Public & Environmental Health Definitions

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Important People in Epidemiology

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HIppocrates - first to identify the relationship between environment and health
John Graunt - studied demography of London, BR, DR, IMR
William Farr - continued Graunt's work in pop statistics for epi "diseases more easily prevented than cured"
John Snow - identified the source of cholera as emitting from an environmental source (drinking water) contaminated with bacteria
Richard Doll - studied link between smoking and lung cancer using epidemiology methods

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Epidemiology

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- understand the distribution of disease in a population
- identify the disease determinants
- use this information to apply as interventions to control and prevent the disease

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Uses of Epi

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PLANNING & POLICY
1. Analyse effectiveness of interventions
2. Health surveillance of pop.
MEDICAL PROGRESSION
3. Natural history of disease
4. Causes and determinants

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Incidence Rate OR Cumulative Incidence

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No. of new cases / No. of ppl at risk x 1000 (in per 1000)
--> rate at which disease occurs

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Incidence Density

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No. of new cases / Total person-time x 1000 (in person-years per 1000)
*as observation duration may differ

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Point Prevalence

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Point prevalence is the number of cases of a disease in a specific point in time in person years / no. of people being observed who are at risk at that time
“do you currently have this disease”
--> probability of a person developing the disease

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Period Prevalence

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Period prevalence is the number of new and existing cases of a disease in a specified time period / no. of people who are under observation for that period of time (even if they dropped out during this period)
“have you ever had this disease”

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Prevalence

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Prevalence = Incidence x Duration

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What affects prevalence of a disease?

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1. Infectivity lambda – how often new cases are added
2. Recovery rho – how quickly people recover from the disease, whether they stay as existing cases (time duration)
3. Immunity of population existing – reduces the denominator of the number of people at risk
4. Movement in and out Immigration and Outmigration of new cases or healthy people
5. High case fatality
6. Better reporting and diagnosis

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What are the risk factors of a disease?

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PPT Place Population (age, gender, ethnicity) Time (year, month, week)

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Why do we use age-standardised figures?

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Account for changes in the population distribution over time so that changes can be compared over time with a common baseline

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Analytic vs Descriptive Epidemiology

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Analytic
- relationship between exposure and outcome (dose-response)
- determinants of distribution of disease
Descriptive
- describe occurrence by time, place, pop PPT
- impact on planning and monitoring population’s health, for allocation of resources and initiating interventions

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Morbidity

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measure of health states of a disease or risk factors for a disease
DALY, QALY, HALE, Disability-free life expectancy (DFLE), Years Potential Life Lost (YLL)

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DALY: disability-adjusted life expectancy

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DALY = YLL + YLD
YLL: years of potential life lost due to premature death = no. of deaths from disease x standard life expectancy at age of death
YLD: years of life lived with disability = incidence rate x disability weight x no. of years lived with disability
1 DALY = 1 year of healthy life lost due to disease

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HALE: healthy life expectancy

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HALE = life expectancy x measurements on quality of life (factor between 0 and 1)
Used as a basis for comparison between different countries

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Disease burden

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impact of health problem as measured by financial cost, mortality and morbidity
can be represented as DALY

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Mortality

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overall deaths due to a certain cause
Source of info: from registries, hospital records

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Mortality rate

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No. of deaths from a pop in a given year / No. of pop in midyear x 1000

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Child mortality rate

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no. of deaths of 1 < children < 4 years of age / 1000 live births

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Infant mortality rate

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no. of deaths of infants <1 year of age / 1000 live births

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Maternal mortality rate

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no. of deaths of women due to childbirth / 1000 live births

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Case-Fatality rate

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No. of deaths among individuals with the disease at specific time / No. of ppl with the disease x 1000

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Health Spectrum

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Susceptible >> Pre-diagnosis >> Symptomatic > Seek Care > Diagnosis >> Treatment >> Cure/Control/Death/Disability

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Measures of association

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Absolute or Relative comparison
Disease Risk Ratio
Odds Ratio

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Risk Ratio

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Absolute comparison in risk difference: risk ratio exposed – risk ratio unexposed
Relative comparison in risk ratio: risk ratio exposed/risk ratio of unexposed
Risk ratio is (a/a+b)/(c/c+d)

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Incidence rate ratio

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Incidence rate in person years of exposed / incidence rate in person years of unexposed

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Odds Ratio

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Odds ratio is (a/c)/(b/d). Out of people who are diseased, how many are exposed and the same out of non-diseased population (refer to case-control study)

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What does the ratio tell us?

