scholarly journals Association between Air Pollution and the Development of Rheumatic Disease: A Systematic Review

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Gavin Sun ◽  
Glen Hazlewood ◽  
Sasha Bernatsky ◽  
Gilaad G. Kaplan ◽  
Bertus Eksteen ◽  
...  
Keyword(s):  
Air Pollution ◽  
Rheumatic Diseases ◽  
Air Pollutants ◽  
Population Sample ◽  
Case Control ◽  
Air Pollutant ◽  
Case Control Studies ◽  
Mesh Terms ◽  
Increased Risk ◽  
American Children

Objective. Environmental risk factors, such as air pollution, have been studied in relation to the risk of development of rheumatic diseases. We performed a systematic literature review to summarize the existing knowledge.Methods. MEDLINE (1946 to September 2016) and EMBASE (1980 to 2016, week 37) databases were searched using MeSH terms and keywords to identify cohort, case-control, and case cross-over studies reporting risk estimates for the development of select rheumatic diseases in relation to exposure of measured air pollutants (n=8). We extracted information on the population sample and study period, method of case and exposure determination, and the estimate of association.Results. There was no consistent evidence of an increased risk for the development of rheumatoid arthritis (RA) with exposure to NO2, SO2, PM2.5, or PM10. Case-control studies in systemic autoimmune rheumatic diseases (SARDs) indicated higher odds of diagnosis with increasing PM2.5exposure, as well as an increased relative risk for juvenile idiopathic arthritis (JIA) in American children <5.5 years of age. There was no association with SARDs and NO2exposure.Conclusion. There is evidence for a possible association between air pollutant exposures and the development of SARDs and JIA, but relationships with other rheumatic diseases are less clear.

scholarly journals Relationship between Air Pollutant Exposure and Gynecologic Cancer Risk

2021 ◽  
Vol 18 (10) ◽  
pp. 5353
Author(s):  
Qiwei Yu ◽  
Liqiang Zhang ◽  
Kun Hou ◽  
Jingwen Li ◽  
Suhong Liu ◽  
...  
Keyword(s):  
Air Pollution ◽  
Cancer Risk ◽  
Air Pollutants ◽  
Gynecological Cancer ◽  
Gynecologic Cancer ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Short Term Exposure ◽  
Increased Risk

Exposure to air pollution has been suggested to be associated with an increased risk of women’s health disorders. However, it remains unknown to what extent changes in ambient air pollution affect gynecological cancer. In our case–control study, the logistic regression model was combined with the restricted cubic spline to examine the association of short-term exposure to air pollution with gynecological cancer events using the clinical data of 35,989 women in Beijing from December 2008 to December 2017. We assessed the women’s exposure to air pollutants using the monitor located nearest to each woman’s residence and working places, adjusting for age, occupation, ambient temperature, and ambient humidity. The adjusted odds ratios (ORs) were examined to evaluate gynecologic cancer risk in six time windows (Phase 1–Phase 6) of women’s exposure to air pollutants (PM2.5, CO, O3, and SO2) and the highest ORs were found in Phase 4 (240 days). Then, the higher adjusted ORs were found associated with the increased concentrations of each pollutant (PM2.5, CO, O3, and SO2) in Phase 4. For instance, the adjusted OR of gynecological cancer risk for a 1.0-mg m−3 increase in CO exposures was 1.010 (95% CI: 0.881–1.139) below 0.8 mg m−3, 1.032 (95% CI: 0.871–1.194) at 0.8–1.0 mg m−3, 1.059 (95% CI: 0.973–1.145) at 1.0–1.4 mg m−3, and 1.120 (95% CI: 0.993–1.246) above 1.4 mg m−3. The ORs calculated in different air pollution levels accessed us to identify the nonlinear association between women’s exposure to air pollutants (PM2.5, CO, O3, and SO2) and the gynecological cancer risk. This study supports that the gynecologic risks associated with air pollution should be considered in improved public health preventive measures and policymaking to minimize the dangerous effects of air pollution.

