Social Epidemiologic Aims

Descriptive
Existence of social differences in health

Etiologic
Causes of social differences in health

Interventions
Policies and programs to address causes

Enough already?

Nevertheless, health inequalities are socially produced, and therefore, also potentially avoidable. However, effective political interventions require a scientific understanding of the causal mechanisms generating the strong and persistent correlations between social conditions and health outcomes.

How can we find out?

Eikemo and Øversveen (2019)

Decomposition: from description to explanation

What changed?
Explaining growing or shrinking gaps

Which ‘components’?
Bridge between descriptive and causal

What if?
Techniques often involve ‘counterfactual’ scenarios

Danish smoking has declined from 21% (2010) to 11% (2025)

Source: Den Nationale Sundhedsprofil 2010 (Tabel 4.1.1) and 2025 (Tabel 3.1.3), Statens Institut for Folkesundhed / Sundhedsstyrelsen.

Covered Today

1. Kitagawa’s Decomposition

If standardization alters a difference between two rates, it should be possible … to break it up into components attributable to the various factors for which the data were standardized.


‘Unpacking’ the difference between crude rates of two groups

Seminal paper by Kitagawa (1955)

Potential consequences of ignoring composition

may give a distorted view of the overall level of health inequality due to social class differentials as it does not take into account the changing distribution of social class within the whole population.

changes in the distribution of social class across the population are an important contributor to recent reductions in mortality

Heller, McElduff, and Edwards (2002)

Group rate: \(R_{i} = y_{i}/n_{i}\)

Group share: \(P_{i} = n_{i}/\sum_{i} n_{i}\)


Crude rate: \(\frac{\sum_{i=1}^{I} y_{i}}{\sum_{i=1}^{I} n_{i}} = \sum_{i=1}^{I} P_{i}R_{i}\)


Standardized rate: \(\frac{\sum_{i=1}^{I} y_{i}}{\sum_{i=1}^{I} s_{i}} = \sum_{i=1}^{I} S_{i}R_{i}\)


where \(S_{i}\) is the share of group i in a standard population (\(\sum_{i} S_{i} = 1\))

Data for crude rates

Stratum Pop Count Rate
\(1\) \(n_{i}\) \(y_{i}\) \(r_{i}\)
\(\vdots\) \(\vdots\) \(\vdots\) \(\vdots\)
\(I\) \(N\) \(Y\) \(R\)

Group A Group B
Age Share Rate Share Rate
Young 30% 10 50% 20
Old 70% 40 50% 30
Crude 31 25
Standardized to A 31 27


Standardization question:

What would the \(A-B\) difference be if \(B\) had \(A\)’s age distribution?

Kitagawa’s key insight

…if the difference between two standardized rates is subtracted from the corresponding difference in crude rates…the result is a weighted average of differences between the composition of the two groups.

But what are the weights?

Crude difference = \(\sum P_{Ai}R_{Ai} - \sum P_{Bi}R_{Bi}\)

→ Reflects differences in both rates and composition


\(A\)-Standardized difference = \(\sum P_{Ai}R_{Ai} - \sum P_{Ai}R_{Bi}\)

→ Reflects only differences in rates (\(P_{Ai}\) is constant)


Crude - Standardized = \(\sum R_{Bi}(P_{Ai}-P_{Bi})\)

→ Differences in composition, weighted by \(B\)s rates!

Applying the decomposition

\[\begin{aligned} \underbrace{\text{Rate}_A - \text{Rate}_B}_{\text{crude difference}} &= \overbrace{\sum_i \left(\frac{R_{Ai}+R_{Bi}}{2}\right)(P_{Ai}-P_{Bi})}^{\text{composition effect}} \\ &+ \underbrace{\sum_i \left(\frac{P_{Ai}+P_{Bi}}{2}\right)(R_{Ai}-R_{Bi})}_{\text{rate effect}} \end{aligned}\]

\(R_{Ai}\) is the rate for group A in stratum i.
\(P_{Ai}\) is the i-stratum-specific weight in group A.

Group A Group B
Age Share Rate Share Rate
Young 30% 10 50% 20
Old 70% 40 50% 30


Composition effect
Group \(\frac{R_{Ai}+R_{Bi}}{2}\) \(P_{Ai}-P_{Bi}\) Contribution
Young 15 −0.20 −3.0
Old 35 +0.20 +7.0
Sum +4.0
Rate effect
Group \(\frac{P_{Ai}+P_{Bi}}{2}\) \(R_{Ai}-R_{Bi}\) Contribution
Young 0.40 −10 −4.0
Old 0.60 +10 +6.0
Sum +2.0


Total = +6.0 = crude gap (31 − 25) →67% due to composition

Rate effect (+2) = standardized gap (avg reference) (28 − 26)

Kitagawa: does the reference group matter?

