Few studies have explored temperature–mortality relationships in China, especially at the multi-large city level. This study was based on the data of seven typical, large Chinese cities to examine temperature-mortality relationships and optimum temperature of China. A generalized additive model (GAM) was applied to analyze the acute-effect of temperature on non-accidental mortality, and meta-analysis was used to merge data. Furthermore, the lagged effects of temperature up to 40 days on mortality and optimum temperature were analyzed using the distributed lag non-linear model (DLNM). We found that for all non-accidental mortality, high temperature could significantly increase the excess risk (ER) of death by 0.33% (95% confidence interval: 0.11%, 0.56%) with the temperature increase of 1 °C. Similar but non-significant ER of death was observed when temperature decreased. The lagged effect of temperature showed that the relative risk of non-accidental mortality was lowest at 21 °C. Our research suggests that high temperatures are more likely to cause an acute increase in mortality. There was a lagged effect of temperature on mortality, with an optimum temperature of 21 °C. Our results could provide a theoretical basis for climate-related public health policy.

The influence of excess iodine on human health has been paid more and more attention. Although numerous studies have reported that excess iodine may cause deleterious effects, the mental damage and its mechanism is yet to be identified. Using Sprague-Dawley rats exposed to excess iodine from pregnancy to 6 months post-delivery as in vivo model, this study explored the impacts of long-term repetitive excess iodine administration on the hippocampus of offspring rats, focusing on mitochondrial apoptosis pathway, with changes in monoamine neurotransmitters. The results showed that excess iodine could increase urinary iodine and brain organ coefficient in offspring of both genders, change the hippocampal cell structure, and damage the spatial learning and memory capacities. Poly ADP-ribose polymerase (PARP), P53, Cleaved Caspase-3, and cytochrome C proteins expression increased and Bcl2 protein expression decreased in hippocampus of excess iodine-treated offspring, indicating that excess iodine could activate the mitochondrial apoptosis pathway. Besides, excess iodine showed different effects on monoamine neurotransmitter in different gender. Collectively, our experimental data indicated that the learning and memory impairment induced by excess iodine may be mediated via mitochondrial apoptotic pathway. Long-term repetitive excess iodine exposure affected monoamine neurotransmitters in hippocampus of offspring rats.