Occupational Epidemiology for CIH: From Workplace Questions to Useful Evidence
A group of workers reports breathing problems. Is the number unusual? Are exposed workers affected more often? Could smoking, worker turnover or different diagnostic practices explain the pattern? Which controls should the hygienist recommend?
How to use this page
Epidemiology provides a structured way to answer these questions. This guide teaches the reasoning first, then the calculations.
BGC lists Biostatistics & Epidemiology as a CIH technical subject area: principles of epidemiology, techniques used to study the distribution of occupationally induced diseases and the factors that influence their frequency, prospective and retrospective studies, morbidity and mortality, animal experimental studies, the distribution of data, and basic biostatistics and statistical interpretation of data in the evaluation of hazards. The learning priorities below are an educational synthesis of that scope; they are not a guarantee of individual examination questions. This chapter covers occupational epidemiology and supporting statistics, while detailed exposure-distribution statistics belong in the companion Exposure Assessment chapter. BGC Subject Area Definitions.
- First pass: read each example and memory aid. Second pass: cover the calculations and work them yourself. All numerical workplace examples are invented for teaching.
- Original wording, not a copy of any course text, BGC material or standard. Source links are in the text and listed on the CIH References page.
Your learning route
Define the health question
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Count cases with the right denominator
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Choose the study design
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Calculate and explain the comparison
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Check uncertainty, bias and causal reasoning
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Use exposure evidence to guide prevention
| Learning stage | What you should be able to do |
|---|---|
| 1–2: Foundations | Define a case; distinguish prevalence, risk and person-time rate. |
| 3–5: Comparisons | Identify study designs; calculate RR, OR, risk difference, SMR and PMR. |
| 6–8: Interpretation | Explain bias, confounding, uncertainty and the evidence needed for causation. |
| 9–10: Application | Interpret screening tests and construct a useful occupational exposure history. |
| 11–12: Retrieval | Apply the concepts to short cases and recall the key formulas. |
How to use it: On your first pass, read each example and memory aid. On your second pass, cover the calculations and work them yourself. All numerical workplace examples below are invented for teaching.
01 Define What You Are Trying to Learn
People, exposure, outcome and time, plus the case definition and the terms to learn early.
Start with people, exposure, outcome and time
Epidemiology examines patterns of health outcomes in populations and factors associated with those patterns. A useful occupational question specifies:
| Part | Example |
|---|---|
| Population | Employees in two production departments. |
| Exposure | Tasks involving a suspected respiratory sensitizer. |
| Comparison | Workers with little or no exposure to that sensitizer. |
| Outcome | Newly diagnosed asthma meeting a consistent case definition. |
| Time | Two years of follow-up. |
“Are workers getting sick?” is a starting concern. “Is the two-year incidence of defined asthma higher among exposed workers?” is a question that guides a study.
A case definition states the criteria used to count an outcome consistently. It can include clinical findings, test results and relevant person/place/time boundaries. Apply comparable outcome criteria to both groups. When testing whether a particular exposure is associated with disease, avoid defining disease status by that very exposure in a way that predetermines the answer. CDC: case definitions.
Distinctions to learn early
| Term | Meaning | Example |
|---|---|---|
| Morbidity | Illness or impaired health. | Asthma diagnoses or hearing impairment. |
| Mortality | Death. | Deaths attributed to lung cancer. |
| Exposure | The factor being studied in relation to an outcome. It may be a harmful agent, a personal characteristic or a protective intervention. | Solvent exposure, vaccination or participation in a respirator program. |
| Risk | Probability of a defined outcome over a specified period. | A 5% two-year risk. |
| Descriptive epidemiology | Describes who is affected, where and when. | Symptoms cluster in one department after a process change. |
| Analytic epidemiology | Compares groups to investigate possible explanations. | Compare outcome occurrence by exposure category. |
Memory aid: Define the people, the exposure, the outcome and the clock before calculating.
02 Count Disease: New Cases, Existing Cases or Person-Time
Prevalence, risk and incidence rate answer different questions, with a worked person-time example.
Three denominators that answer different questions
| Measure | Calculation | Meaning |
|---|---|---|
| Point prevalence | Existing cases now ÷ population now | “What fraction currently has the condition?” |
| Incidence proportion / cumulative incidence / risk | New cases during follow-up ÷ initially disease-free people at risk | “What fraction developed it during this period?” |
| Incidence rate | New cases ÷ accumulated person-time at risk | “How rapidly did new cases occur?” |
Period prevalence includes people who had the condition at any time in a defined interval. Point and period prevalence need clearly defined populations and time boundaries. Prevalence is a proportion, although older sources often call it a “prevalence rate.” CDC: disease-frequency measures.
