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PSM - Epidemiology & Biostatistics

Based on Park's Textbook of Preventive and Social Medicine

1. DEFINITION & AIMS OF EPIDEMIOLOGY

Epidemiology is the study of the distribution and determinants of health-related states or events in specified populations, and the application of this study to the control of health problems.

Three main aims (IEA):

Describe the distribution and magnitude of health/disease problems in populations
Identify aetiological factors (risk factors) in disease pathogenesis
Provide data for planning, implementing, and evaluating health services

Key distinction from clinical medicine: Epidemiology studies populations; clinical medicine studies individuals. The epidemiologist is interested in the relationship between cases and the population - expressed as a rate.

2. TYPES OF EPIDEMIOLOGICAL STUDIES

A. Descriptive Epidemiology

Describes distribution of disease by:

When - time distribution
Where - place distribution
Who - person distribution

Descriptive studies are usually the first phase of investigation. They formulate hypotheses rather than test them.

B. Analytical Epidemiology

Tests hypotheses. Studies individuals within a population. Two main types:

1. Case-Control Study ("Retrospective")

Both exposure and outcome have already occurred before study starts
Proceeds backwards from effect to cause
Starts with cases (with disease) and controls (without disease), then looks back at exposure
Measure of association: Odds Ratio (OR) = ad/bc
OR approximates Relative Risk when the disease is rare

Advantages: Rapid, cheap, few subjects needed, good for rare diseases, can study multiple aetiological factors, no follow-up needed

Disadvantages: Recall bias, selection of control group difficult, cannot calculate incidence directly, one outcome at a time

Biases specific to case-control:

Recall/Memory bias - cases remember past exposure better than controls
Selection bias - cases/controls may not represent the general population
Berkesonian bias - different hospital admission rates for different diseases
Interviewer bias - knowing who is a case leads to more thorough questioning (eliminated by double-blinding)
Confounding bias - controlled by matching

2. Cohort Study ("Prospective")

Starts with exposed and non-exposed people (all disease-free)
Follows forward in time to see who develops disease
Directly calculates Relative Risk (RR)
RR = Incidence among exposed / Incidence among non-exposed
RR > 1 = positive association; RR = 1 = no association; RR < 1 = protective

Advantages: Direct RR calculation, temporal relationship clear, dose-response can be calculated, can study multiple outcomes

Disadvantages: Expensive, time-consuming, attrition (loss to follow-up), inefficient for rare diseases

C. Experimental Epidemiology

Investigator controls conditions - applies/withdraws the intervention
Gold standard: Randomised Controlled Trial (RCT)
Experimental group vs. control group; outcome compared
Can be in animals or humans
Advantages: strongest causal evidence
Disadvantages: costly, ethical issues, feasibility

3. MEASURES OF DISEASE FREQUENCY

Incidence Rate

"The number of new cases occurring in a defined population during a specified period of time"

Formula: $$\text{Incidence Rate} = \frac{\text{Number of new cases in a given period}}{\text{Population at risk during that period}} \times 1000$$

Restricted to acute conditions
Must always state the unit of time (e.g., per 1000 per year)

Special incidence rates:

Rate	Formula	Use
Attack Rate	New cases / Population at risk × 100	During epidemics
Secondary Attack Rate	New cases among contacts / Total susceptible contacts × 100	Household spread

Prevalence Rate

"All current cases (old and new) existing at a given point in time or over a period"

More accurately a ratio, not a rate

Types:

Point prevalence - all cases at a single point in time (most common use)
Period prevalence - all cases during a defined period

Formula (point prevalence): $$\text{Point Prevalence} = \frac{\text{All current cases at a given point in time}}{\text{Estimated population at same point}} \times 100$$

Prevalence-Incidence Relationship

$$\boxed{P = I \times D}$$

P = Prevalence, I = Incidence, D = Mean duration of disease
Long duration disease → high prevalence (e.g., tuberculosis)
Short/rapidly fatal disease → prevalence ≈ incidence (e.g., food poisoning)
Analogy: Prevalence = photograph (snapshot); Incidence = film (continuous record)

4. MEASURES OF ASSOCIATION

Measure	Used In	Formula	Interpretation
Relative Risk (RR)	Cohort study	Incidence (exposed) / Incidence (unexposed)	Strength of association
Odds Ratio (OR)	Case-control study	ad/bc	Approximates RR for rare diseases
Attributable Risk (AR)	Cohort	Incidence (exposed) - Incidence (unexposed)	Excess risk due to exposure
Population Attributable Risk	Cohort	AR × Prevalence of exposure	Impact at population level