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When ratio = 1 there is no relationship
When ratio > 1 there is a positive relationship
When ratio < 1 there is a negative relationship
BETWEEN EXPOSURE and OUTCOME

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Methods of Study Design

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1. Randomised controlled trial (experiment)
(all observational study)
2. Cohort study
3. Case control study
4. Cross-sectional study
5. Ecological study

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RCT

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randomly select people and allocate them randomly to exposure or non-exposure and then follow-up to see if they develop the disease (they are not aware of the exposure or non-exposure – given a placebo)
--> incidence rate ratio

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Cohort

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a cohort of people is selected for the study, they self-select whether they are exposed to a disease, follow up prospectively until they develop the disease and through the course of development, captures person-years, is longitudinal
--> incidence rate ratio

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Case-control Study

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select a group of people who have the disease (cases) and another group of comparable individuals with the same background but do not have the disease (controls), is less valid as there could be bias in the selection process of these two groups of individuals, is longitudinal but is retrospective (asking people whether they were exposed in the past)
--> odds ratio

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Cross-sectional study

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study a specific population at a point in time by surveying everyone, is quick and cheap, shows a snapshot in time, measures risk factor and disease concurrently – but we don’t know the pathway of causation as it could be reversed (causation = exposure must be BEFORE outcome)
 relative risk ratio or odds ratio, but not incidence rate ratio

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Ecological study

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comparison between populations instead of within it, eg. Between different countries, no direct link between individual health exposure and outcome, problem with ecological fallacy, where the characteristics of one population at the population level cannot be extrapolated to an individual level, is useful for generating hypothesis for further study

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Bias

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any systematic error in design, conduct or analysis of a study that results in a distorted estimate of an exposure’s effect on the risk of the disease

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Selection Bias
(2 types: initial design + sick people excluded from participation)

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i) Initial selection where the sample selected is unrepresentative of the entire population, lack of external validity for cohort studies and case-control studies
ii) Self-selection to follow-up “healthy worker effect” where sick people are unable to report for follow-up study interviews, impt for longitudinal prospective studies

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Information Bias

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i) non-differential misclassification: eg. ambiguous phrasing of questionnaire questions, accuracy of measurement test resulting in false positives and negatives, wrongly classifying people into either group (exposed or non-exposed, and diseased or non-diseased)
random error for both groups’ data
ii) differential misclassification: interviewer and recall bias; different quality and extent of information
systematic error for one group’s data

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Confounding

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when a third factor explains the relationship between exposure and outcome
Confounding must be: not on the pathway between exposure and outcome, associated with outcome, related to exposure

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Necessary cause

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when the cause is required in order to produce the outcome, but may not necessarily do so alone

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Sufficient cause

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when cause is capable of producing the outcome, but is not the only one that can do so

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Hill’s criteria of causality

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1. Temporality, cause must precede the effect
2. Consistency with other studies done on other populations
3. Whether experimental evidence was subject to bias during study design
4. Strength of association between cause and effect: is the risk ratio > 1 or <1?
5. Dose-response sensitivity/biological gradient, as degree of exposure increases, the degree of outcome increases
6. Coherence or conflict with existing mainstream knowledge
7. Plausibility according to known information regarding biology and pharmacology
8. Analogous to effects of exposures on other diseases, external validity
9. Specificity of the cause to effect and vice versa

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What does the sufficient cause or pie model of causality show us?

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Diseases are multi-factorial causation
Combination of exposures and interactions can change from pie to pie unless they are a necessary cause

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Levels of prevention

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Primordial - controlling env factors outside an indiv's control
Primary - reducing the onset of the disease by reducing risk factors
Secondary - early detection of the disease
Tertiary - treatment and rehab

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Primordial

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controlling environmental factors outside of an individual’s control that lead to disease, usually interventions at government level eg Smoking bans
Includes interventions relating to social, economic and cultural behaviour
Eliminate risk factors known to increase disease

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Primary

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Prevents onset of disease by reducing the chance of disease occurrence on the entire pop / high risk individuals
eg. smoking cessation programmes, vaccination (risk reduction by altering behavior or exposures that can lead to disease or enhancing resistance to effects of exposure)

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Secondary

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detecting early stages of the disease (preclinical stage) or individuals with high risk factors for developing disease, lead to early interventions that improve the lives of patients and are more cost-effective eg. Mass, multiphasic, targeted screening

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Tertiary

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slow down and prevent the progress of a disease by treatment or rehabilitation to reduce the impact of the disease on quality of life and disability

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Types of interventions

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Screening (2) - done on people who are pre-symptomatic (otherwise it is a diagnosis)
Risk factor reduction (0, 1, 2) - reduce the pop exposed to substance/lifestyle that is a risk factor
Genetic counseling (2) - detect early stages of the disease given that this is a risk factor

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Types of Screening (2)

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Mass screening screens everyone in the population
Multiphasic screening is a suite of different tests that are conducted at once during a screening exercise
Targeted screening where a selected group of high risk individuals are sent for testing

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When to conduct screening? (2)

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- when screening actually improves the quality of life for a patient with early diagnosis
- when early treatment is available for the disease and has proven to improve outcomes
- acceptable to patients in terms of invasiveness, degree of risk (eg. X-rays for lung cancer), cost
- feasible testing strategy
*need to identify high risk groups and sequentially

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Demographic transition theory

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DESCRIBES the changes in mortality with time.
Moves through 5 stages:
1. High BR & DR, fluctuating
2. Declining DR, BR is still high - pop increases overall
3. DR decreases further at a faster rate than decline in BR, overall pop is still increasing but slower
4. Population growth has reached a constant as BR and DR both fall to a low number.
5. Declining local population numbers as life expectancy increases but BR is lower than DR.

