Econometrics II
Department of Economics, WU Vienna
Department of Economics, WU Vienna
October 23, 2025
Consider a binary treatment X, and outcome Y. We can think of the causal effect \(\tau\) as the difference in potential outcomes:
\[ \tau = Y(X=1) - Y(X=0) \]
In reality, only one outcome is realized, the other is counterfactual. Thus, we have to estimate this missing outcome to learn about the causal effect.
The potential outcomes framework is called the Neyman-Rubin causal model.
| i | \(X_i\) | \(Y_i\) | \(Y_i(1)\) | \(Y_i(0)\) |
|---|---|---|---|---|
| 1 | 0 | 1 | ? | 1 |
| 2 | 0 | 1 | ? | 1 |
| 3 | 1 | 1 | 1 | ? |
| 4 | 1 | 0 | 0 | ? |
| … | ||||
| N | 1 | 1 | 1 | ? |
A treatment X is ignorable, conditional on covariates Z, if:
Potential outcomes are independent of X, conditional on Z, and there are both treated and untreated subjects.
If X is ignorable, we can use the sample averages \(\mathrm{E}[Y_i(0)]\) and \(\mathrm{E}[Y_i(1)]\) as estimates for Y(0) and Y(1), then the estimate of \(\tau_{ATE}\) will be causally identified.
Randomization
When designing an experiment, we can use prior information to get more precise and accurate estimates. Imagine an experiment to test the efficacy of a training program:
If we conduct an experiment with B blocks:
\[ \hat{\tau}^b_{ATE}= \mathrm{E}[Y_j(1)] - \mathrm{E}[Y_j(0)] \text{ where } j\in B_b \\ \hat{\tau}_{ATE}=\frac{\sum_iN_i \hat{\tau}^i}{\sum_iN_i}. \]
\[ y_i= \alpha + x_i \tau_{ATE} + 𝟙 (i \in B_1)\gamma_1 + ...+ 𝟙 (i \in B_b)\gamma_b + e_i. \]
Below are 2 causal questions:
Practice task
The effect of media on voting preferences?
The effect of gang presence on income?
The Potential Outcomes (PO) framework, which we covered last week, is one way to view causal questions.
The potential outcomes framework relates very clearly to the notion of a randomized experiment.
Today, we are discussing a different framework that has its strengths elsewhere: the Directed Acyclical Graphs (DAG) framework.
To give you an intuition before we start with the theory, a DAG looks like this:
What you see on the right is what we call a graph.
This graph has three nodes. They are labeled \(i\), \(j\), and \(k\). Sometimes, we call the nodes “vertices,” “agents,” “points,” etc.
Some of the nodes in a graph are usually connected to each other, while others are not. We call those connections edges. Alternatively, they can be called “links,” “connections,” “lines,” etc.
Edges are pairs of two nodes. In the second graph, there is one edge from \(i\) to \(j\). We call this edge \(\{i,j\}\).
This edge does not have a direction.
However, we can easily give edges a direction. We call an edge like this a directed edge. When an edge is directed, the corresponding pair of nodes is no longer an unordered pair, but an ordered pair: \(\{j,i\}\neq\{i,j\}\).
A walk is a sequence of edges that joins a sequence of nodes. A cycle is a special case of a walk where all edges are distinct and the initial and final node are equal. In this graph, \(\left\{\{a,b\},\{b,c\},\{c,a\}\right\}\) is a cycle.
A graph that does not contain any cycles is called an acyclic graph.
If a graph contains only directed edges, we call it a directed graph.
The following graph is both directed and acyclic. We therefore call it a
Directed Acyclic Graph (DAG).
Think
Why is \(\{\{A,B\},\{B,C\},\)\(\{C,E\},\{E,A\}\}\) not a cycle?
Why do we talk about DAGs in an Econometrics class? Because they are really useful for causal modeling.
In the following DAG, nodes represent (random) variables, and edges represent (hypothesized) causal effects.
Missing edges also convey information: the assumption of no causal effect.
DAGs are a very useful framework for causal inference because
It turns out that there are two paths from \(X\) to \(Y\),
We call it a backdoor path because it enters \(X\) trough the “back door,” via an arrow pointed at \(X\).
In this DAG, when we want to isolate the effect \(X\rightarrow Y\), there is one open backdoor path.
This path confounds the causal effect of interest. We therefore call the variable \(U\) a confounder.
Confounder
A confounder is a variable that influences both the dependent and the explanatory variables.
If we just look at the connection between \(X\) and \(Y\), two effects are mixed together:
We can close the backdoor by controlling for the confounder. We only run into problems when we cannot control for the confounder.
We would run a regression along the lines of:
\[ \boldsymbol{y} \sim \boldsymbol{x} + \boldsymbol{u}. \]
Now imagine a different situation: There is a third variable, \(V\), that is jointly influenced by \(X\) and \(Y\).
Effects of both variables collide at \(V\). We therefore call \(V\) a collider. There is again one direct path and one backdoor path, but since the backdoor collides at \(V\), it is already closed.
Collider
A collider is a variable that is influenced by both the dependent and the explanatory variables.
Open backdoors between two variables introduce systematic, non-causal correlation between them. If we want to estimate a causal effect, we need to close them. There are three cases we have to consider:
Confounders
We close backdoor paths by controlling for confounders.
Colliders
We can (and need to) leave colliders alone. The backdoor path is already closed.
Mediators
A mediator mediates part of the effect. If we control for the mediator, we remove the mediated effect and leave only the direct effect.
How does this framework look like if we apply it to an example? Let us look at the following graph on the effect of gender (\(F\)) based discrimination (\(X\)) on earnings (\(Y\)).
We account for occupation (\(O\)) and aptitude (\(A\)).
Note that aptitude is not observed.
How many paths from \(X\) to \(Y\) can we enumerate?
How many paths between \(X\) and \(Y\) can we enumerate?
Which models can we use to isolate the effect of interest?
Without \(A\), we cannot isolate the causal effect of \(X\) on \(Y\) in this model. DAGs can highlight what cannot be done.
How come?
How is this possible?
| No Drug | Took Drug | |||
|---|---|---|---|---|
| Heart Attack | No Heart Attack | Heart Attack | No Heart Attack | |
| Female | 1 | 19 | 3 | 37 |
| Male | 12 | 28 | 8 | 12 |
| Total | 13 | 47 | 11 | 49 |
How does this “Bad-Bad-Good (BBG)” drug paradox arise?
| No Drug | Took Drug | |||
|---|---|---|---|---|
| Heart Attack | No Heart Attack | Heart Attack | No Heart Attack | |
| Female | 1 | 19 | 3 | 37 |
| Male | 12 | 28 | 8 | 12 |
| Total | 13 | 47 | 11 | 49 |