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Objectives It is unclear which chemical components of ambient fine particulate matter, PM2.5 may be most harmful in diseases like SLE, and whether other air pollutants play additional roles. We evaluated the association between mixture of PM2.5 components and SLE onset, quantifying their relative contributions to SLE risk, and potential effect modification by ambient ozone levels.Methods Using MarketScan® administrative health data, we assembled an urban open cohort of all enrollees 18-year-old and older (without prior SLE) with residential core-based statistical area (CBSA) information. Each year after 2013, eligible individuals entered the cohort, followed until SLE onset, death, insurance disenrollment, study end (Dec. 2023). SLE incident cases identified by at least 1 hospitalization or at least 2 physician billing diagnostic codes. From the cohort, all SLE cases and 20% random baseline sub-cohort were combined into case-cohort sample. Concentrations of PM2.5 components (ammonium, black carbon, mineral dust, sulfate, nitrate, organic matter, sea salt) and ambient ozone for 2 years before cohort entry were estimated by satellite- and ground-based models and assigned based on CBSAs at cohort entry. Extended quantile g-computation models assessed associations of SLE onset with mixture of PM2.5 components, ozone and interaction, adjusting for sex, age, baseline chronic obstructive pulmonary disease (smoking proxy), geographic region, year of cohort entry. Index weights estimated by quantile g-computation models quantified the relative contributions of individual PM2.5 components to SLE risk.Results Our case-cohort sample n=8,345,067 individuals including 21,485 new SLE cases. At median ozone referent level (i.e., 36.1 parts per billion), adjusted hazard ratio for SLE onset was 1.142 (95% confidence interval, CI1.107-1.179) per every quartile increase in all PM2.5 components ( table 1). Ozone was associated with increased risk of SLE (HR 1.009, 95% CI1.001-1.017). Effect modification such that HR for PM2.5 was highest when ozone level was lowest. Similar results seen in sub-groups stratified by sex/age. Mineral dust had largest index weight across different sub-groups and ozone levels.Abstract PT5:08 Table 1Systemic lupus erythematosus risk: hazard ration (HR) estimates for effects of PM2.5 component mixture, ozone, and the interaction between the exposures, at different referent levels of ozoneConclusions PM2.5 and ozone were associated with SLE onset. Mineral dust, an important contributor, triggers pulmonary inflammation, is plausible trigger of autoimmunity and SLE onset. Addressing sources of ambient mineral dust may help reduce SLE incidence.