To examine the role of prenatal and postnatal second-hand tobacco smoke (SHS) exposure on asthma, rhinitis, and eczema development up to 16 years of age.
A birth cohort of 4089 children was followed ...for 16 years. Information on parental smoking habits, lifestyle factors, and symptoms of allergic disease was gathered using repeated parental questionnaires. Generalized estimating equations assessed the overall and age-specific associations between SHS exposure and allergic disease at ages 1 to 16 years.
Exposure to SHS in utero was associated with an overall elevated risk of developing asthma up to 16 years (odds ratio OR = 1.45; 95% confidence interval CI, 1.15-1.83) but not for rhinitis or eczema. After additional adjustment for parental smoking throughout childhood, excess overall risks for asthma remained statistically significant. Moreover, a dose-dependent pattern with SHS was observed. Exposure to SHS during infancy was associated with an overall elevated risk of asthma (OR = 1.23; 95% CI, 1.01-1.51), rhinitis (OR = 1.18; 95% CI, 1.01-1.39), and eczema (OR = 1.26; 95% CI, 1.09-1.45) up to 16 years. When age-specific associations were examined, the elevated risks related to SHS exposure in utero or during infancy were mostly confined to early childhood for asthma and rhinitis, whereas the excess risk of eczema appeared greatest at later ages.
Our findings indicate that early SHS exposure, in utero or during infancy, influences the development of allergic disease up to adolescence. Excess risks for asthma and rhinitis were seen primarily in early childhood, whereas those for eczema occurred at later ages.
Obesity-related inflammation is associated with cardiovascular, metabolic, and pulmonary diseases. The aim of this study was to demonstrate associations between adiposity measurements and levels of ...inflammation-related plasma proteins in a population of young adults. Subjects from a population-based birth cohort with a mean age of 22.5 years were included in the study population (n = 2074). Protein levels were analyzed using the Olink Proseek Multiplex Inflammation panel. Percentage body fat (%BF) and visceral fat rating (VFR) measurements were collected using Tanita MC 780 body composition monitor. Linear regression of standardized values was used to investigate associations. Potential effect modifications by sex and BMI category were assessed. Of 71 investigated proteins, 54 were significantly associated with all adiposity measurements %BF, body mass index (BMI), VFR and waist circumference. Among proteins associated with %BF, seven showed a larger or unique association in overweight/obese subjects and three showed a significant effect modification by sex. Fourteen proteins more strongly associated with VFR in females compared to males. Adipose-associated systemic inflammation was observed in this young adult population. Sex and adiposity localization influenced some of the associations. Our results highlight specific proteins as suitable biomarkers related to adiposity.
Exposure to air pollution during infancy has been related to lung function decrements in 8-year-old children, but whether the negative effects remain into adolescence is unknown.
To investigate the ...relationship between long-term air pollution exposure and lung function up to age 16 years.
A total of 2,278 children from the Swedish birth cohort BAMSE (Children, Allergy, Milieu, Stockholm, Epidemiological Survey) performed spirometry at age 16 years. Levels of outdoor air pollution from local road traffic were estimated (nitrogen oxides NOx and particulate matter with an aerodynamic diameter of <10 μm PM10) for residential, daycare, and school addresses during the lifetime using dispersion modeling. Associations between exposure in different time windows and spirometry indexes were analyzed by linear regression and mixed effect models.
Exposure to traffic-related air pollution during the first year of life was associated with FEV1 at age 16 years of -15.8 ml (95% confidence interval CI, -33.6 to 2.0 for a 10 μg/m(3) difference in NOx), predominately in males (-30.4 ml; 95% CI, -59.1 to -1.7), and in subjects not exposed to maternal smoking during pregnancy or infancy. Later exposures appeared to have had an additional negative effect. High exposure during the first year of life was also associated with odds ratios for FEV1 and FVC less than the lower limit of normal (LLN) (defined as a z-score < -1.64 SD) of 3.8 (95% CI, 1.3-10.9) and of 4.3 (95% CI, 1.2-15.0), respectively. The results for PM10 were similar to those for NOx.
Exposure to traffic-related air pollution in infancy is negatively associated with FEV1 at age 16 years, leading to increased risk of clinically important deficits.
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.
Background The role of exposure to air pollution in the development of allergic sensitization remains unclear. Objective We sought to assess the development of sensitization until school age related ...to longitudinal exposure to air pollution from road traffic. Methods More than 2500 children in the birth cohort BAMSE (Children, Allergy, Milieu, Stockholm, Epidemiological Survey) from Stockholm, Sweden, were followed with repeated questionnaires and blood sampling until 8 years of age. Outdoor concentrations of nitrogen oxides, as a marker of exhaust particles, and particles with an aerodynamic diameter of less than 10 μm (PM10 ), mainly representing road dust, were assigned to residential, day care, and school addresses by using dispersion models. Time-weighted average exposures were linked to levels of IgE against common inhalant and food allergens at 4 and 8 years of age. Results Air pollution exposure during the first year of life was associated with an increased risk of pollen sensitization at 4 years of age (odds ratio, 1.83; 95% confidence interval, 1.02-3.28) for a 5th to 95th difference in exposure to nitrogen oxides. At 8 years, there was no general increase in the risk of sensitization; however, the risk of food sensitization was increased, particularly among children free of sensitization at 4 years of age (odds ratio, 2.30; 95% confidence interval, 1.10-4.82). Results were similar by using PM10 . No associations between air pollution exposure after the first year of life and sensitization were seen. Conclusion Traffic-related air pollution exposure does not seem to increase the overall risk of sensitization to common inhalant and food allergens up to school age, but sensitization to certain allergens might be related to exposure during infancy.