5. SCREENING & DIAGNOSTIC TESTS

2x2 Contingency Table

	Disease +	Disease -
Test +	a (True Positive)	b (False Positive)
Test -	c (False Negative)	d (True Negative)

Key Formulae

Parameter	Formula	Meaning
Sensitivity	a/(a+c) × 100	Ability to detect true positives - "does the test pick up disease?"
Specificity	d/(b+d) × 100	Ability to detect true negatives - "does the test exclude disease?"
PPV (Positive Predictive Value)	a/(a+b) × 100	If test is +ve, probability truly has disease
NPV (Negative Predictive Value)	d/(c+d) × 100	If test is -ve, probability truly disease-free
False-negative rate	c/(a+c) × 100	= 1 - Sensitivity
False-positive rate	b/(b+d) × 100	= 1 - Specificity

Example from Park's (hypothetical figures):

a=40, b=20, c=100, d=9840, Total=10,000
Sensitivity = 40/140 × 100 = 28.57%
Specificity = 9840/9860 × 100 = 99.79%
PPV = 40/60 × 100 = 66.66%
NPV = 9840/9940 × 100 = 98.9%

Key Points About Screening

Sensitivity and specificity are properties of the test itself - they do not change with disease prevalence
PPV increases with increasing prevalence of disease in the population - the same test has higher PPV in a high-risk group
High sensitivity = good for ruling OUT disease (SNOUT: Sensitive test, Negative result, rules OUT)
High specificity = good for ruling IN disease (SPIN: Specific test, Positive result, rules IN)

Difference: Screening vs. Case-finding vs. Diagnosis

Screening - testing asymptomatic people NOT seeking care (e.g., neonatal screening)
Case-finding - testing people seeking care for OTHER reasons (e.g., VDRL in antenatal clinic)
Diagnosis - confirming disease in people with signs/symptoms

6. BIAS & CONFOUNDING

Bias = any systematic error in determining the association between exposure and disease.

Types of Bias

Type	Description	Control
Recall/Memory bias	Cases recall past exposures better than controls	Objective records
Selection bias	Cases/controls not representative of general population	Careful selection criteria
Berkesonian bias	Different hospital admission rates for different diseases	Population-based studies
Interviewer bias	Interviewer probes cases more thoroughly knowing the hypothesis	Double-blinding
Confounding	Third variable associated with both exposure and outcome	Matching, stratification, multivariate analysis

Confounding is a key concept: A confounder is a variable that is associated with both the exposure and the disease but is not on the causal pathway. For example, in studying alcohol and lung cancer, smoking is a confounder.

7. QUICK REVISION TABLE - Study Designs at a Glance

Feature	Cross-sectional	Case-Control	Cohort	RCT
Direction	Snapshot	Backward	Forward	Forward
Measure	Prevalence	OR	RR, AR	RR
Cost	Cheap	Moderate	Expensive	Very expensive
Time	Short	Short	Long	Varies
Rare disease	Poor	Good	Poor	Poor
Rare exposure	Poor	Poor	Good	Good
Causality proof	Weakest	Moderate	Strong	Strongest
Bias risk	Moderate	High	Moderate	Lowest

Source: Park's Textbook of Preventive and Social Medicine, 9789382219163

Enumerate the waterborne disease. Write down the principle of chlorination of drinking water. Define breakpoint chlorination in PSM. The long question is answer choice. Hmm.

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PSM - Water Hygiene: Waterborne Diseases & Chlorination

Park's Textbook of Preventive and Social Medicine

1. WATERBORNE DISEASES (Enumeration)

Water-related diseases are classified as follows:

A. Biological (Water-borne) Diseases

1. Those caused by the presence of an infective agent:

Category	Diseases
(a) Viral	Viral hepatitis A, Hepatitis E, Poliomyelitis, Rotavirus diarrhoea (infants)
(b) Bacterial	Typhoid fever, Paratyphoid fever, Bacillary dysentery (Shigella), E. coli diarrhoea, Cholera
(c) Protozoal	Amoebiasis, Giardiasis
(d) Helminthic	Roundworm (Ascaris), Threadworm (Enterobius), Hydatid disease
(e) Leptospiral	Weil's disease (Leptospirosis)

2. Those due to the presence of an aquatic host:

Aquatic Host	Disease
Snail	Schistosomiasis
Cyclops	Guinea worm (Dracunculiasis), Fish tapeworm

B. Chemical Water-related Diseases

Fluoride excess → Dental fluorosis (mottling of enamel)
Fluoride deficiency (< 0.5 mg/L) → Dental caries
High nitrates → Methaemoglobinaemia (cyanosis in infants)
Industrial/agricultural pollutants (heavy metals, cyanides, organic acids, dyes)

2. PRINCIPLES OF CHLORINATION OF DRINKING WATER

"The mere addition of chlorine to water is not chlorination. There are certain rules which should be obeyed in order to ensure proper chlorination."

