Exposure to air pollution - trigger for acute coronary syndromes. Longitude study in two cohorts of industrial and non-industrial cities
Authors: Kuzma L , Wanha W , Kurasz A , Kralisz P , Gajewska-Bachorzewska H , Wojakowski W , Dobrzycki S 
Published: May 2023

Funding Acknowledgements

Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Science Center in Poland.

Background

Poland is one of the most polluted countries in Europe [1]. The most polluted cities are located in the south of the country, with the main sources of pollution associated with the industrial branch, and in the eastern part where non-industrial regions with low emissions sources are related to the effect of Polish smog [2,3].

Objectives

A comparison of the short-term impact of air pollution exposure on the incidence of acute coronary syndromes (ACS) in two cohorts with different sources of air pollution.

Materials and methods

The study covered two voivodship cities with different sources of air pollution. Analyze included 7,200,000 person-years of follow-up and four pollutants NO2, SO2, and particulate matter with a diameter of 2.5 mm or less (PM2.5) and 10 mm or less (PM10) between 2008 and 2018. A time-stratified (simple indicator variables) Poisson regression analysis with 3-lag was used to assess the effects of air pollution on ACS. We adjusted our model for the day of the week and public holidays, as confounders, we used daily relative humidity, atmospheric pressure, and temperature. The analysis was done separately for each city in the NSTEMI and STEMI groups. To avoid the co-linearity effect, each pollutant was modeled separately.

Results

A total of 10,582 patients with ACS were included in the analysis, of whom 5,153 (48.9%) had STEMI. The age-standardized rate per 100,000 population per year for ACS was higher in industrial city (238.8 vs. 82.5, P&lt;0.001). The WHO 2021 daily norms for PM2.5 (75.6% vs. 24.2%), PM10 (32.3% vs. 11.2%), NO2 (61.5% vs. 6%), and SO2 (3.4% vs. 0.1%) were more often exceed in the industrial area (P&lt;0.001). In the non-industrial city, an increase of 10 µg/m3 in SO2 (ORLAG0=1.02, 95%CI 1.016–1097; P&lt;0.001), PM2.5 (ORLAG0=1.016, 95%CI 1.001–1.031; P&lt;0.001) and PM10 concentration (ORLAG1=1.006, 95%CI 1.004–1.027; P=0.01) were associated with an increase in the number of hospitalizations due to STEMI. The effect of SO2 was observed up to 2 days [(ORLAG1=1.019, 95%CI 1.053–1.134; P&lt;0.001); (ORLAG2=1.113, 95%CI 1.037–1.193, P&lt;0.001)] and up to 1 day in case of the PM2.5 (ORLAG1=1.007, 95%CI 1.012–1.041; P&lt;0.001). The influence of NO2 was observed in NSTEMI patients in industrial city (ORLAG0=1.02, 95CI 1.05–1.136; P&lt;0.001) as well as in the non-industrial city (ORLAG0=1.058, 95%CI 1.047–1.308; P=0.01). No effect on STEMI incidence was noted in the non-industrial city.

Conclusion

The effect of air pollution on the incidence of ACS was observed in both areas despite of source and level of air pollution. The risk of air pollution-related ACS was higher in the industrial over the non-industrial area. A clinical effect was more delayed in time in patients with STEMI, especially after exposure to SO2.