Example: prevalence. On one survey date, 30 of 300 workers have asthma. Prevalence = 30/300 = 10%. You cannot tell from that snapshot when their asthma began.
Example: risk. A separate group of 100 workers is free of the outcome at baseline. Four develop it during complete two-year follow-up. Risk = 4/100 = 4% over two years.
Why person-time matters
Workers do not always contribute equal follow-up. They may develop the outcome, die, leave observation or reach study end. For a first-event analysis, count their time only while they are observed and still at risk of that first event. Study entry is set by the protocol; it need not coincide with first exposure.
Suppose the same 100 workers are followed for up to two years:
| Workers | Time contributed per worker | Total |
|---|---|---|
| 96 remain disease-free through study end | 2 years | 192 person-years |
| 4 develop the outcome exactly one year after entry | 1 year | 4 person-years |
| Total | 196 person-years |
The 4% risk and 20.4 per 1,000 person-years rate are both valid here, but answer different questions. Do not label the rate as a percentage. More complex follow-up may require survival-analysis methods rather than a simple baseline denominator. CDC: person-time.
Why high prevalence does not necessarily mean high incidence
Prevalence depends on new cases and how long people remain cases. Longer survival or longer disease duration can increase prevalence even without an increase in new disease. In a stable population with an uncommon condition, prevalence ≈ incidence rate × average duration can be a useful approximation; it is not a universal formula.
Memory aid: Prevalence = present. Incidence = incoming cases. Rate = person-time.
03 Choose the Design by How Participants Enter the Study
Cohort, case-control and cross-sectional, plus the other labels worth recognizing.
The main designs at a glance
| Design / approach | Starts from | Direction | Can measure | Reports |
|---|---|---|---|---|
| Cohort (prospective or retrospective) | A defined population, grouped by exposure | Exposure → later disease; also when both are reconstructed from old records | New cases: risk, or cases per person-time | RR or IRR |
| Case-control | Disease status: cases and controls | Disease → earlier exposure | Exposure odds in each group | OR |
| Cross-sectional | A population at one moment | Snapshot: exposure and disease assessed together | Existing cases: prevalence | Prevalence, PR; a prevalence OR is not a prevalence ratio |
| Case report / case series | One patient or a small group | Describes history and course | Clinical findings and exposure clues | Description; no comparative risk |
| Meta-analysis (evidence synthesis) | Results from several studies | Study results → pooled estimate | Combined estimates from suitable studies | Pooled RR or OR with a confidence interval; it does not select workers |
Watch for: a cohort needs follow-up and enough events; case-control controls must represent the source population's exposure experience; a cross-sectional study cannot show which came first.
A rare exposure often suits a cohort; a rare disease often suits case-control. These are selection guides, not guarantees. A cohort has no automatic advantage in statistical power. CDC: analytic study design.
Retrospective cohort versus case-control
Both may use old records. The distinction is how the study population is assembled:
- A historical employee roster is classified by earlier job exposure, and later disease records are examined → retrospective cohort.
- Workers with a disease and sampled controls are selected, then prior jobs are compared → case-control.
In a conventional case-control study, controls are not chosen merely because they are unexposed. Selecting them that way would distort the exposure comparison. CDC: cohort and case-control investigation.
Other labels worth recognizing
| Term | What it adds | Caution |
|---|---|---|
| Ecological study | Compares groups, such as plants or regions, using aggregate data. | A group association does not establish the same association in individual workers: ecological fallacy. |
| Intervention study | Evaluates a deliberate change, such as improved ventilation. | A comparison group and repeated observations help distinguish intervention effects from other changes. |
| Randomized trial | Assigns an eligible intervention by chance. | Can reduce confounding on average; cannot ethically assign workers to known harmful exposure. |
| Nested case-control | Samples cases and controls within an established cohort. | Useful when detailed measurements are costly; interpretation follows the sampling design. |
| Mortality study | Uses death as the outcome. | This is an outcome focus, often within a cohort—not a mutually exclusive design category. |
Sources: NIOSH CIB 69, NIOSH Practices in Occupational Risk Assessment, CDC-hosted ecological-methods guide (violence research; the method applies generally), CDC design guidance.
Memory aid: Disease-selected → case-control. Defined workforce followed over time → cohort. One snapshot → cross-sectional.
04 Compare Groups: One Table, Several Questions
Risk ratio, risk difference, attributable fraction and odds ratio from one 2 x 2 table.