Reference Composition Rate Total
A's rates 6.0 0.0 6.0
B's rates 2.0 4.0 6.0
Average (Kitagawa) 4.0 2.0 6.0

Crude gap = 31 − 25 = 6 in every row; only the split changes

Single references differ an interaction, \(\sum_i (P_{Ai}-P_{Bi})(R_{Ai}-R_{Bi})\) = 4.0, which the average splits evenly

What accounts for differences in neonatal mortality rates across European countries?


GA-specific rates or distribution?


Implications for interventions?

Sartorius et al. (2024)

Hiding in plain sight?

Both DK and AT similar and ~0.3 deaths per 1000 higher than “Top 3”

But completely different contributions to the difference

Sartorius et al. (2024)

Denmark has much worse rates at early GA

Sartorius et al. (2024)

Austria more births at earlier GA

Sartorius et al. (2024)

Implications for interventions

DK: improving care at early GA

AT: shifting the distribution of GA later

Summary: Kitagawa’s decomposition

When to use
Comparing rates across groups or over time when their composition differs

Extensions
More than two groups or factors; three-part decomposition

Caveats
Not causal; results depend on the strata used and on the reference weights

Kitagawa (1955); Das Gupta (1993)

Covered Today

2. Oaxaca–Blinder Decomposition

Oaxaca-Blinder: Basic Idea

What explains average differences in outcomes? In a regression context:


1. Means

Differences in the prevalence of determinants of outcome


2. Coefficients

Differences in the coefficient of a given determinant on the outcome (i.e., effect measure modification)

Our findings show that unexplained factors associated to immigrant status determine to a great extent disparities in the probability of using hospital, specialist and emergency services of immigrants relative to Spaniards, while individual characteristics, in particular self-reported health and chronic conditions, are much more important in explaining the differences in the probability of using general practitioner services between immigrants and Spaniards

Jiménez-Rubio and Hernández-Quevedo (2010)

Origins

Studies by R. Oaxaca (1973) and Blinder (1973) applied regression-based decomposition methods to analyze the wage gap between men and women and between whites and blacks in the USA.


Focused on how much of wage gap was ‘explained’ by differences in observable characteristics


Recent attempts to reconcile O-B with Kitagawa (equivalent for binary outcome and categorical covariates)

R. L. Oaxaca and Sierminska (2025)

Brief note on interpretation


Decomposition methods are based on regression analyses, and thus all of the usual caveats about good specification apply.


If regressions are purely descriptive, they reveal the associations that characterize the health inequality. Then inequality is explained in a statistical sense but implications for policies to reduce inequality are limited.

O’Donnell et al. (2008)

Why does this work?


OLS regression line always passes through \((\bar{x}, \bar{y})\) because residuals sum to zero.

Why does this work?


The gap decomposes into endowments (different \(\bar{x}\), same coefficients) and coefficients (same \(\bar{x}\), different slopes/intercepts).

Equally valid to use the exposed group’s slope


Same total gap, but different split

See R. Oaxaca (1973), Blinder (1973) and Cotton (1988) for details.

Example: Educational Differences in BMI in Italy



What is the average difference in body mass index (BMI) between those with low vs. high education?


How much is due to differing determinants of BMI (age, gender, smoking, drinking, income)?


Any residual difference is due to education differences in the associations between those risk factors and BMI — i.e., the coefficients differ.

Example data

European Social Survey Round 11, Italy (n = 1743)

Body mass index as outcome (kg/m²): weight / height²

Overall difference by education: High ed (ISCED 5–7) vs Low ed (ISCED 1–4)

Potential determinants (the \(X\)s):

  • age (years)
  • gender (female = 1)
  • smoking (1 = current smoker)
  • binge drinking (1 = monthly or more)
  • married (1 = currently married)
  • income decile (1–10)

