scholarly journals Epidemiological evidence relating environmental smoke to COPD in lifelong non-smokers: a systematic review

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 146 ◽  
Author(s):  
Peter N. Lee ◽  
Barbara A. Forey ◽  
Katharine J. Coombs ◽  
Jan S. Hamling ◽  
Alison J. Thornton

Background: Some evidence suggests environmental tobacco smoke (ETS) might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers. Methods: We identified epidemiological studies providing estimates of relative risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition. Results: Twenty-eight relevant studies were identified; nine European or Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS. Conclusions: Although the evidence suggests ETS increases COPD, study weaknesses and absence of well-designed large studies precludes reliable inference of causality. More definitive evidence is required.

F1000Research ◽  
2020 ◽  
Vol 7 ◽  
pp. 146
Author(s):  
Peter N. Lee ◽  
Barbara A. Forey ◽  
Katharine J. Coombs ◽  
Jan S. Hamling ◽  
Alison J. Thornton

Background: Some evidence suggests environmental tobacco smoke (ETS) might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers. Methods: We identified epidemiological studies providing estimates of relative risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition. Results: Twenty-eight relevant studies were identified; nine European or Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS. Conclusions: Although the evidence strongly suggests that ETS increases COPD, study weaknesses and absence of well-designed large studies preclude reliable effect estimation. More definitive evidence is required.


F1000Research ◽  
2019 ◽  
Vol 7 ◽  
pp. 146
Author(s):  
Peter N. Lee ◽  
Barbara A. Forey ◽  
Katharine J. Coombs ◽  
Jan S. Hamling ◽  
Alison J. Thornton

Background: Some evidence suggests environmental tobacco smoke (ETS) might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers. Methods: We identified epidemiological studies providing estimates of relative risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition. Results: Twenty-eight relevant studies were identified; nine European or Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS. Conclusions: Although the evidence suggests ETS increases COPD, study weaknesses and absence of well-designed large studies preclude reliable estimation of the effect. More definitive evidence is required.


2018 ◽  
Vol 5 (1) ◽  
pp. e000246 ◽  
Author(s):  
Adama Sana ◽  
Serge M A Somda ◽  
Nicolas Meda ◽  
Catherine Bouland

IntroductionChronic obstructive pulmonary disease (COPD) is a major and growing cause of morbidity and mortality worldwide. The global prevalence of COPD is growing faster in women than in men. Women are often exposed to indoor pollutants produced by biomass fuels burning during household activities.MethodsWe conducted a meta-analysis to establish the association between COPD and exposure to biomass smoke in women.Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, we searched MEDLINE and Scopus databases in 31December 2016, with the terms: “wood”, “charcoal”, “biomass”, “solid fuels”, “organic fuel”, “biofuel”, “female”, “women”, “COPD”, “chronic bronchitis”, “emphysema”, “chronic obstructive pulmonary disease”. Studies were eligible if they were case–control or cross-sectional studies involving exposure to indoor biomass smoke, conducted at any time and in any geographic location. Fixed-effects or random-effects meta-analysis was used to generate pooled OR.Results24 studies were included: 5 case–control studies and 19 cross-sectional studies. Biomass-exposed individuals were 1.38 times more likely to be diagnosed with COPD than non-exposed (OR 1.38, 95% CI 1.28 to 1.57).Spirometry-diagnosed COPD studies failed to show a significant association (OR 1.20, 95% CI 0.99 to 1.40). Nevertheless, the summary estimate of OR for chronic bronchitis (CB) was significant (OR 2.11, 95% CI 1.70 to 2.52). The pooled OR for cross-sectional studies and case–control studies were respectively 1.82 (95% CI 1.54 to 2.10) and 1.05 (95% CI 0.81 to 1.30). Significant association was found between COPD and biomass smoke exposure for women living as well in rural as in urban areas.ConclusionsThis study showed that biomass smoke exposure is associated with COPD in rural and urban women.In many developing countries, modern fuels are more and more used alongside traditional ones, mainly in urban area. Data are needed to further explore the benefit of the use of mixed fuels for cooking on respiratory health, particularly on COPD reduction.


Cancers ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 471
Author(s):  
B. Krishna ◽  
Samir Jana ◽  
Aditya Panda ◽  
David Horne ◽  
Sanjay Awasthi ◽  
...  