scholarly journals The first 1000 days of life: traffic-related air pollution and development of wheezing and asthma in childhood. A systematic review of birth cohort studies

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Alessandra Bettiol ◽  
Elena Gelain ◽  
Erika Milanesio ◽  
Federica Asta ◽  
Franca Rusconi
Keyword(s):  
Systematic Review ◽  
Air Pollution ◽  
Cohort Studies ◽  
Exposure Assessment ◽  
Birth Cohort ◽  
Early Life ◽  
Air Pollutants ◽  
Air Pollutant ◽  
Increased Risk ◽  
The Relationship

Abstract Background The first 1000 days of life -including pregnancy and the first 2 years after birth- represent a critical window for health interventions. This systematic review aimed to summarize the evidence on the relationship between traffic-related air pollutants exposure in the first 1000 days of life and the development of wheezing and asthma, with a particular focus on windows of exposure. Methods Medline and Embase were searched from January 2000 to May 2020 to retrieve population-based birth-cohort studies, including registries, providing quantitative information on the association between exposure to traffic-related air pollutants during pregnancy or early life, and the risk of developing wheezing and asthma in childhood. Screening and selection of the articles were completed independently by three reviewers. The quality of studies was assessed using the Newcastle-Ottawa scale. Results Out of 9681 records retrieved, 26 studies from 21 cohorts were included. The most common traffic-related air pollutant markers were particulate matter (PM) and nitric oxides (NOx). The variability in terms of pollutants, exposure assessment methods, and exposure levels chosen to present the results did not allow a meta-analysis. Exposure to PM and NOx in pregnancy (10 cohorts) was consistently associated with an increased risk of asthma development, while the association with wheezing development was unclear. The second trimester of pregnancy seemed to be particularly critical for asthma risk. As for exposure during early life (15 cohorts), most studies found a positive association between PM (7/10 studies) and NOx (11/13 studies) and the risk of asthma development, while the risk of wheezing development was controversial. The period of postnatal exposure, however, was less precisely defined and a partial overlap between the period of exposure measurement and that of outcome development was present in a consistent number of studies (14 out of 15) raising doubts on the associations found. Conclusions Traffic-related air pollution during pregnancy is associated with an increased risk of asthma development among children and adolescents. The relationship between exposure in the first two years of life and the development of wheezing and asthma needs to be confirmed in studies with more precise exposure assessment.

scholarly journals Air Pollution, Road Proximity, Greenspace, Indoor Air Pollution and Reduced Lung Function Incidence in Children : A Case-control Study

2021 ◽  
Author(s):  
Jingwei Zhang ◽  
Yuming Wang ◽  
Lihong Feng ◽  
Changchun Hou ◽  
Qing Gu
Keyword(s):  
Air Pollution ◽  
Lung Function ◽  
Indoor Air ◽  
Air Pollutants ◽  
Indoor Air Pollution ◽  
Case Control Study ◽  
Conditional Logistic Regression ◽  
Case Control ◽  
Increased Risk ◽  
Control Study

Abstract Objectives Reduced lung function during childhood could substantially influence the health states of the respiratory system in adults, so, the relationships between air pollution, road proximity, greenspace, indoor air pollution and reduced lung function incidence in children were investigated in this study. Methods The lung function of children was tested every year from 2015 to 2018 and the method of case-control study was applied. Propensity score matching (PSM) was performed to minimize confounding bias and the conditional logistic regression model was carried out to evaluate the effects of indoor and outdoor environmental risk factors on reduced lung function of children. Results Each-one quartile increment in the mixture of the six air pollutants at lag1, lag2 and lag3 periods were related to 46.2%, 9.57% and 8.28% increased risk levels of getting the unhealthy outcome. The protective effect of greenness at lag2 period (Odds ratios (OR) = 0.01 (95% confidence interval (CI): 0–0.02)) was stronger than that at lag1 period (OR = 0.03 (95% CI: 0.01–0.05)). Conclusions Separate and combined effects of most air pollutants at different lag periods represented the hazard effects to the lung function of students. And the distance band of 101–200 m between the home address of each student and the major road could be detrimental to the health of the lung of children significantly. Exposure levels of greenness had protective effects on lung health for students. Only the indoor factor of secondhand smoke exposure was significantly associated with an elevated risk of having reduced lung function.

