ABSTRACT
BACKGROUND: Cardiovascular disease (CVD) has evolved into a serious public health issue that demands the use of suitable methods to estimate the risk of the disease. As a result, in a sample of individuals who completed a 3-year low-sodium salt or conventional salt intervention in a hypertensive environment, we constructed a 13-year cardiovascular (CV) event risk prediction model with a 10-year follow-up. METHODS: A Cox proportional hazards model was used to build a prediction model based on data from 306 participants who matched the inclusion criteria. Both the discriminating power and the calibration of the prediction models were assessed. The discriminative power of the prediction model was measured using the area under the curve (AUC). Brier scores and calibration plots were used to assess the prediction model's calibration. The model was internally validated using the tenfold cross-validation method. The nomogram served as a tool for visualising the model. RESULTS: Among the 306 total individuals, there were 100 cases and 206 control. In the model, there were six predictors including age, smoking, LDL-C (low-density lipoprotein cholesterol), baseline SBP (systolic blood pressure), CVD (cardiovascular history), and CNV (genomic copy number variation) nsv483076. The fitted model has an AUC of 0.788, showing strong model discrimination, and a Brier score of 0.166, indicating that it was well-calibrated. According to the results of internal validation, the prediction model utilised in this study had a good level of repeatability. According to the model integrating the interaction of CNVs and baseline blood pressure, the effect of baseline SBP on CV events may be greater when nsv483076 was normal double copies than when nsv483076 was copy number variation. CONCLUSIONS: The efficacy of risk prediction models for CV events that include environmental and genetic components is excellent, and they may be utilised as risk assessment tools for CV events in specific groups to offer a foundation for tailored intervention strategies.
Subject(s)
Cardiovascular Diseases , Hypertension , Humans , DNA Copy Number Variations , Cardiovascular Diseases/genetics , Cardiovascular Diseases/epidemiology , Risk Assessment/methods , Smoking , Risk FactorsABSTRACT
Objective: The association between occupational noise exposure and hypertension is controversial. Thus, we aimed to assess the relationship between occupational noise exposure and hypertension. Methods: This was a caseâcontrol study, and 509 cases and 1,018 controls from an automobile company were included between July and October 2013. Occupational noise exposure was defined as exposure to noise level ≥80 dB(A) (Lex, 8 h) or cumulative noise exposure (CNE) ≥ 80 dB(A)-years. To assess the associations of noise level and CNE with hypertension, univariate and multivariate logistic regression were performed to calculate odds ratios (ORs) and 95% confidence intervals (CIs). The restricted cubic spline function was used to establish doseâresponse curves. Results: A noise level ≥80 dB (A) (Lex, 8 h) was significantly associated with hypertension (OR 2.48, 95% CI 1.89-3.24). CNE ≥80 dB (A)-years was significantly associated with hypertension (OR 1.53, 95% CI 1.18-2.00). Nonlinear relationships between noise level, CNE and hypertension were found (p- nonlinear<0.05). Conclusion: Our study suggests that occupational noise exposure is a potential risk factor for hypertension in automobile company workers.
Subject(s)
Hypertension , Noise, Occupational , Occupational Exposure , Humans , Noise, Occupational/adverse effects , Case-Control Studies , Hypertension/epidemiology , Hypertension/etiology , Occupational Exposure/adverse effects , Odds RatioABSTRACT
Objective: The effects of e-cigarettes on lung function were compared between the e-cigarette and the non-e-cigarette group, as well as self-changes after inhaling e-cigarettes. Method: From March 1st, 2022, relevant literature was selected from four databases through a predefined retrieval strategy. Strict literature screening and quality evaluation were conducted. The study followed PRISMA guidelines. Results: Our results showed that CO (SMD: -1.48, 95%: -2.82-0.15) and FeNO (SMD: -0.66, 95%: -1.32, -0.01) were significantly decreased after e-cigarette usage. Only asthmatic smokers showed a statistically significant increase in flow resistance after inhaling e-cigarettes. Conversely, the decrease of FEV1/FVC% in the non-e-cigarette groups exceeded that in the e-cigarette group (SMD:1.18, 95%: 0.11-2.26). The degree of O2 saturation decrease was also less than that for the cigarette groups (SMD:0.32, 95%: 0.04-0.59), especially when compared to the conventional cigarette group (SMD:0.56, 95%: 0.04-1.08). Conclusion: The current findings indicate that short-term e-cigarette inhalation has a similar (but not significant) effect on lung function, as compared with non-e-cigarettes. More clinical studies are needed to explore the safety of inhaling e-cigarettes, especially in vulnerable populations.
