Environmental Health Research Fund of the Chinese University of Hong Kong and PhD Studentship of the Chinese University of Hong Kong.

Study Objectives: There is limited information on the relationship between risk of cardiovascular disease and the joint effects of sleep quality and sleep duration, especially from large, prospective, cohort studies. This study is to prospectively investigate the joint effects of sleep quality and sleep duration on the development of coronary heart disease. Methods: This study examined 60,586 adults aged 40 years or older. A self-administered questionnaire was used to collect information on sleep quality and sleep duration as well as a wide range of potential confounders. Events of coronary heart disease were self-reported in subsequent medical examinations. Two types of Sleep Score (multiplicative and additive) were constructed to reflect the participants' sleep profiles, considering both sleep quality and sleep duration. The Cox regression model was used to estimate the hazard ratio (HR) and the 95% confidence interval (CI). Results: A total of 2,740 participants (4.5%) reported new events of coronary heart disease at follow-up. For sleep duration, participants in the group of < 6 h/d was significantly associated with an increased risk of coronary heart disease (HR: 1.13, 95% CI: 1.04-1.23). However, the association in the participants with long sleep duration (> 8 h/d) did not reach statistical significance (HR: 1.11, 95% CI: 0.98-1.26). For sleep quality, both dreamy sleep (HR: 1.21, 95% CI: 1.10-1.32) and difficult to fall asleep/use of sleeping pills or drugs (HR: 1.40, 95% CI: 1.25-1.56) were associated with an increased risk of the disease. Participants in the lowest quartile of multiplicative Sleep Score (HR: 1.31, 95% CI: 1.16-1.47) and of additive sleep score (HR: 1.31, 95% CI: 1.16-1.47) were associated with increased risk of coronary heart disease compared with those in the highest quartile. Conclusions: Both short sleep duration and poor sleep quality are associated with the risk of coronary heart disease. The association for long sleep duration does not reach statistical significance. Lower Sleep Score (poorer sleep profile) increases the risk of coronary heart disease, suggesting the importance of considering sleep duration and sleep quality together when developing strategies to improve sleep for cardiovascular disease prevention. Keywords: cohort study, coronary heart disease, sleep duration, sleep quality, sleep score Citation: Lao XQ, Liu X, Deng HB, Chan TC, Ho KF, Wang F, Vermeulen R, Tam T, Wong MC, Tse LA, Chang LY, Yeoh EK. Sleep quality, sleep duration, and the risk of coronary heart disease: a prospective cohort study with 60,586 adults.

This study aimed to analyze the epidemiology and virology of fatal and nonfatal hand, foot, and mouth disease (HFMD) cases in Mainland China. A total of 10,714,237 survivors and 3046 deaths were reported from 2008 to 2014 June, with a case fatality rate of 0.03%. The morbidity of the survivors increased from 37.6/100,000 in 2008 to 139.6/100,000 in 2013 and peaked in 2012 at 166.8/100,000. However, the mortality varied around 0.03-0.04/100,000 across the time. Most of the survivors were distributed in the southern and eastern China, predominantly in the Guangxi and Hainan Province, whereas deaths were dominant in southern (Guangxi) and southwestern (Guizhou) China. The two groups showed similar seasonal fluctuations from 2008 to 2014, peaking in spring and early summer. Of the total cases, 93.97% were children less than 5 years of age, with those ≤ 2 years old accounting for 60.08% versus 84.02% in the survivor and death groups, respectively. Boys were at higher risk of infection than girls in both groups. Five years of virological surveillance showed that 43.73%, 22.04%, and 34.22% of HFMD cases were due to EV71, CoxA16 and other enteroviruses, respectively. EV71 was encountered in most deaths, with no substantial effect of age, gender, month, and year on incidence. Subgenotype C4a was the prevalent EV71 strain in Mainland China, with no significant difference in the VP1 gene related to virulence between the two groups. In conclusion, based on the largest population study, fatal and nonfatal HFMD cases, mainly caused by C4a of EV71, are circulating in Mainland China with a low-cause fatality rate.

National Key R&D Plan of China Science and key epidemiological disciplines of Zhejiang Provincial Health of China.

Sleep duration may be a significant determinant of metabolic health.

