Impact of ground-level ozone exposure on sleep quality and electroencephalogram patterns at different time scales.

Ozone exposure is associated with various adverse health outcomes, but its impact on sleep quality is uncertain. Here we assessed the causal effect of long-term (yearly and monthly) exposure to ozone on nocturnal workday sleep time in a national representative sample from the China Family Panel Study, using a difference-in-differences approach. We further followed ninety healthy Chinese young adults four times in four seasons from September 2020 to June 2021, measured their daily sleep architecture using accelerometers, ascertained daily ozone exposure, recorded 5-min eye-closed resting-state electroencephalogram (EEG) signals at the last day of each one-week-long measurement session, and explored the effect of ozone exposure on objectively-measured sleep architecture. In the national sample, we found that every 1 interquartile range (IQR) µg/m3 increase in yearly and monthly ozone exposure was causally associated with 7.31 (p = 0.0039) and 4.19 (p = 0.040) minutes decline in nocturnal workday sleep time; the dose-response curve represented a quasi-linear pattern with no safety threshold, and plateaued at higher concentrations. In the small-scale study with objectively-measured sleep architecture, we found that every 1 IQR µg/m3 increase in the weekly ozone exposure was associated with 5.33 min decrease in night-time total sleep time (p = 0.031), 1.63 percentage points decrease in sleep efficiency (p < 0.001), 1.99 min increase in sleep latency (p = 0.0070), and 5.34 min increase in wake after sleep onset time (p = 0.0016) in a quasi-linear pattern. Notably, we found the accumulating trend of ozone exposure on sleep quality during both the short-term and long-term periods. We also found that short-term ozone exposure was associated with altered EEG patterns, mediated by sleep quality. This study indicates that long-term and short-term ozone exposures have negative and accumulating impacts on sleep quality and might impair brain functioning. More hidden health burdens of ozone are worth exploring.

Causal effects of prenatal and chronic PM2.5 exposures on cognitive function.

Growing evidence indicated an association between PM2.5 exposure and cognitive function, but the causal effect and the cognitive effect of prenatal PM2.5 exposure remain elusive. We obtained 15,099 subjects from a nationally representative sample of China and measured their cognitive performance. We ascertained subjects' prenatal PM2.5 exposure and chronic PM2.5 exposure of the recent two years. Using this national sample, we found that PM2.5 exposure during the mid- to late-pregnancy was significantly associated with declined cognition and income; chronic PM2.5 exposure was also independently associated with cognition and income measured at adulthood with greater magnitude. Negative effect modification was observed between prenatal and chronic PM2.5 exposure. Instrumental variable approach and difference-in-difference study verified causal effects: every 1 µg/m3 increase in prenatal and chronic PM2.5 exposures were causally associated with -0.22% (-0.38%, -0.06%) and -0.17% (-0.31%, -0.03%) changes in cognitive function, respectively. People with low cognition and low income were more vulnerable to PM2.5 exposure with greater cognitive and income decline. In the future, although China's improved air quality continues to benefit people and reduce cognitive decline induced by chronic PM2.5 exposure, high prenatal PM2.5 exposure will continue to hurt the overall cognition of Chinese population, since in total 360 million people were born during the 2000-2020 polluted era. Prenatal PM2.5-induced cognitive decline would remain largely unchanged before 2050 and gradually reduce after 2065, regardless of environmental policy scenarios. The long-lasting cognitive impact of PM2.5 is worth considering while enacting environmental policies.

Heat stroke-induced cerebral cortex nerve injury by mitochondrial dysfunction: A comprehensive multi-omics profiling analysis.

In recent years, global warming has led to frequent instances of extremely high temperatures during summer, arousing significant concern about the adverse effects of high temperature. Among these, heat stroke is the most serious, which has detrimental effects on the all organs of human body, especially on brain. However, the comprehensive pathogenesis leading to brain damage remains unclear. In this study, we constructed a mouse model of heat stroke and conducted multi-omics profiling to identify relevant pathogenesis induced by heat stroke. The mice were placed in a constant temperature chamber at 42 °C with a humidity of 50 %, and the criteria for success in modeling were that the rectal temperature reached 42 °C and that the mice were trembling. Then the mice were immediately taken out for further experiments. Firstly, we conducted cFos protein localization and identified the cerebral cortex, especially the anterior cingulate cortex as the region exhibiting the most pronounced damage. Secondly, we performed metabolomics, transcriptomics, and proteomics analysis on cerebral cortex. This multi-omics investigation unveiled noteworthy alterations in proteins and metabolites within pathways associated with neurotransmitter systems, heatstroke-induced mitochondrial dysfunction, encompassing histidine and pentose phosphate metabolic pathways, as well as oxidative stress. In addition, the cerebral cortex exhibited pronounced Reactive Oxygen Species (ROS) production, alongside significant downregulation of the mitochondrial outer membrane protein Tomm40 and mitochondrial permeability transition pore, implicating cerebral cortex mitochondrial dysfunction as the primary instigator of neural impairment. This study marks a significant milestone as the first to employ multi-omics analysis in exploring the molecular mechanisms underlying heat stroke-induced damage in cerebral cortex neurons. It comprehensively identifies all potentially impacted pathways by heat stroke, laying a solid foundation for ensuing research endeavors. Consequently, this study introduces a fresh angle to clinical approaches in heatstroke prevention and treatment, as well as establishes an innovative groundwork for shaping future-forward environmental policies.

