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Register a new userCausal Inference by Surrogate Experiments: z-Identifiability
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We address the problem of estimating the effect of intervening on a set of variables X from experiments on a different set, Z, that is more accessible to manipulation. This problem, which we call z-identifiability, reduces to ordinary identifiability when Z = empty and, like the latter, can be given syntactic characterization using the do-calculus [Pearl, 1995; 2000]. We provide a graphical necessary and sufficient condition for z-identifiability for arbitrary sets X,Z, and Y (the outcomes). We further develop a complete algorithm for computing the causal effect of X on Y using information provided by experiments on Z. Finally, we use our results to prove completeness of do-calculus relative to z-identifiability, a result that does not follow from completeness relative to ordinary identifiability.
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We consider the problem of identifying the causal direction between two discrete random variables using observational data. Unlike previous work, we keep the most general functional model but make an assumption on the unobserved exogenous variable: Inspired by Occams razor, we assume that the exogenous variable is simple in the true causal direction. We quantify simplicity using Renyi entropy. Our main result is that, under natural assumptions, if the exogenous variable has low $H_0$ entropy (cardinality) in the true direction, it must have high $H_0$ entropy in the wrong direction. We establish several algorithmic hardness results about estimating the minimum entropy exogenous variable. We show that the problem of finding the exogenous variable with minimum entropy is equivalent to the problem of finding minimum joint entropy given $n$ marginal distributions, also known as minimum entropy coupling problem. We propose an efficient greedy algorithm for the minimum entropy coupling problem, that for $n=2$ provably finds a local optimum. This gives a greedy algorithm for finding the exogenous variable with minimum $H_1$ (Shannon Entropy). Our greedy entropy-based causal inference algorithm has similar performance to the state of the art additive noise models in real datasets. One advantage of our approach is that we make no use of the values of random variables but only their distributions. Our method can therefore be used for causal inference for both ordinal and also categorical data, unlike additive noise models.
I propose a framework, estimators, and inference procedures for the analysis of causal effects in a setting with spatial treatments. Many events and policies (treatments), such as opening of businesses, building of hospitals, and sources of pollution, occur at specific spatial locations, with researchers interested in their effects on nearby individuals or businesses (outcome units). However, the existing treatment effects literature primarily considers treatments that could be assigned directly at the level of the outcome units, potentially with spillover effects. I approach the spatial treatment setting from a similar experimental perspective: What ideal experiment would we design to estimate the causal effects of spatial treatments? This perspective motivates a comparison between individuals near realized treatment locations and individuals near unrealized candidate locations, which is distinct from current empirical practice. Furthermore, I show how to find such candidate locations and apply the proposed methods with observational data. I apply the proposed methods to study the causal effects of grocery stores on foot traffic to nearby businesses during COVID-19 lockdowns.
The Ladder of Causation describes three qualitatively different types of activities an agent may be interested in engaging in, namely, seeing (observational), doing (interventional), and imagining (counterfactual) (Pearl and Mackenzie, 2018). The inferential challenge imposed by the causal hierarchy is that data is collected by an agent observing or intervening in a system (layers 1 and 2), while its goal may be to understand what would have happened had it taken a different course of action, contrary to what factually ended up happening (layer 3). While there exists a solid understanding of the conditions under which cross-layer inferences are allowed from observations to interventions, the results are somewhat scarcer when targeting counterfactual quantities. In this paper, we study the identification of nested counterfactuals from an arbitrary combination of observations and experiments. Specifically, building on a more explicit definition of nested counterfactuals, we prove the counterfactual unnesting theorem (CUT), which allows one to map arbitrary nested counterfactuals to unnested ones. For instance, applications in mediation and fairness analysis usually evoke notions of direct, indirect, and spurious effects, which naturally require nesting. Second, we introduce a sufficient and necessary graphical condition for counterfactual identification from an arbitrary combination of observational and experimental distributions. Lastly, we develop an efficient and complete algorithm for identifying nested counterfactuals; failure of the algorithm returning an expression for a query implies it is not identifiable.
In this work, we consider the problem of robust parameter estimation from observational data in the context of linear structural equation models (LSEMs). LSEMs are a popular and well-studied class of models for inferring causality in the natural and social sciences. One of the main problems related to LSEMs is to recover the model parameters from the observational data. Under various conditions on LSEMs and the model parameters the prior work provides efficient algorithms to recover the parameters. However, these results are often about generic identifiability. In practice, generic identifiability is not sufficient and we need robust identifiability: small changes in the observational data should not affect the parameters by a huge amount. Robust identifiability has received far less attention and remains poorly understood. Sankararaman et al. (2019) recently provided a set of sufficient conditions on parameters under which robust identifiability is feasible. However, a limitation of their work is that their results only apply to a small sub-class of LSEMs, called ``bow-free paths. In this work, we significantly extend their work along multiple dimensions. First, for a large and well-studied class of LSEMs, namely ``bow free models, we provide a sufficient condition on model parameters under which robust identifiability holds, thereby removing the restriction of paths required by prior work. We then show that this sufficient condition holds with high probability which implies that for a large set of parameters robust identifiability holds and that for such parameters, existing algorithms already achieve robust identifiability. Finally, we validate our results on both simulated and real-world datasets.
Risk modeling with EHR data is challenging due to a lack of direct observations on the disease outcome, and the high dimensionality of the candidate predictors. In this paper, we develop a surrogate assisted semi-supervised-learning (SAS) approach to risk modeling with high dimensional predictors, leveraging a large unlabeled data on candidate predictors and surrogates of outcome, as well as a small labeled data with annotated outcomes. The SAS procedure borrows information from surrogates along with candidate predictors to impute the unobserved outcomes via a sparse working imputation model with moment conditions to achieve robustness against mis-specification in the imputation model and a one-step bias correction to enable interval estimation for the predicted risk. We demonstrate that the SAS procedure provides valid inference for the predicted risk derived from a high dimensional working model, even when the underlying risk prediction model is dense and the risk model is mis-specified. We present an extensive simulation study to demonstrate the superiority of our SSL approach compared to existing supervised methods. We apply the method to derive genetic risk prediction of type-2 diabetes mellitus using a EHR biobank cohort.
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