Environmental exposures and risks for the idiopathic inflammatory myopathies and its phenotypes: a narrative review

The delineation of myositis-specific autoantibody (MSA) subgroups over the past two decades has reframed environmental research in idiopathic inflammatory myopathies (IIMs), making it plausible to examine discrete exposure-phenotype pairings within serologically defined subgroups. This review synthesises evidence on environmental, occupational, infectious, and pharmacological exposures, with attention to phenotypic specificity.

Ultraviolet radiation shapes MSA-specific geographic distributions at the population level and associates with dermatomyositis onset at the individual level. Disease onset follows MSA-specific seasonal patterns, replicated across geographically independent cohorts. Smoking amplifies antisynthetase syndrome risk through a gene-environment interaction with HLA-DRB1*03:01, whilst protecting against anti-TIF1-γ autoantibodies. Gestational and early-life tobacco smoke exposure is consistently implicated as risks for juvenile IIM. Occupational silica exposure associates with antisynthetase syndrome and overlap myositis, with synergistic lung disease risk when combined with smoking. Statins, immune checkpoint inhibitors, anti-TNFα agents, and interferons each induce immunopathologically distinct myositis phenotypes. Postpandemic surveillance has documented a rise in anti-MDA5 autoantibody-positive disease following SARS-CoV-2 infection.

Environmental exposures in IIM act preferentially in specific serological and genetic contexts, consistent with discrete exposure-phenotype pairings shaped by genetic background and age at exposure. Prospective, MSA-stratified studies with direct exposure quantification represent priority directions for the field.