Compared to the previous studies, our results are the smallest in magnitude, likely because of the high geographical precision that allows more accurate confounding and spatial autocorrelation adjustment. In addition, we report weak evidence of an effect, which could also be due to lack of power and individual exposure data. Nevertheless, as for NO2 we find a high posterior probability of an effect on mortality, we argue that a potential explanation might be the mediation effect of pre-existing conditions. While in our analysis the inclusion of area-level prevalence of hypertension, diabetes and COPD did not change the results, the ecological nature of the pre-existing conditions data does not allow us to account for the mediation effect at the individual level. Our study focuses on the mortality after contracting SARS-CoV-2, however we cannot rule out individual susceptibility to becoming infected as an explanation to the uncertainty in the effect estimates (Villeneuve and Goldberg 2020). Such susceptibility can reflect immunosuppression, leading to later increases in inflammation (Edoardo Conticini et al. 2020) and thus worse prognosis, or even disease spread, as recent studies have suggested that PM2.5 can proliferate COVID-19 transmission (Bianconi et al. 2020).