Dataset Information

Ambient air pollution in gastrointestinal endoscopy unit; rationale and design of a prospective study.

ABSTRACT: BACKGROUND:A gastrointestinal endoscopy unit is frequently exposed to gastrointestinal gas expelled from patients and electrocoagulated tissue through carbonation for the treatment of gastrointestinal neoplasms or hemostasis of gastrointestinal bleeding. This can be potentially harmful to the health of not only the healthcare personnel but also patients who undergo endoscopic examinations. However, there has been scarce data on air quality in the endoscopy unit. This study aimed to measure the air quality in the gastrointestinal endoscopy unit. METHODS:This is a prospective study using conventional portable passive air quality monitoring sensors in the gastrointestinal endoscopy unit. We will check the 6 main indoor air quality indices, as well as the atmospheric temperature, pressure, and humidity in the endoscopy unit of a single hospital in Korea. These indices are as follows: carbon dioxide (CO2), total volatile organic compounds (VOCs), particulate matter that has a diameter of <2.5??m, nitrogen dioxide (NO2), carbon monoxide (CO), and ozone. The indices will be checked in the endoscopy unit, including the procedural area, recovery area, and area for disinfection and cleansing of equipment, at 1-minute intervals for at least 1 week, and the type and number of endoscopic procedures will also be recorded. The primary outcome of this study is to determine whether the air quality indices exceed safety thresholds and whether there is any association between ambient air pollution and the type and number of endoscopic procedures. CONCLUSION:The results of this study will provide evidence for health-related protective strategies for medical practitioners and patients in the endoscopy unit.

SUBMITTER: Bang CS

PROVIDER: S-EPMC6310590 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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Ambient air pollution in gastrointestinal endoscopy unit; rationale and design of a prospective study.

Bang Chang Seok CS Lee Keunwook K Choi Jae Ho JH Soh Jae Seung JS Hong Ji Young JY Baik Gwang Ho GH Kim Dong Joon DJ

Medicine 20181201 49

<h4>Background</h4>A gastrointestinal endoscopy unit is frequently exposed to gastrointestinal gas expelled from patients and electrocoagulated tissue through carbonation for the treatment of gastrointestinal neoplasms or hemostasis of gastrointestinal bleeding. This can be potentially harmful to the health of not only the healthcare personnel but also patients who undergo endoscopic examinations. However, there has been scarce data on air quality in the endoscopy unit. This study aimed to measu ...[more]

PMID: 30544484

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Project description:Study questionTo what extent are ambient concentrations of particulate matter <2.5 microns (PM2.5), nitrogen dioxide (NO2) and ozone (O3) associated with risk of self-reported physician-diagnosed uterine leiomyomata (UL)?Summary answerIn this large prospective cohort study of Black women, ambient concentrations of O3, but not PM2.5 or NO2, were associated with increased risk of UL.What is known alreadyUL are benign tumors of the myometrium that are the leading cause of gynecologic inpatient care among reproductive-aged women. Black women are clinically diagnosed at two to three times the rate of white women and tend to exhibit earlier onset and more severe disease. Two epidemiologic studies have found positive associations between air pollution exposure and UL risk, but neither included large numbers of Black women.Study design, size, durationWe conducted a prospective cohort study of 21 998 premenopausal Black women residing in 56 US metropolitan areas from 1997 to 2011.Participants/material, setting, methodsWomen reported incident UL diagnosis and method of confirmation (i.e. ultrasound, surgery) on biennial follow-up questionnaires. We modeled annual residential concentrations of PM2.5, NO2 and O3 throughout the study period. We used Cox proportional hazards regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for a one-interquartile range (IQR) increase in air pollutant concentrations, adjusting for confounders and co-pollutants.Main results and the role of chanceDuring 196 685 person-years of follow-up, 6238 participants (28.4%) reported physician-diagnosed UL confirmed by ultrasound or surgery. Although concentrations of PM2.5 and NO2 were not appreciably associated with UL (HRs for a one-IQR increase: 1.01 (95% CI: 0.93, 1.10) and 1.05 (95% CI: 0.95, 1.16), respectively), O3 concentrations were associated with increased UL risk (HR for a one-IQR increase: 1.19, 95% CI: 1.07, 1.32). The association was stronger among women age <35 years (HR: 1.26, 95% CI: 0.98, 1.62) and parous women (HR: 1.28, 95% CI: 1.11, 1.48).Limitations, reasons for cautionOur measurement of air pollution is subject to misclassification, as monitoring data are not equally spatially distributed and we did not account for time-activity patterns. Our outcome measure was based on self-report of a physician diagnosis, likely resulting in under-ascertainment of UL. Although we controlled for several individual- and neighborhood-level confounding variables, residual confounding remains a possibility.Wider implications of the findingsInequitable burden of air pollution exposure has important implications for racial health disparities, and may be related to disparities in UL. Our results emphasize the need for additional research focused on environmental causes of UL.Study funding/competing interest(s)This research was funded by the National Cancer Institute (U01-CAA164974) and the National Institute of Environmental Health Sciences (R01-ES019573). L.A.W. is a fibroid consultant for AbbVie, Inc. and accepts in-kind donations from Swiss Precision Diagnostics, Sandstone Diagnostics, FertilityFriend.com and Kindara.com for primary data collection in Pregnancy Study Online (PRESTO). M.J. declares consultancy fees from the Health Effects Institute (as a member of the review committee). The remaining authors declare they have no actual or potential competing financial interests.Trial registration numberN/A.

