Chronic respiratory disorders (CRDs) are a major contributor to the burden of non-communicable diseases worldwide, drastically reducing quality of life with no known cures on the market. Numerous data from clinical studies reveal that metabolic dysregulation and the associated inflammatory response contribute to CRD pathogenesis. Notably, asthma, chronic obstructive pulmonary disease (COPD), and sleep apnoea have been linked to metabolic, low-grade inflammatory conditions including obesity and diabetes. Additionally, the brain-lung axis also represents a complex bi-directional network linked via inflammatory pathways. While these systems have been identified as tractable therapeutic targets, these relationships are largely supported through observational studies, meaning further work is needed to confirm these mechanisms are causally linked to respiratory outcomes. With the advent of the genome wide association study (GWAS) it became possible to compare genomes between biological traits, allowing for a hypothesis free approach to map genetic variations to disease aetiology and identify new treatment targets. This project aimed to identify statistical associations between GWAS for 1960 metabolic and brain measure traits and CRDs. Linkage disequilibrium score regression and latent causal variable modelling were employed to test for genetic correlation and partial genetic causality between two recent metabolite cohorts, and brain traits from the ENIMGA consortium and Oxford Big 40 Project, and asthma, COPD, and sleep apnoea GWAS from the FinnGen Project, respectively. This revealed 19, 45, and 43 significant partially genetically causal traits for asthma, COPD, and sleep apnoea GWAS, respectively, when testing significantly genetically correlated trait pairs. Utilising Mendelian randomisation for causal inference modelling on significantly partially causal pairs indicated a trend of increased CRD severity negatively impacting brain dimensions, while circulating metabolites influenced CRD genetic severity in both positive and negative directions. Together, these results provide further evidence for the causal relationship between metabolic and immunological regulation and CRDs.