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Epidemiologic transition theory

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EXPLAINS the changes in patterns of mortality and mortality factors in countries as they develop. Says that as a country becomes more advanced and developed, mortality caused by communicable diseases is reduced and a corresponding increase in non-communicable, chronic diseases occurs.

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Reasons for decrease in communicable diseases

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- Greater sanitation, hygiene, sewage systems
- Better healthcare facilities
- Greater access to healthcare
- Better living conditions
- Increase in standard of nutrition
- Medical advancement and technology
- Better interventions: vector control programs and vaccinations

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Reasons for increase in chronic diseases

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- Greater affluence leading to unhealthy, rich diets
- Increase in sedentary lifestyles
- Increase in life expectancy, more likely to develop chronic diseases at a later age
- Increase in tobacco use, alcohol abuse

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Classic Epi Trans Model

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UK
slow transition
mainly due to improvements in sanitation, housing

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Accelerated Epi Trans Model

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Japan, Asian Tigers
fast transition
mainly due to better public health infrastructure, access

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Delayed/Contemporary Epi Trans Model

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LDCS: Africa, South America, China, India
still in process of transition, not yet
most impt: medical advancements eg. vaccinations

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Social Model of Health / Health Determinants

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General socioeconomic, cultural + env conditions >> Social & Community networks >> Individual lifestyle factors >> Age, Sex & Constitutional factors

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Purpose of Theories of Behaviour Change

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1. Contextualise and understand specific health behaviours
2. Identify push and pull factors that promote or hinder certain health behaviours
3. Create or design interventions that address or alter behaviour change

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Context of Health Behaviour

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Society > Community > Interpersonal > Intrapersonal and Individual

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Types of Models: Explanatory and change or Planning

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Explanatory/change models:
Individual - Health Belief Model, Stages of Change, Community - Diffusion of innovation
Interpersonal - Social Cognitive Model
Planning models: PRECEDE-PROCEED

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Health Belief Model
EXPLANATORY + INDVIDUAL

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Perceived susceptibility, severity, benefits, barriers, cues to action, self-efficacy

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Stages of Change Model
EXPLANATION + INDIVIDUAL

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Pre-contemplaton, Contemplation, Action, Maintenance, Relapse

5'A's: Ask, Advice, Assess, Assist, Arrange

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Social Cognitive Theory

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- Reciprocal Determinism (interrelated links between environment, personal factors and behaviour)
- Behavioural Capability - knowledge and skills to make a change
- Expectations - anticipated consequences
- Self-efficacy - confidence in one's ability
- Reinforcements - social persuasions
- Observational learning- role models

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Diffusion of Innovation

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Innovators > Early adopters > Early Majority > Late Majority > Laggards
phase of adoption: awareness, interest, trial, review, adoption/rejection

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PRECEDE-PROCEED Model

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PRECEDE stands for Predisposing, Reinforcing, and Enabling Constructs in Educational/Environmental Diagnosis and Evaluation [leading up to an intervention]
Phase 1: Identify desired outcomes in behavioural, environmental, epidemiological and social domains
Phase 2: Identify behaviour, lifestyle and environmental factors that influence the achievement of these desired outcomes, or conditions that have to be attained in order to achieve them
Phase 3: Identify the predisposing, reinforcing and enabling factors that are related to the behaviour, lifestyle and environmental factors from Phase 2
Phase 4: Identify the administrative and policy factors that influence what can be implemented (policies, resources, organization, service or programme components)

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PRECEDE-PROCEED Model

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PROCEED spells out Policy, Regulatory, and Organizational Constructs in Educational and Environmental Development [to design and implement an intervention]
Phases should move backward and correspond to the earlier phases on Outcome > Impact > Process
Phase 5: Implementation of the programme: design and conducting
Phase 6: Process evaluation of gaps, relationship between components of programme
Phase 7: Impact of the programme on changing the influencing factors of environmental, behavioural and personal factors
Phase 8: Outcome evaluation of whether the intended desirable outcomes are achieved

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Interventions (use the context of health behaviour to classify)

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Classified into institutional/community, interpersonal level and individual level
OR: environmental, social, institutional

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Risk Factors

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Classified into modifiable and non-modifiable

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What is a healthy environment?