Reports on the association of TGF-β1 polymorphisms with breast cancer (BC) have been conflicting, inconsistent, inconclusive, and controversial. PubMed, EMBASE, and Google Scholar were used to identify studies on TGF-β1 polymorphisms and BC risk. Data were extracted independently, and of the initial 3043 studies, 39 case-control studies were eligible for inclusion in the meta-analysis. Information from these studies was extracted, and the overall associations of three TGF-β1 polymorphisms (TGF-β1 29>T/C, TGF-β1-509 C/T, and TGF-β1*6A) with BC risk were analyzed using overall allele, homozygous, heterozygous, recessive, and dominant models. None of the three TGF-β1 polymorphisms studied had a significant influence on the development of BC. However, stratified analysis revealed a positive correlation between the TGF-β1 29T>C polymorphism and BC risk according to a heterozygous model of the Asian population (odds ratio (OR) = 1.115, 95% confidence interval (CI) = 1.006–1.237, p = 0.039). Interestingly, this polymorphism was associated with lower odds of BC according to a heterozygous model of the Middle Eastern population (OR = 0.602, 95% CI = 0.375–0.966, p = 0.035). Thus, our analysis of large datasets indicates that the TGF-β1 29T>C polymorphism is significantly associated with BC risk in the Asian population. In contrast, the TGF-β1*6A and TGF-β1-509 C/T polymorphisms failed to show an association with BC.


Author(s):  
Damiano Pizzol ◽  
Jacopo Demurtas ◽  
Stefano Celotto ◽  
Stefania Maggi ◽  
Lee Smith ◽  
...  

Abstract Background Urinary incontinence (UI) and low quality of life (QoL) are two common conditions. Some recent literature proposed that these two entities can be associated. However, no attempt was made to collate this literature. Therefore, the aim of this study was to conduct a systematic review and meta-analysis of existing data to estimate the strength of the association between UI and QoL. Methods An electronic search of major databases up to 18th April 2020 was carried out. Meta-analysis of cross-sectional and case–control studies comparing mean values in QoL between patients with UI and controls was performed, reporting random-effects standardized mean differences (SMDs) ± 95% confidence intervals (CIs) as the effect size. Heterogeneity was assessed with the I2. Results Out of 8279 articles initially screened, 23 were finally included for a total of 24,983 participants, mainly women. The mean age was ≥ 50 years in 12/23 studies. UI was significantly associated with poor QoL as assessed by the short-form 36 (SF-36) total score (n = 6 studies; UI: 473 vs. 2971 controls; SMD = − 0.89; 95% CI − 1.3 to − 0.42; I2 = 93.5) and by the sub-scales of SF-36 and 5/8 of the domains included in the SF-36. Similar results were found using other QoL tools. The risk of bias of the studies included was generally high. Conclusions UI is associated with a poor QoL, with a strong level of certainty. This work, however, mainly based on cross-sectional and case–control studies, highlights the necessity of future longitudinal studies for better understanding the importance of UI on QoL.


Author(s):  
Yun-A Kim ◽  
Yoon Jeong Cho ◽  
Sang Gyu Kwak

The association of Helicobacter pylori (H. pylori) infection with functional dyspepsia has been well studied. However, the data on the relationship between H. pylori infection and irritable bowel syndrome (IBS) are conflicting. This study aims to elucidate the association between H. pylori infection and IBS. PubMed, Cochrane Library, CINAHL and SCOPUS databases were searched to identify eligible English articles published up to December 2019. Cross-sectional studies, case–control studies and cohort studies reporting both prevalence of H. pylori infection and IBS were selected for the detailed review. The pooled odds ratio (ORs) and their 95% confidence interval (CI) were calculated. A total of 7269 individuals in four cross-sectional studies and six case-control studies were included. The prevalence of H. pylori infection ranged from 12.8% to 73.4% in the control group, and 9.7% to 72.1% in the IBS group. The combined OR for H. pylori infection was 1.10 (95% CI: 0.93–1.29, I2: 37.5%). In a subgroup analysis of IBS defined according to Rome criteria, the OR for H. pylori infection was 1.10 (95% CI: 0.93–1.30, I2 = 31.7%). In this meta-analysis, H. pylori infection was not significantly associated with IBS. Well-designed studies are needed to identify the relationship between H. pylori infection and IBS.


2013 ◽  
Vol 23 (3) ◽  
pp. 437-441 ◽  
Author(s):  
Maria Inês Rosa ◽  
Geraldo Doneda Silva ◽  
Priscyla Waleska Targino de Azedo Simões ◽  
Meriene Viquetti Souza ◽  
Ana Paula Ronzani Panatto ◽  
...  