Heat exposure intervention, anxiety level, and multi-omic profiles: A randomized crossover study.

BACKGROUND: Climate change has led to the frequent occurrence of high-temperature weather, which has various adverse effects on health, ranging from blood metabolism to systemic organ function. In particular, the sequelae of heat stress injury in most people are related to the nervous system. However, the mechanisms between heat stress and mental health conditions, especially heat stress and anxiety, remain unclear. OBJECTIVE: We attempted to elucidate the effect of heat exposure intervention on anxiety levels in the population and its mechanism. METHODS: We first carried out a randomized controlled trial in 20 college students in Beijing, China, to observe the results of the effects of heat exposure intervention on human anxiety. Then, we collected blood samples before and after heat exposure experiment and used metabolomic and transcriptomic approaches to quantify serum metabolites and ELISA measurements to explore the underlying mechanisms. RESULTS: We found that even 1.5-hour heat exposure intervention significantly increased anxiety levels. Heat stress-induced anxiety was mediated by the activation of the HPA axis, inflammation, oxidative stress, and subsequently unbalanced neurotransmitters. Metabolites such as BDNF, GABA, and glucocorticoids released by the adrenal glands are biomarkers of heat stress-induced anxiety. CONCLUSIONS: We have demonstrated a causal link between heat stress and anxiety, explored possible biological pathway between heat stress and anxiety. Heat stress can cause the activation of the HPA axis and lead to changes in the body's metabolism, resulting in a series of changes such as inflammation and oxidative stress, leading to anxiety. This study reveals hidden health cost of climate change that has been underexplored, and also reminds us the importance of immediate climate actions.

Interactive Compensation Effects of Physical Activity and Sleep on Mental Health: A Longitudinal Panel Study among Chinese College Students during the COVID-19 Pandemic.

Physical activity (PA) and sleep are both important to mental health. However, their joint effects on mental distress have not been well explored. The aim of this study was to investigate the joint effects of PA and sleep on mental health, as well as the dose-response relationships between PA and mental health under different sleep health statuses. A longitudinal panel study was adopted to evaluate the relationship between PA, sleep, and mental health among 66 healthy Chinese college students with four online questionnaire surveys. A mixed-effect model with individual-level random effect was used to analyze the interactive regulation effect of PA and sleep on mental health, and a generalized additive model with splines was further fitted to analyze dose-response relationships between variables. When sleep was at a healthy level, no significant difference in mental health was observed between different levels of PA (p > 0.05). However, poor sleepers with moderate and high PA levels indicated significantly fewer negative emotions than those with low PA levels (p = 0.001, p = 0.004). Likewise, poor sleepers who engaged in more moderate intensity PA could significantly reduce negative emotions (ß = -0.470, p = 0.011) in a near-linear trend. In summary, both sleep and PA benefit mental health, and they probably regulate mental health through an interactive compensation mode. For good and poor sleepers, PA plays a different role in maintaining and improving mental health. Increasing moderate intensity PA up to moderate-and-high levels is recommended for those who simultaneously suffer from sleep and psychological health problems.

Physical activity attenuates negative effects of short-term exposure to ambient air pollution on cognitive function.

BACKGROUND: As physical activity benefits brain health whereas air pollution damages it, the cognitive response to these exposures may interact. PURPOSE: This study aimed to assess the short-term joint effect of physical activity and air pollution on cognitive function in a panel of healthy young adults. METHODS: We followed ninety healthy subjects aged around 22 years from September 2020 to June 2021 and measured their personal exposure to fine particulate matter (PM2.5) (µg/m3) and daily accelerometer-based moderate-to-vigorous physical activity (MVPA) (min/day) in 4 one-week-long sessions over the study period. At the end of each measurement session, we assessed executive function using Stroop color-word test and collected resting-state electroencephalogram (EEG) signals. RESULTS: We found short-term PM2.5 exposure damaged executive function (ßPM25 = 0.0064, p = 0.039) but physical activity could counterbalance it (ßMVPA = -0.0047, p = 0.048), whereby beta-3 wave played as a potential mediating role. MVPA-induced improvement on executive function was larger in polluted air (ßMVPA = -0.010, p = 0.035) than that in clean air (ßMVPA = -0.003, p = 0.45). To offset the negative effect of air pollution on cognitive function, individuals should do extra 13.6 min MVPA every day for every 10 µg/m3 increase in daily PM2.5. CONCLUSION: This study implies that physical activity could be used as a preventive approach to compensate the cognitive damages of air pollution.

