scholarly journals Relationship Between Secondhand Smoke Exposure and Depressive Symptoms: A Systematic Review and Dose–Response Meta-Analysis

Author(s):  
Han ◽  
Liu ◽  
Gong ◽  
Ye ◽  
Zhou

Previous studies have suggested an association between secondhand smoke (SHS) exposure and risk of depressive symptoms. However, it remains unclear whether there is a dose–response relationship. The effect estimates were pooled using fixed-effect or random-effect models based on homogeneity analysis. The dose–response meta-analysis was performed by linear and non-linear regression. Subgroup analyses were conducted to explore the possible sources of heterogeneity. Twenty-four studies were included in this meta-analysis. SHS exposure was significantly associated with increased odds of depressive symptoms (odds ratio (OR) = 1.32, 95% confidence interval (CI) 1.25–1.39). For SHS exposure expressed as an ordinal variable, the dose–response meta-analysis revealed a monotonically increasing relationship between SHS exposure and depressive symptoms. A similar dose–response relationship was observed for SHS exposure expressed as a continuous variable (OR = 1.57, 95% CI = 1.26–1.87). Our findings suggest that SHS exposure is associated with increasing odds of depressive symptoms in a dose–response manner.

Author(s):  
Xiaohua Ye ◽  
Jingya Huang ◽  
Liang Xia ◽  
Xiaojun Xu ◽  
Xiao Gong ◽  
...  

Few studies have focused on the potential relationship between secondhand smoke (SHS) exposure and depressive symptoms. This study aimed to explore the potential association between SHS exposure and depressive symptoms and differentiate this association in setting-specific exposure and symptom-specific outcomes. A cross-sectional study was conducted in Guangdong province of China from September to December 2010 using a multistage sampling method to randomly sample adults aged 18 years and older. SHS exposure was defined as inhalation by non-smokers of the smoke exhaled from smokers for at least 1 day a week in the past 30 days. Depressive symptoms were measured using the nine-item Patient Health Questionnaire. The zero-inflate negative binomial regression models were used to explore the associations between SHS exposure and depressive symptoms. A total of 2771 non-smokers were included in this study, with mean age of 49.6 ± 14.0 years and 70.3% of females. The prevalence of depressive symptoms was significantly higher in participants with SHS exposure than in those without exposure (incidence rate ratio (IRR) = 1.32, 95% confidence interval (CI) 1.16–1.51), and there were similar positive associations for SHS exposure in medical facilities (IRR = 1.37, 95% CI 1.17–1.61) and in schools (IRR = 1.46, 95% CI 1.20–1.77). Notably, there was a monotonically increasing dose-response relationship between frequency of SHS exposure and depressive symptoms. When differentiating this relationship by the dimensions of depressive symptoms, there were similar dose-response relationships for cognitive-affective and somatic symptoms. When differentiating this relationship by sex, only females showed a significant dose-response relationship. Our findings suggest dose-response relationships between SHS exposure and depressive symptoms in sex-specific and symptom-specific manners. Future longitudinal studies are needed to establish the biological mechanisms of the impact of SHS exposure.


2020 ◽  
Vol 55 (5) ◽  
pp. 457-467
Author(s):  
Xiaohui Yu ◽  
Jiahao Chen ◽  
Wenjie Jiang ◽  
Dongfeng Zhang

Abstract Aims We conducted a dose–response meta-analysis to explore the association between alcohol and particular alcoholic beverages with risk of esophageal cancer (EC) by histological type [esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC)] and whether the association differs according to gender. Methods PubMed and Web of Science databases were searched for relevant articles published between January 1960 and December 2019. The pooled relative ratios (RRs) and 95% confidence interval (CI) were calculated with the fixed or random effect model. The dose–response relationship was assessed by restricted cubic spline. Results A total of 74 published articles involving 31,105 cases among 3,369,024 participants were included in this meta-analysis. The pooled RRs of the highest versus lowest alcohol intake were 3.67 (95% CI, 2.89,4.67) for EC, 5.11 (95% CI, 3.60,7.25) for ESCC and 0.96 (95% CI, 0.79,1.16) for EAC. The above-mentioned associations were observed in cohort design, for different alcoholic beverages (beer, wine and liquor/spirits) and gender. Evidence of a nonlinear dose–response relationship for EC risk with alcohol intake was found (Pnon-linearity < 0.001), and a linear relationship (Pnon-linearity = 0.216) suggested that the risk of ESCC increased by 33% for every 12.5 g/day increment of alcohol intake. Conclusions This meta-analysis suggests that alcohol intake might significantly increase the incidence of EC, especially for ESCC.