scholarly journals Is childhood wheeze and asthma in Latin America associated with poor hygiene and infection? A systematic review

2018 ◽  
Vol 5 (1) ◽  
pp. e000249 ◽  
Author(s):  
Cristina Ardura-Garcia ◽  
Paul Garner ◽  
Philip J Cooper
Keyword(s):  
Systematic Review ◽  
Latin American ◽  
Observational Studies ◽  
Case Control ◽  
Asthma Prevalence ◽  
Selective Reporting ◽  
Case Control Studies ◽  
Cross Sectional ◽  
Increased Risk ◽  
American Children

IntroductionHigh asthma prevalence in Latin-American cities is thought to be caused by poor hygiene and infections. This contradicts the widely accepted ‘hygiene hypothesis’ for asthma aetiology.MethodsSystematic review of observational studies evaluating the association between poor hygiene exposures or infections and asthma/wheeze among Latin-American children aged 4–16 years. MEDLINE, EMBASE, LILACS and CINAHL electronic databases were searched following a predefined strategy to 18 December 2017. We quantified outcomes measured and reported, assessed risk of bias and tabulated the results.ResultsForty-five studies included: 6 cohort, 30 cross-sectional and 9 case–control studies. 26 cross-sectional studies were school-based surveys (14 of over 3000 children), whereas 5 case–control studies were hospital/health centre-based. Exposures measured and reported varied substantially between studies, and current wheeze was the most common outcome reported. Data showed selective reporting based on statistical significance (P value <0.05): 17/45 studies did not clearly describe the number of exposures measured and 15/45 studies reported on less than 50% of the exposures measured. Most exposures studied did not show an association with wheeze or asthma, except for a generally increased risk associated with acute respiratory infections in early life. Contradictory associations were observed frequently between different studies.ConclusionSelective reporting is common in observational studies exploring the association between environmental exposures and risk of wheeze/asthma. This, together with the use of different study outcomes (wheeze/asthma) associated with possibly distinct causal mechanisms, complicates inferences about the role of poor hygiene exposures and childhood infections in explaining asthma prevalence in Latin-American children.

scholarly journals The importance and challenge of carcinogenic air pollutants for health risk and impact assessment

2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
P Mudu ◽  
R Pérez Velasco ◽  
I Zastenskaya ◽  
D Jarosinska
Keyword(s):  
Lung Cancer ◽  
Air Pollution ◽  
Impact Assessment ◽  
Air Pollutants ◽  
Air Pollutant ◽  
Sufficient Evidence ◽  
International Agency ◽  
Outdoor Air ◽  
Outdoor Air Pollution ◽  
Increased Risk

Abstract Along the years, the International Agency for Research on Cancer (IARC) has classified many air pollutants components as carcinogens, including solvents, diesel engine exhaust, metals, such as chromium, nickel, arsenic, and cadmium. The IARC list of Group 1 carcinogens includes benzene, diesel exhaust, benzo[a]pyrene (B[a]P, a polycyclic aromatic hydrocarbon [PAH]), indoor emissions from coal combustion, and 1,3-buta-diene. Sources, mainly combustion-related, that emit airborne carcinogens can be both in indoor and outdoor. In 2013, the IARC has classified outdoor air pollution and one of its major components, particulate matter (PM), as carcinogenic. In its evaluation, the IARC suggested sufficient evidence showing that exposure to outdoor air pollution and PM causes lung cancer and it noted that a positive association between such pollution and an increased risk of bladder cancer. The association between exposure to air pollutant and cancer risk has been investigated in cohort studies and the results are generally consistent, indicating that long-term exposure to air pollution can cause lung cancer and increase risks of cancer in other locations. The use of the information on carcinogenicity is fundamental to produce estimates to quantify risks and impacts on exposed population. WHO in several recent activities has addressed this issue. For example, it is also under consideration by various experts in the framework of the Task Force for Health (TFH) of the UNECE Convention on Long-range Transboundary Air Pollution. The discussion of this session will focus on the implications and the challenges to integrate toxicological and epidemiological evidence of identified air carcinogens in health in risk and impact assessment.

