BACKGROUND: Extreme temperature events (ETEs), including heat wave and cold spell, have been linked to myocardial infarction (MI) morbidity; however, their effects on MI mortality are less clear. Although ambient fine particulate matter (PM _2.5 ) is suggested to act synergistically with extreme temperatures on cardiovascular mortality, it remains unknown if and how ETEs and PM _2.5 interact to trigger MI deaths. METHODS: A time-stratified case-crossover study of 202 678 MI deaths in Jiangsu province, China, from 2015 to 2020, was conducted to investigate the association of exposure to ETEs and PM _2.5 with MI mortality and evaluate their interactive effects. On the basis of ambient apparent temperature, multiple temperature thresholds and durations were used to build 12 ETE definitions. Daily ETEs and PM _2.5 exposures were assessed by extracting values from validated grid datasets at each subject’s geocoded residential address. Conditional logistic regression models were applied to perform exposure-response analyses and estimate relative excess odds due to interaction, proportion attributable to interaction, and synergy index. RESULTS: Under different ETE definitions, the odds ratio of MI mortality associated with heat wave and cold spell ranged from 1.18 (95% CI, 1.14–1.21) to 1.74 (1.66–1.83), and 1.04 (1.02–1.06) to 1.12 (1.07–1.18), respectively. Lag 01-day exposure to PM _2.5 was significantly associated with an increased odds of MI mortality, which attenuated at higher exposures. We observed a significant synergistic interaction of heat wave and PM _2.5 on MI mortality (relative excess odds due to interaction >0, proportion attributable to interaction >0, and synergy index >1), which was higher, in general, for heat wave with greater intensities and longer durations. We estimated that up to 2.8% of the MI deaths were attributable to exposure to ETEs and PM _2.5 at levels exceeding the interim target 3 value (37.5 μg/m ³ ) of World Health Organization air quality guidelines. Women and older adults were more vulnerable to ETEs and PM _2.5 . The interactive effects of ETEs or PM _2.5 on MI mortality did not vary across sex, age, or socioeconomic status. CONCLUSIONS: This study provides consistent evidence that exposure to both ETEs and PM _2.5 is significantly associated with an increased odds of MI mortality, especially for women and older adults, and that heat wave interacts synergistically with PM _2.5 to trigger MI deaths but cold spell does not. Our findings suggest that mitigating both ETE and PM _2.5 exposures may bring health cobenefits in preventing premature deaths from MI.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is currently a global pandemic, and there are limited laboratory studies targeting pathogen resistance. This study aimed to investigate the effect of selected disinfection products and methods on the inactivation of SARS-CoV-2 in the laboratory. We used quantitative suspension testing to evaluate the effectiveness of the disinfectant/method. Available chlorine of 250 mg/L, 500 mg/L, and 1000 mg/L required 20 min, 5 min, and 0.5 min to inactivate SARS-CoV-2, respectively. A 600-fold dilution of 17% concentration of di-N-decyl dimethyl ammonium bromide (283 mg/L) and the same concentration of di-N-decyl dimethyl ammonium chloride required only 0.5 min to inactivate the virus efficiently. At 30% concentration for 1 min and 40% and above for 0.5 min, ethanol could efficiently inactivate SARS-CoV-2. Heat takes approximately 30 min at 56 °C, 10 min above 70 °C, or 5 min above 90 °C to inactivate the virus. The chlorinated disinfectants, Di-N-decyl dimethyl ammonium bromide/chloride, ethanol, and heat could effectively inactivate SARS-CoV-2 in the laboratory test. The response of SARS-CoV-2 to disinfectants is very similar to that of SARS-CoV.

To study the association between short-term exposure to air pollutants and mortality of Chronic Ischemic Heart Disease (CIHD). Using a case-crossover design, we investigated 148,443 CIHD deaths from 2015 to 2020 in Jiangsu Province, China. Exposure to six ambient pollutants, including PM₁₀, PM_2.5, NO₂, CO, SO₂, and O_3, was assessed by extracting daily concentrations from validated 10 km × 10 km pollutant grids at each subject's residential address. A conditional logistic regression approach was used to explore the exposure-response relationship with adjustment for temperature and relative humidity. We calculated the Population Attributable Fractions (PAFs) and the attributable deaths number of CIHD. An increase of 10 μg/m³ in PM₁₀ and PM_2.5 exposure was associated with a 1.16% (95% CI: 0.85-1.48%) and 1.80% (1.36-2.24%) increase in CIHD mortality, respectively. A threshold value of 123 µg/m³ was identified for the association between O₃ exposure and CIHD mortality. Controlling for PM_2.5, each increase of 10 µg/m³ in O₃ (>threshold) was statistically significantly associated with a 0.94% (0.19-1.71%) increase in CIHD mortality, however there was no association between NO₂, SO₂, CO exposure and CIHD mortality. Reducing PM_2.5, PM₁₀ and O₃ to the WHO air quality guidelines would prevent 6.16% (95% CI: 4.70-7.58%), 4.30% (3.18-5.43%) and 1.29% (0.48-4.20%) of CIHD deaths, respectively. During the warm season, mortality and PAFs of CIHD associated with PM_2.5, PM₁₀, and O₃ were significantly higher. Short-term exposure to ambient PM_2.5, PM_10, and O₃ might trigger deaths from CIHD. These findings indicate that the premature deaths of CIHD patients can be alleviated by reducing exposure to polluted air.

Exposure to non-optimum ambient temperature has been linked to increased risk of total cardiovascular disease (CVD) mortality; however, the adverse effects on mortality from specific types of CVD remain less understood. To comprehensively investigate the association of ambient temperature with cause-specific CVD mortality, and to estimate and compare the corresponding mortality burden. We conducted a time-stratified case-crossover study of 1000,014 CVD deaths in Jiangsu province, China during 2015-2019 using data from the China National Mortality Surveillance System. Residential daily 24-hour average temperature for each subject was extracted from a validated grid data at a spatial resolution of 0.0625° × 0.0625°. We fitted distributed lag non-linear models (DLNM) based on conditional logistic regression to quantitatively investigate the association of ambient temperature with total and cause-specific CVD mortality, which was used to further estimate mortality burden attributable to non-optimum ambient temperatures. With adjustment for relative humidity, we observed reverse J-shaped exposure-response associations of ambient temperature with total and cause-specific CVD mortality, with minimum mortality temperatures ranging from 19.5 °C to 23.0 °C. An estimated 20.3% of the total CVD deaths were attributable to non-optimum temperatures, while the attributable fraction (AF) of mortality from chronic rheumatic heart diseases, hypertensive diseases, ischemic heart diseases (IHD), pulmonary heart disease, stroke, and sequelae of stroke was 22.4%, 23.2%, 23.3%, 20.9%, 17.6% and 21.3%, respectively. For total and cause-specific CVDs, most deaths were attributable to moderate cold temperature. We observed significantly higher mortality burden from total and certain cause-specific CVDs in adults 80 years or older and those who were widowed. Exposure to ambient temperature was significantly associated with increased risk of cause-specific CVD mortality. The burden of CVD mortality attributable to non-optimum temperature was substantial especially in older and widowed adults, and significantly varied across specific types of CVD.