Author(s):  
Makoto Hibino ◽  
Yoichiro Otaki ◽  
Elsa Kobeissi ◽  
Han Pan ◽  
Hiromi Hibino ◽  
...  

Background: Hypertension or elevated blood pressure (BP) is an important risk factor for aortic dissection (AD); however, few prospective studies concerning this topic have been published. We investigated the association between hypertension/elevated BP and AD in two cohorts and conducted a meta-analysis of published prospective studies, including these two studies. Methods: We analyzed data from the Japan Specific Health Checkups (J-SHC) Study and UK Biobank, which prospectively followed 534,378 and 502,424 participants, respectively. Multivariable Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) for the association of hypertension/elevated BP with AD incidence in the UK Biobank and AD mortality in the J-SHC Study. In the meta-analysis, summary relative risks (RRs) were calculated using random effects models. A potential nonlinear dose-response relationship between BP and AD was tested using fractional polynomial models, and the best-fitting second-order fractional polynomial regression model was determined. Results: In the J-SHC Study and UK Biobank, there were 84 and 182 ADs during 4- and 9-year follow-up, and the adjusted HRs of AD were 3.57 (95% CI, 2.17-6.11) and 2.68 (95% CI: 1.78-4.04) in hypertensive individuals, 1.33 (95% CI: 1.05-1.68) and 1.27 (95% CI: 1.11-1.48) per 20-mmHg increase in systolic BP (SBP), and 1.67 (95% CI: 1.40-2.00) and 1.66 (95% CI: 1.46-1.89) per 10-mmHg increase in diastolic BP (DBP), respectively. In the meta-analysis, the summary RRs were 3.07 (95% CI 2.15-4.38, I2=76.7%, n=7 studies, 2,818 ADs, 4,563,501 participants) for hypertension and 1.39 (95% CI: 1.16-1.66, I2=47.7%, n=3) and 1.79 (95% CI: 1.51-2.12, I2=57.0%, n=3) per 20-mmHg increase in SBP and per 10-mmHg in DBP, respectively. The AD risk showed a strong, positive dose-response relationship with SBP and even more so with DBP. The risk of AD in the nonlinear dose-response analysis was significant at SBP >132 mmHg and DBP >75 mmHg. Conclusions: Hypertension and elevated SBP and DBP are associated with a high risk of AD. The risk of AD was positively dose-dependent, even within the normal BP range. These findings provide further evidence for the optimization of BP to prevent AD.


Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Jingkai Wei ◽  
Yuzhi Xi ◽  
Ruixue Hou ◽  
Alysse Kowalski ◽  
Hao Sun ◽  
...  

Introduction: Previous studies show that alpha-linolenic acid (ALA) is associated with reduced risk of coronary heart disease (CHD). However, it remains unclear whether and how dietary ALA doses are related to CHD. Hypothesis: We hypothesized that higher dietary ALA intake is associated with a greater reduction in risk of CHD. Methods: We searched PubMed, EMBASE, and Web of Science for prospective studies examining the association between dietary ALA intake and CHD risk. Dietary ALA intake was assigned or measured by self-report. Outcomes were reported as total and fatal CHD and/or myocardial infarction, which were obtained from blinded endpoint assessments or medical records. Two-stage fixed-effects dose-response meta-analyses were conducted to estimate the association between increasing ALA intake (relative to study-specific referents) and CHD. Results: Fifteen published articles were identified and included in the meta-analysis (13 cohort studies and 2 randomized controlled trials). The pooled analysis was based on 310,768 individuals with 12,049 events with a mean length of follow-up of 9.6 years. The analysis showed a J-shaped curve between ALA intake and relative risk of total CHD (Chi-square=21.08, p<0.001). ALA intake from 0.3-1.4g/day showed reduced risk of total CHD, while intake ≥2.5g/day was associated with increased risk of CHD, compared to people without ALA intake (Figure 1A). Approximately 1g/day of ALA intake was associated with the lowest risk of total CHD. ALA intake was linearly associated with fatal CHD - every 1g/day increase in ALA intake was associated with an 11% decrease in fatal CHD risk (95% CI: -0.16, -0.05) (Figure 1B). Conclusion: The J-shaped dose-response relationship based on our pooled analysis suggests that 1g/day of dietary ALA may be optimal for total CHD prevention. Though a higher dietary ALA intake was associated with reduced risk of fatal CHD, the excess total CHD risk at higher ALA intakes warrants further investigation, especially through randomized controlled trials.