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- Clean air – pollution
- Clean and sufficient water – pollution from chemical, physical, biological sources
- Safe and sufficient food
- Safe and peaceful settlements – work environment: stress, psychosocial, ergonomic/posture
- Stable global environment

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How is environmental health different from public health?

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Only deal with physical and natural environment, doesn’t modify social and cultural aspects of community and prevent disease by creating health-supportive environments

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Types of Hazards:

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1. Biological: parasites, bacteria, viruses, fungi
2. Chemical: toxic heavy metals, POPs, EDCs, pesticides, solvents
3. Physical: radiation, temperature/heat, noise
4. Ergonomic: awkward postures, repetitive motions, lifting
5. Psychosocial: stress, lifestyle disruption, discrimination, unemployment
6. Safety Hazards: motor accidents, sports/high risk activities, workplace safety

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Routes/pathways of exposure:

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1. Inhalation from the air
- Trapped/dislodged/direct effect on lungs
- Absorbed into bloodstream

2. Ingestion through food/drink
- Absorbed via intestines/digestive system
Eg. Mercury and Minamata disease – bioaccumulation from food chain
Eg. Consuming contaminated water and drink – waterborne diseases (diarrhea, gastroenteritis) or biological pollutants (salmonella, bacteria)

3. Dermal through contact with skin
- Absorbed through cuts, cracks in skin
- Can also burn and irritate skin
Eg. Agent Orange (herbicide/foliage remover used in Vietnam War) and chloroacne

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Major Environmental Contaminations

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a) Water Pollution: contamination of waterways, leaching/washing off of agricultural runoff, nutrient loading, water quality problems, direct dumping of pollutants from sources

b) Air Pollution: tranboundary air pollution (haze), indoor air pollution in LDCs – indoor cooking from stoves, incomplete combustion, indoor air pollution in DCs – secondhand smoke exposure, link to lung cancer

c) Food Pollution – intentional addition of toxic chemicals (eg. Melamine in milk powder for children) or non-intentional (eg. Food poisoning caused by Salmonella contaminated food products)

d) Soil/Land Pollution – leachates from landfill disposal, garbage-tainted soil, direct disposal of chemicals from factories or industry, overuse of herbicides and fertilisers (causing land degradation)

e) Plastic Pollution – microplastics in waste

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Hierarchy of Control

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Elimination > Substitution > Engineering Controls > Administrative Controls > Personal Protective Equipment

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What is occupational health?

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- Identify workplace hazards and potential dangers
- Prevent disease and injury
- Promote a healthy and productive workforce

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Occupational, Work-Related and General Diseases

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Occupational Disease: Your work DIRECTLY causes the disease
Work-related Disease: Work is A FACTOR that causes the disease (but is not the only one)
General Disease: Disease is caused by factors other than work, but work PLAYS A PART or IS AFECTED BY your disease

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How does your health affect your work?

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- Decrease in productivity (eg. Factory line)
- Danger to self (eg. Operating machinery)
- Danger to others in the community (eg driving bus)

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How does your work affect your health?

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- Accidents and injuries from workplace safety
- Obvious diseases that are clearly due to work (eg. Psychosomatic stress from work demands)
- Hidden diseases (eg. Sick building syndrome)
- Incurable diseases

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Risk

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Risk is a function of likelihood of a hazard occurring x severity of this hazard.

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Risk Assessment

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1. Identify the hazards to health
2. Assess how likely they are to occur and how severe they would be
3. Control by applying interventions (refer to hierarchy of control) to reduce the risk (severity and likelihood)
4. Evaluate whether the risk is in an acceptable range or whether activity should be carried out

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Evaluation of Risk

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Acceptable – carry on but monitor to ensure that risk does not change due to circumstances
Moderately acceptable – carry on only if the risk can be reduced to a minimum acceptable level “as is practicable” through controls
Not acceptable – do not carry out the activity unless you can reduce the risk to a more acceptable level

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How can we control risk?

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Substitution
Engineering Methods  Controlling at source
Environmental Monitoring  Reduce exposure
Biological Monitoring  Measure exposure
Personal Protection Equipment
Workers’ Training + Education

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What is public health surveillance?

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Continuous, systematic collection, analysis and interpretation of health-related data needed for planning, implementation and evaluation of public health

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Purpose of surveillance

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- Serve as early warning system for potential epidemics/future problems; monitor progress towards desirable outcomes
- Monitor and clarify epidemiology of health problems (Determinants and Distribution), in order to set decisions on priorities and strategies

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Medical surveillance

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Pre-employment medical examination
Pre-placement medical examination
Periodic examination
Fitness-to-return-to-work examination