In this paper, we analyze the applicability of the Causal Identification algorithm to causal time series graphs with latent confounders. Since these graphs extend over infinitely many time steps, deciding whether causal effects across arbitrary time intervals are identifiable appears to require computation on graph segments of unbounded size. Even for deciding the identifiability of intervention effects on variables that are close in time, no bound is known on how many time steps in the past need to be considered. We give a first bound of this kind that only depends on the number of variables per time step and the maximum time lag of any direct or latent causal effect. More generally, we show that applying the Causal Identification algorithm to a constant-size segment of the time series graph is sufficient to decide identifiability of causal effects, even across unbounded time intervals.
We measure the association between generative AI (GAI) tool adoption and four metrics spanning security operations, information protection, and endpoint management: 1) number of security alerts per incident, 2) probability of security incident reopenings, 3) time to classify a data loss prevention alert, and 4) time to resolve device policy conflicts. We find that GAI is associated with robust and statistically and practically significant improvements in the four metrics. Although unobserved confounders inhibit causal identification, these results are among the first to use observational data from live operations to investigate the relationship between GAI adoption and security operations, data loss prevention, and device policy management.
We measure the association between generative AI (GAI) tool adoption and security operations center productivity. We find that GAI adoption is associated with a 30.13% reduction in security incident mean time to resolution. This result is robust to several modeling decisions. While unobserved confounders inhibit causal identification, this result is among the first to use observational data from live operations to investigate the relationship between GAI adoption and security worker productivity.
The supply of politicians affects the quality of democratic institutions. Yet little is known about the economic motivations that drive individuals into politics. This paper examines how experiencing a job loss affects individuals' decisions to enter political life and explores its implications for political selection. Using highly granular administrative data linking individual records of political participation with comprehensive employer-employee data for all formal workers in Brazil, and leveraging mass layoffs for causal identification, we find that job loss significantly increases the likelihood of joining a political party and running for local office. Layoff-induced candidates are positively selected on various competence measures, suggesting that economic shocks improve the quality of political entrants. Further, we observe that the increase in candidacies is more pronounced among laid-off individuals with greater financial incentives from holding office and higher predicted income losses. Finally, using a regression discontinuity design, we find that eligibility for unemployment benefits increases the likelihood of becoming a party member and running for local office. These results are consistent with the reduction in private-sector opportunity costs and the increased time resources explaining the rise in political entry.
Identifying causal relations is crucial for a variety of downstream tasks. In additional to observational data, background knowledge (BK), which could be attained from human expertise or experiments, is usually introduced for uncovering causal relations. This raises an open problem that in the presence of latent variables, what causal relations are identifiable from observational data and BK. In this paper, we propose two novel rules for incorporating BK, which offer a new perspective to the open problem. In addition, we show that these rules are applicable in some typical causality tasks, such as determining the set of possible causal effects with observational data. Our rule-based approach enhances the state-of-the-art method by circumventing a process of enumerating block sets that would otherwise take exponential complexity.
Event Causality Identification (ECI) aims to detect whether there exists a causal relation between two events in a document. Existing studies adopt a kind of identifying after learning paradigm, where events' representations are first learned and then used for the identification. Furthermore, they mainly focus on the causality existence, but ignoring causal direction. In this paper, we take care of the causal direction and propose a new identifying while learning mode for the ECI task. We argue that a few causal relations can be easily identified with high confidence, and the directionality and structure of these identified causalities can be utilized to update events' representations for boosting next round of causality identification. To this end, this paper designs an *iterative learning and identifying framework*: In each iteration, we construct an event causality graph, on which events' causal structure representations are updated for boosting causal identification. Experiments on two public datasets show that our approach outperforms the state-of-the-art algorithms in both evaluations for causality existence identification and direction identification.
Causal inference from observational data following the restricted structural causal models (SCM) framework hinges largely on the asymmetry between cause and effect from the data generating mechanisms, such as non-Gaussianity or non-linearity. This methodology can be adapted to stationary time series, yet inferring causal relationships from nonstationary time series remains a challenging task. In this work, we propose a new class of restricted SCM, via a time-varying filter and stationary noise, and exploit the asymmetry from nonstationarity for causal identification in both bivariate and network settings. We propose efficient procedures by leveraging powerful estimates of the bivariate evolutionary spectra for slowly varying processes. Various synthetic and real datasets that involve high-order and non-smooth filters are evaluated to demonstrate the effectiveness of our proposed methodology.