A two-year cohort example
All 400 workers are free of the outcome initially, and follow-up is complete.
| Develop outcome | Do not develop outcome | Total | |
|---|---|---|---|
| Exposed | a = 20 | b = 180 | 200 |
| Unexposed | c = 10 | d = 190 | 200 |
First calculate the two risks
The denominator includes all initially at-risk people in that exposure group, not only the cases.
| Question | Measure | Calculation | Interpretation |
|---|---|---|---|
| How many times the risk? | Risk ratio, RR | 10%/5% = 2 | Exposed risk is twice the comparison risk. |
| How much extra absolute risk? | Risk difference, RD (in some texts called attributable risk) | 10% − 5% = 5 percentage points | Five additional observed cases per 100 exposed workers over two years. |
| What fraction of exposed-group risk is the excess? | Attributable fraction among exposed, AFₑ | (10% − 5%)/10% = 50% | Under causal assumptions, half the exposed-group cases would be attributed to exposure. |
In some texts the risk difference is called attributable risk; this is not the attributable fraction AFₑ in the table above. RR below 1 means lower risk in the numerator group; the example below shows why. RR = 1 means no difference. Multiply AFₑ by 100 for a percentage. The term “attributable” requires a valid causal interpretation; an unadjusted association alone does not establish preventable cases. Five percentage points is an absolute difference; the relative increase from 5% to 10% is 100%. CDC: association measures, CDC: attributable proportion.
Why can an "exposed" group have lower risk?
The example above showed higher disease risk among exposed workers, but the factor being studied does not have to be harmful. In industrial hygiene, "exposure" often means dust, chemicals or noise. In epidemiology it means the factor whose relationship with an outcome we are investigating. That can be vaccination, training or a protective program. Put the group with the factor on top and the comparison group underneath, and always read the group labels.
Hypothetical example: vaccination and flu over one season. Both groups start free of flu and are completely followed over the same season.
| Group | New flu cases | People followed | Risk during the season |
|---|---|---|---|
| Vaccinated (the factor studied) | 50 | 10,000 | 0.5%, or 5 per 1,000 |
| Unvaccinated (comparison) | 200 | 10,000 | 2%, or 20 per 1,000 |
The vaccinated group had one-quarter of the comparison group's risk, which is 75% lower. This is an association in the protective direction; showing that vaccination caused the drop also requires considering study design, uncertainty, bias and confounding. The same arithmetic applies at work: 4 per 1,000 with a respirator program against 16 per 1,000 without it gives RR = 0.25. CDC: measures of association.
Memory aid: "Exposed" names the factor being compared, not "harmed". For a disease outcome, RR below 1 means lower risk in the numerator group.
Odds are different from probability
At 10% risk, odds are 0.10/0.90 = 1/9. In the cohort table:
RR = 2 and OR = 2.11 are close, but not identical. When outcomes are common, the difference can be substantial: risks of 60% and 30% give RR = 2, but OR = 3.5.
How to read an odds ratio
Memory aid:
- Odds = yes ÷ no.
- OR = one group's odds ÷ the comparison group's odds.
- OR tells us the association; the confidence interval tells us its precision.
In the cohort table above, the exposed odds are 20 ÷ 180 = 0.111 and the unexposed odds are 10 ÷ 190 = 0.053, so OR = 0.111 ÷ 0.053 = 2.11.
| Result | Interpretation, for the comparison defined |
|---|---|
| OR = 1 | Equal odds; no observed association. |
| OR > 1 | Higher odds in the numerator group. |
| OR < 1 | Lower odds in the numerator group. |
| 95% CI includes 1 | Not statistically significant at the usual two-sided 5% level. |
| 95% CI excludes 1 | Statistically significant at that level, under the analysis assumptions. |
An OR above 1 alone does not establish statistical significance or causation. Also, "not significant" does not prove there is no effect. Source: CDC: interpreting study results.
Why case-control studies usually use OR
Suppose a case-control study enrolls:
| Cases | Controls | |
|---|---|---|
| Previously exposed | 30 | 20 |
| Previously unexposed | 20 | 80 |
Step 1: odds = yes ÷ no. Here "yes" is previously exposed and "no" is previously unexposed, and we take the odds separately in each column.
Step 2: the odds of exposure in each group.
Step 3: OR = one group's odds ÷ the comparison group's odds.
Step 4: simplify. Dividing by a fraction is the same as multiplying by its flip, so the two fractions cross-multiply into one:
Both routes give the same answer: OR = 6. In the 2 × 2 table, this is the top-left cell times the bottom-right cell, divided by the top-right cell times the bottom-left cell.