ObjectiveWe performed a systematic review and a meta-analysis to estimate the prevalence of human papillomavirus (HPV) in ovarian cancer.MethodsA comprehensive search of the Cochrane Library, MEDLINE, CANCERLIT, LILACS, Grey literature and EMBASE was performed for articles published from January 1990 to March 2012. The following MeSH (Medical Subject Headings) terms were searched: “ovarian tumor” or “ovarian cancers” and “HPV” or “human papillomavirus.” Included were case-control and cross-sectional studies, prospective or retrospective, that evaluated clinical ovarian cancer and provided a clear description of the use of in situ hybridization, Southern blot hybridization, and polymerase chain reaction. The statistical analysis was performed using REVMAN 5.0.ResultsIn total, 24 primary studies were included in this meta-analysis. Studies from 11 countries on 3 continents contained data on HPV and ovarian cancer, including 889 subjects. Overall, the HPV prevalence in patients with ovarian cancer was 17.5 (95% confidence interval [CI], 15.0%–20.0%). Human papillomavirus prevalence ranged from 4.0% (95% CI, 1.7%–6.3%) in Europe to 31.4% (95% CI, 26.9%–35.9%) in Asia. An aggregate of 4 case-control studies from Asia showed an odds ratio of 2.48 (95% CI, 0.64–9.57).ConclusionsWe found a high prevalence of HPV-positive DNA in ovarian cancer cases, but the role of HPV in ovarian cancer remains inconclusive. Further studies are needed to control case to answer this question.


2019 ◽  
Vol 53 (2) ◽  
Author(s):  
Leah Antoinette M. Caro-Chang ◽  
Mia Katrina R. Gervasio ◽  
Claudine Yap-Silva

Objectives. The study aimed to confirm the association between androgenetic alopecia (AGA) and Metabolic Syndrome (MetS). It also aimed to determine if early-onset AGA among males and AGA among females increases the risk of developing MetS, and if severity of AGA increases the odds of developing MetS. Methods. Observational studies from electronic databases were selected by the consensus of three independent review authors. The Newcastle-Ottawa Scale for assessing the quality of non-randomized studies in meta-analysis was used. Statistical analyses were accomplished using Review Manager software. Results. A total of 11 case-control studies, one prospective cohort study, and five cross-sectional studies were selected. In the meta-analysis of ten case-control studies and three cross-sectional studies (3840 participants), AGA was significantly correlated with MetS (OR 2.59, 95% CI 1.51 to 4.44; p<0.0005). Early-onset AGA among males (<35 years old) showed significant association (OR 3.69, 95% CI 2.15 to 6.33; p<0.00001). AGA among females also increased the odds of developing MetS (OR 5.59, 95% CI 2.06 to 15.12; p<0.0007). Moderate to severe AGA in males, Norwood-Hamilton IV or higher, was also significant (OR 1.65, 95% CI 1.12 to 2.42; p=0.01). The same trend was noted for females with Ludwig II and III (OR 5.82, 95% CI 2.54 to 13.34; p<0.00001). Conclusion. Although the pathophysiology still remains under investigation, the present study points to an association between AGA and MetS. It can be used as a marker to identify patients who should be screened for MetS and managed accordingly.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Meng-Han Shen ◽  
Chau Yee Ng ◽  
Kuo-Hsuan Chang ◽  
Ching-Chi Chi

Abstract Polyautoimmunity implicates that some autoimmune diseases share common etiopathogenesis. Some studies have reported an association between multiple sclerosis (MS) and vitiligo; meanwhile, other studies have failed to confirm this association. We performed a systemic review and meta-analysis to examine the association of MS with vitiligo. We searched the MEDLINE and Embase databases on March 8, 2020 for relevant case–control, cross-sectional, and cohort studies. The Newcastle–Ottawa Scale was used to evaluate the risk of bias of the included studies. Where applicable, we performed a meta-analysis to calculate the pooled odds ratio (OR) for case–control/cross-sectional studies and risk ratio for cohort studies with 95% confidence interval (CI). Our search identified 285 citations after removing duplicates. Six case–control studies with 12,930 study subjects met our inclusion criteria. Our meta-analysis found no significant association of MS with prevalent vitiligo (pooled OR 1.33; 95% CI 0.80‒2.22). Analysis of the pooled data failed to display any increase of prevalent vitiligo in MS patients compared with controls. Ethnic and genetic factors may play an important role for sporadically observed associations between MS and vitiligo. Future studies of this association should therefore consider stratification by ethnic or genetic factors.


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