Abstract
Background
Acute aortic dissection (AAD) is a fatal cardiovascular emergency whose environmental triggers remain poorly understood. Although particulate air pollution has been implicated, the role of gaseous pollutants, such as carbon monoxide (CO), remains unclear. This study was performed to determine whether short‐term exposure to ambient CO and other air pollutants triggers the onset of AAD.
Methods
We conducted a time‐stratified case‐crossover study of 798 patients with emergency department–confirmed AAD in an industrial metropolitan area from 2018 to 2021. Individual exposures to fine particulate matter (aerodynamic diameter ≤2.5 μm), particulate matter (aerodynamic diameter ≤10 μm), CO, nitrogen dioxide, ozone, sulfur dioxide, temperature, humidity, and wind speed were assigned from 24 monitoring stations. Conditional logistic regression models evaluated associations across lag 0 to 3 days, adjusting for meteorological factors. Effects were assessed using mean and interquartile range increments.
Results
No air pollutants were associated with AAD on the event day. However, ambient CO exhibited a strong delayed effect: at a 2‐day lag, each 1‐ppm increase in CO was associated with a 2.67‐fold increase in AAD risk (95% CI, 1.207–5.900), and each interquartile range increase of 0.19 ppm increased risk by 113% (95% CI, 1.075–4.239). The other pollutants showed no significant associations at any lag. Apparent temperature effects in mean‐based models were not confirmed by interquartile range–based analysis, indicating no robust thermal trigger.
Conclusions
Ambient CO is a potent delayed trigger of acute aortic dissection, likely acting through subacute inflammatory and oxidative vascular injury rather than immediate hypoxia. These findings suggest targeted public health alerts and emission control for CO in industrialized cities.