The Spectral Structure of Latent Treatment Effects

Estimating causal effects from real-world spatiotemporal data is challenging due to hidden confounders and interference. Standard causal identification methods assume conditional exchangeability given observed covariates, which fails whenever hidden confounders affect both treatment and outcomes - a common setting in domains such as climate, environmental policy, epidemiology, and regional economics. In this paper, we propose a novel spatiotemporal proximal causal inference framework that extends proximal identification theory to spatiotemporal settings. The proposed method jointly captures local and neighborhood-level confounding information by introducing treatment- and outcome-inducing proxies, and we derive a spatiotemporal outcome confounding bridge function that identifies the potential outcome without requiring direct recovery of the hidden confounder. We establish the identifiability of this bridge function under proxy exclusion restrictions and a spatiotemporal completeness condition, and show that the resulting estimator recovers the outcome through a proximal generalization of the g-computation formula. To operationalize this identification result, we propose a neural architecture that learns proxies via transformer-based spatiotemporal encoders - coupled with a conditional mutual information critic to enforce exclusion restrictions and a moment-matching network to guarantee that the learned bridge function satisfies the underlying identifying equation. We further introduce a stabilized weighting scheme to address treatment support imbalance. Experiments on synthetic datasets demonstrate that our approach achieves comparable performance to baseline causal inference methods, while providing, to our knowledge, the first theoretically grounded outcomes for the hidden confounding in the presence of spatiotemporal interference through a proximal causal inference framework.

A central goal of modern causal inference is estimating heterogeneous treatment effects to answer questions like "how does an intervention affect each unit," rather than only on average. We study this problem with panel-data where we observe $n$ units across $m$ times under unknown, non-uniform treatment assignments. The data in this setting is naturally represented as a matrix of all unit--time treatment effects. Estimating heterogeneous treatment effects can then be expressed as obtaining a good estimation of each row's average in this matrix. This allows us to formulate the problem as matrix completion, which can be solved under natural low-rankness assumptions. However, existing matrix-completion guarantees are not powerful enough to get meaningful bounds for the per-row guarantee required for estimating the heterogeneous treatment effect; roughly speaking, they are only useful for estimating average treatment effect bounds, as also illustrated in a recent line of work. We give a simple, computationally efficient estimator that, without knowledge of the propensities and under standard low-rankness and regularity assumptions, achieves a row-wise $\ell_2$ error of $\tilde{O}(\sqrt{\frac{1}{n} + \frac{n}{m^2}})$. Technically, our analysis establishes the first sharp row-wise $\ell_2$-perturbation bound for low-rank approximation, complementing existing spectral-, Frobenius-, and entrywise perturbation theory.

We propose \textbf{CaSPECT}, a causal spectral clustering framework for discovering causally homogeneous subgroups from observational data. Rather than clustering in covariate space, CaSPECT defines similarity through the topology of a learned directed acyclic graph (DAG); a bootstrap-stabilised PC algorithm recovers the causal skeleton; a novel \emph{Orientation Validation Score} (OVS) combines PC bootstrap evidence with DirectLiNGAM to orient edges robustly; directed edges are weighted by backdoor-identified average treatment effects estimated via OLS or double machine learning. Chung's directed Laplacian provides a spectral embedding in which individuals close together share the same causal propagation pathways. We establish almost-sure consistency of the full pipeline and validate the method through a controlled simulation study and on LaLonde CPS1, IHDP, and 401(k) datasets, where CaSPECT recovers a positive and statistically significant treatment effect within the causally comparable subpopulation and corrects for severe confounding without requiring a pre-specified propensity score model.