Asthma has become the most common, childhood chronic disease in the industrialized world, and it is also increasing in developing regions. There are huge differences in the prevalence of childhood ...asthma across countries and continents, and there is no doubt that the prevalence of asthma was strongly increasing during the past decades worldwide. Asthma, as a complex disease, has a broad spectrum of potential determinants ranging from genetics to life style and environmental factors. Environmental factors are likely to be important in explaining the regional differences and the overall increasing trend towards asthma's prevalence. Among the environmental conditions, indoor factors are of particular interest because people spend more than 80% of their time indoors globally. Increasing prices for oil, gas and other sources of primary energy will further lead to better insulation of homes, and ultimately to reduced energy costs. This will decrease air exchange rates and will lower the dilution of indoor air mass with ambient air. Indoor air quality and potential health effects will therefore be an area for future research and for gaining a better understanding of asthma epidemics. This strategic review will summarize the current knowledge of the effects of a broad spectrum of indoor factors on the development of asthma in childhood in Western countries based on epidemiological studies. In conclusion, several epidemiological studies point out, that indoor factors might cause asthma in childhood. Stronger and more consistent findings are seen when exposure to these indoor factors is assessed by surrogates for the source of the actual toxicants. Measurement-based exposure assessments for several indoor factors are less common than using surrogates of the exposure. These studies, however, mainly showed heterogeneous results. The most consistent finding for an induction of asthma in childhood is related to exposure to environmental tobacco smoke, to living in homes close to busy roads, and in damp homes where are visible moulds at home. The causing agents of the increased risk of living in damp homes remained uncertain and needs clarification. Exposure to pet-derived allergens and house dust mites are very commonly investigated and thought to be related to asthma onset. The epidemiological evidence is not sufficient to recommend avoidance measures against pet and dust mites as preventive activities against allergies. More research is also needed to clarify the potential risk for exposure to volatile and semi-volatile organic compounds due to renovation activities, phthalates and chlorine chemicals due to cleaning.
Air pollutants are suggested to be related to type 2 diabetes (T2D). Since several high quality papers on air pollutants and T2D have been published beyond the last reviews, an extended systematic ...review is highly warranted. We review epidemiological studies to quantify the association between air pollutants and T2D, and to answer if diabetes patients are more vulnerable to air pollutants.
We systematically reviewed the databases of PubMed and Web of Science based on the guidelines of the Preferred Reporting Items for Systematic review and Meta-analysis (PRISMA). We calculated odds ratios (OR) or hazard ratios (HR) and their 95% confidence intervals (CI) to assess the strength of the associations between air pollutants e.g., particulate matter with diameter ≤ 2.5 μm (PM2.5), particulate matter with diameter ≤ 10 μm (PM10), and nitrogen dioxide (NO2) and T2D. We evaluated the quality and risk of bias of the included studies and graded the credibility of the pooled evidence using several recommended tools. We also performed sensitivity analysis, meta-regression analysis, and publication bias test.
Out of 716 articles identified, 86 were used for this review and meta-analysis. Meta-analyses showed significant associations of PM2.5 with T2D incidence (11 studies; HR = 1.10, 95% CI = 1.04–1.17 per 10 μg/m3 increment; I2 = 74.4%) and prevalence (11 studies; OR = 1.08; 95% CI = 1.04–1.12 per 10 μg/m3 increment; I2 = 84.3%), of PM10 with T2D prevalence (6 studies; OR = 1.10; 95% CI = 1.03–1.17 per 10 μg/m3 increment; I2 = 89.5%) and incidence (6 studies; HR = 1.11; 95% CI = 1.00–1.22 per μg/m3 increment; I2 = 70.6%), and of NO2 with T2D prevalence (11 studies; OR = 1.07; 95% CI = 1.04–1.11 per 10 μg/m3 increment; I2 = 91.1%). The majority of studies on glucose-homoeostasis markers also showed increased risks with higher air pollutants levels, but the studies were too heterogeneous for meta-analysis. Overall, patients with diabetes might be more vulnerable to PM.
Recent publications strengthened the evidence for adverse effects of ambient air pollutants exposure (especially for PM) on T2D and that diabetic patients might be more vulnerable to air pollutants exposure.
•Evidence on ambient air pollution and diabetes is still inconsistent.•We reviewed 86 studies on air pollution and diabetes and its traits.•We meta-analyzed 29 studies for PM and NO2 with diabetes.•Air pollutants (e.g., PM and NO2) are associated with higher odds of diabetes.•Air pollution is associated with dysregulation of glucose metabolism.