Cases have six times the exposure odds of controls. The investigator chose how many cases and controls to enroll, so 30/(30+20) is not the population disease risk among exposed workers. For conventional cumulative case-control sampling, OR approximates RR when the outcome is uncommon in the source population. In risk-set sampling, OR estimates a rate ratio without requiring a rare disease; this is an optional advanced distinction. CDC published study illustrating risk-set sampling. CDC: OR interpretation, NIOSH CIB 69, NIOSH Practices in Occupational Risk Assessment.
Read labels, not just letters. Transposing the table preserves the same comparison. Reversing exposed and unexposed reference groups takes the reciprocal of the ratio.
Other ratios and population impact
- Incidence rate ratio: divide exposed cases/person-time by comparison cases/person-time. For example, 20/1,000 PY ÷ 10/1,000 PY = 2.
- Prevalence ratio: divide the two prevalence proportions in a cross-sectional study. Do not describe this as new-disease risk.
- Population attributable fraction: (population risk − unexposed risk) ÷ population risk, under appropriate causal/comparability assumptions. It differs from AFₑ because it considers the entire population, including how common exposure is. In the 400-worker example, population risk is 30/400 = 7.5%, giving (7.5 − 5) ÷ 7.5 = 33.3%.
Memory aid: Ratio asks “how many times?” Difference asks “how many extra?” Attributable fraction asks “what share?”
05 Compare Mortality Fairly: SMR, SIR and PMR
Observed against expected deaths or cases, and why PMR is not a risk.
SMR: observed deaths versus expected deaths
An older workforce naturally has more deaths than a younger one. Standardization accounts for differences such as age and calendar period before interpreting excess deaths.
For indirect standardization, apply reference death rates to the cohort's corresponding person-time strata and add the results:
| Teaching stratum | Cohort person-years | Reference deaths per 1,000 PY | Expected deaths |
|---|---|---|---|
| Younger workers | 2,000 | 1 | 2 |
| Older workers | 1,000 | 8 | 8 |
| Total | 10 |
If 15 deaths are observed:
This is 50% above expected, not a 150% increase. Real studies commonly use more detailed age, sex and calendar-period strata. The result depends on the reference rates and needs an uncertainty interval. NIOSH-hosted SMR methods study.
SIR—standardized incidence ratio—uses observed and expected incident cases, rather than deaths. Do not confuse this with an infection-specific metric that happens to use the same acronym. CDC: SIR and statistical investigation.
PMR: what share of deaths was from this cause?
Suppose 20 of 100 workforce deaths were due to a particular cause. In the reference population, that cause accounts for 10% of deaths:
The cause represents twice the share of deaths. This does not establish twice the mortality risk among living workers. If deaths from other causes fall, the share from this cause can rise without its own rate increasing. Adjusted PMRs require appropriate stratum-specific methods. CDC: proportionate mortality.
| Measure | What goes into the denominator? | Null value |
|---|---|---|
| Cause-specific mortality rate | Population-time at risk | Depends on comparison |
| SMR or SIR | Expected deaths or cases | 1, or 100 on index scale |
| PMR | Reference proportion of deaths from the cause | 1, or 100 on index scale |
Memory aid: SMR counts deaths against expectation; PMR compares shares of deaths.
Memory Aid: Which Measure Is the Question Asking For? Memory aid
Read the question for its key words first. The words usually name the measure before you calculate anything.
| Measure | What does it ask? | Words to recognize in a question | Example meaning |
|---|---|---|---|
| Risk ratio (RR) | Which group is more likely to develop the disease during the stated period, and by how much? | New cases; initially disease-free workers; risk over five years | RR = 2: twice the risk. |
| Odds | Within one group, how many "yes" for every "no"? | Cases compared with noncases; exposed compared with unexposed | 20 cases and 80 noncases: odds = 20/80 = 0.25, or 1:4. |
| Odds ratio (OR) | How do the "yes-to-no" odds compare between two groups? | Odds; cases and controls; previous exposure | OR = 3: three times the odds, not necessarily three times the risk. |
| Prevalence ratio (PR) | Which group has a larger percentage of workers with the disease today? | Currently; existing cases; survey; snapshot | PR = 2: the percentage currently affected is twice as high. |
| Incidence rate ratio (IRR) | Which group develops new cases faster, allowing for time followed? | New cases per person-year; person-time | IRR = 2: twice the new-case rate per person-time. |
| Standardized mortality ratio (SMR) | Did more workers die than expected? | Observed deaths; expected deaths; reference death rates | SMR = 1.5, or 150: 50% more deaths than expected. |
| Standardized incidence ratio (SIR) | Were there more new disease cases than expected? | Observed new cases; expected new cases | SIR = 2: twice the expected number of new cases. |
| Proportionate mortality ratio (PMR) | Does this cause account for a bigger share of deaths than in the comparison population? | Deaths from one cause as a share of all deaths | PMR = 2: twice the share of deaths, not necessarily twice the risk of dying. |
For the other measures, the questions are just as direct:
| Measure | What does it ask? |
|---|---|
| Risk difference (RD) | How many extra cases per 100 workers over the same period? |
| Attributable fraction among exposed (AFₑ) | What percentage of the exposed group's risk is above the comparison group's risk? |
| Population attributable fraction (PAF) | What percentage of the whole population's risk is above the baseline expected without the exposure? |
| Case fatality proportion (often called "case fatality rate") | Of the people who developed this disease, what percentage died from it? |
Calling excess cases "caused by the exposure," or "preventable by removing it," requires causal evidence.
