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Aim: This study aimed to identify the epidemiological characteristics and transmission dynamics of paediatric cases.Methods: Information on 1369 paediatric cases with COVID-19 from 8 December 2019 to 7 March 2020 in Hubei province was extracted from the National Infectious Disease Surveillance System. The analysis included epidemic curves, temporal-spatial distribution, clinical classification and interval times between onset and diagnosis.Results: Among 1369 paediatric cases, the median age was 9 years and 58.2% of them were males. The proportion of severe and critical cases in children was lower than that in adults and the proportion of asymptomatic cases in children was five times greater than for adult cases. The first paediatric case was reported on 2 January 2020, and the daily number of new paediatric cases remained high from 1 February through to 22 February. The epidemiological curve of paediatric cases lagged behind that of adults by 19 days, and the first spike of the epidemic curve in senior high school students occurred 1 week earlier than in other paediatric groups. The proportion of clustered cases among children was about twice that for adults. The median of the interval in paediatric cases between onset and diagnosis, isolation and notification were 3, 0 and 3 days, respectively, and all of those were significantly shorter than in adults.Conclusions: The epidemic curve of child cases lagged behind that of adult cases by 19 days, and the major form of transmission observed was in clusters. [ABSTRACT FROM AUTHOR]

Background Disease caused by SARS-CoV-2 broke out in Wuhan in December 2019. We utilized confirmed cases outside Hubei Province to analyze epidemiologic characteristics and evaluate the effect of traffic restrictions implemented in Hubei beginning on 23 January 2020. Methods Information on 7015 confirmed cases from 19 January to 8 February 2020 in all provinces outside Hubei was collected from the national and local health commissions in China. Incubation period and interval times were calculated using dates of the following events: contact with an infected person, onset, first visit, and diagnosis. We evaluated changes in incubation period and interval times. Results The average age of all cases was 44.24 years. The median incubation period was 5 days and extended from 2 days on 23 January to 15 days on 8 February. The proportion of imported cases decreased from 85.71% to 33.19% after 23 January. In addition, lengths of intervals between onset and diagnosis, onset and first visit, and first visit and diagnosis decreased over time. Conclusions Rapidly transmitting COVID-19 has a short incubation period. The onset mainly occurred among young to middle-aged adults. Traffic restrictions played an important role in the decreased number of imported cases outside Hubei. [ABSTRACT FROM AUTHOR]

PM 2.5 exposure leads to lung function alteration. The potential pathway underlying above association, especially the role of DNA methylation is unclear. The objectives of this study are to evaluate the associations of personal PM 2.5 concentrations with DNA methylation at the epigenome-wide level, and investigate how PM 2.5 -related DNA methylation affects lung function. A total of 402 observations of non-smokers were selected from the Wuhan-Zhuhai cohort. PM 2.5 exposure was estimated through a model established in the same population. Blood DNA methylation levels were determined through Illumina Infinium MethylationEPIC BeadChips. Lung function was tested through spirometry on the day of blood sampling. The associations of PM 2.5 exposure with DNA methylation and DNA methylation with lung function were determined through linear mixed models. Ten PM 2.5 -related CpG sites (mapped to 7 different genes) were observed with false discovery rate <0.05. Methylation levels of cg24821877, cg24862131, cg23530876, cg11149743 and cg10781276 were positively associated with PM 2.5 concentrations. While methylation levels of cg10314909, cg08968107, cg18362281, cg24663971 and cg17834632 were negatively associated with PM 2.5 concentrations. The top CpG was cg24663971 (P = 1.51✕10−9). Among the above 10 sites, significantly positive associations of methylation levels of cg24663971 with FVC%pred and FEV 1 %pred, and cg10314909 with FVC, FVC%pred, and FEV 1 %pred were observed. Age had modification effect on the associations between cg24663971 methylation and FVC%pred, and the associations were more obvious among participants with age ≥58 years. In conclusion, PM 2.5 exposure was associated with DNA methylation, and PM 2.5 -related DNA methylation was associated with lung function among Wuhan urban non-smokers. [Display omitted] • Ten CpGs were linked to PM 2.5 exposure with false discovery rate <0.05. • Cg24663971 and cg10314909 methylation was positively associated with lung function. • PM 2.5 exposure concentrations at the individual level were estimated. • Blood DNA methylation at the epigenome level were determined. [ABSTRACT FROM AUTHOR]

