Abstract Background Epidemiological studies suggest an association between sleep duration and risk of coronary heart disease, however, the results are controversial. We conducted this systematic ...review and meta-analysis to summarize the potential dose–response relationship between sleep duration and risk of coronary heart disease. Methods The electronic reference databases (PubMed and Embase) were searched through January 2016 with selection criteria for relevant studies. Both semiparametric and parametric methods were used to calculate the pooled risk estimates. Results Seventeen articles with 22 independent reports involving 17,841 incident cases of coronary heart disease among 517,440 participants were included in our meta-analysis. A U-shaped relationship was detected between sleep duration and risk of coronary heart disease, with the lowest risk at 7–8 h per day. Compared with 7 h sleep duration per day, the combined relative risk of coronary heart disease were 1.11 (95%CI = 1.05–1.16) for an reduction of one hour and 1.07 (95%CI = 1.00–1.15) for an increment of one hour. And the results almost did not change in the subgroup analysis of gender and fatal cases. Exclusion of any single study did not alter the combined relative risk. In addition, visual inspection of funnel plots, Begg's and Egger's tests failed to identify publication bias. Conclusions Both short and long sleep duration are significantly associated with increased risk of coronary heart disease. Compared with 7 h sleep duration per day, the risk of coronary heart disease increases 11% for an hour decrease and increases 7% for an hour increase.
Fine particulate matter (PM2.5) exposure has been associated with lung function decline, but impact of PM2.5 constituents especially for polycyclic aromatic hydrocarbons (PAHs) on lung function is ...unclear among community population. We enrolled 224 Chinese participants who participated in two study periods (2014–2015 and 2017–2018) of the Wuhan-Zhuhai cohort as a panel, and quantified the associations of personal PM2.5 and sixteen PM2.5-bound PAHs with lung function levels as well as lung function change in three years by linear mixed models. Diagnostic ratios were calculated to identify potential sources of PM2.5-bound PAHs in Wuhan and Zhuhai separately. In single-constituent models, we found that each one interquartile-range increase of naphthalene, acenaphthene, fluoranthene and pyrene were associated with 26.82, 60.99, 45.25 and 23.37 mL decline in FVC respectively; while fluoranthene and pyrene were associated with 27.43 and 15.49 mL decline in FEV1 respectively. Similar results were observed in consitituent-PM2.5 joint models and single-constituent residual models. Persistently long-term high levels of three HMW-PAHs (benzoaanthracene, dibenzoa,hanthracene, and benzoghiperylene) were associated with 214.65, 226.13, and 265.00 mL decline in FVC decline in three years, compared with persistently low exposure level groups. The associations were different between Wuhan and Zhuhai. The results of diagnostic ratios suggested the differences in PAH emissions between two cities. Our findings provide evidence that both short- and long-term PM2.5-bound PAH exposures might affect lung function.
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•Personal PM2.5 exposure and sixteen PM2.5-bound PAHs were measured.•FVC and FEV1 declined when acute exposure to PM2.5-bound PAHs, but not for PM2.5.•Persistently high exposure to HMW-PAHs (BaA, DhA and BgP) linked with FVC decline.•Potential sources of PM2.5-bound PAHs in Wuhan and Zhuhai were different.
Cadmium is a recognized human carcinogen, raising global concern for its ubiquitously environmental exposure on public health. Diabetogenic effects of cadmium have been suggested in previous studies, ...but the longitudinal associations of chronic cadmium exposure with fasting blood glucose changes and type 2 diabetes mellitus have not been fully elucidated.
To investigate the effects of long-term cadmium exposure on the fasting blood glucose changes and type 2 diabetes mellitus risk in a longitudinal prospective study of China.
A total of 3521 urban adults were included as baseline study population from the Wuhan-Zhuhai cohort, and followed up three years later. Urinary cadmium concentrations were determined repeatedly during the follow-up of a three-year period. The within-person and between-person variability of urinary cadmium concentrations over three years was estimated using multilevel random-effects mixed models. Multivariate regression models were performed to evaluate the associations of cadmium exposure with fasting blood glucose changes and type 2 diabetes mellitus risk.
