Exposure to Particulate Matter and Risk of Anorexia Nervosa: A Mendelian Randomization Study
Author:
Affiliation:
1. Barts and The London School of Medicine and Dentistry, Queen Mary University of London
2. William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London
Abstract
Background Exposure to particulate matter is linked to mental health outcomes through observational and Mendelian randomization studies. In this study, the causal association between particulate matter 2.5 (PM2.5) and particulate matter 10 (PM10) exposure and anorexia nervosa (AN) was explored. Methods Two-Sample Mendelian randomization analysis was performed using genetic instrumental variables for PM2.5 and PM10 as exposures to test for a potential causal association with AN using the inverse variance weighted method (IVW), with additional methods including the weighted median and MR-Egger. Association data for PM2.5 included 455 314 participants and 423,796 participants for PM10. Summary data for AN derived from the Psychiatric Genomics Consortium (PGC) meta-analysis genome-wide association study comprising 16 992 cases and 55 525 controls. Sensitivity analyses for pleiotropy and heterogeneity were conducted using MR-Egger intercepts, Cochrane’s Q, MR- Pleiotropy RESidual Sum and Outlier (MR-PRESSO) and least absolute shrinkage and selection operator (LASSO) regression. Results Genetically predicted increase in PM10 (one standard deviation) exposure was associated with an increased risk of anorexia nervosa at Bonferroni significance (p = 0.003, OR = 2.5, 95% CI = 1.38–4.54) using the IVW method. Sensitivity analysis detected no pleiotropy or heterogeneity. There was no suggestion of a causal role for PM2.5 and AN (p = 0.57). Conclusion We provide for the first-time evidence for a potential role of genetically predicted exposure to PM10 in the development of AN, with no evidence of a causal effect of PM2.5 on AN. More robust epidemiological and biological studies are needed to understand the mechanism of this effect and neurobiological basis for disease.
Publisher
Springer Science and Business Media LLC
Reference44 articles.
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