As a polycyclic aromatic hydrocarbon, environmental exposure to phenanthrene is widespread worldwide. The potential effects and mechanism of phenanthrene exposure on fasting plasma glucose (FPG) have not been well determined. In this study, we aim to explore the effects of phenanthrene exposure and AMER3 variants on fasting plasma glucose (FPG) through a longitudinal epidemiological study. Repeated measurements of five urinary hydroxyphenanthrene (OHPh) for 5739 participants with 7083 observations from the Wuhan-Zhuhai cohort were performed to analyze the relationships between total OHPh (ΣOHPh) and FPG using linear mixed models and restricted cubic spline functions. Then, we genotyped 2777 participants (4104 observations) using the Infinium OmniZhongHua-8 BeadChip and included all 14 single nucleotide polymorphisms (SNPs) within the AMER3 gene to analyze the interaction of the AMER3 on the relationship between ΣOHPh and FPG. We observed a U-shaped relationship between ΣOHPh and FPG, and the turning point of ΣOHPh was 2.512 μg/mmol Cr. When lower than the turning point, ΣOHPh was negatively associated with FPG, while higher than the turning point, ΣOHPh was positively associated with FPG. Furthermore, we observed interactions (P int <0.05) between two common variants (rs72854995 and rs72854999) of the AMER3 and ΣOHPh on FPG change: the U-shaped relationship was still observed in the GG genotype groups but not in the allele A carriers. Our results suggested that the AMER3 gene can modify the U-shaped relationship between phenanthrenes exposure and FPG, which showed a new gene-environment interaction and will provide a new perspective on the relationship between phenanthrene exposure and FPG. [Display omitted] • A U-shaped relationship was observed between ΣOHPh and FPG. • AMER3 variants modify the U-shaped relationship between ΣOHPh and FPG. • The role of AMER3 in glucose metabolism warrants further investigation. [ABSTRACT FROM AUTHOR]

Environmental risk factors have been implicated in adverse health effects. Previous epidemiological studies on environmental risk factors mainly analyzed the impact of single pollutant exposure on health, while in fact, humans are constantly exposed to a complex mixture consisted of multiple pollutants/chemicals. In recent years, environmental epidemiologists have sought to assess adverse health effects of exposure to multi-pollutant mixtures based on the diversity of real-world environmental pollutants. However, the statistical challenges are considerable, for instance, multicollinearity and interaction among components of the mixture complicate the statistical analysis. There is currently no consensus on appropriate statistical methods. Here we summarized the practical statistical methods used in environmental epidemiology to estimate health effects of exposure to multi-pollutant mixture, such as Bayesian kernel machine regression (BKMR), weighted quantile sum (WQS) regressions, shrinkage methods (least absolute shrinkage and selection operator, elastic network model, adaptive elastic-net model, and principal component analysis), environment-wide association study (EWAS), etc. We sought to review these statistical methods and determine the application conditions, strengths, weaknesses, and result interpretability of each method, providing crucial insight and assistance for addressing epidemiological statistical issues regarding health effects from multi-pollutant mixture. [Display omitted] • Mixture analysis is challenged by high-dimensionality, multicollinearity, interaction, etc. • BKMR and WQS-based methods developed for mixture analysis are increasingly used. • Method selection should be based on its features, data traits, study purposes, etc. • Combined use of multiple statistical methods proposed in this study is recommended. • Measurement error deserves attention when assessing multi-pollutant mixture effects. [ABSTRACT FROM AUTHOR]

Exposure to heavy metals was reported to be associated with heart rate variability (HRV) alteration. However, possible pathway of such association remains unclear. In this research, we investigated the possible role of lipid peroxidation in the associations between urinary heavy metals and HRV. We performed a cross-sectional study using baseline data of Wuhan-Zhuhai cohort. Urinary heavy metals (including lead, barium, antimony, cadmium, zinc, copper, iron and manganese), urinary 8-iso-prostaglandin-F2α levels (common biomarker for lipid peroxidation) and HRV indices (SDNN, r-MSSD, low frequency, high frequency and total power) were measured among 3022 participants. We conducted multivariable linear regression models to quantify associations between urinary 8-iso-prostaglandin-F2α (8-iso-PGF2α) and heavy metals or HRV indices. The potential role of 8-iso-PGF2α in the association of urinary heavy metals with HRV was evaluated through mediation analyses. After adjusting for potential confounders, urinary manganese, iron, copper, zinc, cadmium, antimony and barium were identified to be negatively associated with one or more HRV parameters. Each one-unit growth of log-transformed levels of urinary manganese, iron, copper, zinc, antimony and barium was associated with a 1.9%, 1.5%, 4.7%, 4.0%, 2.7% and 1.3% decrease in SDNN, respectively. We observed positive dose-response relationships between all eight urinary heavy metals and 8-iso-PGF2α, as well as negative association of urinary 8-iso-PGF2α with SDNN and total power (all P trend<0.05). The proportions mediated by 8-iso-PGF2α on SDNN were 4.6% for manganese, 9.3% for iron, 19.8% for antimony and 11.0% for barium. The proportions mediated by 8-iso-PGF2α on total power were 6.9% for manganese and 10.1% for cadmium (all P value < 0.05). This study suggested that urinary manganese, iron, copper, zinc, cadmium, antimony and barium were negatively associated with HRV indices. Lipid peroxidation may partly mediate the associations of urinary manganese, iron, cadmium, antimony and barium with specific HRV indices. [ABSTRACT FROM AUTHOR]