The geometric means of creatinine-corrected urinary cadmium concentration at baseline were 1.13 μg/g creatinine, which were close to the levels of follow-up (1.14 μg/g creatinine). The intra-class correlation coefficient of creatinine-corrected urinary cadmium concentrations was 0.71, achieving good reproducibility of cadmium over three years. With adjustment for potential confounders, each one-unit increase in log10-transformed cadmium was associated with a 0.11 (95%CI: 0.03 to 0.19) elevation in fasting blood glucose concentration, and was associated with a 42% (95%CI: 1.16 to 1.73) increase in risk of prevalent type 2 diabetes mellitus. Upward trends of fasting blood glucose changes and type 2 diabetes mellitus incidence were observed with increasing cadmium exposure. Individuals with the highest urinary cadmium exposure had a significant increase in fasting blood glucose change at follow-up β (95% CI): 0.49 (0.31–0.67). Risk of incident type 2 diabetes mellitus were gradually elevated across increasing quartiles of cadmium exposure, though associations did not reach statistical significance (P = 0.15).
Our findings suggested that relatively high chronic cadmium exposure for general population adults might contribute to elevated changes of fasting blood glucose resulting in the development of type 2 diabetes mellitus.
•Excellent reproducibility was achieved for urinary Cd levels over three years.•Significant associations observed for urinary Cd with FBG and prevalent T2DM risk.•Individuals with high Cd exposure had a significant increase in FBG at follow-up.•Risk of incident T2DM were gradually elevated across increasing urinary Cd.•Associations were further confirmed in penalized regression splines models.
Silicosis is one of the most severe interstitial lung fibrosis diseases worldwide, caused by crystalline silica exposure. While the mechanisms and pathogenesis underlying silicosis remained unknown. ...N6-methyladenosine (m6A) methylation has received significant attention in a variety of human diseases. However, whether m6A methylation is involved in silicosis has not been clarified. In this study, we conducted methylated RNA immunoprecipitation sequencing (MeRIP-Seq) and transcriptome sequencing (RNA-Seq) to profile the m6A modification in normal and silicosis mouse models (n = 3 pairs). The global levels of m6A methylation were further assessed by m6A RNA methylation quantification kits, and the major regulators of m6A RNA methylation were verified by qRT-PCR. Our results showed that long-term exposure to crystalline silica led to silicosis, accompanied by increasing levels of m6A methylation. Upregulation of METTL3 and downregulation of ALKBH5, FTO, YTHDF1, and YTHDF3 might contribute to aberrant m6A modification. Compared with controls, 359 genes showed differential m6A methylation peaks in silicosis (P < 0.05 and FC ≥ 2). Among them, 307 genes were hypermethylated, and 52 genes were hypomethylated. RNA-Seq analysis revealed 1091 differentially expressed genes between the two groups, 789 genes were upregulated and 302 genes were downregulated in the lungs of silicosis mice (P < 0.05 and FC ≥ 2). In the conjoint analysis of MeRIP-Seq and RNA-Seq, we identified that 18 genes showed significant changes in both m6A modification and mRNA expression. The functional analysis further noted that these 18 m6A-mediated mRNAs regulated pathways that were closely related to “phagosome”, “antigen processing and presentation”, and “apoptosis”. All findings suggested that m6A methylation played an essential role in the formation of silicosis. Our discovery with multi-omics approaches not only gives clues for the epigenetic mechanisms underlying the pathogenesis of silicosis but also provides novel and viable strategies for the prevention and treatment of silicosis.
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•We firstly found that m6A methylation level was increased in silicosis.•We conducted MeRIP-Seq and RNA-Seq to identify the gene changes in silicosis.•Functional analyses found altered genes were related to immune response and fibrosis.