Park's Textbook

The 5 Principles:

Principle 1 - Clarity of Water

The water to be chlorinated must be clear and free from turbidity. Turbidity impedes efficient chlorination because suspended particles protect bacteria from the action of chlorine.

Principle 2 - Chlorine Demand Must Be Met

The "chlorine demand" of water must first be estimated and satisfied.

"The chlorine demand of water is the difference between the amount of chlorine added to the water and the amount of residual chlorine remaining at the end of a specific contact period (usually 60 minutes) at a given temperature and pH."

In simple terms: it is the amount of chlorine needed to destroy bacteria AND oxidize all organic matter and ammoniacal substances present in the water. The point at which the chlorine demand is fully met is the "break-point" (see below).

Principle 3 - Adequate Contact Period

The presence of free residual chlorine for a contact period of at least ONE HOUR is essential to kill bacteria and viruses.

Note: Chlorine has no effect on spores, protozoal cysts, and helminthic ova except in higher doses.

Principle 4 - Minimum Free Residual Chlorine

The minimum recommended concentration of free residual chlorine = 0.5 mg/L for one hour.

Free residual chlorine provides a margin of safety against subsequent microbial contamination during storage and distribution.

Principle 5 - Correct Dosage Formula

$$\boxed{\text{Correct dose} = \text{Chlorine demand of water} + \text{Free residual chlorine (0.5 mg/L)}}$$

Additional Key Points on Action of Chlorine:

When chlorine is added to water, the chemical reactions are:

$$\text{H}_2\text{O} + \text{Cl}_2 \rightarrow \text{HCl} + \text{HOCl}$$ $$\text{HOCl} \rightarrow \text{H}^+ + \text{OCl}^-$$

The HCl is neutralized by the alkalinity of the water
Disinfecting action is mainly due to HOCl (hypochlorous acid) - the most effective form
HOCl is 70-80 times more effective than the hypochlorite ion (OCl⁻)
Chlorine acts best when pH is around 7 (predominance of HOCl)
When pH exceeds 8.5, it becomes unreliable because ~90% of HOCl gets ionized to OCl⁻

3. BREAKPOINT CHLORINATION (Definition)

(Exam-favourite long question topic)

Step-by-step Explanation:

When chlorine is added to water containing ammonia, it forms chloramines (combined chlorine). Chloramines do not have the same efficiency as free chlorine.

What happens as chlorine dose is progressively increased:

Stage	What Happens
1	Chlorine added → reacts with ammonia → forms chloramines (combined residual chlorine rises)
2	More chlorine added → chloramines are destroyed by the added chlorine → residual chlorine falls
3	Further increase in dose → residual keeps falling → end products carry no residual chlorine
4	A minimum (the "breakpoint") is reached → all combined chlorines are completely destroyed
5	Beyond this point → residual chlorine begins to rise again in direct proportion to chlorine added = free chlorine

Definition (Park's):

"The point at which the residual chlorine appears and when all combined chlorines have been completely destroyed is the breakpoint, and the corresponding dosage is the breakpoint dosage."

Significance:

Breakpoint chlorination achieves the same results as superchlorination but in a rational, controlled manner
It can therefore be construed as "controlled superchlorination"
Beyond the breakpoint, any additional chlorine added remains as free available chlorine (the most effective germicidal form)
It removes all taste and odour caused by chloramines
It ensures true disinfection by free HOCl rather than the less efficient chloramines

Graphical Concept:

Residual Cl
    ↑
    |  /‾‾‾‾‾‾
    | /  Combined Cl (chloramines)
    |/
    |   ↘          /‾‾‾‾ Free Cl begins
    |    ↘        /
    |     [BREAKPOINT]
    |________________________→ Chlorine dose added

At the breakpoint, all ammonia-nitrogen is oxidised, chloramines are destroyed, and every additional unit of chlorine now appears as free residual chlorine.

Methods of Chlorination (for completeness)

Agent	Notes
Chlorine gas	First choice - cheap, quick, efficient, easy to apply; needs special equipment (Paterson's chloronome)
Chloramine	Slower action, less chlorinous taste, more persistent residual; less commonly used
Perchloron / HTH (High Test Hypochlorite)	Calcium compound with 60-70% available chlorine; used as solution for disinfection

Source: Park's Textbook of Preventive and Social Medicine, Chapter on Water Hygiene

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