Ambient Carbon Monoxide as a Delayed Trigger of Acute Aortic Dissection: A Time‐Stratified Case‐Crossover Study in a Tropical Industrial Metropolis
7 affiliations
- 1Department of Emergency Medicine Kaohsiung Chang Gung Memorial Hospital Kaohsiung Taiwan
- 2Department of Public Health, College of Health Sciences Kaohsiung Medical University Kaohsiung Taiwan
- 3Department of Medical Research, Kaohsiung Medical University Hospital Kaohsiung Medical University Kaohsiung Taiwan
- 4Center for Big Data Research Kaohsiung Medical University Kaohsiung Taiwan
- 5Department of Occupational and Environmental Medicine Kaohsiung Medical University Hospital Kaohsiung Taiwan
- 6Ph.D. Program in Environmental and Occupational Medicine, College of Medicine, and Research Center for Precision Environmental Medicine Kaohsiung Medical University Kaohsiung Taiwan
- 7National Center for High‐Performance Computing National Institutes of Applied Research Tainan Taiwan
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.
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BibTeX
@article{chiang2026ambient,
title = {{Ambient Carbon Monoxide as a Delayed Trigger of Acute Aortic Dissection: A Time‐Stratified Case‐Crossover Study in a Tropical Industrial Metropolis}},
author = {Charng‐Yen Chiang and Fu‐Jen Cheng and Shih‐Chiang Hung and Chin‐Wei Chen and Fu‐Wen Liang and Hung‐Yi Chuang},
journal = {Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease},
year = {2026},
month = sep,
doi = {10.1161/jaha.126.049936},
url = {https://doi.org/10.1161/jaha.126.049936},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Ambient Carbon Monoxide as a Delayed Trigger of Acute Aortic Dissection: A Time‐Stratified Case‐Crossover Study in a Tropical Industrial Metropolis
AU - Charng‐Yen Chiang
AU - Fu‐Jen Cheng
AU - Shih‐Chiang Hung
AU - Chin‐Wei Chen
AU - Fu‐Wen Liang
AU - Hung‐Yi Chuang
PY - 2026
DA - 2026/09/09
JO - Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
DO - 10.1161/jaha.126.049936
UR - https://doi.org/10.1161/jaha.126.049936
AB - 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.
SN - 2047-9980
ER -