Project description:BackgroundRecent studies suggest potential interactions of air pollutants with dietary factors and genetic susceptibility on mortality risk; however, evidence from prospective studies is still lacking. We aimed to assess the association between air pollution and mortality, and investigate the modification effects of a healthy diet and genetic susceptibility.MethodsA total of 386 937 participants were enrolled from 2006 to 2010 and followed up to 2018 in the UK Biobank study. The annual average air pollutant concentrations of particulate matter (PM) with diameters ≤2.5 (PM2.5), ≤10 (PM10) and between 2.5 and 10 µm (PM2.5-10) and nitrogen oxides (NO2 and NOx) were calculated and linked to participants' residential addresses. Healthy dietary patterns were evaluated by a healthy diet score (HDS) based on intakes of vegetables, fruit, fish, unprocessed red meat and processed meat. We also calculated genetic risk score (GRS) of the lifespan. We examined potential interactions by setting variable cross-product terms of air pollutants with diets or GRS in the models.ResultsWe identified 11 881 deaths [2426 from cardiovascular diseases (CVD), 1211 from coronary heart disease (CHD) and 466 from stroke] during a median follow-up of 8.9 years. We found that PM2.5 [hazard ratio (HR), 1.27; 95% CI, 1.05-1.55], PM10 (HR, 1.18; 95% CI, 1.04-1.34), NO2 (HR, 1.05; 95% CI, 1.01-1.08), and NOx (HR, 1.02; 95% CI, 1.01-1.03) were associated with all-cause mortality. PM2.5 was also associated with increased risks of CVD mortality (HR, 1.68; 95% CI, 1.10-2.56) and CHD mortality (HR, 2.08; 95% CI, 1.16-3.75). In addition, we found that adherence to healthy dietary patterns modified associations of PM2.5, NO2 and NOx with all-cause mortality (P-interaction = 0.006, 0.006 and 0.02, respectively). Among the individual dietary components, vegetable intakes showed interactions with PM2.5, NO2 and NOx (P-interaction = 0.007, 0.004 and 0.02, respectively). The associations between air pollutants and increased risks of all-cause mortality were attenuated among participants with higher vegetable intakes. We did not observe interactions between air pollutants and HDS on CVD, CHD or stroke mortality (P-interaction > 0.05). Besides, we did not find interactions between air pollutants and genetic risk for lifespan on mortality risk.ConclusionThis study provides evidence linking long-term exposure to various air pollutants to the risk of all-cause, CVD and CHD mortality, and the potential attenuation of a healthy diet, especially high vegetable intakes, on such relations. Our findings highlight the importance of adherence to a healthy diet in lowering ambient air-pollution-related mortality risk.

Project description:BackgroundPrevious studies indicated that air pollution plausibly increases the risk of adverse outcomes in inflammatory bowel disease (IBD) via proinflammatory mechanisms. However, there is scant epidemiological data and insufficient prospective evidence assessing associations between ambient air pollution and clinical outcomes of IBD.ObjectivesWe aimed to investigate the associations between ambient air pollution and clinical outcomes among individuals with IBD.MethodsLeveraging data from the UK Biobank, we included 4,708 individuals with IBD recruited in the period 2006-2010 in this study. A land use regression model was used to assess annual mean concentrations of ambient air pollutants nitrogen including oxides (NOx), nitrogen dioxide (NO2), and particulate matter (PM) with aerodynamic diameter ≤10μm (PM10) and PM with aerodynamic diameter ≤2.5μm (PM2.5). Individuals with IBD were followed up for incident clinical outcomes of enterotomy, gastrointestinal cancer, and all-cause mortality, ascertained via death registry, inpatient, primary care, and cancer registry data. Cox proportional hazard model was used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for the magnitude of the associations.ResultsDuring a mean follow-up of 12.0 y, 265 enterotomy events, 124 incident gastrointestinal cancer, and 420 death events were documented among individuals with IBD. We found that each interquartile range (IQR) increase in exposure to PM2.5 was associated with increased risk of enterotomy (HR=1.16; 95% CI: 1.00, 1.34, p=0.043), whereas an IQR increase in exposure to NOx (HR=1.10; 95% CI: 1.01, 1.20, p=0.016), NO2 (HR=1.16; 95% CI: 1.03, 1.29, p=0.010), PM10 (HR=1.15; 95% CI: 1.03, 1.30, p=0.015), and PM2.5 (HR=1.14; 95% CI: 1.02, 1.28, p=0.019) was associated with increased risk of all-cause mortality among individuals with IBD. We did not observe any significant associations between air pollutants and gastrointestinal cancer in the primary analyses. Consistent results were observed in subgroup and sensitivity analyses.ConclusionsAmbient pollution exposure was associated with an increased risk of enterotomy and all-cause mortality among individuals with IBD, highlighting the important role of environmental health in improving the prognosis of IBD. https://doi.org/10.1289/EHP12215.