Subject(s)
Electronic Nicotine Delivery Systems , Tobacco Products , Vaping , Humans , Lung , Vaping/adverse effectsABSTRACT
There is no consensus on the role of bilirubin in acute ischemic stroke. Higher levels of serum bilirubin may provide a treatment advantage in oxidative-stress-mediated diseases but also may simply reflect the strength of the oxidative stress. As of 28 February 2022, the relevant studies were selected from four databases (PubMed, Web of science, Cochrane, and CNKI) through a retrieval strategy, and strict literature screening and quality evaluation were carried out. The dose-response relationship was fitted with a restricted cubic splines function. We found that the serum total bilirubin level and the direct bilirubin level were positively correlated with the severity of ischemic stroke. The direct bilirubin level was linearly correlated with the severity of stroke (P for non-linearity = 0.55), and the direct bilirubin increase of 1 µmol/L may be related to the 1% increase in the possibility of having moderate or severe ischemic stroke. High bilirubin levels are associated with stroke severity in patients with ischemic stroke and may serve as a marker of the intensity of initial oxidative stress.
ABSTRACT
BACKGROUND: Many epidemiological studies have investigated the relationship between occupational noise and hypertension, but with conflicting findings. This study aimed to assess the relationship between occupational noise exposure and the risk of hypertension. METHODS: A case-control study was conducted to explore hypertension predictors, and then sensitivity analysis was performed based on propensity score matching (PSM). Data were collected from participants' annual physical examinations and occupational noise exposure measurements. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression analysis. A restricted cubic spline (RCS) function was used to fit the dose-effect relationship. RESULTS: 500 cases and 4,356 controls were included in the study. Multivariate logistic regression showed that an increase in the level of occupational noise [range 68-102 dB(A)] of 1 dB(A), corresponded to an increase in hypertension risk of 8.3% (OR: 1.083, 95% CI: 1.058-1.109). Compared to the first quartile, the risk of hypertension in the fourth quartile was 1.742 (95% CI: 1.313-2.310). After applying PSM to minimize bias, we obtained a population of 500 cases and 1,000 controls. Noise level was significantly associated with the risk of hypertension. In addition, the RCS curve showed the risk of hypertension was relatively stable until a predicted noise level of around 80 dB(A) and then started to increase rapidly afterward (P nonlinear = 0.002). CONCLUSIONS: Occupational noise exposure was significantly associated with hypertension risk and there was a positively correlated dose-response relationship.
ABSTRACT
Background: Evidence suggests that the total bilirubin has a protective effect on coronary heart disease (CHD), but the dose-response relationship remains controversial, and there is no meta-analysis to assess the relationship. Methods: As of October 1, 2021, relevant literature was selected from four databases (PubMed, Web of Science, Cochrane Library, and Embase) by using a retrieval strategy. The dose-response curve between the total bilirubin and CHD was fitted by a restricted cubic spline. Stata 12.0 was used for statistical analysis. Results: A total of 170,209 (6,342 cases) participants from 7 prospective studies were analyzed in our meta-analysis. We calculated the pooled relative risks (RRs) and 95% CIs for the association between serum bilirubin level and risk of CHD using random-effects models. Compared with the first quantile, the bilirubin level in the third quantile had a protective effect on the risk of CHD (RR, 0.90; 95% CI, 0.82-0.99). The restricted cubic spline functions depicted a U-type curve relationship between bilirubin (3.42-49 µmol/L) and CHD (P linear < 0.001). When the bilirubin level was in the range of 3.42-13µmol/L, the protective effect of bilirubin on CHD was enhanced with increasing bilirubin levels. When the bilirubin level exceeded 13µmol/L, the protective effect of bilirubin weakened, and a dangerous effect gradually appeared with further increases in bilirubin levels. Conclusions: Compared with a low bilirubin level, a high bilirubin level has a protective effect on the risk of CHD, and there was a U-shaped dose-response relationship between them.