No Arabic abstract
In causal mediation studies that decompose an average treatment effect into a natural indirect effect (NIE) and a natural direct effect (NDE), examples of post-treatment confounding are abundant. Past research has generally considered it infeasible to adjust for a post-treatment confounder of the mediator-outcome relationship due to incomplete information: it is observed under the actual treatment condition while missing under the counterfactual treatment condition. This study proposes a new sensitivity analysis strategy for handling post-treatment confounding and incorporates it into weighting-based causal mediation analysis without making extra identification assumptions. Under the sequential ignorability of the treatment assignment and of the mediator, we obtain the conditional distribution of the post-treatment confounder under the counterfactual treatment as a function of not just pretreatment covariates but also its counterpart under the actual treatment. The sensitivity analysis then generates a bound for the NIE and that for the NDE over a plausible range of the conditional correlation between the post-treatment confounder under the actual and that under the counterfactual conditions. Implemented through either imputation or integration, the strategy is suitable for binary as well as continuous measures of post-treatment confounders. Simulation results demonstrate major strengths and potential limitations of this new solution. A re-analysis of the National Evaluation of Welfare-to-Work Strategies (NEWWS) Riverside data reveals that the initial analytic results are sensitive to omitted post-treatment confounding.
Establishing cause-effect relationships from observational data often relies on untestable assumptions. It is crucial to know whether, and to what extent, the conclusions drawn from non-experimental studies are robust to potential unmeasured confounding. In this paper, we focus on the average causal effect (ACE) as our target of inference. We build on the work of Franks et al. (2019)and Robins (2000) by specifying non-identified sensitivity parameters that govern a contrast between the conditional (on measured covariates) distributions of the outcome under treatment (control) between treated and untreated individuals. We use semiparametric theory to derive the non-parametric efficient influence function of the ACE, for fixed sensitivity parameters. We use this influence function to construct a one-step bias-corrected estimator of the ACE. Our estimator depends on semiparametric models for the distribution of the observed data; importantly, these models do not impose any restrictions on the values of sensitivity analysis parameters. We establish sufficient conditions ensuring that our estimator has root-n asymptotics. We use our methodology to evaluate the causal effect of smoking during pregnancy on birth weight. We also evaluate the performance of estimation procedure in a simulation study.
Although the exposure can be randomly assigned in studies of mediation effects, any form of direct intervention on the mediator is often infeasible. As a result, unmeasured mediator-outcome confounding can seldom be ruled out. We propose semiparametric identification of natural direct and indirect effects in the presence of unmeasured mediator-outcome confounding by leveraging heteroskedasticity restrictions on the observed data law. For inference, we develop semiparametric estimators that remain consistent under partial misspecifications of the observed data model. We illustrate the proposed estimators through both simulations and an application to evaluate the effect of self-efficacy on fatigue among health care workers during the COVID-19 outbreak.
In employing spatial regression models for counts, we usually meet two issues. First, ignoring the inherent collinearity between covariates and the spatial effect would lead to causal inferences. Second, real count data usually reveal over or under-dispersion where the classical Poisson model is not appropriate to use. We propose a flexible Bayesian hierarchical modeling approach by joining non-confounding spatial methodology and a newly reconsidered dispersed count modeling from the renewal theory to control the issues. Specifically, we extend the methodology for analyzing spatial count data based on the gamma distribution assumption for waiting times. The model can be formulated as a latent Gaussian model, and consequently, we can carry out the fast computation using the integrated nested Laplace approximation method. We also examine different popular approaches for handling spatial confounding and compare their performances in the presence of dispersion. We use the proposed methodology to analyze a clinical dataset related to stomach cancer incidence in Slovenia and perform a simulation study to understand the proposed approachs merits better.
Analyses of environmental phenomena often are concerned with understanding unlikely events such as floods, heatwaves, droughts or high concentrations of pollutants. Yet the majority of the causal inference literature has focused on modelling means, rather than (possibly high) quantiles. We define a general estimator of the population quantile treatment (or exposure) effects (QTE) -- the weighted QTE (WQTE) -- of which the population QTE is a special case, along with a general class of balancing weights incorporating the propensity score. Asymptotic properties of the proposed WQTE estimators are derived. We further propose and compare propensity score regression and two weighted methods based on these balancing weights to understand the causal effect of an exposure on quantiles, allowing for the exposure to be binary, discrete or continuous. Finite sample behavior of the three estimators is studied in simulation. The proposed methods are applied to data taken from the Bavarian Danube catchment area to estimate the 95% QTE of phosphorus on copper concentration in the river.
While a randomized controlled trial (RCT) readily measures the average treatment effect (ATE), this measure may need to be generalized to the target population to account for a sampling bias in the RCTs population. Identifying this target population treatment effect needs covariates in both sets to capture all treatment effect modifiers that are shifted between the two sets. Standard estimators then use either weighting (IPSW), outcome modeling (G-formula), or combine the two in doubly robust approaches (AIPSW). However such covariates are often not available in both sets. Therefore, after completing existing proofs on the complete case consistency of those three estimators, we compute the expected bias induced by a missing covariate, assuming a Gaussian distribution and a semi-parametric linear model. This enables sensitivity analysis for each missing covariate pattern, giving the sign of the expected bias. We also show that there is no gain in imputing a partially-unobserved covariate. Finally we study the replacement of a missing covariate by a proxy. We illustrate all these results on simulations, as well as semi-synthetic benchmarks using data from the Tennessee Student/Teacher Achievement Ratio (STAR), and with a real-world example from critical care medicine.