Background:Chronic kidney disease (CKD) is a serious global public health challenge, but there is limited information on the connection between air pollution and risk of CKD.Objective:The aim of this study was to investigate the association between long-term exposure to particulate matter (PM) with an aerodynamic diameter of less than 2.5μm (PM2.5) and the development of CKD in a large cohort.Methods:A total of 100,629 nonCKD Taiwanese residents age 20 y or above were included in this study between 2001 and 2014. Ambient PM2.5 concentration was estimated at each participant’s address using a satellite-based spatiotemporal model. Incident CKD cases were identified by an estimated glomerular filtration rate (eGFR) of less than 60mL/min/1.73 m2. We collected information on a wide range of potential confounders/modifiers during the medical examinations. Cox proportional hazard regression was applied to calculate hazard ratios (HRs).Results:During the follow-up, 4,046 incident CKD cases were identified, and the incidence rate was 6.24 per 1,000 person-years. In contrast with participants with the first quintile exposure of PM2.5, participants with the fourth and fifth quintiles exposure of PM2.5 had increased risk of CKD development, adjusting for age, sex, educational level, smoking, drinking, body mass index, systolic blood pressure, fasting glucose, total cholesterol, and self-reported heart disease or stroke, with an HR [95% confidence interval (CI)] of 1.11 (1.02, 1.22) and 1.15 (1.05, 1.26), respectively. A significant concentration–response trend was observed (p<0.001). Every 10 μg/m3 increment in the PM2.5 concentration was associated with a 6% higher risk of developing CKD (HR: 1.06, 95% CI: 1.02, 1.10). Sensitivity and stratified analyses yielded similar results.Conclusions:Long-term exposure to ambient PM2.5 was associated with an increased risk of CKD development. Our findings reinforce the urgency to develop global strategies of air pollution reduction to prevent CKD. https://doi.org/10.1289/EHP3304

Background:Long-term exposure to particulate matter (PM) air pollution may increase blood pressure and the risk of hypertension. However, epidemiological evidence is scarce and inconsistent.Objectives:We investigated the associations between long-term exposure to PM with an aerodynamic diameter <2.5μm (PM2.5), blood pressure, and incident hypertension in a large Taiwanese cohort.Methods:We studied 361,560 adults ≥18y old from a large cohort who participated in a standard medical examination program during 2001 to 2014. Among this group, 125,913 nonhypertensive participants were followed up. A satellite-based spatiotemporal model was used to estimate the 2-y average PM2.5 concentrations at each participant’s address. Multivariable linear regression was used in the cross-sectional data analysis with the 361,560 participants to investigate the associations between PM2.5 and systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP), and Cox proportional hazard regression was used in the cohort data analysis with the 125,913 participants to investigate the associations between PM2.5 and incident hypertension.Results:Each 10−μg/m3 increment in the 2-y average PM2.5 concentration was associated with increases of 0.45 mmHg [95% confidence interval (CI): 0.40, 0.50], 0.07 mmHg (95% CI: 0.04, 0.11), and 0.38 mmHg (95% CI: 0.33, 0.42) in SBP, DBP, and PP, respectively, after adjusting for a wide range of covariates and possible confounders. Each 10-μg/m3 increment in the 2-y average PM2.5 concentration was associated with an increase of 3% in the risk of developing hypertension [hazard ratio=1.03 (95% CI: 1.01, 1.05)]. Stratified and sensitivity analyses yielded similar results.Conclusions:Long-term exposure to PM2.5 air pollution is associated with higher blood pressure and an increased risk of hypertension. These findings reinforce the importance of air pollution mitigation strategies to reduce the risk of cardiovascular disease. https://doi.org/10.1289/EHP2466

BackgroundParticulate matter (PM) air pollution is associated with the risk of cardiovascular morbidity and mortality. However, the biological mechanism underlying the associations remains unclear. Atherosclerosis, the underlying pathology of cardiovascular disease, is a chronic inflammatory process. We therefore investigated the association of long-term exposure to fine PM (PM2.5) with C-reactive protein (CRP), a sensitive marker of systemic inflammation, in a large Taiwanese population.MethodsParticipants were from a large cohort who participated in a standard medical examination programme with measurements of high-sensitivity CRP between 2007 and 2014. We used a spatiotemporal model to estimate 2-year average PM2.5 exposure at each participant’s address, based on satellite-derived aerosol optical depth data. General regression models were used for baseline data analysis and mixed-effects linear regression models were used for repeated data analysis to investigate the associations between PM2.5 exposure and CRP, adjusting for a wide range of potential confounders.ResultsIn this population of 30 034 participants with 39 096 measurements, every 5 μg/m3 PM2.5 increment was associated with a 1.31% increase in CRP [95% confidence interval (CI): 1.00%, 1.63%) after adjusting for confounders. For those participants with repeated CRP measurements, no significant changes were observed between the first and last measurements (0.88 mg/l vs 0.89 mg/l, P = 0.337). The PM2.5 concentrations remained stable over time between 2007 and 2014.ConclusionsLong-term exposure to PM2.5 is associated with increased level of systemic inflammation, supporting the biological link between PM2.5 air pollution and deteriorating cardiovascular health. Air pollution reduction should be an important strategy to prevent cardiovascular disease.