Exposure profile–specific associations of epicardial and pericardial adipose tissue with spirometric function in pneumoconiosis: a retrospective cross-sectional study

Background We investigated the association between cardiac adiposity and spirometric function in pneumoconiosis and whether this association varied by occupational exposure profile. Methods This retrospective observational study included 214 male patients with pneumoconiosis classified into silica-predominant and mixed inorganic dust/metal-fume exposure profiles. Epicardial adipose tissue (EAT) and total pericardial adipose tissue (PAT) volumes were measured on non-contrast chest CT and evaluated in separate linear regression models. The outcomes were FEV1 percent predicted, FVC percent predicted, and FEV1/FVC. Pooled main-effect, exposure profile-stratified, and interaction models were adjusted for age, smoking pack-years, pneumoconiosis-related work duration, body mass index, and three-level ILO radiographic category; pooled models additionally included exposure profile. Main analyses included 182 patients with complete data. Results In pooled and stratified models, neither EAT nor PAT volume was significantly associated with any spirometric outcome. The EAT × mixed profile interaction was significantly negative for FEV1/FVC (β = −0.112, 95% CI − 0.197 to −0.028; p = 0.009), whereas the corresponding PAT interaction was not significant (β = −0.048, 95% CI − 0.099 to 0.002; p = 0.062). No comparable interactions were observed for FEV1 or FVC percent predicted. In sensitivity analyses excluding patients with airflow obstruction, documented chronic obstructive pulmonary disease, or asthma (n = 146), both interaction estimates were attenuated and nonsignificant (EAT: β = −0.041, 95% CI − 0.102 to 0.020, p = 0.186; PAT: β = −0.017, 95% CI − 0.056 to 0.021, p = 0.380). Conclusions Exploratory interaction analysis suggested that the EAT–FEV1/FVC association varied by occupational exposure profile. Non-significant within-profile associations and attenuation in sensitivity analyses limit the strength of this evidence. These findings require confirmation in prospective studies with quantitative exposure and airway imaging assessments.