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•We found an inverted U-shaped association of ambient temperature with semen quality.•Both low and high ambient temperatures were inversely associated with semen quality.•An “optimal” ...ambient air temperature of 13 °C was suggested for semen quality.
Semen quality is a vital determinant for male fertility. The process of spermatogenesis is highly sensitive to fluctuations in temperature. However, the impact of ambient temperature on semen quality remains unclear. We aimed to quantitatively assess the association between ambient temperature and semen quality. Using data from Hubei provincial human sperm bank in Wuhan, China, we conducted a longitudinal study including 10 802 volunteers who lived in Wuhan and passed the initial physical examination for sperm donation between Mar 27, 2013 and April 9, 2018. Semen quality parameters including sperm concentration, total sperm number, total motility, progressive motility, total motile sperm count and progressively motile sperm count were determined in the sperm bank. We used linear mixed models to identify estimate changes of outcomes in relation to ambient temperature (i.e., air temperature and apparent temperature) exposure measured as the mean daily temperature during the 0–90 days before semen collection. Among 10 802 subjects who underwent 41 689 semen examinations, we observed inverted U-shaped exposure-response associations between air temperature exposure and all semen quality parameters, with an identical threshold exposure of 13 °C. For air temperature exposure <13 °C, each 5 °C lower temperature was significantly associated with 1.94 × 106/ml, 7.12 × 106, 0.77%, 0.81%, 6.48 × 106, and 5.87 × 106 decrease in sperm concentration, total sperm count, total motility, progressive motility, total motile sperm count and progressively motile sperm count, respectively. When air temperature exposure was ≥13 °C, each 5 °C higher temperature was significantly associated with 0.70 × 106/ml, 4.09 × 106, 1.01%, 1.06%, 4.31 × 106, and 4.20 × 106 decrease in sperm concentration, total sperm count, total motility, progressive motility, total motile sperm count and progressively motile sperm count, respectively. Age, BMI and smoking did not significantly modify these associations. Similar results were observed for apparent temperature. This study provides a comprehensive picture of nonlinear association between ambient temperature and semen quality, as well as an optimal temperature for the benefit of semen quality. Both lower and higher ambient temperature exposures compared with the optimal temperature were significantly associated with decreased semen quality. The findings highlight the needs and importance to reduce extreme ambient temperature exposures in maintaining optimal semen quality for men. Further investigation is warranted to determine the causality of the association and the underlying mechanisms.
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•Urinary copper and zinc were positively associated with MetS prevalence.•Urinary copper and zinc were positively associated with plasma CRP.•Higher concentration of plasma CRP was ...positively related to MetS prevalence.•Associations of copper and zinc with MetS was partly mediated through CRP.
Essential metals have been reported to be associated with metabolic diseases. However, the relationships between essential metals exposure and Metabolic Syndrome (MetS) is still uncertain, and the underlying mechanisms of the association remain unclear.
To investigate the associations of urinary essential metals with MetS prevalence; and further to explore potential role of systemic inflammation biomarker, C-reactive protein (CRP), in relationships between essential metals exposure and MetS prevalence in a cross-sectional study.
Concentrations of 8 urinary essential metals and plasma C-reactive protein (CRP) were quantified in 3272 adults from Wuhan-Zhuhai cohort. Urinary essential metals were adjusted by the corresponding urinary creatinine concentrations and reported as μg/mmol creatinine. Multivariable logistic regression and linear regression models were used to evaluate dose–response relationships between essential metals, plasma CRP, and MetS prevalence. Mediation analysis was performed to investigate the role of plasma CRP in the associations between urinary essential metals and MetS prevalence.