Causal identification in causal Bayes nets (CBNs) is an important tool in causal inference allowing the derivation of interventional distributions from observational distributions where this is possible in principle. However, most existing formulations of causal identification using techniques such as d-separation and do-calculus are expressed within the mathematical language of classical probability theory on CBNs. However, there are many causal settings where probability theory and hence current causal identification techniques are inapplicable such as relational databases, dataflow programs such as hardware description languages, distributed systems and most modern machine learning algorithms. We show that this restriction can be lifted by replacing the use of classical probability theory with the alternative axiomatic foundation of symmetric monoidal categories. In this alternative axiomatization, we show how an unambiguous and clean distinction can be drawn between the general syntax of causal models and any specific semantic implementation of that causal model. This allows a purely syntactic algorithmic description of general causal identification by a translation of recent formulations of the general ID algorithm through fixing. Our description is given entirely in terms of the non-parametric ADMG structure specifying a causal model and the algebraic signature of the corresponding monoidal category, to which a sequence of manipulations is then applied so as to arrive at a modified monoidal category in which the desired, purely syntactic interventional causal model, is obtained. We use this idea to derive purely syntactic analogues of classical back-door and front-door causal adjustment, and illustrate an application to a more complex causal model.
With the rise of Large Language Models(LLMs), it has become crucial to understand their capabilities and limitations in deciphering and explaining the complex web of causal relationships that language entails. Current methods use either explicit or implicit causal reasoning, yet there is a strong need for a unified approach combining both to tackle a wide array of causal relationships more effectively. This research proposes a novel architecture called Context Aware Reasoning Enhancement with Counterfactual Analysis(CARE CA) framework to enhance causal reasoning and explainability. The proposed framework incorporates an explicit causal detection module with ConceptNet and counterfactual statements, as well as implicit causal detection through LLMs. Our framework goes one step further with a layer of counterfactual explanations to accentuate LLMs understanding of causality. The knowledge from ConceptNet enhances the performance of multiple causal reasoning tasks such as causal discovery, causal identification and counterfactual reasoning. The counterfactual sentences add explicit knowledge of the not caused by scenarios. By combining these powerful modules, our model aims to provide a deeper understanding of causal relationships, enabling enhanced interpretability. Evaluation of benchmark datasets shows improved performance across all metrics, such as accuracy, precision, recall, and F1 scores. We also introduce CausalNet, a new dataset accompanied by our code, to facilitate further research in this domain.
In the 1990s, Joshua Angrist and Guido Imbens studied the causal interpretation of Instrumental Variable estimates (a widespread methodology in economics) through the lens of potential outcomes (a classical framework to formalize causality in statistics). Bridging a gap between those two strands of literature, they stress the importance of treatment effect heterogeneity and show that, under defendable assumptions in various applications, this method recovers an average causal effect for a specific subpopulation of individuals whose treatment is affected by the instrument. They were awarded the Nobel Prize primarily for this Local Average Treatment Effect (LATE). The first part of this article presents that methodological contribution in-depth: the origination in earlier applied articles, the different identification results and extensions, and related debates on the relevance of LATEs for public policy decisions. The second part reviews the main contributions of the authors beyond the LATE. J. Angrist has pursued the search for informative and varied empirical research designs in several fields, particularly in education. G. Imbens has complemented the toolbox for treatment effect estimation in many ways, notably through propensity score reweighting, matching, and, more recently, adapting machine learning procedures.
Scientists often want to learn about cause and effect from hierarchical data, collected from subunits nested inside units. Consider students in schools, cells in patients, or cities in states. In such settings, unit-level variables (e.g. each school's budget) may affect subunit-level variables (e.g. the test scores of each student in each school) and vice versa. To address causal questions with hierarchical data, we propose hierarchical causal models, which extend structural causal models and causal graphical models by adding inner plates. We develop a general graphical identification technique for hierarchical causal models that extends do-calculus. We find many situations in which hierarchical data can enable causal identification even when it would be impossible with non-hierarchical data, that is, if we had only unit-level summaries of subunit-level variables (e.g. the school's average test score, rather than each student's score). We develop estimation techniques for hierarchical causal models, using methods including hierarchical Bayesian models. We illustrate our results in simulation and via a reanalysis of the classic "eight schools" study.