Background
Air pollutants such as particulate matter (PM
2.5
) and nitrogen dioxide (NO
2
) in outdoor air have long been suspected of causing the development of asthma and allergic rhinitis. ...However, a variety of systematic reviews have reached different conclusions in the last 15 years on whether these air pollutants do in actual fact play a causal role in the onset of asthma, allergic rhinitis, and eczema.
Methods
Based on published systematic reviews and the most recent publications, the current state of knowledge on epidemiological evidence is presented and the potential for primary prevention of these allergic diseases by reducing or avoiding exposure to these air pollutants evaluated.
Results
Despite conducting an extensive literature search, analyzing the most recent results, and focusing on the birth cohort studies most relevant to the question in hand, epidemiological results do not adequately support the concept of a causal relationship between the two air pollutants in question, PM
2.5
and NO
2
, and asthma. Epidemiological studies predominantly show no effect of these air pollutants on allergic sensitization and the onset of allergic rhinitis. The small number of studies that have investigated the link between air pollutants and eczema largely revealed there to be no link.
Conclusion
If the evidence for the causal role of air pollutants in the onset of allergies is inconclusive, one must assume that it is probably not possible to achieve primary prevention of allergies by improving air quality. However, there is sufficient evidence to show that air pollutants can trigger exacerbations of allergic diseases. This alone justifies ensuring that the existing threshold values for air pollutants are adhered to, in order to protect particularly allergy sufferers from health impairments.
Background
Real‐world evidence is sparse on the benefits of allergen immunotherapy AIT; subcutaneous/sublingual immunotherapy (SCIT/SLIT), the only disease‐modifying intervention for allergic ...rhinitis (AR) with long‐term efficacy. This real‐life study evaluated the effect of six AITs (native pollen SLIT/SCIT, four allergoid SCITs) vs symptomatic medication use, on AR symptoms and asthma symptoms/onset, in patients with birch pollen‐associated AR and/or asthma.
Methods
In this retrospective cohort analysis of a German longitudinal prescription database, AIT patients received ≥2 successive seasonal treatment cycles; non‐AIT patients had ≥3 AR prescriptions in three seasons or previous month. Patients were matched for: index year, age, gender, main indication at index, number of seasonal cycles within treatment period, baseline AR/asthma treatment prescriptions. Multiple regression analysis compared prescription data in AIT and non‐AIT groups as proxy for clinical status/disease progression.
Results
Up to 6 years of follow‐up, significantly more AIT (65.4%) vs non‐AIT (47.4%) patients were AR medication‐free; odds ratio (OR) 95% confidence interval (CI): 0.51 (0.48‐0.54); P < 0.001 (28.6% covariate‐adjusted reduction vs non‐AIT; P < 0.001), and significantly more AIT (49.1%) vs non‐AIT (35.1%) patients were asthma medication‐free OR (95% CI): 0.59 (0.55‐0.65); P < 0.001 (32% reduction vs non‐AIT; P < 0.001), or reduced existing asthma medication use (32% covariate‐adjusted reduction vs non‐AIT; P < 0.001). During treatment, new‐onset asthma risk was significantly reduced in the AIT vs non‐AIT group (OR: 0.83; P = 0.001).
Conclusions
Birch pollen AIT demonstrated real‐world benefits up to 6 years post‐treatment cessation through significantly reduced AR and asthma medication intake, and significantly decreased risk of new‐onset asthma medication use on‐treatment.
In this retrospective, real‐world study in Germany, birch pollen allergen immunotherapy (AIT) demonstrated significant benefits up to 6 years post‐treatment in patients with birch pollen‐associated allergic rhinitis (AR) and/or asthma. AIT was associated with significantly improved AR and asthma symptoms as the medication dispensing decreased; nearly two‐thirds and one‐half of patients initially using AR or asthma medications, respectively, no longer required them at study end. During the period in which they were receiving AIT, patients with AR but not asthma had a significantly decreased risk of new‐onset asthma medication dispensing.
In a rapidly urbanizing world, many people have little contact with natural environments, which may affect health and well-being. Existing reviews generally conclude that residential greenspace is ...beneficial to health. However, the processes generating these benefits and how they can be best promoted remain unclear.
During an Expert Workshop held in September 2016, the evidence linking greenspace and health was reviewed from a transdisciplinary standpoint, with a particular focus on potential underlying biopsychosocial pathways and how these can be explored and organized to support policy-relevant population health research.