scholarly journals 1235Household air pollution and lung cancer mortality among never-smokers: findings from the China Kadoorie Biobank

2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Elvin Cheng ◽  
Ka Hung Chan ◽  
Marianne Weber ◽  
Julia Steinberg ◽  
Karen Canfell ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Air Pollution ◽  
Risk Factor ◽  
Cox Regression ◽  
Total Duration ◽  
Case Control ◽  
Mortality Data ◽  
Case Control Studies ◽  
Increased Risk ◽  
Never Smokers

Abstract Background Household air pollution (HAP) has been classified as a major risk factor for lung cancer (LC) among never-smokers, however, evidence is largely from case-control studies. Using the prospective cohort China Kadoorie Biobank (CKB), we investigated the association of HAP with LC death among never-smokers. Methods The CKB, a large-scale cohort study, recruited 512,715 adults aged 30–79 years from ten regions in China during 2004-2008. Self-reported never-smoking participants were followed up to 31/12/2016 with linkage to mortality data. Total duration of HAP exposure was calculated from self-reported solid fuel use in domestic cooking and slow-burning stoves in participants’ three most recent residences, and self-reported coal-smoky home in winter during their lifetime. Hazard ratios (HR) and 95% confidence intervals (CI) of LC death associated with HAP exposure were estimated using Cox regression, adjusting for key confounders including several demographic, environmental and lifestyle factors. Results There were 979 LC deaths among 323,794 never-smokers without prior cancer during a median follow-up of 10.2 years. There was a log-linear positive association between HAP exposure and LC death (p-trend=0.0034), with 4% increased risk per 5-year longer exposure (HR = 1.04; 95% CI 1.01-1.06); and participants with 40.1-50.0 years of exposure had the highest risk compared to the never-exposed (HR = 1.53; 95% CI 1.13-2.07). Conclusions This study provides new prospective evidence that HAP exposure is associated with LC death among Chinese never-smokers, and strengthens the previous evidence largely based on case-control studies. Key messages This study supports HAP as an important risk factor for LC development among never-smokers.

scholarly journals Population-Based Estimates of the Age-Specific Cumulative Risk of Breast Cancer for Pathogenic Variants in CHEK2: Findings from the Australian Breast Cancer Family Registry

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1378
Author(s):  
Tú Nguyen-Dumont ◽  
James G. Dowty ◽  
Jason A. Steen ◽  
Anne-Laure Renault ◽  
Fleur Hammet ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cumulative Risk ◽  
Population Based ◽  
Case Control ◽  
Cancer Information ◽  
Case Control Studies ◽  
Breast Cancer Family ◽  
Pathogenic Variants ◽  
Increased Risk ◽  
Control Family

Case-control studies of breast cancer have consistently shown that pathogenic variants in CHEK2 are associated with about a 3-fold increased risk of breast cancer. Information about the recurrent protein-truncating variant CHEK2 c.1100delC dominates this estimate. There have been no formal estimates of age-specific cumulative risk of breast cancer for all CHEK2 pathogenic (including likely pathogenic) variants combined. We conducted a population-based case-control-family study of pathogenic CHEK2 variants (26 families, 1071 relatives) and estimated the age-specific cumulative risk of breast cancer using segregation analysis. The estimated hazard ratio for carriers of pathogenic CHEK2 variants (combined) was 4.9 (95% CI 2.5–9.5) relative to non-carriers. The HR for carriers of the CHEK2 c.1100delC variant was estimated to be 3.5 (95% CI 1.02–11.6) and the HR for carriers of all other CHEK2 variants combined was estimated to be 5.7 (95% CI 2.5–12.9). The age-specific cumulative risk of breast cancer was estimated to be 18% (95% CI 11–30%) and 33% (95% CI 21–48%) to age 60 and 80 years, respectively. These findings provide important information for the clinical management of breast cancer risk for women carrying pathogenic variants in CHEK2.