The shortest memory aid, one cue per measure:
- RR: developing it. How much more likely?
- OR: yes versus no. How much higher are the odds?
- PR: having it today. Which group has more?
- IRR: new cases per person-time. Which group develops them faster?
- SMR: deaths. More than expected?
- SIR: new cases. More than expected?
- PMR: this cause. What share of all deaths?
06 Ask Whether the Comparison Is Distorted
Selection and information bias, confounding, random error and the healthy-worker effect.
| Problem | What happens | Workplace example | How to reduce it |
|---|---|---|---|
| Selection bias | Who enters or remains changes the exposure–outcome comparison. | Symptomatic workers leave the exposed department before a survey. | Study former workers where possible; examine participation and follow-up. |
| Information bias | Exposure or outcome is measured systematically incorrectly. | Cases receive a more detailed job-history interview than controls. | Apply consistent methods; blind assessors when feasible; validate records. |
| Confounding | Another factor mixes with the exposure association. | Exposed workers smoke more, and smoking affects the disease outcome. | Use subject knowledge, suitable design and adjusted/stratified analysis. |
| Random error | Estimates fluctuate because data are limited. | Five cases yield an unstable estimate. | Evaluate precision, study size and confidence intervals. |
Recall bias and interviewer bias are information-bias mechanisms. Detection/surveillance bias can occur if one group is examined much more intensively. Larger samples improve precision but do not automatically fix systematic error. CDC: interpreting study results.
The healthy-worker effect, explained simply
People healthy enough to obtain employment can have lower mortality than the general population, which includes people unable to work. Separately, healthier people may remain in demanding jobs while ill workers leave or transfer. These are commonly taught as occupational selection effects:
- Healthy hire effect: who starts work.
- Healthy-worker survivor effect: who remains exposed over time.
Therefore, low overall mortality does not prove that a workplace is harmless. Internal worker comparisons can help, but do not automatically remove survivor bias. Detailed analysis can involve both selection and time-varying confounding. Healthy-worker survivor methods paper.
Confounding versus effect modification
| Pattern | Meaning | Action |
|---|---|---|
| An apparent exposure effect changes after accounting for smoking differences. | Smoking may have confounded the original comparison. | Report an appropriately adjusted estimate, if assumptions support it. |
| The exposure association differs between smokers and nonsmokers. | Possible effect modification on the chosen risk or rate scale. | Report the subgroup results; the difference may matter for prevention. |
A classical confounder relates to exposure and outcome and is not an intermediate step in the causal pathway being studied. For example, adjusting for a biological effect caused by the exposure can remove part of the very effect you intend to estimate. Matching needs appropriate analysis; it does not automatically eliminate confounding.
Exposure misclassification: assigning a worker to the wrong category can conceal or distort an association. Under common simple assumptions, nondifferential binary misclassification tends to dilute an effect, but “misclassification always biases toward the null” is false.
Memory aid: Selection = who is included; information = what is measured; confounding = another explanation mixed in.
07 Read the Uncertainty Before Accepting the Headline
Confidence intervals, Type I and II error, power, p-values, SD versus SE.
Effect size and precision answer different questions
| Result | What it tells you |
|---|---|
| RR = 2.0; 95% CI 1.4–2.8 | Higher risk estimate; interval excludes 1 under the model used. |
| RR = 2.0; 95% CI 0.6–6.7 | Same point estimate, much less precision; compatible with both lower and substantially higher risk. |
| RD = 0.05; 95% CI −0.01 to 0.11 | Difference interval includes 0; the study has not clearly distinguished the difference from the null. |
The null is 1 for ratios (above 1 is higher, below 1 is lower) and 0 for differences. “Not statistically significant” does not demonstrate absence of an effect, especially when the interval is wide. A 95% CI is generated by a method that covers the true parameter in 95% of repeated samples under its assumptions; it is not the range containing 95% of workers. CDC: confidence intervals.
