Background
Industrialization has been linked to the etiology of inflammatory bowel disease (IBD).
Aim
We investigated the association between air pollution exposure and IBD.
Methods
The European ...Prospective Investigation into Cancer and Nutrition cohort was used to identify cases with Crohn’s disease (CD) (
n
= 38) and ulcerative colitis (UC) (
n
= 104) and controls (
n
= 568) from Denmark, France, the Netherlands, and the UK, matched for center, gender, age, and date of recruitment. Air pollution data were obtained from the European Study of Cohorts for Air Pollution Effects. Residential exposure was assessed with land-use regression models for particulate matter with diameters of <10 μm (PM
10
), <2.5 μm (PM
2.5
), and between 2.5 and 10 μm (PM
coarse
), soot (PM
2.5 absorbance
), nitrogen oxides, and two traffic indicators. Conditional logistic regression analyses were performed to calculate odds ratios (ORs) with 95 % confidence intervals (CIs).
Results
Although air pollution was not significantly associated with CD or UC separately, the associations were mostly similar. Individuals with IBD were less likely to have higher exposure levels of PM
2.5
and PM
10
, with ORs of 0.24 (95 % CI 0.07–0.81) per 5 μg/m
3
and 0.25 (95 % CI 0.08–0.78) per 10 μg/m
3
, respectively. There was an inverse but nonsignificant association for PM
coarse
. A higher nearby traffic load was positively associated with IBD OR 1.60 (95 % CI 1.04–2.46) per 4,000,000 motor vehicles × m per day. Other air pollutants were positively but not significantly associated with IBD.
Conclusion
Exposure to air pollution was not found to be consistently associated with IBD.
Healing of burn wounds is often associated with scar formation due to excessive inflammation and delayed wound closure. To date, no effective treatment is available to prevent the fibrotic process. ...The Renin Angiotensin System (RAS) was shown to be involved in fibrosis in various organs. Statins (e.g. Atorvastatin), Angiotensin receptor antagonists (e.g. Losartan) and the combination of these drugs are able to reduce the local RAS activation, and reduced fibrosis in other organs. We investigated whether inhibition of the RAS could improve healing of burn wounds by treatment with Atorvastatin, Losartan or the combination of both drugs. Therefore, full and partial thickness burn wounds were inflicted on both flanks of Yorkshire pigs. Oral administration of Atorvastatin, Losartan or the combination was started at post-burn day 1 and continued for 28 days. Full thickness wounds were excised and transplanted with an autologous meshed split-thickness skin graft at post-burn day 14. Partial thickness wounds received conservative treatment. Atorvastatin treatment resulted in enhanced graft take and wound closure of the full thickness wounds, faster resolution of neutrophils compared to all treatments and reduced alpha-smooth muscle actin positive cells compared to control treatment. Treatment with Losartan and to a lesser extent the combination therapy resulted in diminished graft take, increased wound contraction and poorer scar outcome. In contrast, Losartan treatment in partial thickness wounds decreased the alpha-smooth muscle actin+ fibroblasts and contraction. In conclusion, we showed differential effects of Losartan and Atorvastatin in full and partial thickness wounds. The extensive graft loss seen in Losartan treated wounds is most likely responsible for the poor clinical outcome of these full thickness burn wounds. Therefore, Losartan treatment should not be started before transplantation in order to prevent graft loss. Atorvastatin seems to accelerate the healing process in full thickness wounds possibly by dampening the pro-inflammatory response.
Current day concentrations of ambient air pollution have been associated with a range of adverse health effects, particularly mortality and morbidity due to cardiovascular and respiratory diseases. ...In this review, we summarize the evidence from epidemiological studies on long-term exposure to fine and coarse particles, nitrogen dioxide (NO2) and elemental carbon on mortality from all-causes, cardiovascular disease and respiratory disease. We also summarize the findings on potentially susceptible subgroups across studies. We identified studies through a search in the databases Medline and Scopus and previous reviews until January 2013 and performed a meta-analysis if more than five studies were available for the same exposure metric.
Abstract
Background
Uraemia induces endothelial cell (EC) injury and impaired repair capacity, for which the underlying mechanism remains unclear. Active vitamin D (VD) may promote endothelial ...repair, however, the mechanism that mediates the effects of VD in chronic kidney disease are poorly understood. Thus, we investigated uraemia-induced endothelial damage and the protection against such damage by active VD.