Polycyclic aromatic hydrocarbon (PAH) exposure has been considered a risk factor for cardiovascular diseases (CVD), whereas possible mechanisms for this association have not been fully understood. This study focused on exploring the potential effect of oxidatively damaged DNA on the relationships between PAH exposure and the 10-year atherosclerotic CVD (ASCVD) risk. Urinary levels of monohydroxy PAH metabolites (OH-PAHs) and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG, the typical biomarker for oxidatively damaged DNA) were measured among 3052 subjects in the baseline of the Wuhan-Zhuhai cohort. The relationships between urinary OH-PAHs, 8-oxodG and 10-year risk of ASCVD were analyzed by linear mixed models and logistic regression models, respectively. The mediation analysis was further applied to explore the role of 8-oxodG in the relationship between urinary OH-PAHs and 10-year ASCVD risk. After controlling for potential confounders, the log-transformed level of total urinary low molecular weight OH-PAHs (∑LMW OH-PAHs) was significantly associated with an elevated risk of 10-year ASCVD [odds ratio (OR) = 1.222, 95% confidence interval (CI): 1.065–1.402]. More specifically, significantly positive dose-response relationships between total urinary hydroxynaphthalene (∑OHNa), hydroxyfluorene (∑OHFlu), hydroxyphenanthrene (∑OHPh) and 10-year ASCVD risk were observed (all P for trend <0.05). We also found positive relationships between urinary OH-PAH levels and 8-oxodG, as well as between urinary 8-oxodG levels and 10-year risk of ASCVD. Moreover, mediation analyses indicated that urinary 8-oxodG mediated 14.49%, 12.62% and 10.55% of the associations between urinary ∑LMW OH-PAHs, ∑OHNa, ∑OHFlu and 10-year ASCVD risk, respectively. These findings suggest that the oxidatively damaged DNA pathway may be a possible mechanism underlying PAH-associated ASCVD risk elevation. Image 1 • Urinary levels of low molecular weight OH-PAHs were positively associated with the 10-year ASCVD risk. • Urinary 8-oxodG levels were both positively associated with urinary OH-PAHs and 10-year ASCVD risk. • Urinary 8-oxodG partially mediated the associations between urinary low molecular weight OH-PAHs and 10-year ASCVD risk. Urinary 8-oxodG may partially mediate the association between low molecular weight PAH exposure and elevated risk of 10-year ASCVD in a Chinese population. [ABSTRACT FROM AUTHOR]

[Display omitted] • Exposure to PAHs is associated with increased blood lipid profiles over 6 years. • Individual with higher lipid-PRS could be more susceptible to hyperlipidemias. • Higher lipid-PRS aggravate and modify blood lipid when exposure to PAHs. We aim to analyze the effects of polycyclic aromatic hydrocarbons (PAHs) exposure and genetic predisposition on blood lipid through a longitudinal epidemiological study. We enrolled 4,356 observations who participated at baseline (n = 2,435) and 6-year follow-up (n = 1,921) from Wuhan-Zhuhai cohort. Ten urinary PAHs metabolites and blood lipid (i.e. , total cholesterol [TC], triglycerides [TG], low-density lipoprotein cholesterol [LDL-C], and high-density lipoprotein cholesterol [HDL-C]) were measured at both baseline and follow-up. The polygenic risk scores (PRS) of blood lipid were constructed by the corresponding genome-wide association studies. Linear mixed models were fit to identify associations between urinary PAHs metabolites, blood lipid, and lipid-PRSs in the repeated-measure analysis. Besides, longitudinal relationships of blood lipid with urinary PAHs metabolites and respective lipid-PRSs were examined by using linear regression models. Compared with subjects who had persistently low urinary total hydroxyphenanthrene (ΣOHPh), those with persistently high levels had an average increase of 0.137 mmol/l for TC and 0.129 mmol/l for LDL-C over 6 years. Each 1-unit increase of TC-, TG-, LDL-C-, and HDL-C-specific PRS were associated with an average increase of 0.438 mmol/l for TC, 0.264 mmol/l for TG, 0.198 mmol/l for LDL-C, and 0.043 mmol/l for HDL-C over 6 years, respectively. Compared with subjects who had low genetic risk and persistently low ΣOHPh, subjects with high LDL-specific PRS and persistently high ΣOHPh had an average increase of 0.652 mmol/l for LDL-C. Our results suggest that high-level ΣOHPh exposure is associated with an average increase of LDL-C over 6 years, and those relationships can be aggravated by a higher LDL-C-genetic risk. No significant relationships were observed between other PAHs metabolites (including hydroxynaphthalene, hydroxyfluorene, and hydroxypyrene) and blood lipid changes over 6 years. Our findings emphasize the importance of preventing PAHs exposure, particularly among those with a higher genetic predisposition of hyperlipidemia. [ABSTRACT FROM AUTHOR]