Type I error, Type II error and power
| Concept | Meaning | Memory aid |
|---|---|---|
| Null hypothesis | Usually no difference or association in the specified comparison. | Baseline statistical claim. |
| Type I error; α | Rejecting a true null. | False alarm. |
| Type II error; β | Failing to reject a false null for a specified alternative. | Missed effect. |
| Power = 1 − β | Probability of detecting the specified effect with the planned method. | Ability to detect. |
| p-value | Probability, under the null and model assumptions, of data at least as incompatible with the null as those observed. | Not the probability the null is true. |
Power depends on effect size, sample size/events, variability and the chosen significance level. Repeatedly testing many outcomes can generate chance positives. Statistical significance cannot correct poor exposure assessment or establish practical importance. CDC: statistical considerations.
SD versus SE: a short bridge to biostatistics
Standard deviation (SD) describes spread among observations. Standard error (SE) describes uncertainty in an estimate. For an ordinary sample mean of independent observations:
If SD = 10 and n = 100, SE = 1. That does not mean individual values vary by only 1. Repeated measurements on the same worker are not automatically 100 independent workers. Confidence intervals require an appropriate method; do not apply mean formulas to RR or OR without the correct transformation/model. NIST: confidence limits for a mean.
08 Decide How Strongly the Evidence Supports Causation
Temporality, the Bradford Hill viewpoints, latency and lagging.
Exposure must precede the outcome. This is temporality. A diagnosis today may reflect exposure years earlier, so a clean air sample today does not reconstruct the relevant history.
The Bradford Hill viewpoints help organize evidence:
| Viewpoint | Useful question |
|---|---|
| Temporality | Did relevant exposure occur before disease developed? |
| Strength | How large is the association, and how uncertain is it? |
| Consistency | Do other populations and methods show compatible findings? |
| Biological gradient | Does disease occurrence change with exposure level? |
| Plausibility | Is there a credible biological explanation? |
| Coherence | Does the interpretation fit other clinical, toxicological and population evidence? |
| Experiment | Does reducing exposure produce evidence consistent with benefit? |
| Specificity | Is a particular exposure–outcome link distinctive? Limited specificity does not rule out causation. |
| Analogy | Do similar agents or mechanisms provide supporting context? |
These are viewpoints, not a scorecard that must reach nine checks. A weak or absent exposure gradient can reflect latency, thresholds or exposure error; strong associations can still be biased. Hill AB, The environment and disease: association or causation? Proc R Soc Med, 1965.
Latency is the delay between relevant exposure and detectable disease, as operationally defined in a study. Exposure lagging excludes recent exposure from a cumulative metric when it is assumed too recent to affect the outcome; select and justify the lag rather than searching only for a significant result.
09 Understand Screening and Surveillance
Sensitivity, specificity, PPV and NPV, and lead-time bias.
Screening looks for possible disease in people who may not yet have recognized symptoms. A positive screen often requires further assessment. Surveillance repeatedly collects, interprets and communicates health information to guide action. A screening programme can supply surveillance data; collecting results without interpreting or acting on them is incomplete. CDC: surveillance functions.
Four results, four useful measures
| Condition present by reference assessment | Condition absent | |
|---|---|---|
| Test positive | True positive: TP | False positive: FP |
| Test negative | False negative: FN | True negative: TN |
| Measure | Formula | Question answered |
|---|---|---|
| Sensitivity | TP/(TP+FN) | Of people with the condition, how many test positive? |
| Specificity | TN/(TN+FP) | Of people without it, how many test negative? |
| Positive predictive value, PPV | TP/(TP+FP) | Of positive tests, how many truly have it? |
| Negative predictive value, NPV | TN/(TN+FN) | Of negative tests, how many truly lack it? |
Example: Of 1,000 workers, 100 have the condition. A test detects 90 of them and incorrectly flags 90 of the other 900. Sensitivity = 90%; specificity = 90%; PPV = 90/180 = 50%; NPV = 810/820 = 98.8%.
Why can a positive test be wrong when the test catches every case?
A test answers two different questions. Sensitivity: if someone has the disease, will the test catch it? PPV: if someone tests positive, do they actually have the disease? The two start with different groups.