Methods
We applied electric cell-substrate impedance sensing (ECIS) to study real-time responses of human ECs exposed to pooled uraemic and non-uraemic plasma with or without the addition of active VD. The effects of indoxyl sulphate and p-cresol were tested in non-uraemic plasma. Structural changes for vascular endothelial (VE)-cadherin and F-actin were assessed by immunostaining and quantified.
Results
The exposure of ECs to uraemic media significantly decreased endothelial barrier function after 24 h. Cell migration after electrical wounding and recovery of the barrier after thrombin-induced loss of integrity were significantly impaired in uraemic-medium stimulated cells and cells exposed to indoxyl sulphate and p-cresol. This effect on ECIS was dependent on loss of cell–cell interaction. Mechanistically, we found that EC, exposed to uraemic media, displayed disrupted VE-cadherin interactions and F-actin reorganization. VD supplementation rescued both endothelial barrier function and cell–cell interactions in ECs exposed to uraemic media. These events were associated with an increment of VE-cadherin at intercellular junctions.
Conclusions
Our data demonstrate a potentially clinically relevant mechanism for uraemia-induced endothelial damage. Furthermore, active VD rescued the uraemic medium-induced loss of cell–cell adhesion, revealing a novel role of active VD in preservation of endothelial integrity during uraemia.
The evidence from observational epidemiological studies of a link between long-term air pollution exposure and diabetes prevalence and incidence is currently mixed. Some studies found the strongest ...associations of diabetes with fine particles, other studies with nitrogen dioxide and some studies found no associations.
Our aim was to investigate associations between long-term exposure to multiple air pollutants and diabetes prevalence in a large national survey in the Netherlands.
We performed a cross-sectional analysis using the 2012 Dutch national health survey to investigate the associations between the 2009 annual average concentrations of multiple air pollutants (PM10, PM2.5, PM10−2.5, PM2.5 absorbance, OPDTT, OPESR and NO2) and diabetes prevalence, among 289,703 adults. Air pollution exposure was assessed by land use regression models. Diabetes was defined based on a combined measure of self-reported physician diagnosis and medication prescription from an external database. Using logistic regression, we adjusted for potential confounders, including neighborhood- and individual socio-economic status and lifestyle-related risk factors such as smoking habits, alcohol consumption, physical activity and BMI.
After adjustment for potential confounders, all pollutants (except PM2.5) were associated with diabetes prevalence. In two-pollutant models, NO2 and OPDTT remained associated with increased diabetes prevalence. For NO2 and OPDTT, single-pollutant ORs per interquartile range were 1.07 (95% CI: 1.05, 1.09) and 1.08 (95% CI: 1.05, 1.10), respectively. Stratified analysis showed no consistent effect modification by any of the included known diabetes risk factors.
Long-term residential air pollution exposure was associated with diabetes prevalence in a large health survey in the Netherlands, strengthening the evidence of air pollution being an important diabetes risk factor. Most consistent associations were observed for NO2 and oxidative potential of PM2.5 measured by the DTT assay. The finding of an association with the oxidative potential of fine particles but not with PM2.5, suggests that particle composition may be important for a potential effect on diabetes.
•Air pollution was associated with diabetes prevalence in a large Dutch health survey.•Most consistent associations were observed for NO2 and oxidative potential of PM2.5.•We found no evidence that associations were stronger in women than in men•We found stronger associations in physically active subjects.•Particle composition may play an important role in the potential effects on diabetes.
There is evidence for adverse effects of outdoor air pollution on lung function of children. Quantitative summaries of the effects of air pollution on lung function, however, are lacking due to large ...differences among studies.
We aimed to study the association between residential exposure to air pollution and lung function in five European birth cohorts with a standardized exposure assessment following a common protocol.