Potential pathways linking greenspace to health are here presented in three domains, which emphasize three general functions of greenspace: reducing harm (e.g. reducing exposure to air pollution, noise and heat), restoring capacities (e.g. attention restoration and physiological stress recovery) and building capacities (e.g. encouraging physical activity and facilitating social cohesion). Interrelations between among the three domains are also noted. Among several recommendations, future studies should: use greenspace and behavioural measures that are relevant to hypothesized pathways; include assessment of presence, access and use of greenspace; use longitudinal, interventional and (quasi)experimental study designs to assess causation; and include low and middle income countries given their absence in the existing literature. Cultural, climatic, geographic and other contextual factors also need further consideration.
While the existing evidence affirms beneficial impacts of greenspace on health, much remains to be learned about the specific pathways and functional form of such relationships, and how these may vary by context, population groups and health outcomes. This Report provides guidance for further epidemiological research with the goal of creating new evidence upon which to develop policy recommendations.
•Although it appears that greenspace benefits health, the pathways are unclear.•We have organized pathways into three domains that emphasize greenspace functions.•Pathways likely intertwine and vary by context, populations and health outcomes.•We identify diverse challenges in measurement and analysis that require attention.•Research guided by our discussion will better efforts to enable greenspace-related health benefits.
There are a few epidemiological studies that (1) link increased ambient air pollution (AP) with an increase in lung cancer incidence rates and (2) investigate whether residing in green spaces could ...be protective against cancer. However, it is completely unclear whether other forms of cancer are also affected by AP and if residential green spaces could lower cancer incidence rates in general. Therefore, the objective was to estimate whether AP and green space are associated with several cancer types.
The analysis was based on routine health care data from around 1.9 million people from Saxony who were free of cancer in 2008 and 2009. Incident cancer cases (2010-2014) of mouth and throat, skin (non-melanoma skin cancer - NMSC), prostate, breast, and colorectum were defined as: (1) one inpatient diagnosis, or (2) two outpatient diagnoses in two different quarters within one year and a specific treatment or death within two quarters after the diagnosis. Exposures, derived from freely available 3rd party data, included particulate matter with aerodynamic diameter of less than 10 μm (PM
) and nitrogen dioxide (N0
) as well as green space (Normalized Difference Vegetation Index - NDVI). Associations between air pollutants, green space, and cancer incidence were assessed by multilevel Poisson models. Age, sex, physician contacts, short- and long-term unemployment, population density, and having an alcohol-related disorder were considered as potential confounders.
Three thousand one hundred seven people developed mouth and throat cancer, 33,178 NMSC, 9611 prostate cancer, 9577 breast cancer, and 11,975 colorectal cancer during the follow-up period (2010-2014). An increase in PM
of 10 μg/m
was associated with a 53% increase in relative risk (RR) of mouth and throat cancer and a 52% increase in RR of NMSC. Prostate and breast cancer were modestly associated with PM
with an increase in RR of 23 and 19%, respectively. The associations with N0
were in the same direction as PM
but the effect estimates were much lower (7-24%). A 10% increase in NDVI was most protective of mouth and throat cancer (- 11% RR) and of NMSC (- 16% RR). Colorectal cancer was not affected by any of the exposures.
In addition to the studies carried out so far, this study was able to provide evidence that higher ambient AP levels increase the risk of mouth and throat cancer as well as of NMSC and that a higher residential green space level might have a protective effect for NMSC in areas with low to moderate UV intensity. Nevertheless, we cannot rule out residual confounding by socioeconomic or smoking status.
Abstract Tissue availability of polyunsaturated fatty acids (PUFAs) depends on dietary intake and metabolic turnover and has a major impact on human health. Strong associations between variants in ...the human genes fatty acid desaturase 1 ( FADS1 , encoding Δ-5 desaturase) and fatty acid desaturase 2 ( FADS2 , encoding Δ-6 desaturase) and blood levels of PUFAs and long-chain PUFAs (LC-PUFAs) have been reported. The most significant associations and the highest proportion of genetically explained variability (28%) were found for arachidonic acid (20:4n-6), the main precursor of eicosanoids. Subjects carrying the minor alleles of several single nucleotide polymorphisms had a lower prevalence of allergic rhinitis and atopic eczema. Therefore, blood levels of PUFAs and LC-PUFAs are influenced not only by diet, but to a large extent also by genetic variants common in a European population. These findings have been replicated in independent populations. Depending on genetic variants, requirements of dietary PUFA or LC-PUFA intakes to achieve comparable biological effects may differ. We recommend including analyses of FADS1 and FADS2 polymorphism in future cohort and intervention studies addressing biological effects of PUFAs and LC-PUFAs.
