Residential Greenspace in Childhood Reduces Risk of Pediatric Inflammatory Bowel Disease: A Population-Based Cohort Study.

INTRODUCTION: Environmental factors related to urbanization and industrialization are believed to be involved in inflammatory bowel disease (IBD) development, but no study has looked at the association between greenspace and IBD. METHODS: We conducted a retrospective cohort study using linked population-based health administrative and environmental data sets. The study population comprised 2,715,318 mother-infant pairs from hospital births in Ontario, Canada, between April 1, 1991, and March 31, 2014. We measured the exposure to residential greenspace using the normalized difference vegetation index derived using remote-sensing methods. Average greenspace was estimated for the pregnancy and childhood periods. We used mixed-effects Cox proportional hazard models to assess potential associations between residential greenspace and the risk of developing IBD before 18 years while adjusting for covariates including sex, maternal IBD, rural/urban residence at birth, and neighborhood income. RESULTS: There were 3,444 IBD diagnoses that occurred during follow-up. An increase in the interquartile range of residential greenspace during the childhood period was associated with a lower risk of developing pediatric-onset IBD (hazard ratio [HR] 0.77, 95% confidence interval [CI] 0.74-0.81). This relationship was significant for both ulcerative colitis (HR 0.72 95% CI 0.67-0.78) and Crohn's disease (HR 0.81, 95% CI 0.76-0.87). There was a linear dose response across increasing quartiles of greenspace (P < 0.0001). No consistent association was detected between maternal intrapartum greenspace exposure and pediatric-onset IBD. DISCUSSION: Higher exposure to residential greenspace during childhood was associated with a reduced risk of IBD, suggesting a novel avenue to prevent IBD in children.

The effect of ginger (Zingiber officinale Roscoe) in patients with advanced cancer.

BACKGROUND: Anorexia-cachexia syndrome (ACS) is a complex condition in advanced cancer patients, defined by disproportionate loss of skeletal muscle mass, and a lack or loss of appetite. This condition greatly lowers the quality of life and limits the treatment options. ACS is commonly associated with gastrointestinal symptoms such as nausea and vomiting. Ginger has been successful in treating these symptoms but has not yet been tested on patients with advanced cancer. Electrogastrography is a technology that allows the direct recording of the gastric myoelectrical activity (GMA). PURPOSE: The aim of this study is to (1) determine the effects of ginger on the GMA in these patients, (2) evaluate the subjective symptoms using 3 validated scales, and (3) correlate the level of inflammatory factors and ghrelin in this patient population. METHODS: Patients with ACS and advanced cancer were recruited from the Palliative Rehabilitation outpatient program at Elisabeth Bruyère Hospital. Patients were instructed to take a daily capsule of 1650 mg of ginger for 14 days and outcome measures were recorded at pre- and post-intervention, which included a blood test for analysis of CRP, albumin and ghrelin levels, 3 self-administered surveys (DSSI, PG-SGA, ESAS), patient-reported symptoms, and an EGG diagnosis. RESULTS: Fifteen patients with a median age of 58 and varying cancer diagnoses were enrolled. EGG diagnosis showed that 9 of the 15 patients had a direct improvement in their GMA, and all patients showed improvement in reported symptoms, most notably nausea, dysmotility- and reflux-like symptoms. There was no correlation found for ginger administration and inflammatory factors. CONCLUSION: These findings suggest that ginger may improve GMA as measured by EGG and may have a notable effect on symptom improvement.

Ambient air pollution and incidence of early-onset paediatric type 1 diabetes: A retrospective population-based cohort study.

BACKGROUND: Studies have reported increasing incidence rates of paediatric diabetes, especially among those aged 0-5 years. Epidemiological evidence linking ambient air pollution to paediatric diabetes remains mixed. OBJECTIVE: This study investigated the association between maternal and early-life exposures to common air pollutants (NO2, PM2.5, O3, and oxidant capacity [Ox; the redox-weighted average of O3 and NO2]) and the incidence of paediatric diabetes in children up to 6 years of age. METHODS: All registered singleton births in Ontario, Ca nada occurring between April 1st, 2006 and March 31st, 2012 were included through linkage from health administrative data. Monthly exposures to NO2, PM2.5, O3, and Ox were estimated across trimesters, the entire pregnancy period and during childhood. Random effects Cox proportional hazards models were used to assess the relationships with paediatric diabetes incidence while controlling for important covariates. We also modelled the shape of concentration-response (CR) relationships. RESULTS: There were 1094 children out of a cohort of 754,698 diagnosed with diabetes before the age of six. O3 exposures during the first trimester of pregnancy were associated with paediatric diabetes incidence (hazard ratio (HR) per interquartile (IQR) increase = 2.00, 95% CI: 1.04-3.86). The CR relationship between O3 during the first trimester and paediatric diabetes incidence appeared to have a risk threshold, in which there was little-to-no risk below 25 ppb of O3, while above this level risk increased sigmoidally. No other associations were observed. CONCLUSION: O3 exposures during a critical period of development were associated with an increased risk of paediatric diabetes incidence.

