Although epidemiological studies have reported associations between mortality and both ambient air pollution and air temperature, it remains uncertain whether the mortality effects of air pollution are modified by temperature and vice versa. Moreover, little is known on the interactions between ultrafine particles (diameter ≤ 100 nm, UFP) and temperature. We investigated whether the short-term associations of particle number concentration (PNC in the ultrafine range (≤100 nm) or total PNC ≤ 3000 nm, as a proxy for UFP), particulate matter ≤ 2.5 μm (PM2.5) and ≤ 10 μm (PM10), and ozone with daily total natural and cardiovascular mortality were modified by air temperature and whether air pollution levels affected the temperature-mortality associations in eight European urban areas during 1999-2013. We first analyzed air temperature-stratified associations between air pollution and total natural (nonaccidental) and cardiovascular mortality as well as air pollution-stratified temperature-mortality associations using city-specific over-dispersed Poisson additive models with a distributed lag nonlinear temperature term in each city. All models were adjusted for long-term and seasonal trend, day of the week, influenza epidemics, and population dynamics due to summer vacation and holidays. City-specific effect estimates were then pooled using random-effects meta-analysis. Pooled associations between air pollutants and total and cardiovascular mortality were overall positive and generally stronger at high relatively compared to low air temperatures. For example, on days with high air temperatures (>75th percentile), an increase of 10,000 particles/cm3 in PNC corresponded to a 2.51% (95% CI: 0.39%, 4.67%) increase in cardiovascular mortality, which was significantly higher than that on days with low air temperatures (50th percentile), both heat- and cold-related mortality risks increased. Our findings showed that high temperature could modify the effects of air pollution on daily mortality and high air pollution might enhance the air temperature effects.

Improved understanding of the effects of meteorological conditions on the transmission of SARS-CoV-2, the causative agent for COVID-19 disease, is needed. Here, we estimate the relationship between air temperature, specific humidity, and ultraviolet radiation and SARS-CoV-2 transmission in 2669 U.S. counties with abundant reported cases from March 15 to December 31, 2020. Specifically, we quantify the associations of daily mean temperature, specific humidity, and ultraviolet radiation with daily estimates of the SARS-CoV-2 reproduction number (R_t) and calculate the fraction of R_t attributable to these meteorological conditions. Lower air temperature (within the 20–40 °C range), lower specific humidity, and lower ultraviolet radiation were significantly associated with increased R_t. The fraction of R_t attributable to temperature, specific humidity, and ultraviolet radiation were 3.73% (95% empirical confidence interval [eCI]: 3.66–3.76%), 9.35% (95% eCI: 9.27–9.39%), and 4.44% (95% eCI: 4.38–4.47%), respectively. In total, 17.5% of R_t was attributable to meteorological factors. The fractions attributable to meteorological factors generally were higher in northern counties than in southern counties. Our findings indicate that cold and dry weather and low levels of ultraviolet radiation are moderately associated with increased SARS-CoV-2 transmissibility, with humidity playing the largest role.

Aims: The association between air temperature and mortality has been shown to vary over time, but evidence of temporal changes in the risk of myocardial infarction (MI) is lacking. We aimed to estimate the temporal variations in the association between short-term exposures to air temperature and MI in the area of Augsburg, Germany. Methods and results: Over a 28-years period from 1987 to 2014, a total of 27 310 cases of MI and coronary deaths were recorded. Daily meteorological parameters were measured in the study area. A time-stratified case-crossover analysis with a distributed lag non-linear model was used to estimate the risk of MI associated with air temperature. Subgroup analyses were performed to identify subpopulations with changing susceptibility to air temperature. Results showed a non-significant decline in cold-related MI risks. Heat-related MI relative risk significantly increased from 0.93 [95% confidence interval (CI): 0.78–1.12] in 1987–2000 to 1.14 (95% CI: 1.00–1.29) in 2001–14. The same trend was also observed for recurrent and non-ST-segment elevation MI events. This increasing population susceptibility to heat was more evident in patients with diabetes mellitus and hyperlipidaemia. Future studies using multicentre MI registries at different climatic, demographic, and socioeconomic settings are warranted to confirm our findings. Conclusion: We found evidence of rising population susceptibility to heat-related MI risk from 1987 to 2014, suggesting that exposure to heat should be considered as an environmental trigger of MI, especially under a warming climate.

Older adults are generally amongst the most vulnerable to heat and cold. While temperature-related health impacts are projected to increase with global warming, the influence of population aging on these trends remains unclear. Here we show that at 1.5 °C, 2 °C, and 3 °C of global warming, heat-related mortality in 800 locations across 50 countries/areas will increase by 0.5%, 1.0%, and 2.5%, respectively; among which 1 in 5 to 1 in 4 heat-related deaths can be attributed to population aging. Despite a projected decrease in cold-related mortality due to progressive warming alone, population aging will mostly counteract this trend, leading to a net increase in cold-related mortality by 0.1%–0.4% at 1.5–3 °C global warming. Our findings indicate that population aging constitutes a crucial driver for future heat- and cold-related deaths, with increasing mortality burden for both heat and cold due to the aging population.