In the single-metal models, we observed positive dose-dependent relationships of urinary copper and zinc with MetS prevalence. Compared with the lowest quartiles of urinary metals, the ORs (95% CI) of MetS in the highest quartiles were 1.40 (1.03, 1.91) for urinary copper and 2.07 (1.51, 2.84) for zinc, respectively. The dose-dependent relationships of zinc and copper with MetS remained significant in the multiple-metal models and Bayesian kernel machine regression (BKMR) models. No significant associations were observed between others essential metals (e.g. manganese, iron, cobalt, selenium, chromium, molybdenum) and MetS in this general population (all P value > 0.05). In addition, urinary copper and zinc increased monotonically with plasma CRP elevation, and plasma CRP was positively associated with the MetS prevalence. Mediation analysis indicated that plasma CRP mediated 5.2% and 3.2% in the associations of urinary copper and zinc with MetS prevalence, respectively.
Elevated concentrations of urinary copper and zinc were associated with increased prevalence of MetS. Systemic inflammation may play an important role in the associations of copper and zinc exposure with MetS.
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•Urinary acrolein metabolites (UAMs) were repeatedly measured over a period of 3 years.•UAMs were cross-sectionally associated with pulmonary function (PF) reduction.•UAMs were ...longitudinally associated with PF decline in 3 years.•8-OHdG, CRP, and CC16 aggravated and/or mediated acrolein-associated PF reduction.•This is the first study to report the associations of UAMs with PF.
Acrolein is a significant high priority hazardous air pollutant with pulmonary toxicity and the leading cause of most noncancer adverse respiratory effects among air toxics that draws great attention. Whether and how acrolein exposure impacts pulmonary function remain inconclusive.
To assess the association of acrolein exposure with pulmonary function and the underlying roles of oxidative DNA damage, inflammation, and pulmonary epithelium integrity.
Among 3,279 Chinese adults from the Wuhan-Zhuhai cohort, associations of urinary acrolein metabolites (N-Acetyl-S-(2-carboxyethyl)-L-cysteine, CEMA; N-Acetyl-S-(3-hydroxypropyl)-L-cysteine, 3HPMA) as credible biomarkers of acrolein exposure with pulmonary function were analyzed by linear mixed models. Joint effects of biomarkers of oxidative DNA damage (8-hydroxy-deoxyguanosine), inflammation (C-reactive protein, CRP), and pulmonary epithelium integrity (Club cell secretory protein, CC16) with acrolein metabolites on pulmonary function and the mediating roles of these biomarkers were assessed. Besides, a subgroup (N = 138) was randomly recruited from the cohort to assess the stabilities of acrolein metabolites and their longitudinal associations with pulmonary function change in three years.
Significant inverse dose–response relationships between acrolein metabolites and pulmonary function were found. Each 10-fold increment in CEMA, 3HPMA, or ΣUACLM (CEMA + 3HPMA) was cross-sectionally related to a 68.56-, 40.98-, or 46.02-ml reduction in FVC and a 61.54-, 43.10-, or 50.14-ml reduction in FEV1, respectively (P < 0.05). Furthermore, acrolein metabolites with fair to excellent stabilities were found to be longitudinally associated with pulmonary function decline in three years. Joint effects of acrolein metabolites with 8-hydroxy-deoxyguanosine, CRP, and CC16 on pulmonary function were identified. CRP significantly mediated 5.97% and 5.51% of CEMA-associated FVC and FEV1 reductions, respectively. 8-hydroxy-deoxyguanosine significantly mediated 6.78%, 6.88%, and 7.61% of CEMA-, 3HPMA-, and ΣUACLM-associated FVC reductions, respectively.
Acrolein exposure of general adults was cross-sectionally and longitudinally related to pulmonary function decline, which was aggravated and/or partly mediated by oxidative DNA damage, inflammation, and pulmonary epithelium injury.
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•Acrylamide (ACR) exposure was associated with increased cardiovascular (CV) risk.•Long-term daily ACR exposure could longitudinally increase CV risk over 3 years.•ACR exposure was ...related to oxidative stress, inflammation, and TGF-β1 induction.•Oxidative stress, inflammation, and TGF-β1 mediated ACR-associated CV risk increase.