High ed BMI: 23.6, Low ed BMI: 25.2, Gap = 1.6

Source: Author’s calculations

Differences in determinants

Differences in age, smoking, etc. could explain part of the BMI gap

Source: Author’s calculations

Differences in coefficients

Differences in returns (i.e., coefficients) form the ‘unexplained’ component

Decomposition results: variable contributions

Overall gap = 1.61 kg/m². Endowments: 38%; Coefficients: 62%

Endowments Coefficients
Est SE Est SE
Total 0.608 0.108 1.030 0.259
   Age (years) 0.415 0.074 0.865 0.691
   Female 0.080 0.051 0.466 0.181
   Current smoker 0.004 0.008 -0.145 0.115
   Binge drinking (monthly+) 0.001 0.007 0.003 0.104
   Married 0.012 0.016 -0.037 0.208
   Income (decile) 0.095 0.071 0.133 0.425
   Intercept -0.256 0.837

Note: Low ed betas used as reference

Summary: Endowments = 38%, Coefficients = 62%

Endowments
Est SE
Total 0.608 0.108
Age (years) 0.415 0.074
Female 0.080 0.051
Current smoker 0.004 0.008
Binge drinking (monthly+) 0.001 0.007
Married 0.012 0.016
Income (decile) 0.095 0.071

If the low-educated had the same covariate means as the high-educated (keeping the low-educated group’s own coefficients), their BMI would be 0.608 \(kg/m^2\) lower (38% of the gap).


Most of this is due to older age among the low-educated, which predicts higher BMI.

Summary: Endowments = 38%, Coefficients = 62%

If the high-educated group’s covariates had the same relationship with BMI as they do in the low-educated group, their BMI would be 1.030 higher, accounting for 62% of the gap.


Smoking is negative, since smoking predicts higher BMI among the high-educated and is more common among high educated.

Coefficients
Est SE
Total 1.030 0.259
Age (years) 0.865 0.691
Female 0.466 0.181
Current smoker -0.145 0.115
Binge drinking (monthly+) 0.003 0.104
Married -0.037 0.208
Income (decile) 0.133 0.425
Intercept -0.256 0.837

Which covariates drive the endowments?

  • Variables where groups differ and that predict BMI contribute most

  • Income and age are the biggest drivers

Decomposition results: does the reference group matter?

Endowments account for 36–44% of it; interaction is negligible

Summary: Oaxaca–Blinder decomposition

When to use
Explaining average gaps with potential determinants

Extensions
Nonlinear outcomes (binary, counts); pooled reference coefficients

Caveats
Not causal; specification errors; reference matters for categorical covariates

R. Oaxaca (1973); Blinder (1973); Cotton (1988)

Covered Today

3. Concentration Index Decomposition

Relative Concentration Curve


Explicitly accounts for changing composition

We want to understand this:

By evaluating something like this:

Research Question:

How much of inequality is due to other factors that are differential by \(x\) (income) and also affect \(y\) (health)?

Relative Concentration Index

\[RCI= \frac{2}{n\mu} \sum_{i=1}^{n}y_{i}R_{i}-1\]

where

  • \(\mu\) is the mean of \(y_{i}\) (e.g., smoking);
  • \(R_{i}\) is the fractional rank of the ith person in the socioeconomic (i.e., income) distribution.

Decomposition:

Develop a model for predicting \(y\) using several determinants, then plug back into the \(RCI\) equation

Estimates how much of the overall inequality in \(y\) is due to the association between income and other factors that predict health

Kakwani, Wagstaff, and Doorslaer (1997)

RCI Decomposition


\(RCI\) is a function of health \((y_{i})\) and socioeconomic rank \((R_{i})\), i.e. \[RCI= \frac{2}{n\mu} \sum_{i=1}^{n}{\color{red}{y_{i}}}R_{i}-1\]

Then write a regression expressing health \((y_{i})\) as a function of several \(k_{i}\) determinants (e.g., age, gender, urban/rural status): \[\color{red}{y_{i}}=\alpha + \sum{\beta_{x}x_{k_{i}}}+\epsilon_{i}\]

Wagstaff, Doorslaer, and Watanabe (2003)

RCI Decomposition

Now re-express \(RCI\) as:

\[RCI=\sum{(\beta_{k}\bar{x}_{k}/\mu)RCI_{k}}+gRCI_{e}/\mu\]

Where

  • \(\mu\) is the mean of \(y\),
  • \(\bar{x}_{k}\) is the mean of determinant \(x_{k}\),
  • \(\beta_{k}\) is the regression coefficient for \(x_{k}\), and
  • \(RCI_{k}\) is the relative concentration index for \(x_{k}\).

