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Upper gastrointestinal bleeding due to peptic ulcer disease is not associated with air pollution: a case-crossover
Samuel Quan1, Hong Yang2, Divine Tanyingoh3
1Departments of Medicine and Community Health Sciences, University of Calgary, 3280 Hospital Drive NW, Room 6D56, Calgary, AB, T2N-4N1, Canada. squan15@gmail.com.
Background:
Recent studies have demonstrated an association between short-term elevations in air pollution and an increased risk of exacerbating gastrointestinal disease. The objective of the study was to evaluate if day-to-day increases in air pollution concentrations were positively associated with upper gastrointestinal bleeding (UGIB) secondary to peptic ulcer disease (PUD).
Methods:
A time-stratified case-crossover study design was used. Adults presenting to hospitals with their first UGIB secondary to PUD from 2004-2010 were identified using administrative databases from Calgary (n = 1374; discovery cohort) and Edmonton (n = 1159; replication cohort). Daily concentrations of ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, and particulate matter (PM10 and PM2.5) were estimated in these two cities. Conditional logistic regression models were employed, adjusting for temperature and humidity. Odds ratios (OR) with 95 % confidence intervals (CI) were expressed relative to an interquartile range increase in the concentration of each pollutant.
Results:
No statistically significant associations were observed for any of the individual pollutants based on same-day, or 1-day lag effects within the Calgary discovery cohort. When the air pollution exposures were assessed as 3-, 5-, and 7-day averages, some pollutants were inversely associated with UGIB in the discovery cohort; for example, 5-day averages of nitrogen dioxide (OR = 0.68; 95 % CI: 0.53-0.88), and particulate matter <2.5 μm (OR = 0.75; 95 % CI: 0.61-0.90). However, these findings could not be reproduced in the replication cohort.
Conclusion:
Our findings suggest that short-term elevations in the level of ambient air pollutants does not increase the incidence of UGIB secondary to PUD.
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