Short-term effects of fine particulate matter (PM 2.5) exposure on lung function have been reported. However, few studies have assessed PM 2.5 exposure on the personal level, and the mechanism underlying the effects of PM 2.5 exposure on lung function remains less clear. To evaluate the association between personal PM 2.5 exposure and lung function alteration in general population and to explore the roles of systematic inflammation and oxidative damage in this association. A total of 7685 lung function tests were completed among 4697 urban adults in Wuhan, China. Plasma C-reactive protein (CRP), urinary 8-iso-prostaglandin-F 2α (8-iso-PGF 2α) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels were measured. Personal PM 2.5 exposure levels were estimated using an estimation model from the actual measurements of individual PM 2.5 levels in 191 participants. Mixed linear models were used to evaluate the association between personal PM 2.5 exposure and lung function. Mediation analyses were conducted to investigate the roles of CRP, 8-iso-PGF 2α and 8-OHdG in above associations. After adjusting for confounders, each 10 μg/m3 increase in the previous-day personal PM 2.5 exposure was associated with 2.94 mL, 2.02 mL and 16.14 mL/s decreases in forced vital capacity (FVC), forced expiration volume in 1 s (FEV 1) and peak expiratory flow, respectively. The associations were more obvious among never smokers compared with current smokers. Cumulative 7-day exposure to PM 2.5 led to the strongest adverse effects on lung function. Among never smokers with high PM 2.5 exposure levels, a positive relationship was observed between personal PM 2.5 level and urinary 8-iso-PGF 2α , and 8-iso-PGF 2α meditated 4.69% and 12.30% of the association between the 7-day moving PM 2.5 concentration and FVC and FEV 1 , respectively. We did not observe a significant positive association between PM 2.5 exposure and plasma CRP or urinary 8-OHdG. Short-term personal exposure to PM 2.5 is associated with reduced pulmonary ventilation function. Urinary 8-iso-PGF 2α partly mediates these associations. Unlabelled Image • Personal PM 2.5 exposure was estimated using a model from actual measurements. • Cumulative 7 days PM 2.5 exposure showed greatest effect on FVC, FEV 1 and PEF. • PM 2.5 -related declines in both FEV 1 and FVC were stronger among never smokers. • Urinary 8-iso-PGF 2α mediated the associations among nonsmokers with high PM 2.5 level. [ABSTRACT FROM AUTHOR]

• PAH exposure at high level was significantly associated with plasma IL-22 decline. • Down-regulated IL-22 was associated with a higher level of FPG and T2D prevalence. • IL-22 partially mediated the association between PAH exposure with FPG and T2D. Previous studies found that exposure to polycyclic aromatic hydrocarbons (PAHs) was associated with type 2 diabetes (T2D) prevalence. However, the potential mechanism is still unclear. In this study, we investigated 3031 Chinese urban adults to discover the relationship between PAH exposure and plasma Interleukin-22 (IL-22) and potential role of IL-22 in the association between PAH and fasting plasma glucose (FPG) or risk of T2D. After adjustment for potential confounders, significant dose-response relationships were observed between several urinary PAH metabolites with FPG and the prevalence of T2D. Each 1-U increase in ln-transformed value of 2-hydroxynaphthalene (2-OHNa), 2-hydroxyphenanthrene (2-OHPh), 3-hydroxyphenanthrene (3-OHPh), 4-hydroxyphenanthrene (4-OHPh), 9-hydroxyphenanthrene (9-OHPh), 1-hydroxypyrene (1-OHP) or total PAH metabolites was significantly associated with a 0.053, 0.026, 0.037, 0.045, 0.051, 0.041 or 0.047 unit decrease in IL-22 level, respectively. In addition, plasma IL-22 level was negatively associated with FPG and prevalence of T2D in a dose-dependent manner. Mediation analysis showed that IL-22 mediated 8.48 %, 3.87 %, 6.64 %, 6.47 %, and 8.67 % of the associations between urinary 2-OHNa, 1-OHPh, 3-OHPh, 4-OHPh, and 9-OHPh with the prevalence of T2D, respectively. These results indicated that urinary PAHs metabolites were inversely associated with plasma levels of IL-22, but positively related to FPG and the T2D prevalence. Downregulation of IL-22 might play a significant role in mediating PAHs exposure-associated risk increasement of T2D. [ABSTRACT FROM AUTHOR]