Hydrogen sulfide and traffic-related air pollutants in association with increased mortality: a case-crossover study in Reykjavik, Iceland

OBJECTIVES: To study the association between daily mortality and short-term increases in air pollutants, both traffic-related and the geothermal source-specific hydrogen sulfide (H(2)S). DESIGN: Population-based, time stratified case-crossover. A lag time to 4 days was considered. Seasonal, gender and age stratification were calculated. Also, the best-fit lag when introducing H(2)S >7 µg/m(3) was selected by the Akaike Information Criterion (AIC). SETTING: The population of the greater Reykjavik area (n=181 558) during 2003–2009. PARTICIPANTS: Cases were defined as individuals living in the Reykjavik capital area, 18 years or older (N=138 657), who died due to all natural causes (ICD-10 codes A00-R99) other than injury, poisoning and certain other consequences of external causes, or cardiovascular disease (ICD-10 codes I00-I99) during the study period. MAIN OUTCOME MEASURE: Percentage increases in risk of death (IR%) following an interquartile range increase in pollutants. RESULTS: The total number of deaths due to all natural causes was 7679 and due to cardiovascular diseases was 3033. The interquartile range increased concentrations of H(2)S (2.6 µg/m(3)) were associated with daily all natural cause mortality in the Reykjavik capital area. The IR% was statistically significant during the summer season (lag 1: IR%=5.05, 95% CI 0.61 to 9.68; lag 2: IR%=5.09, 95% CI 0.44 to 9.97), among males (lag 0: IR%=2.26, 95% CI 0.23 to 4.44), and among the elderly (lag 0: IR%=1.94, 95% CI 0.12 to 1.04; lag 1: IR%=1.99, 95% CI 0.21 to 1.04), when adjusted for traffic-related pollutants and meteorological variables. The traffic-related pollutants were generally not associated with statistical significant IR%s. CONCLUSIONS: The results suggest that ambient H(2)S air pollution may increase mortality in Reykjavik, Iceland. To the best of our knowledge, ambient H(2)S exposure has not previously been associated with increased mortality in population-based studies and therefore the results should be interpreted with caution. Further studies are warranted to confirm or refute whether H(2)S exposure induces premature deaths.