Inferring causal structures from time series data is the central interest of many scientific inquiries. A major barrier to such inference is the problem of subsampling, i.e., the frequency of measurement is much lower than that of causal influence. To overcome this problem, numerous methods have been proposed, yet either was limited to the linear case or failed to achieve identifiability. In this paper, we propose a constraint-based algorithm that can identify the entire causal structure from subsampled time series, without any parametric constraint. Our observation is that the challenge of subsampling arises mainly from hidden variables at the unobserved time steps. Meanwhile, every hidden variable has an observed proxy, which is essentially itself at some observable time in the future, benefiting from the temporal structure. Based on these, we can leverage the proxies to remove the bias induced by the hidden variables and hence achieve identifiability. Following this intuition, we propose a proxy-based causal discovery algorithm. Our algorithm is nonparametric and can achieve full causal identification. Theoretical advantages are reflected in synthetic and real-world experiments.
Predicting the effect of unseen interventions is a fundamental research question across the data sciences. It is well established that in general such questions cannot be answered definitively from observational data. This realization has fuelled a growing literature introducing various identifying assumptions, for example in the form of a causal diagram among relevant variables. In practice, this paradigm is still too rigid for many practical applications as it is generally not possible to confidently delineate the true causal diagram. In this paper, we consider the derivation of bounds on causal effects given only observational data. We propose to take as input a less informative structure known as a Partial Ancestral Graph, which represents a Markov equivalence class of causal diagrams and is learnable from data. In this more ``data-driven'' setting, we provide a systematic algorithm to derive bounds on causal effects that exploit the invariant properties of the equivalence class, and that can be computed analytically. We demonstrate our method with synthetic and real data examples.
Assessing causal effects in the presence of unobserved confounding is a challenging problem. Existing studies leveraged proxy variables or multiple treatments to adjust for the confounding bias. In particular, the latter approach attributes the impact on a single outcome to multiple treatments, allowing estimating latent variables for confounding control. Nevertheless, these methods primarily focus on a single outcome, whereas in many real-world scenarios, there is greater interest in studying the effects on multiple outcomes. Besides, these outcomes are often coupled with multiple treatments. Examples include the intensive care unit (ICU), where health providers evaluate the effectiveness of therapies on multiple health indicators. To accommodate these scenarios, we consider a new setting dubbed as multiple treatments and multiple outcomes. We then show that parallel studies of multiple outcomes involved in this setting can assist each other in causal identification, in the sense that we can exploit other treatments and outcomes as proxies for each treatment effect under study. We proceed with a causal discovery method that can effectively identify such proxies for causal estimation. The utility of our method is demonstrated in synthetic data and sepsis disease.
Finding the parameters of a latent variable causal model is central to causal inference and causal identification. In this article, we show that existing graphical structures that are used in causal inference are not stable under marginalization of Gaussian Bayesian networks, and present a graphical structure that faithfully represent margins of Gaussian Bayesian networks. We present the first duality between parameter optimization of a latent variable model and training a feed-forward neural network in the parameter space of the assumed family of distributions. Based on this observation, we develop an algorithm for parameter optimization of these graphical structures based on a given observational distribution. Then, we provide conditions for causal effect identifiability in the Gaussian setting. We propose an meta-algorithm that checks whether a causal effect is identifiable or not. Moreover, we lay a grounding for generalizing the duality between a neural network and a causal model from the Gaussian to other distributions.
Causality and eXplainable Artificial Intelligence (XAI) have developed as separate fields in computer science, even though the underlying concepts of causation and explanation share common ancient roots. This is further enforced by the lack of review works jointly covering these two fields. In this paper, we investigate the literature to try to understand how and to what extent causality and XAI are intertwined. More precisely, we seek to uncover what kinds of relationships exist between the two concepts and how one can benefit from them, for instance, in building trust in AI systems. As a result, three main perspectives are identified. In the first one, the lack of causality is seen as one of the major limitations of current AI and XAI approaches, and the "optimal" form of explanations is investigated. The second is a pragmatic perspective and considers XAI as a tool to foster scientific exploration for causal inquiry, via the identification of pursue-worthy experimental manipulations. Finally, the third perspective supports the idea that causality is propaedeutic to XAI in three possible manners: exploiting concepts borrowed from causality to support or improve XAI, utilizing counterfactuals for explainability, and considering accessing a causal model as explaining itself. To complement our analysis, we also provide relevant software solutions used to automate causal tasks. We believe our work provides a unified view of the two fields of causality and XAI by highlighting potential domain bridges and uncovering possible limitations.