Ambient air pollution and the risk of pediatric-onset inflammatory bowel disease: A population-based cohort study.

BACKGROUND: High-income nations have the highest rates of inflammatory bowel disease (IBD). The incidence of pediatric-onset IBD is increasing faster than IBD diagnosed in older individuals. Previous epidemiological studies have shown that air pollution might be a risk factor for development of earlier-onset IBD, but results remain mixed. OBJECTIVES: The objective of this study was to evaluate the associations between maternal and early-life exposures to nitrogen dioxide (NO2), fine particulate matter (PM2.5), ozone (O3,) and oxidant capacity (Ox) and risk of pediatric-onset IBD diagnosis. METHODS: We conducted a retrospective cohort study using linked population-based health administrative data. Singleton livebirths in Ontario, Canada between April 1st, 1991 and March 31st, 2014 were included. We investigated the association between weekly exposures during pregnancy and annual exposures from birth until the age of 18 years, and IBD diagnosed <18 years of age using Cox proportional hazards models. We reported hazard ratios (HR) and 95% confidence intervals (CI) for an associated increase in the interquartile range (IQR) of each pollutant. Models were mutually adjusted for exposures in both prenatal and postnatal periods, as well as for sex, rurality of residence at birth, maternal IBD, and neighborhood income. RESULTS: 2,218,789 newborns were included in this study, of whom 2491 developed IBD during follow-up. Increased associations with pediatric-onset IBD were noted for childhood exposure to Ox (HR 1.08, 95% CI 1.01-1.16). IBD development was also associated with Ox during the second trimester (HR 1.21, 95% CI 1.03-1.42), but not the overall pregnancy period (HR 1.12, 95% CI 0.79-1.59). There were no associations of IBD with exposure to NO2, PM2.5, or O3. DISCUSSION: Exposure to Ox during childhood was associated with IBD < 18 years. This suggests that air pollution may impact the developing child physiology in such a way that leads to early onset of IBD.

Spatial variations in ambient ultrafine particle concentrations and risk of congenital heart defects.

BACKGROUND: Cardiovascular malformations account for nearly one-third of all congenital anomalies, making these the most common type of birth defects. Little is known regarding the influence of ambient ultrafine particles (<0.1 µm) (UFPs) on their occurrence. OBJECTIVE: This population-based study examined the association between prenatal exposure to UFPs and congenital heart defects (CHDs). METHODS: A total of 158,743 singleton live births occurring in the City of Toronto, Canada between April 1st 2006 and March 31st 2012 were identified from a birth registry. Associations between exposure to ambient UFPs between the 2nd and 8th week post conception when the foetal heart begins to form and CHDs identified at birth were estimated using random-effects logistic regression models, adjusting for personal- and neighbourhood-level covariates. We also investigated multi-pollutant models accounting for co-exposures to PM2.5, NO2 and O3. RESULTS: A total of 1468 CHDs were identified. In fully adjusted models, UFP exposures during weeks 2 to 8 of pregnancy were not associated with overall CHDs (Odds Ratio (OR) per interquartile (IQR) increase = 1.02, 95% CI: 0.96-1.08). When investigating subtypes of CHDs, UFP exposures were associated with ventricular septal defects (Odds Ratio (OR) per interquartile (IQR) increase = 1.13, 95% CI: 1.03-1.33), but not with atrial septal defect (Odds Ratio (OR) per interquartile (IQR) increase = 0.89, 95% CI: 0.74-1.06). CONCLUSION: This is the first study to evaluate the association between prenatal exposure to UFPs and the risk of CHDs. UFP exposures during a critical period of embryogenesis were associated with an increased risk of ventricular septal defect.