Environmental triggers of acute Stanford type A aortic dissection: The roles of ambient temperature, air pollution, and workplace thermal conditions.
This study examines the short-term associations and potential long-term causal effects of environmental temperature and air pollution exposures on the risk of acute Stanford Type A Aortic Dissection (AAAD). We conducted a time-series analysis in Shenyang, Northeast China, using daily meteorological and air quality data matched with hospital admissions for AAAD from Shengjing Hospital of China Medical University. Daily mean temperature ranged from approximately - 20 °C to 20 °C, while PM2.5 concentrations exhibited episodic spikes up to 600 µg/m³. A distributed lag non-linear model (DLNM) evaluated lagged exposure - response relationships over a 28-day period. The DLNM revealed a pronounced inverse J-shaped relationship between mean temperature and AAAD risk: exposure to cold temperatures below 0 °C was associated with a significantly elevated relative risk (RR), with persistent effects noted from lag 5 to lag 20 days. PM2.5 exhibited a U-shaped association with AAAD, with the highest risks observed at concentrations near 250 µg/m³ within 0-4 days post-exposure. Joint exposure surfaces demonstrated complex interplay between cold and particulate matter on AAAD incidence. To explore potential long-term causal effects, we performed two-sample Mendelian randomization analyses using genetic instruments for workplace temperature conditions and for chronic exposure to air pollutants (PM2.5, PM10 and NO2). The primary inverse-variance weighted analysis showed non-significant associations for genetically instrumented "often cold" workplace exposure (e.g., OR = 0.23; 95% CI: 0.0004-142.62; P = 0.655) and likewise provided no robust evidence for causal effects of long-term PM2.5, PM10 or NO2 exposure on AAAD risk, with wide confidence intervals encompassing the null. These findings highlight significant short-term associations of cold and high pollution exposures with AAAD incidence, whereas long-term causal links inferred from genetic proxies for workplace temperature and air pollutants remain unconfirmed and require further investigation.