In consequential domains, it is often impossible to compel individuals to take treatment, so that optimal policy rules are merely suggestions in the presence of human non-adherence to treatment recommendations. Under heterogeneity, covariates may predict take-up of treatment and final outcome, but differently. While optimal treatment rules optimize causal outcomes across the population, access parity constraints or other fairness considerations on who receives treatment can be important. For example, in social services, a persistent puzzle is the gap in take-up of beneficial services among those who may benefit from them the most. We study causal identification and robust estimation of optimal treatment rules, including under potential violations of positivity. We consider fairness constraints such as demographic parity in treatment take-up, and other constraints, via constrained optimization. Our framework can be extended to handle algorithmic recommendations under an often-reasonable covariate-conditional exclusion restriction, using our robustness checks for lack of positivity in the recommendation. We develop a two-stage algorithm for solving over parametrized policy classes under general constraints to obtain variance-sensitive regret bounds. We illustrate the methods in three case studies based on data from reminders of SNAP benefits recertification, randomized encouragement to enroll in insurance, and from pretrial supervised release with electronic monitoring. While the specific remedy to inequities in algorithmic allocation is context-specific, it requires studying both take-up of decisions and downstream outcomes of them.
This paper serves as a starting point for machine learning researchers, engineers and students who are interested in but not yet familiar with causal inference. We start by laying out an important set of assumptions that are collectively needed for causal identification, such as exchangeability, positivity, consistency and the absence of interference. From these assumptions, we build out a set of important causal inference techniques, which we do so by categorizing them into two buckets; active and passive approaches. We describe and discuss randomized controlled trials and bandit-based approaches from the active category. We then describe classical approaches, such as matching and inverse probability weighting, in the passive category, followed by more recent deep learning based algorithms. By finishing the paper with some of the missing aspects of causal inference from this paper, such as collider biases, we expect this paper to provide readers with a diverse set of starting points for further reading and research in causal inference and discovery.
Confounding is a significant obstacle to unbiased estimation of causal effects from observational data. For settings with high-dimensional covariates -- such as text data, genomics, or the behavioral social sciences -- researchers have proposed methods to adjust for confounding by adapting machine learning methods to the goal of causal estimation. However, empirical evaluation of these adjustment methods has been challenging and limited. In this work, we build on a promising empirical evaluation strategy that simplifies evaluation design and uses real data: subsampling randomized controlled trials (RCTs) to create confounded observational datasets while using the average causal effects from the RCTs as ground-truth. We contribute a new sampling algorithm, which we call RCT rejection sampling, and provide theoretical guarantees that causal identification holds in the observational data to allow for valid comparisons to the ground-truth RCT. Using synthetic data, we show our algorithm indeed results in low bias when oracle estimators are evaluated on the confounded samples, which is not always the case for a previously proposed algorithm. In addition to this identification result, we highlight several finite data considerations for evaluation designers who plan to use RCT rejection sampling on their own datasets. As a proof of concept, we implement an example evaluation pipeline and walk through these finite data considerations with a novel, real-world RCT -- which we release publicly -- consisting of approximately 70k observations and text data as high-dimensional covariates. Together, these contributions build towards a broader agenda of improved empirical evaluation for causal estimation.
Identifying the causal variables of an environment and how to intervene on them is of core value in applications such as robotics and embodied AI. While an agent can commonly interact with the environment and may implicitly perturb the behavior of some of these causal variables, often the targets it affects remain unknown. In this paper, we show that causal variables can still be identified for many common setups, e.g., additive Gaussian noise models, if the agent's interactions with a causal variable can be described by an unknown binary variable. This happens when each causal variable has two different mechanisms, e.g., an observational and an interventional one. Using this identifiability result, we propose BISCUIT, a method for simultaneously learning causal variables and their corresponding binary interaction variables. On three robotic-inspired datasets, BISCUIT accurately identifies causal variables and can even be scaled to complex, realistic environments for embodied AI.