
not die
Total number of people with bedsore
b
745
a+b
824
c
286
d
8290
c+d
8576
a/(a+b)
9.6%
(c/(c+d)
3.3%
No of people without a bedsore who
died
No of people without bedsore who did
not die
Total No. of people without a bedsore
Proportion of people with a bedsore
who died
Proportion of people without a bedsore
who died
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RR = (79/824)/(286/8576) = 2.9
This suggests that the probability of death was 2.9
times as high in people with bedsores as in people
without bedsores. This may imply a strong
association between bedsores and death.
Do not rush with conclusions as there is a possibility
of a confounding factor; where when patients where
admitted to hospital the medical severity of their
cases was recorded, leading to two categories: high
severity and low severity groups. Our task now is to
check whether medical severity is a confounding
factor or not. Two tables will be necessary, one for
each category:
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Collected info:
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Of the 79 people who had bedsores and died 55 had high
medical severity and 24 had low medical severity
Of the 745 people who had bedsores and did not die, 51 had
high medical severity and 694 had low medical severity
Of the 286 people who had no bedsores and died, 5 had high
medical severity and 281 had low medical severity
Of the 8290 people who had no bedsores and did not die, 5 had
high medical severity and 8285 had low medical severity.
Now construct a table for each category:
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High medical severity group
died
Did not
die
Total
Bedsore
55
51
106
No bedsore
5
5
10
Total
60
56
116
77

The relative risk in the high medical severity
group

RR = (55/106)/(5/10) = 1.04
78
Low medical severity group
died
Did not
die
Total
Bedsore
24
694
718
No bedsore
281
8285
8566
Total
305
8979
9284
79

The relative risk in the low medical severity
group

RR = (24/718)/(281/8566) = 1.02
80



This process is called stratification where two strata
where created. In each stratum, the association
between bedsores and death cannot be explained by
medical severity because in each stratum medical
severity was kept constant.
Stratification is used to adjust for a confounding
factor.
Both relative risks of both strata are close to 1. This
means that the risk of death has no association to
bedsores, provided that adjustment is made for
medical severity.
81
Association of interest
Bedsores
Death
association
association
Medical severity
82



1.
2.
The unadjusted relative risk of 2.9 is thus
misleading. Therefore, trying to eliminate bedsores
will not affect probability of death. If A does not
cause B, then eliminating A will not affect the
occurrence of B. Bedsores are said to be guilty by
association.
If the adjusted and unadjusted relative risk have
been similar, this means that medical severity did
not confound the association between bedsores and
death.
For confounding to occur:
There must be an association between cofounder
and the disease
There must be an association between cofounder
and exposure
83
4. Cross-sectional study
A cross-sectional study examines the relationship between
diseases (or other health-related characteristics) and other
variables of interest as they exist in a defined population at one
particular time. Disease prevalence rather than incidence is
normally recorded in a cross-sectional study and the temporal
sequence of cause and effect cannot necessarily be determined.
A type of study that is referenced about a single point in time. In
other words, information about the exposure factor and
outcome variables are collected at the same point of time.
Example: conducting a survey in which information about
exposure and information about disease outcome are collected
at the same time.
84