Elucidating the environmental risk factors for rheumatic diseases: An umbrella review of meta‐analyses

2018 ◽  
Vol 21 (8) ◽  
pp. 1514-1524 ◽  
Author(s):  
Lazaros Belbasis ◽  
Vasilios Dosis ◽  
Evangelos Evangelou
2017 ◽  
Vol 13 (4) ◽  
pp. 406-418 ◽  
Author(s):  
Vanesa Bellou ◽  
Lazaros Belbasis ◽  
Ioanna Tzoulaki ◽  
Lefkos T. Middleton ◽  
John P.A. Ioannidis ◽  
...  

2016 ◽  
Vol 23 ◽  
pp. 1-9 ◽  
Author(s):  
Vanesa Bellou ◽  
Lazaros Belbasis ◽  
Ioanna Tzoulaki ◽  
Evangelos Evangelou ◽  
John P.A. Ioannidis

Author(s):  
David Rojas-Rueda ◽  
Emily Morales-Zamora ◽  
Wael Abdullah Alsufyani ◽  
Christopher H. Herbst ◽  
Salem M. AlBalawi ◽  
...  

Background: Environmental health is a growing area of knowledge, continually increasing and updating the body of evidence linking the environment to human health. Aim: This study summarizes the epidemiological evidence on environmental risk factors from meta-analyses through an umbrella review. Methods: An umbrella review was conducted on meta-analyses of cohort, case-control, case-crossover, and time-series studies that evaluated the associations between environmental risk factors and health outcomes defined as incidence, prevalence, and mortality. The specific search strategy was designed in PubMed using free text and Medical Subject Headings (MeSH) terms related to risk factors, environment, health outcomes, observational studies, and meta-analysis. The search was limited to English, Spanish, and French published articles and studies on humans. The search was conducted on September 20, 2020. Risk factors were defined as any attribute, characteristic, or exposure of an individual that increases the likelihood of developing a disease or death. The environment was defined as the external elements and conditions that surround, influence, and affect a human organism or population’s life and development. The environment definition included the physical environment such as nature, built environment, or pollution, but not the social environment. We excluded occupational exposures, microorganisms, water, sanitation and hygiene (WASH), behavioral risk factors, and no-natural disasters. Results: This umbrella review found 197 associations among 69 environmental exposures and 83 diseases and death causes reported in 103 publications. The environmental factors found in this review were air pollution, environmental tobacco smoke, heavy metals, chemicals, ambient temperature, noise, radiation, and urban residential surroundings. Among these, we identified 65 environmental exposures defined as risk factors and 4 environmental protective factors. In terms of study design, 57 included cohort and/or case-control studies, and 46 included time-series and/or case-crossover studies. In terms of the study population, 21 included children, and the rest included adult population and both sexes. In this review, the largest body of evidence was found in air pollution (91 associations among 14 air pollution definitions and 34 diseases and mortality diagnoses), followed by environmental tobacco smoke with 24 associations. Chemicals (including pesticides) were the third larger group of environmental exposures found among the meta-analyses included, with 19 associations. Conclusion: Environmental exposures are an important health determinant. This review provides an overview of an evolving research area and should be used as a complementary tool to understand the connections between the environment and human health. The evidence presented by this review should help to design public health interventions and the implementation of health in all policies approach aiming to improve populational health.


2017 ◽  
Vol 19 (2) ◽  
pp. 84-96 ◽  
Author(s):  
Beatrice Bortolato ◽  
Cristiano A. Köhler ◽  
Evangelos Evangelou ◽  
Jordi León-Caballero ◽  
Marco Solmi ◽  
...  