scholarly journals Relevance of hMLH1 -93G>A, 655A>G and 1151T>A polymorphisms with colorectal cancer susceptibility: a meta-analysis based on 38 case-control studies

2018 ◽  
Vol 64 (10) ◽  
pp. 942-951 ◽  
Author(s):  
Mohammad Zare ◽  
Jamal Jafari-Nedooshan ◽  
Mohammadali Jafari ◽  
Hossein Neamatzadeh ◽  
Seyed Mojtaba Abolbaghaei ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Asian Population ◽  
Case Control ◽  
Biomedical Literature ◽  
Case Control Studies ◽  
Increased Risk ◽  
Comprehensive Search ◽  
Meta Analyses

SUMMARY OBJECTIVE: There has been increasing interest in the study of the association between human mutL homolog 1 (hMLH1) gene polymorphisms and risk of colorectal cancer (CRC). However, results from previous studies are inconclusive. Thus, a meta-analysis was conducted to derive a more precise estimation of the effects of this gene. METHODS: A comprehensive search was conducted in the PubMed, EMBASE, Chinese Biomedical Literature databases until January 1, 2018. Odds ratio (OR) with 95% confidence interval (CI) was used to assess the strength of the association. RESULTS: Finally, 38 case-control studies in 32 publications were identified met our inclusion criteria. There were 14 studies with 20668 cases and 19533 controls on hMLH1 −93G>A, 11 studies with 5,786 cases and 8,867 controls on 655A>G and 5 studies with 1409 cases and 1637 controls on 1151T>A polymorphism. The combined results showed that 655A>G and 1151T>A polymorphisms were significantly associated with CRC risk, whereas −93G>A polymorphism was not significantly associated with CRC risk. As for ethnicity, −93G>A and 655A>G polymorphisms were associated with increased risk of CRC among Asians, but not among Caucasians. More interestingly, subgroup analysis indicated that 655A>G might raise CRC risk in PCR-RFLP and HB subgroups. CONCLUSION: Inconsistent with previous meta-analyses, this meta-analysis shows that the hMLH1 655A>G and 1151T>A polymorphisms might be risk factors for CRC. Moreover, the −93G>A polymorphism is associated with the susceptibility of CRC in Asian population.

scholarly journals Association between Risk Factors for Vascular Dementia and Adiponectin

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Juhyun Song ◽  
Won Taek Lee ◽  
Kyung Ah Park ◽  
Jong Eun Lee
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Signal Transduction ◽  
Vascular Dementia ◽  
Case Control ◽  
Case Control Studies ◽  
Insulin Signal Transduction ◽  
Increased Risk ◽  
The Brain

Vascular dementia is caused by various factors, including increased age, diabetes, hypertension, atherosclerosis, and stroke. Adiponectin is an adipokine secreted by adipose tissue. Adiponectin is widely known as a regulating factor related to cardiovascular disease and diabetes. Adiponectin plasma levels decrease with age. Decreased adiponectin increases the risk of cardiovascular disease and diabetes. Adiponectin improves hypertension and atherosclerosis by acting as a vasodilator and antiatherogenic factor. Moreover, adiponectin is involved in cognitive dysfunction via modulation of insulin signal transduction in the brain. Case-control studies demonstrate the association between low adiponectin and increased risk of stroke, hypertension, and diabetes. This review summarizes the recent findings on the association between risk factors for vascular dementia and adiponectin. To emphasize this relationship, we will discuss the importance of research regarding the role of adiponectin in vascular dementia.

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