Variants in the
gene cluster modify the activity of polyunsaturated fatty acid (PUFA) desaturation and the lipid composition in human blood and tissue.
variants have been associated with plasma lipid ...concentrations, risk of cardiovascular diseases, overweight, eczema, pregnancy outcomes, and cognitive function. Studies on variations in the
genecluster provided some of the first examples for marked gene-diet interactions in modulating complex phenotypes, such as eczema, asthma, and cognition. Genotype distribution differs markedly among ethnicities, apparently reflecting an evolutionary advantage of genotypes enabling active long-chain PUFA synthesis when the introduction of agriculture provided diets rich in linoleic acid but with little arachidonic and eicosapentaenoic acids. Discovering differential effects of PUFA supply that depend on variation of
genotypes could open new opportunities for developing precision nutrition strategies based either on an individual's genotype or on genotype distributions in specific populations.
Studies on the association between traffic noise and cardiovascular diseases have rarely considered air pollution as a covariate in the analyses. Isolated systolic hypertension has not yet been in ...the focus of epidemiological noise research.
The association between traffic noise (road and rail) and the prevalence of hypertension was assessed in two study populations with a total of 4,166 participants 25-74 years of age. Traffic noise (weighted day-night average noise level; LDN) at the facade of the dwellings was derived from noise maps. Annual average PM2.5 mass concentrations at residential addresses were estimated by land-use regression. Hypertension was assessed by blood pressure readings, self-reported doctor-diagnosed hypertension, and antihypertensive drug intake.
In the Greater Augsburg, Germany, study population, traffic noise and air pollution were not associated with hypertension. In the City of Augsburg population (n = 1,893), where the exposure assessment was more detailed, the adjusted odds ratio (OR) for a 10-dB(A) increase in noise was 1.16 (95% CI: 1.00, 1.35), and 1.11 (95% CI: 0.94, 1.30) after additional adjustment for PM2.5. The adjusted OR for a 1-μg/m3 increase in PM2.5 was 1.15 (95% CI: 1.02, 1.30), and 1.11 (95% CI: 0.98, 1.27) after additional adjustment for noise. For isolated systolic hypertension, the fully adjusted OR for noise was 1.43 (95% CI: 1.10, 1.86) and for PM2.5 was 1.08 (95% CI: 0.87, 1.34).
Traffic noise and PM2.5 were both associated with a higher prevalence of hypertension. Mutually adjusted associations with hypertension were positive but no longer statistically significant.
Summary Background A close relation between asthma and allergic rhinitis has been reported by several epidemiological and clinical studies. However, the nature of this relation remains unclear. We ...used the follow-up data from the European Community Respiratory Health Survey to investigate the onset of asthma in patients with allergic and non-allergic rhinitis during an 8·8-year period. Methods We did a longitudinal population-based study, which included 29 centres (14 countries) mostly in western Europe. Frequency of asthma was studied in 6461 participants, aged 20–44 years, without asthma at baseline. Incident asthma was defined as reporting ever having had asthma confirmed by a physician between the two surveys. Atopy was defined as a positive skin-prick test to mites, cat, Alternaria, Cladosporium , grass, birch, Parietaria , olive, or ragweed. Participants were classified into four groups at baseline: controls (no atopy, no rhinitis; n=3163), atopy only (atopy, no rhinitis; n=704), non-allergic rhinitis (rhinitis, no atopy; n=1377), and allergic rhinitis (atopy+rhinitis; n=1217). Cox proportional hazards models were used to study asthma onset in the four groups. Findings The 8·8-year cumulative incidence of asthma was 2·2% (140 events), and was different in the four groups (1·1% (36), 1·9% (13), 3·1% (42), and 4·0% (49), respectively; p<0·0001). After controlling for country, sex, baseline age, body-mass index, forced expiratory volume in 1 s (FEV1 ), log total IgE, family history of asthma, and smoking, the adjusted relative risk for asthma was 1·63 (95% CI 0·82–3·24) for atopy only, 2·71 (1·64–4·46) for non-allergic rhinitis, and 3·53 (2·11–5·91) for allergic rhinitis. Only allergic rhinitis with sensitisation to mite was associated with increased risk of asthma independently of other allergens (2·79 1·57–4·96). Interpretation Rhinitis, even in the absence of atopy, is a powerful predictor of adult-onset asthma. Funding UCB Institute of Allergy and Agence Nationale de la Recherche.
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