The health impacts of climate warming are usually quantified based on daily average temperatures. However, extra health risks might result from hot nights. We project the future mortality burden due to hot nights. We selected the hot night excess (HNE) to represent the intensity of night-time heat, which was calculated as the excess sum of high temperature during night time. We collected historical mortality data in 28 cities from three east Asian countries, from 1981 to 2010. The associations between HNE and mortality in each city were firstly examined using a generalised additive model in combination with a distributed lag non-linear model over lag 0-10 days. We then pooled the cumulative associations using a univariate meta-regression model at the national or regional levels. Historical and future hourly temperature series were projected under two scenarios of greenhouse-gas emissions from 1980-2099, with ten general circulation models. We then projected the attributable fraction of mortality due to HNE under each scenario. Our dataset comprised 28 cities across three countries (Japan, South Korea, and China), including 9 185 598 deaths. The time-series analyses showed the HNE was significantly associated with increased mortality risks, the relative mortality risk on days with hot nights could be 50% higher than on days with non-hot nights. Compared with the rise in daily mean temperature (lower than 20%), the frequency of hot nights would increase more than 30% and the intensity of hot night would increase by 50% by 2100s. The attributable fraction of mortality due to hot nights was projected to be 3·68% (95% CI 1·20 to 6·17) under a strict emission control scenario (SSP126). Under a medium emission control scenario (SSP245), the attributable fraction of mortality was projected to increase up to 5·79% (2·07 to 9·52), which is 0·95% (-0·39 to 2·29) more than the attributable fraction of mortality due to daily mean temperature. Our study provides evidence for significant mortality risks and burden in association with night-time warming across Japan, South Korea, and China. Our findings suggest a growing role of night-time warming in heat-related health effects in a changing climate. The National Natural Science Foundation of China, Shanghai International Science and Technology Partnership Project.

Background: Short-term exposure to ambient air pollution has been linked with daily hospitalization and mortality from acute coronary syndrome (ACS); however, the associations of subdaily (hourly) levels of criteria air pollutants with the onset of ACS and its subtypes have rarely been evaluated. Methods: We conducted a time-stratified case-crossover study among 1 292 880 patients with ACS from 2239 hospitals in 318 Chinese cities between January 1, 2015, and September 30, 2020. Hourly concentrations of fine particulate matter (PM _2.5 ), coarse particulate matter (PM _2.5–10 ), nitrogen dioxide (NO ₂ ), sulfur dioxide (SO ₂ ), carbon monoxide (CO), and ozone (O ₃ ) were collected. Hourly onset data of ACS and its subtypes, including ST-segment–elevation myocardial infarction, non–ST-segment–elevation myocardial infarction, and unstable angina, were also obtained. Conditional logistic regressions combined with polynomial distributed lag models were applied. Results: Acute exposures to PM _2.5 , NO ₂ , SO ₂ , and CO were each associated with the onset of ACS and its subtypes. These associations were strongest in the concurrent hour of exposure and were attenuated thereafter, with the weakest effects observed after 15 to 29 hours. There were no apparent thresholds in the concentration–response curves. An interquartile range increase in concentrations of PM _2.5 (36.0 μg/m ³ ), NO ₂ (29.0 µg/m ³ ), SO ₂ (9.0 µg/m ³ ), and CO (0.6 mg/m ³ ) over the 0 to 24 hours before onset was significantly associated with 1.32%, 3.89%, 0.67%, and 1.55% higher risks of ACS onset, respectively. For a given pollutant, the associations were comparable in magnitude across different subtypes of ACS. NO ₂ showed the strongest associations with all 3 subtypes, followed by PM _2.5 , CO, and SO ₂ . Greater magnitude of associations was observed among patients older than 65 years and in the cold season. Null associations of exposure to either PM _2.5–10 or O ₃ with ACS onset were observed. Conclusions: The results suggest that transient exposure to the air pollutants PM _2.5 , NO ₂ , SO ₂ , or CO, but not PM _2.5–10 or O ₃ , may trigger the onset of ACS, even at concentrations below the World Health Organization air quality guidelines.

Although air pollution has been frequently linked to a range of cardiometabolic diseases, its association with the onset, progression, and prognosis of cardiometabolic multimorbidity (CMM) has never been studied. We conducted this prospective analysis based on the UK Biobank cohort. CMM was defined as the coexistence of at least two cardiometabolic diseases, including type 2 diabetes, ischemic heart disease and stroke. Multi-state model was used to analyze the association between air pollution and the trajectory of CMM. 410,494 middle- and old-age participants were included. During a median follow-up of 12.0 years, 56,877 participants developed first cardiometabolic disease (FCMD), 8616 developed CMM, and 22,423 died. The risks of transitions from baseline to FCMD, from FCMD to CMM, and transitions from baseline and FCMD to all-cause mortality increased by 3% (2%, 5%), 3% (1%, 6%), 5% (2%, 7%) and 2% (−1%, 6%), respectively, per interquartile range increase of fine particulate matter. The corresponding increases were 3% (2%, 5%), 6% (3%, 9%), 4% (2%, 7%) and 6% (2%, 10%), respectively, for nitrogen dioxide. Older participants, males, and individuals with excessive alcohol drinking and lower economic levels were more likely to experience these risks. Air pollution exposures could play important roles in almost all transition phases of CMM development. Our results highlight clean air as an upstream approach to mitigate both initiation and progression of CMM, especially in vulnerable populations. Shanghai Municipal Science and Technology Commission (21TQ015); The National Natural Science Foundation of China (92143301 and 92043301).