Suppose a disease affects 1 in 1,000 people. A test catches every true case (sensitivity 100%) but also gives a positive result to 1% of people without the disease (specificity 99%). Test 100,000 people:
| Step | Calculation | Result |
|---|---|---|
| People who have the disease | 100,000 ÷ 1,000 | 100 people |
| True positives (100% sensitivity) | 100 × 100% | 100 |
| People without the disease | 100,000 − 100 | 99,900 people |
| False positives (1% false-positive rate) | 99,900 × 1% | 999 |
| Everyone who tested positive | 100 + 999 | 1,099 positive results |
The test misses no cases, but only about 9 of every 100 positive results are true. The healthy group is so large that its small false-positive percentage produces almost ten false alarms for every true case. Do not mix up the two percentages: 1% false-positive rate means 1% of people without the disease test positive; about 91% of positive results are false means false positives make up about 91% of everyone who tests positive.
When sensitivity and specificity stay the same, a rarer disease gives a lower PPV, which is why a positive screening result may need confirmatory testing. CDC: predictive value and prevalence.
Memory aid: Sensitivity asks, "Did we catch the cases?" PPV asks, "Can we trust this positive?"
Lower prevalence also raises NPV. In practice, test performance can also change with the population and threshold. Sensitivity/specificity are not automatically the same as analytic detection limits. CDC: surveillance-test calculation table, CDC: predictive value and prevalence.
Memory aid: Sensitivity starts with diseased people; specificity starts with disease-free people; predictive value starts with a test result.
When evaluating a screening programme, also recognize lead-time bias: earlier diagnosis can lengthen measured survival from diagnosis without postponing death. A programme should demonstrate meaningful health benefit, not just more diagnoses. NCI: interpreting screening statistics.
10 Connect the Health Findings to the Right Exposure
Exposure metrics, SEGs, job-exposure matrices and what the hygienist does at each stage.
Choose a metric that fits the mechanism
| Metric | What it represents | Limitation |
|---|---|---|
| Ever/never exposed | Any qualifying exposure history. | Hides intensity and duration. |
| Duration | Time in exposed work. | Long time does not guarantee high dose. |
| Average intensity | Typical concentration during the defined exposure period. | Can hide brief peaks. |
| Cumulative exposure | Sum of intensity × duration across periods. | Equal cumulative values can represent different exposure patterns. |
| Peak exposure | Short high-level exposure. | Historical peaks may be poorly documented. |
| Lagged cumulative exposure | Cumulative metric excluding a prespecified recent period. | Depends on biological and analytic assumptions. |
Example: 2 mg/m³ for 3 working-years plus 0.5 mg/m³ for 4 working-years gives 8 mg/m³-years on this defined exposure scale. It is an exposure index, not a measured absorbed dose. State the work schedule and concentration assumptions.
SEG: a similar exposure group shares relevant task, agent and control patterns. JEM: a job-exposure matrix assigns exposure estimates to jobs, often by period or industry. A shared title does not establish identical exposure; workers may perform different tasks. NCI: exposure assessment methods.
The IH's work through the study
| Stage | Practical work | Why it matters |
|---|---|---|
| Frame the question | Agree on agent, route, outcome, time window and comparison. Review earlier evidence and possible confounders. | Aligns the exposure assessment with the disease mechanism. |
| Check feasibility | Inspect employment/medical-linkage records, monitoring data and process histories. Plan staffing, equipment, laboratory support, budget and schedule. | Shows whether the question can be answered. |
| Write the protocol | Define metrics, group rules, sampling, confidentiality, quality checks and decision rules. | Reduces inconsistent decisions after outcomes are known. |
| Build histories | Combine measurements, job changes, ventilation records, material substitutions, production information and interviews. | Reconstructs exposure during the relevant period. |
| Evaluate uncertainty | Separate measured from inferred data; validate estimates; assess alternative classifications and missing information. | Reveals how assumptions might change conclusions. |
| Report and act | Explain limits and prevention implications; document revisions and data provenance; communicate appropriately. | Supports reproducibility and protection of workers. |
Medical information needs authorized handling and confidentiality. Employer reports should communicate prevention findings without unnecessary disclosure of identifiable health information. Regulatory medical-surveillance triggers vary by agent and jurisdiction; a rule such as “30 exposure days” is not a general epidemiologic study requirement.
Exposure reconstruction should preserve historical process changes and the basis for each estimate. Document how uncertain estimates were assigned so future reviewers can understand the reasoning.
11 Apply the Ideas to Three Short Workplace Cases
A process change, a long-latency cancer and a ventilation improvement, then six check questions.
Case A: symptoms after a process change
A factory receives 12 respiratory complaints after introducing a material. First define the symptoms/outcomes, dates, population and tasks; investigate the agent and controls. Counts alone lack a denominator. If a complete workforce is identifiable, compare new outcomes across exposure groups. Check whether increased awareness or medical testing contributed to the apparent rise. Exposure control can proceed while the investigation continues.
