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A key question in many network studies is whether the observed correlations between units are primarily due to contagion or latent confounding. Here, we study this question using a segregated graph (Shpitser, 2015) representation of these mechanisms, and examine how uncertainty about the true underlying mechanism impacts downstream computation of network causal effects, particularly under full interference---settings where we only have a single realization of a network and each unit may depend on any other unit in the network. Under certain assumptions about asymptotic growth of the network, we derive likelihood ratio tests that can be used to identify whether different sets of variables---confounders, treatments, and outcomes---across units exhibit dependence due to contagion or latent confounding. We then propose network causal effect estimation strategies that provide unbiased and consistent estimates if the dependence mechanisms are either known or correctly inferred using our proposed tests. Together, the proposed methods allow network effect estimation in a wider range of full interference scenarios that have not been considered in prior work. We evaluate the effectiveness of our methods with synthetic data and the validity of our assumptions using real-world networks. 

Recent text-based causal methods attempt to mitigate confounding bias by estimating proxies of confounding variables that are partially or imperfectly measured from unstructured text data. These approaches, however, assume analysts have supervised labels of the confounders given text for a subset of instances, a constraint that is sometimes infeasible due to data privacy or annotation costs. In this work, we address settings in which an important confounding variable is completely unobserved. We propose a new causal inference method that uses two instances of pre-treatment text data, infers two proxies using two zero-shot models on the separate instances, and applies these proxies in the proximal g-formula. We prove, under certain assumptions about the instances of text and accuracy of the zero-shot predictions, that our method of inferring text-based proxies satisfies identification conditions of the proximal g-formula while other seemingly reasonable proposals do not. To address untestable assumptions associated with our method and the proximal g-formula, we further propose an odds ratio falsification heuristic that flags when to proceed with downstream effect estimation using the inferred proxies. We evaluate our method in synthetic and semi-synthetic settings---the latter with real-world clinical notes from MIMIC-III and open large language models for zero-shot prediction---and find that our method produces estimates with low bias. We believe that this text-based design of proxies allows for the use of proximal causal inference in a wider range of scenarios, particularly those for which obtaining suitable proxies from structured data is difficult. 

Prior work applying semiparametric theory to causal inference has primarily focused on deriving estimators that exhibit statistical robustness under a prespecified causal model that permits identification of a desired causal parameter. However, a fundamental challenge is correct specification of such a model, which usually involves making untestable assumptions. Evidence factors is an approach to combining hypothesis tests of a common causal null hypothesis under two or more candidate causal models. Under certain conditions, this yields a test that is valid if at least one of the underlying models is correct, which is a form of causal robustness. We propose a method of combining semiparametric theory with evidence factors. We develop a causal null hypothesis test based on joint asymptotic normality of K asymptotically linear semiparametric estimators, where each estimator is based on a distinct identifying functional derived from each of K candidate causal models. We show that this test provides both statistical and causal robustness in the sense that it is valid if at least one of the K proposed causal models is correct, while also allowing for slower than parametric rates of convergence in estimating nuisance functions. We demonstrate the effectiveness of our method via simulations and applications to the Framingham Heart Study and Wisconsin Longitudinal Study.