Two types of ‘explained’ components

Determinant impact depends on:

  1. the strength of the relationship between each factor and income \(\color{blue}{RCI_{k}}\)

  2. the strength of the relationship between each factor and health, and its prevalence in the population (elasticity) \(\color{red}{\beta_{k}\bar{x}_{k}/\mu}\)

Procedure for decomposing the Concentration Index


  1. Regress \(y\) (‘health’) on its determinants \((\beta_{k}x_{k})\):

\[y_{i}=\alpha + \sum{\beta_{x}x_{k_{i}}}+\epsilon_{i}\]

  1. Calculate means of \(y\) \((\mu)\) and all \(x_{k}\) determinants

  2. Calculate (\(RCI\)) for health and for each determinant \((RCI_{k})\), i.e., use each \(x_{k}\) as the “outcome” and estimate a \(RCI\) for age, education, etc.

Procedure for decomposing the Concentration Index


  1. Absolute contribution: for each \(x\) multiply ‘elasticity’ by its concentration index \((RCI_{k})\):

\[(\beta_{k}\bar{x}_{k}/\mu)RCI_{k}\]

  1. Calculate the % contribution of each determinant:

\[[(\beta_{k}\bar{x}_{k}/\mu)RCI_{k}]/RCI\]

Example: Decomposing Socioeconomic Inequality in Current Smoking

Data: European Social Survey Round 11 for Sweden

Unique Missing Pct. Mean SD Min Median Max Histogram
Current smoker 2 0 0.1 0.2 0.0 0.0 1.0
Income decile 10 0 6.6 2.6 1.0 7.0 10.0
Age (years) 76 0 54.4 18.6 15.0 56.0 90.0
Low education (ISCED 1–4) 2 0 0.4 0.5 0.0 0.0 1.0
Female 2 0 0.5 0.5 0.0 0.0 1.0
Binge drinking (monthly+) 2 0 0.5 0.5 0.0 0.0 1.0
Obese (BMI ≥ 30) 2 0 0.1 0.4 0.0 0.0 1.0
Married 2 0 0.5 0.5 0.0 0.0 1.0
Survey weight 132 0 1.0 0.5 0.3 0.8 4.0

Source: Author’s calculations

What are we explaining?


Overall CI = -0.20


Smoking more concentrated among the poor

Step 1: Predictors of current smoking

Variable β OR 95% CI p
Age (years) -0.001 0.999 (0.99, 1.01) 0.906
Female 0.141 1.152 (0.73, 1.83) 0.547
Low education (ISCED 1–4) 0.359 1.432 (0.90, 2.27) 0.130
Married -0.989 0.372 (0.21, 0.65) <0.001
Binge drinking (monthly+) 0.38 1.463 (0.92, 2.32) 0.107
Obese (BMI ≥ 30) 0.495 1.64 (0.90, 2.99) 0.106

Step 2: Estimating elasticity for low education

\[RCI=\sum{ \underbrace{(\beta_{k}\bar{x}_{k}/\mu)}_{\text{elasticity}} RCI_{k}}+gRCI_{e}/\mu\]

  • \(\beta_{\text{low education}}\) = 0.36 (OR = 1.4)
  • Marginal effect: 0.024
  • Mean low education: 0.452
  • Mean smoking rate: 7.3%

Elasticity for low education is: (0.024 * 0.452 / .073) = 0.148

Interpretation: a 1% increase in low education increases smoking by 14.8% (not percentage points!).

What about the RCI for low education?

This is Step (2): Calculate the mean of \(y\) \((\mu)\) and of each of the \(x_{k}\) determinants

Step 3: \(RCI_{k}\)

Note the y-axis is cumulative share of low education


The poorest 50% account for roughly 60% of the share of low educated.

This is Step (3): Calculate the \(CI\) for each of the potential determinants \(x_{k}\)

Step 4: Calculate contributions

Estimation for a specific factor: Low education

\[RCI=\sum{ \underbrace{(\beta_{k}\bar{x}_{k}/\mu)}_{\text{elasticity}} RCI_{k}}+gRCI_{e}/\mu\]

The elasticity of smoking (prior slide) = 0.148

Now we have \(RCI_{k}\) for low education = -0.265

The contribution of low education:

\[\text{Elasticity}\times RCI_{ed} = 0.148 * -0.265 = -.039\]

Thus low education accounts for -.039/ -0.203 = 19% of the overall \(RCI\)

RCI = -0.203


(-) Binge drinking: ↑ smoking but more common at higher incomes


(+) Married: ↓ smoking but more common at higher incomes

Contribution
Variable Elasticity CI_k Absolute %
Logistic regression; marginal effects used as elasticity weights.
Age -0.030 0.001 -0.000 0.0
Binge drinker 0.152 0.103 0.016 -7.7
Female 0.060 -0.031 -0.002 0.9
Obese 0.068 -0.013 -0.001 0.4
Low education 0.144 -0.265 -0.038 18.8
Married -0.353 0.284 -0.100 49.4
Residual -0.077 38.1

Uncertainty in the RCI Decomposition

Each contribution has sampling variability:

\[\underbrace{\frac{\hat{\beta}_k \bar{x}_k}{\hat{\mu}}}_{\text{elasticity}} \times \underbrace{\widehat{RCI}_k}_{\text{inequality in }x_k}\]

Can bootstrap the decomp \(B\) times to get empirical CIs.