Short-term PM2.5 exposure and cognitive function: Association and neurophysiological mechanisms.

BACKGROUND: Although converging evidence has demonstrated that exposure to fine particulate matter (PM2.5) caused adverse effects on brain structure and cognitive function, the association between the short-term exposure to PM2.5 and cognition dysfunction remained underexplored, especially possible neurophysiological mechanisms. METHODS: We conducted a longitudinal observational study with four repeated measurement sessions among 90 young adults from September 2020 to June 2021. During each measurement session, we measured participants' personal-level air pollution exposure for one week with portable monitors, followed by executive function assessment and electrophysiological signal recording at an assessment center. Standard Stroop color-word test was used accompanied with electroencephalogram (EEG) recording to assess performance on executive function. We used linear mixed-effect model with lagged values of PM2.5 levels to analyze the association between PM2.5 exposure and changes in executive function, and mediation analysis to investigate mediation effect by EEG signal. RESULTS: Adjusted mixed-effect models demonstrated that elevated PM2.5 exposure three days prior to cognitive assessment (lag-3) was associated with (1) declined performance in both congruent and incongruent tasks in Stroop test, (2) reduced lower and upper alpha event-related desynchronization (ERD) during 500-1000 ms after stimuli, both indicating impaired executive control. Lower and upper alpha ERD also mediated observed associations between short-term PM2.5 exposure and executive function. No significant associations were found between short-term PM2.5 exposure or aperiodic exponents in tonic and phasic states, or periodic alpha oscillations in tonic state. CONCLUSION: Our results provided evidence that short-term PM2.5 exposure was associated with executive dysfunction. Reduced alpha ERD was likely to be the underlying pathway through which PM2.5 induced adverse effects on neuron activities during cognitive tasks.

Effects of Online Bodyweight High-Intensity Interval Training Intervention and Health Education on the Mental Health and Cognition of Sedentary Young Females.

This study aimed to assess the effectiveness of an online high-intensity interval training (HIIT) intervention and health education on the behaviors, mental health, and cognitive function of sedentary young females. A single-blinded, six-week, randomized controlled pilot trial involving 70 sedentary young Chinese females, aged 18-30 years, was conducted. An intervention group (IG) (n = 33) underwent a HIIT intervention and health education, while a waitlist group (WG) (n = 37) only received health education. In pre-, mid-, and post-tests, both groups filled out questionnaires about physical activity, sedentary behavior, and mental health. Cognitive functions were assessed at the pre- and post-tests by computer-administered cognitive tests. A mixed-effect model with repeated measures was used to analyze outcomes of interest. The retention rate of the IG and WG was 100% and 78.38%, respectively. The IG were found to have significantly increased rates of moderate-to-vigorous physical activity (MVPA) (Mdiff = 940.61, p < 0.001, 95% confidence interval (95% CI): 576.67, 1304.55) from pre-test to post-test, while the WG demonstrated a more marked reduction in sedentary time (Mdiff = -73.02, p = 0.038, 95% CI: -141.90, -4.14) compared with the IG in the post-test. Moreover, anxiety and stress levels were shown to significantly reduce in the IG over the six-week period (Mdiff = -4.73, p = 0.002, 95% CI: -7.30, -2.15 and Mdiff = -5.09, p = 0.001, 95% CI: -8.29, -1.89, respectively). In addition, we observed a significant improvement in verbal ability (p = 0.008, ηp2 = 0.19) following the HIIT intervention and effects of the interaction with time on processing speed (p = 0.050, ηp2 = 0.10) and episodic memory (p = 0.048, ηp2 = 0.11). Moreover, the IG had better global cognitive performance than the WG in the post-test (Mdiff = 8.28, p = 0.003, 95% CI: 3.06, 13.50). In summary, both an online bodyweight HIIT intervention combined with health education, or health education alone, can effectively improve health-related behaviors, but the behavioral consequences may differ based on the emphasis of different intervention modalities. Furthermore, the "bodyweight HIIT plus health education" modality might be a more promising online intervention strategy to mitigate against negative emotions and improve cognitive function.