Case B: long-latency cancer
A small number of workers has an unusual cancer. A case series can alert investigators, but cannot quantify comparative risk. A case-control study may efficiently compare work histories; a historical cohort may be feasible if rosters and follow-up records are strong. A present-day sample alone cannot represent exposure decades earlier.
Case C: improved ventilation
Complaints decline after local exhaust ventilation is installed. This supports further evaluation, but production volume, workforce composition or reporting may also have changed. Check exposure reduction, use comparable outcome definitions, examine repeated observations and consider a suitable comparison department. A single before/after count does not isolate the intervention effect.
Check yourself
- Forty existing cases among 400 workers on one date: which measure and value?
- Four first cases in 196 person-years: what incidence rate per 1,000 PY?
- Exposure risks of 10% and 5%: what RR, RD and AFₑ?
- Fifteen observed deaths and ten expected: what SMR and excess percentage?
- RR 2.0 with 95% CI 0.6–6.7: does this establish no effect?
- Ninety true positives and ninety false positives: what PPV?
Answers: 1. Point prevalence, 10%. 2. 20.4/1,000 PY. 3. RR 2; RD 5 percentage points; AFₑ 50% under causal assumptions. 4. SMR 1.5 or 150; 50% above expected. 5. No: the estimate is imprecise and compatible with a range of effects. 6. 50%.
12 Final Review Card
One line per cue, and where this chapter ends.
| Exam cue | Recall |
|---|---|
| Current disease burden | Prevalence. |
| New cases / initially at-risk people | Risk over the stated period. |
| New cases / person-time | Incidence rate. |
| Select cases and controls, compare earlier exposure | Case-control; usually OR. |
| Defined population followed for outcomes | Cohort, including retrospective cohort. |
| Snapshot | Cross-sectional; check temporality and worker turnover. |
| Aggregate group data | Ecological study; avoid individual inference. |
| RR | Exposed risk / comparison risk. Null = 1. RR < 1 = lower risk (0.5 = half the risk); RR = 1 = no difference. |
| OR | ad/bc with clearly labeled cells. Null = 1. |
| Risk difference (attributable risk) | Exposed risk − comparison risk. Null = 0. |
| AFₑ | (RR−1)/RR; causal assumptions required. |
| SMR / SIR | Observed / expected. Check ratio versus ×100 convention. |
| PMR | Relative proportion of deaths; not risk among living workers. |
| Healthy worker | Healthy hire and survivor processes can distort comparisons. |
| Confounding | Another factor distorts the association. |
| Effect modification | Association differs across strata on the chosen scale. |
| Small p-value | Does not prove causation or freedom from bias. |
| Wide CI | Low precision; null inclusion does not prove no effect. |
| Type I / Type II | False alarm / missed effect. Power = 1−β. |
| SD / SE | Spread of observations / uncertainty in an estimate. |
| Sensitivity / specificity | Start with condition status. |
| PPV / NPV | Start with test result. |
| Causal requirement | Relevant exposure precedes the outcome. |
| IH contribution | Reconstruct meaningful exposure and explain uncertainty. |
Where this chapter ends
For the wider CIH biostatistics area, study arithmetic/geometric means, normal and lognormal distributions, variance and GSD, percentiles, sampling strategies, confidence versus tolerance limits, and selection of statistical tests in a separate chapter. This guide provides the epidemiologic reasoning that makes those tools useful; it does not claim to cover every item in the combined rubric.
Occupational Epidemiology — Frequently asked questions
What is the difference between prevalence and incidence?
Prevalence is the fraction of a population that has a condition at a point in time (existing cases). Incidence counts new cases: risk divides new cases by the people initially at risk, and the incidence rate divides new cases by the person-time at risk.
When do I use a case-control study instead of a cohort study?
A case-control study selects people with the disease and suitable controls and compares their earlier exposure, which often suits an uncommon disease or a long latency. A cohort study follows a defined group, which often suits an uncommon exposure. These are selection guides, not rules.
Why does a case-control study report an odds ratio?
Investigators choose how many cases and controls to enroll, so the study cannot give the disease risk in exposed workers. The odds ratio can still be estimated, and it approximates the risk ratio when the disease is uncommon in the source population.
What does an SMR of 150 mean?
Observed deaths were 1.5 times the expected number, which is 50% above expected, not a 150% increase. The expected number comes from reference death rates applied to the cohort's person-time, and the result needs a confidence interval.
Does a non-significant result prove an exposure has no effect?
No. A wide confidence interval that includes the null means the study was imprecise and is compatible with both small and large effects. Statistical significance also cannot correct poor exposure assessment or establish causation.