See O’Donnell et al. (2008); Hosseinpoor, Doorslaer, and Speybroeck (2006)

Summary: Concentration index decomposition

When to use
Summarizing with RCI and asking which determinants drive it

Extensions
Nonlinear models; Oaxaca-type decomposition of differences and temporal changes

Caveats
‘Explained’ share depends on well-specified model; predictive, not causal

Wagstaff, Doorslaer, and Watanabe (2003); Kakwani, Wagstaff, and Doorslaer (1997); O’Donnell et al. (2008); Erreygers and Kessels (2016)

Covered Today

4. Interventional Decomposition

Origins: Why ‘interventional’?

Prior decompositions (e.g., Kitagawa, O-B) ‘descriptive’


Causal mediation challenges


Challenges with non-manipulable exposures


How much would gaps change if we intervened on a target?

Jackson and VanderWeele (2018)

Many recent developments

Reconciling the descriptive framework of KBO with causal inference.

See Jackson and VanderWeele (2018); Jackson (2021); Lundberg (2024); Yu and Elwert (2025); Jackson et al. (2025); Opacic, Wei, and Zhou (2026)

Youth accident deaths: what would we intervene on?

Danish-origin adolescents die in accidents more often than immigrant-origin peers (IRR 1.7 vs first-generation)


Alcohol is a plausible pathway: 16% of fatal accidents; Danish-origin youth have 4x the odds of an alcohol-related death


But immigrant-origin families are poorer, so adjusting for income widens the gap (IRR 1.7 → 2.6)

What if Danish-origin youth drank like their immigrant-origin peers?

Udesen et al. (2023); Kruckow and Tolstrup (2024) (ethnic IRRs inverted from Kruckow supplementary table 2)

Conceptualizing the DAG (assumptions)

Different from causal mediation (still valid)

Steps for pursuing interventional decomposition

1 Define the gap and intervention
Consider feasibility, implementation

2 Draw the DAG
Which covariates to adjust for (allowability)

3 Defend the assumptions
Exchangeability; positivity; consistency

4 Estimate the model
Outcome model, weighting, doubly robust

5 Compare factual and counterfactual
Consider effect scale, uncertainty

Jackson and VanderWeele (2018); Jackson (2021); Lundberg (2024)

Recent example

we estimate the expected 1-year mortality among the low-income patients in a hypothetical world where they initiated medication as often as high-income patients…

Møller et al. (2026)

Møller results

IDIE-exposed is the expected reduction in 1-year mortality among low-income heart failure patients in a hypothetical world where they initiated medication with the same probability as observed among similar high-income patients, rather than their observed probability.

Møller et al. (2026)

Summary: Interventional decomposition

When to use
Counterfactual inequality under a hypothetical intervention on a mediator

Extensions
Stochastic interventions; weighting framework; nonparametric estimation

Caveats
Causal assumptions; well-defined intervention; choices about ‘allowable’ covariates

Jackson and VanderWeele (2018); Jackson (2021); Lundberg (2024); Yu and Elwert (2025); Møller et al. (2026)

Summary


Various decomposition techniques exist that may be useful for analyzing social inequalities in health

Moves beyond measuring to explanations and interventions

Used responsibly, they can help to provide key evidence on why health inequalities exist and change over time.

References

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Sartorius, Victor, Marianne Philibert, Kari Klungsoyr, Jeannette Klimont, Katarzyna Szamotulska, Zeljka Drausnik, Petr Velebil, et al. 2024. “Neonatal Mortality Disparities by Gestational Age in European Countries.” JAMA Network Open 7 (8): e2424226. https://doi.org/10.1001/jamanetworkopen.2024.24226.
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Yu, Ang, and Felix Elwert. 2025. “Nonparametric Causal Decomposition of Group Disparities.” The Annals of Applied Statistics 19 (1). https://doi.org/10.1214/24-AOAS1990.