Project description:Long-term exposure to air pollution has been associated with several adverse health effects including cardiovascular, respiratory diseases and cancers. However, underlying molecular alterations remain to be further investigated. The aim of this study is to investigate the effects of long-term exposure to air pollutants on (a) average DNA methylation at functional regions and, (b) individual differentially methylated CpG sites. An assumption is that omic measurements, including the methylome, are more sensitive to low doses than hard health outcomes. This study included blood-derived DNA methylation (Illumina-HM450 methylation) for 454 Italian and 159 Dutch participants from the European Prospective Investigation into Cancer and Nutrition (EPIC). Long-term air pollution exposure levels, including NO2, NOx, PM2.5, PMcoarse, PM10, PM2.5 absorbance (soot) were estimated using models developed within the ESCAPE project, and back-extrapolated to the time of sampling when possible. We meta-analysed the associations between the air pollutants and global DNA methylation, methylation in functional regions and epigenome-wide methylation. CpG sites found differentially methylated with air pollution were further investigated for functional interpretation in an independent population (EnviroGenoMarkers project), where (N=613) participants had both methylation and gene expression data available. Exposure to NO2 was associated with a significant global somatic hypomethylation (p-value=0.014). Hypomethylation of CpG island's shores and shelves and gene bodies was significantly associated with higher exposures to NO2 and NOx. Meta-analysing the epigenome-wide findings of the 2 cohorts did not show genome-wide significant associations at single CpG site level. However, several significant CpG were found if the analyses were separated by countries. By regressing gene expression levels against methylation levels of the exposure-related CpG sites, we identified several significant CpG-transcript pairs and highlighted 5 enriched pathways for NO2 and 9 for NOx mainly related to the immune system and its regulation. Our findings support results on global hypomethylation associated with air pollution, and suggest that the shores and shelves of CpG islands and gene bodies are mostly affected by higher exposure to NO2 and NOx. Functional differences in the immune system were suggested by transcriptome analyses.

Project description:OBJECTIVE:To examine associations of proximity to major roadways, sustained exposure to fine particulate matter (PM2.5), and acute exposure to ambient air pollutants with adipokines and measures of glucose homeostasis among participants living in the northeastern United States. METHODS:We included 5958 participants from the Framingham Offspring cohort examination cycle 7 (1998-2001) and 8 (2005-2008) and Third Generation cohort examination cycle 1 (2002-2005) and 2 (2008-2011), who did not have type 2 diabetes at the time of examination visit. We calculated 2003 annual average PM2.5 at participants' home address, residential distance to the nearest major roadway, and daily PM2.5, black carbon (BC), sulfate, nitrogen oxides (NOx), and ozone concentrations. We used linear mixed effects models for fasting glucose, insulin, and homeostasis model assessment of insulin resistance (HOMA-IR) which were measured up to twice, and used linear regression models for adiponectin, resistin, leptin, and hemoglobin A1c (HbA1c) which were measured only once, adjusting for demographics, socioeconomic position, lifestyle, time, and seasonality. RESULTS:The mean age was 51years and 55% were women. Participants who lived 64m (25th percentile) from a major roadway had 0.28% (95% CI: 0.05%, 0.51%) higher fasting plasma glucose than participants who lived 413m (75th percentile) away, and the association appeared to be driven by participants who lived within 50m from a major roadway. Higher exposures to 3- to 7-day moving averages of BC and NOx were associated with higher glucose whereas the associations for ozone were negative. The associations otherwise were generally null and did not differ by median age, sex, educational attainment, obesity status, or prediabetes status. CONCLUSIONS:Living closer to a major roadway or acute exposure to traffic-related air pollutants were associated with dysregulated glucose homeostasis but not with adipokines among participants from the Framingham Offspring and Third Generation cohorts.

Dataset Information

Ambient air pollution in gastrointestinal endoscopy unit; rationale and design of a prospective study.

Publications

Ambient air pollution in gastrointestinal endoscopy unit; rationale and design of a prospective study.

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