Weather characteristics have been suggested by many social scientists to influence criminality. According to a recent study, climate change may cause a substantial increase in criminal activities during the twenty-first century. The additional number of crimes due to climate have been estimated by associational models, which are not optimal to quantify causal impacts of weather conditions on criminality. Using the Rubin Causal Model and crime data reported daily between 2012 and 2017, this study examines whether changes in heat index, a proxy for apparent temperature, and rainfall occurrence, influence the number of violent crimes in Boston. On average, more crimes are reported on temperate days compared to extremely cold days, and on dry days compared to rainy days. However, no significant differences in the number of crimes between extremely hot days versus less warm days could be observed. The results suggest that weather forecasts could be integrated into crime prevention programs in Boston. The weather-crime relationship should be taken into account when assessing the economic, sociological, or medical impact of climate change. Researchers and policy makers interested in the effects of environmental exposures or policy interventions on crime should consider a causal inference approach to analyze their data.

When addressing environmental health‐related questions, most often, only observational data are collected for ethical or practical reasons. However, the lack of randomized exposure often prevents the comparison of similar groups of exposed and unexposed units. This design barrier leads the environmental epidemiology field to mainly estimate associations between environmental exposures and health outcomes. A recently developed causal inference pipeline was developed to guide researchers interested in estimating the effects of plausible hypothetical interventions for policy recommendations. This article illustrates how this multistaged pipeline can help environmental epidemiologists reconstruct and analyze hypothetical randomized experiments by investigating whether an air pollution reduction intervention decreases the risk of multiple sclerosis relapses in Alsace region, France. The epidemiology literature reports conflicted findings on the relationship between air pollution and multiple sclerosis. Some studies found significant associations, whereas others did not. Two case‐crossover studies reported significant associations between the risk of multiple sclerosis relapses and the exposure to air pollutants in the Alsace region. We use the same study population as these epidemiological studies to illustrate how appealing this causal inference approach is to estimate the effects of hypothetical, but plausible, environmental interventions.

Statistical analysis of microbial genomic data within epidemiological cohort studies holds the promise to assess the influence of environmental exposures on both the host and the host-associated microbiome. However, the observational character of prospective cohort data and the intricate characteristics of microbiome data make it challenging to discover causal associations between environment and microbiome. Here, we introduce a causal inference framework based on the Rubin Causal Model that can help scientists to investigate such environment-host microbiome relationships, to capitalize on existing, possibly powerful, test statistics, and test plausible sharp null hypotheses. Using data from the German KORA cohort study, we illustrate our framework by designing two hypothetical randomized experiments with interventions of (i) air pollution reduction and (ii) smoking prevention. We study the effects of these interventions on the human gut microbiome by testing shifts in microbial diversity, changes in individual microbial abundances, and microbial network wiring between groups of matched subjects via randomization-based inference. In the smoking prevention scenario, we identify a small interconnected group of taxa worth further scrutiny, including Christensenellaceae and Ruminococcaceae genera, that have been previously associated with blood metabolite changes. These findings demonstrate that our framework may uncover potentially causal links between environmental exposure and the gut microbiome from observational data. We anticipate the present statistical framework to be a good starting point for further discoveries on the role of the gut microbiome in environmental health.