2015 ◽  
Vol 14 (3) ◽  
pp. 263-273 ◽  
Author(s):  
Lazaros Belbasis ◽  
Vanesa Bellou ◽  
Evangelos Evangelou ◽  
John P A Ioannidis ◽  
Ioanna Tzoulaki

2019 ◽  
Vol 157 (3) ◽  
pp. 647-659.e4 ◽  
Author(s):  
Daniele Piovani ◽  
Silvio Danese ◽  
Laurent Peyrin-Biroulet ◽  
Georgios K. Nikolopoulos ◽  
Theodore Lytras ◽  
...  

2013 ◽  
Vol 12 (1) ◽  
Author(s):  
Mark J Nieuwenhuijsen ◽  
Payam Dadvand ◽  
James Grellier ◽  
David Martinez ◽  
Martine Vrijheid

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 420.1-420
Author(s):  
F. Wouters ◽  
M. Maurits ◽  
L. van Boheemen ◽  
M. Verstappen ◽  
X. Matthijssen ◽  
...  

Background:The HLA shared epitope (SE) and smoking are the best known genetic and environmental risk factors for rheumatoid arthritis (RA) development; however, at which pre-RA stage they exert their effect is unknown. The following stages are discerned: an asymptomatic stage in which autoimmune responses can develop, a symptomatic stage (clinically suspect arthralgia (CSA)), and development of clinically apparent inflammatory arthritis (IA). Studies in the general asymptomatic population revealed contrasting results on the associations between SE-alleles and smoking and the presence of anti-citrullinated protein antibodies (ACPA). Furthermore, studies on these risk factors in the symptomatic pre-RA phase are scarce and these data might teach us whether SE-alleles and smoking are involved in symptom development and/or progression to clinical arthritis.Objectives:We aimed to determine at which pre-RA stage SE and smoking exert their effect. In this respect, the analyses were focused on the presence of ACPA, but associations for other anti-modified protein antibodies (anti-carbamylated and anti-acetylated protein antibodies (anti-CarP and AAPA, respectively)) were also studied.Methods:Results from the literature on the association of SE and smoking with ACPA in the asymptomatic population were summarized in inverse-variance weighted meta-analyses. In addition 577 CSA-patients were studied. Associations of SE and smoking with IgG ACPA were studied at baseline (CSA-onset), to assess an effect on symptom development. Additionally, patients were monitored for the development of clinically apparent inflammatory arthritis (IA) for median 2 years and associations of SE, smoking and auto-antibodies with progression to IA were determined. Analyses were stratified for ACPA-status and associations in ACPA-positive patients were validated in meta-analyses with other arthralgia-cohorts. Finally analyses were repeated for anti-CarP and AAPA.Results:Meta-analyses showed that SE is not associated with ACPA-positivity in the asymptomatic population (OR 1.06 (95%CI 0.69-1.64)), whereas smoking was associated (OR 1.37 (1.15-1.63)). At CSA-onset, both SE and smoking associated with ACPA-positivity (OR 2.08 (1.24-3.49) and OR 2.41 (1.31-4.43), respectively). During follow-up of CSA-patients SE associated with IA-development (HR 1.86 (1.23-2.82)), in contrast to smoking. SE conferred risk for IA-development in ACPA-negative CSA-patients (HR 1.71 (0.99-2.96)) and in ACPA-positive patients (CSA-cohort HR 1.29 (0.67-2.47); meta-analysis three arthralgia-cohorts HR 1.52 (1.08-2.15)). Investigating the other autoantibodies revealed that SE and smoking were not associated with anti-CarP or AAPA-positivity at CSA-onset; longitudinally AAPA associated with progression to IA independent from ACPA and RF (HR 1.79 (1.02-3.16)), whilst anti-Carp did not.Conclusion:SE and smoking act in partly different pre-RA stages. Although SE does not associate with ACPA in the general population, it does mediate symptom-development and further progression to clinical arthritis. Smoking confers risk to development of ACPA and/or joint symptoms, but is not further involved in IA-development. The time-specific biologic pathways that are underlying need further exploration. These data enhance the understanding of the timing of key genetic and environmental risk factors in the trajectory of RA development.Disclosure of Interests:None declared


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