Acrylamide (ACR) exposure and consequent health hazards are alarming public health issues that attract worldwide concern. The World Health Organization urges more researches into health hazards from ACR exposure. However, whether and how ACR exposure increases cardiovascular risk remain unclear, and we sought to address these issues in this prospective cohort study conducted on 3024 general adults with 3-year follow-up (N = 871 at follow-up). Individual urinary ACR metabolites (N-Acetyl-S-(2-carbamoylethyl)-L-cysteine AAMA and N-Acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine GAMA) as credible biomarkers of ACR exposure were detected to assess their cross-sectional and longitudinal relationships with 10-year cardiovascular disease (CVD) risk, a well measure of overall cardiovascular risk. Besides, biomarkers of oxidative stress (urinary 8-hydroxy-deoxyguanosine 8-OHdG and 8-iso-prostaglandin-F2α 8-iso-PGF2α) and inflammation (circulating mean platelet volume MPV and plasma C-reactive protein CRP) as well as plasma transforming growth factor-β1 (TGF-β1) were measured to assess their mediating/mechanistic roles in the relationships of ACR metabolites with 10-year CVD risk. We found AAMA, GAMA, and ΣUAAM (AAMA + GAMA) were cross-sectionally and longitudinally related to increased 10-year CVD risk with odds ratios (95% confidence intervals CIs) of 1.32 (1.04, 1.70), 1.81 (1.36, 2.40), and 1.40 (1.07, 1.82), respectively, and risk ratios (95% CIs) of 1.99 (1.10, 3.60), 2.48 (1.27, 4.86), and 2.13 (1.15, 3.94), respectively. Furthermore, 8-OHdG, 8-iso-PGF2α, MPV, CRP, and TGF-β1 were found to significantly mediate 8.06–48.92% of the ACR metabolites-associated 10-year CVD risk increment. In summary, daily ACR exposure of general adults was cross-sectionally and longitudinally associated with increased cardiovascular risk, which was partly mediated by oxidative stress, inflammation, and TGF-β1, suggesting for the first time that ACR exposure may well increase cardiovascular risk of general adult population partly by mechanisms of inducing oxidative stress, inflammation, and TGF-β1. Our findings have important public health implications that provide potent epidemiological evidence and vital mechanistic insight into cardiovascular risk increment from ACR exposure.
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•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.
Little is known about the effects of night shifts and their interactions with genetic factors on chronic obstructive pulmonary disease (COPD). In this study, we aim to investigate relationships ...between long-term night shift work exposure and COPD risk, and assess modification effects of genetic predisposition.
A total of 277,059 subjects who were in paid employment or self-employed were included in the UK Biobank. Information on current and lifetime employment was obtained, and a weighted COPD-specific genetic risk score (GRS) was constructed. We used Cox proportional hazard models to investigate associations between night shift work and COPD risk, and their interaction with COPD-specific GRS.
The cohort study included 277,059 participants (133,063 men 48.03%; mean SD age, 52.71 7.08 years). During a median follow-up of 12.87 years, we documented 6558 incidents of COPD. From day work, irregular night shifts to regular night shifts, there was an increased trend in COPD incidence (P for trend < 0.001). Compared with day workers, the hazard ratio (HR) and 95% confidence interval (CI) of COPD was 1.28 (1.20, 1.37) for subjects with rarely/sometimes night shifts and 1.49 (1.35, 1.66) for those with permanent night shifts. Besides, the longer durations (especially in subjects with night shifts ≥ 10 years) and increasing monthly frequency of night shifts (in workers with > 8 nights/month) were associated with a higher COPD risk. Additionally, there was an additive interaction between night shifts and genetic susceptibility on the COPD risk. Subjects with permanent night shifts and high genetic risk had the highest risk of COPD (HR: 1.90 95% CI: 1.63, 2.22), with day workers with low genetic risk as a reference.
Long-term night shift exposure is associated with a higher risk of COPD. Our findings suggest that decreasing the frequency and duration of night shifts may offer a promising approach to mitigating respiratory disease incidence in night shift workers, particularly in light of individual susceptibility.
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