2015 ◽  
Vol 181 (6) ◽  
pp. 374-384 ◽  
Author(s):  
Michael Goodman ◽  
K. M. Venkat Narayan ◽  
Dana Flanders ◽  
Ellen T. Chang ◽  
Hans-Olov Adami ◽  
...  

2018 ◽  
Vol 119 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Jingkai Wei ◽  
Ruixue Hou ◽  
Yuzhi Xi ◽  
Alysse Kowalski ◽  
Tiansheng Wang ◽  
...  

AbstractPrevious studies show inconsistent associations between α-linolenic acid (ALA) and risk of CHD. We aimed to examine an aggregate association between ALA intake and risk of CHD, and assess for any dose–response relationship. We searched the PubMed, EMBASE and Web of Science databases for prospective cohort studies examining associations between ALA intake and CHD, including composite CHD and fatal CHD. Data were pooled using random-effects meta-analysis models, comparing the highest category of ALA intake with the lowest across studies. Subgroup analysis was conducted based on study design, geographic region, age and sex. For dose–response analyses, we used two-stage random-effects dose–response models. In all, fourteen studies of thirteen cohorts were identified and included in the meta-analysis. The pooled results showed that higher ALA intake was associated with modest reduced risk of composite CHD (risk ratios (RR)=0·91; 95 % CI 0·85, 0·97) and fatal CHD (RR=0·85; 95 % CI 0·75, 0·96). The analysis showed a J-shaped relationship between ALA intake and relative risk of composite CHD (χ2=21·95, P<0·001). Compared with people without ALA intake, only people with ALA intake <1·4 g/d showed reduced risk of composite CHD. ALA intake was linearly associated with fatal CHD – every 1 g/d increase in ALA intake was associated with a 12 % decrease in fatal CHD risk (95 % CI −0·21, −0·04). Though a higher dietary ALA intake was associated with reduced risk of composite and fatal CHD, the excess composite CHD risk at higher ALA intakes warrants further investigation, especially through randomised controlled trials.


2019 ◽  
Vol 69 (3) ◽  
pp. 182-188 ◽  
Author(s):  
Man Cheng ◽  
Heng He ◽  
Dongming Wang ◽  
Luli Xu ◽  
Bin Wang ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Hongrui Zhai ◽  
Yu Wang ◽  
Wenjie Jiang

Object. Results on the associations of fruit and vegetable intake with risk of chronic obstructive pulmonary disease (COPD) are still in conflict. Hence, we conducted a meta-analysis to quantitatively evaluate the association between fruit and vegetable intake and the risk of COPD. Methods. PubMed, Web of Science, and China National Knowledge Infrastructure (CNKI) were searched for relevant studies published up to September 2019. Combined relative risks (RRs) and 95% confidence intervals (CIs) were calculated with the random effects model (REM). Dose-response relationship was assessed by the restricted cubic spline model. Results. There are 8 studies involving 5,787 COPD cases among 244,154 participants included in this meta-analysis. For the highest versus the lowest level, the pooled RR of COPD was 0.75 (95% CI, 0.68–0.84; I2 = 46.7%) for fruits plus vegetables, 0.72 (95% CI, 0.66–0.79; I2 = 1.3%) for fruits, and 0.76 (95% CI, 0.63–0.92; I2 = 62.7%) for vegetables. In subgroup analysis of fruit plus vegetable intake and COPD risk, the inverse association exists in all three study designs. A nonlinear dose-response relationship was found for COPD risk with fruit (Pnon−linearity<0.01). Conclusions. This meta-analysis indicates that fruit and vegetable intake might be related to a lower risk of COPD.


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