As part of the European Study of Cohorts for Air Pollution Effects (ESCAPE) we analyzed data from birth cohort studies situated in Germany, Sweden, the Netherlands, and the United Kingdom that measured lung function at 6-8 years of age (n = 5,921). Annual average exposure to air pollution nitrogen oxides (NO2, NOx), mass concentrations of particulate matter with diameters < 2.5, < 10, and 2.5-10 μm (PM2.5, PM10, and PMcoarse), and PM2.5 absorbance at the birth address and current address was estimated by land-use regression models. Associations of lung function with estimated air pollution levels and traffic indicators were estimated for each cohort using linear regression analysis, and then combined by random effects meta-analysis.
Estimated levels of NO2, NOx, PM2.5 absorbance, and PM2.5 at the current address, but not at the birth address, were associated with small decreases in lung function. For example, changes in forced expiratory volume in 1 sec (FEV1) ranged from -0.86% (95% CI: -1.48, -0.24%) for a 20-μg/m3 increase in NOx to -1.77% (95% CI: -3.34, -0.18%) for a 5-μg/m3 increase in PM2.5.
Exposure to air pollution may result in reduced lung function in schoolchildren.
Land use regression (LUR) models have become popular to explain the spatial variation of air pollution concentrations. Independent evaluation is important. We developed LUR models for nitrogen ...dioxide (NO2) using measurements conducted at 144 sampling sites in The Netherlands. Sites were randomly divided into training data sets with a size of 24, 36, 48, 72, 96, 108, and 120 sites. LUR models were evaluated using (1) internal “leave-one-out-cross-validation (LOOCV)” within the training data sets and (2) external “hold-out” validation (HV) against independent test data sets. In addition, we calculated Mean Square Error based validation R2s. The mean adjusted model and LOOCV R2 slightly decreased from 0.87 to 0.82 and 0.83 to 0.79, respectively, with an increasing number of training sites. In contrast, the mean HV R2 was lowest (0.60) with the smallest training sets and increased to 0.74 with the largest training sets. Predicted concentrations were more accurate in sites with out of range values for prediction variables after changing these values to the minimum or maximum of the range observed in the corresponding training data set. LUR models for NO2 perform less well, when evaluated against independent measurements, when they are based on relatively small training sets. In our specific application, models based on as few as 24 training sites, however, achieved acceptable hold out validation R2s of, on average, 0.60.
Land use regression (LUR) models typically investigate within-urban variability in air pollution. Recent improvements in data quality and availability, including satellite-derived pollutant ...measurements, support fine-scale LUR modeling for larger areas. Here, we describe NO2 and PM10 LUR models for Western Europe (years: 2005–2007) based on >1500 EuroAirnet monitoring sites covering background, industrial, and traffic environments. Predictor variables include land use characteristics, population density, and length of major and minor roads in zones from 0.1 km to 10 km, altitude, and distance to sea. We explore models with and without satellite-based NO2 and PM2.5 as predictor variables, and we compare two available land cover data sets (global; European). Model performance (adjusted R 2) is 0.48–0.58 for NO2 and 0.22–0.50 for PM10. Inclusion of satellite data improved model performance (adjusted R 2) by, on average, 0.05 for NO2 and 0.11 for PM10. Models were applied on a 100 m grid across Western Europe; to support future research, these data sets are publicly available.
Scarless wound healing is a unique and intrinsic capacity of the fetal skin that is not fully understood. Further insight into the underlying mechanisms of fetal wound healing may lead to new ...therapeutic approaches promoting adult scarless wound healing. Differences between fetal and adult wound healing are found in the extracellular matrix, the inflammatory reaction and the levels of growth factors present in the wound. This review focuses specifically on transforming growth factor β (TGF‐β), as this growth factor is prominently involved in wound healing and fibroblast‐to‐myofibroblast differentiation.
Although fetal fibroblasts do respond to TGF‐β, they lack a proliferative and a contractile response and display short‐lived myofibroblast differentiation, autocrine response, and collagen up‐regulation in comparison with adult fibroblasts. Curiously, prolonged TGF‐β activation is associated with fibrosis, and therefore, this short‐lived response in fetal fibroblasts might contribute to scarless healing. This review gives an overview of the current knowledge on TGF‐β signaling and the intracellular TGF‐β signaling pathway in fetal fibroblasts. Furthermore, this review also describes the various components that regulate the cellular TGF‐β response and hypothesizes about the possible roles these components might play in the altered response of fetal fibroblasts to TGF‐β.