The aim of this study was to determine the effect of six traffic-related air pollution metrics (nitrogen dioxide, nitrogen oxides, particulate matter with an aerodynamic diameter <10 μm (PM10), ...PM2.5, coarse particulate matter and PM2.5 absorbance) on childhood asthma and wheeze prevalence in five European birth cohorts: MAAS (England, UK), BAMSE (Sweden), PIAMA (the Netherlands), GINI and LISA (both Germany, divided into north and south areas). Land-use regression models were developed for each study area and used to estimate outdoor air pollution exposure at the home address of each child. Information on asthma and current wheeze prevalence at the ages of 4-5 and 8-10 years was collected using validated questionnaires. Multiple logistic regression was used to analyse the association between pollutant exposure and asthma within each cohort. Random-effects meta-analyses were used to combine effect estimates from individual cohorts. The meta-analyses showed no significant association between asthma prevalence and air pollution exposure (e.g. adjusted OR (95%CI) for asthma at age 8-10 years and exposure at the birth address (n=10377): 1.10 (0.81-1.49) per 10 μg · m(-3) nitrogen dioxide; 0.88 (0.63-1.24) per 10 μg · m(-3) PM10; 1.23 (0.78-1.95) per 5 μg · m(-3) PM2.5). This result was consistently found in initial crude models, adjusted models and further sensitivity analyses. This study found no significant association between air pollution exposure and childhood asthma prevalence in five European birth cohorts.
Previous published analyses have focused on the effect of air pollution on asthma and rhinoconjunctivitis throughout early and middle childhood. However, the role of exposure to air pollution in the ...development of childhood and adolescent asthma and rhinoconjunctivitis remains unclear. We aimed to assess the longitudinal associations between exposure to air pollution and development of asthma and rhinoconjunctivitis throughout childhood and adolescence.
We did a population-based birth cohort study of 14 126 participants from four prospective birth cohort studies from Germany, Sweden, and the Netherlands with 14–16 years of follow-up. We linked repeated questionnaire reports of asthma and rhinoconjunctivitis with annual average air pollution concentrations (nitrogen dioxide NO2, particulate matter PM with a diameter of less than 2·5 μm PM2·5, less than 10 μm PM10, and between 2·5 μm and 10 μm PMcoarse, and PM2·5 absorbance indicator of soot) at the participants' home addresses. We analysed longitudinal associations of air pollution exposure at participants' birth addresses and addresses at the time of follow-up with asthma and rhinoconjunctivitis incidence and prevalence in cohort-specific analyses, with subsequent meta-analysis and pooled analyses.
Overall, the risk of incident asthma up to age 14–16 years increased with increasing exposure to NO2 (adjusted meta-analysis odds ratio OR 1·13 per 10 μg/m3 95% CI 1·02–1·25) and PM2·5 absorbance (1·29 per 1 unit 1·00–1·66) at the birth address. A similar, albeit non-significant, trend was shown for PM2·5 and incident asthma (meta-analysis OR 1·25 per 5 μg/m3 95% CI 0·94–1·66). These associations with asthma were more consistent after age 4 years than before that age. There was no indication of an adverse effect of air pollution on rhinoconjunctivitis.
Exposure to air pollution early in life might contribute to the development of asthma throughout childhood and adolescence, particularly after age 4 years, when asthma can be more reliably diagnosed. Reductions in levels of air pollution could help to prevent the development of asthma in children.
The European Union.
Background: There are limited prospective data on long-term exposure to air pollution and effects on childhood respiratory morbidity. We investigated the development of asthma and related symptoms ...longitudinally over the first 12 years of life in relation to air pollution from road traffic. Methods: The Swedish birth cohort BAMSE (Children, Allergy, Milieu, Stockholm, Epidemiological Survey) includes 4089 children who were followed up with repeated questionnaires and blood samples for up to 12 years of age. Residential, daycare, and school addresses, time-activity patterns, emission databases, and dispersion models were used to estimate individual exposure to particulate matter with aerodynamic diameter <10 μm (PM₁₀) and nitrogen oxides (NO x ) from traffic. Results: Overall, the data suggested possible associations between exposure to air pollution during the first year of life and asthma and wheezing in children up to 12 years of age. Asthma risks seemed to be particularly increased in children age 8 to 12 years; the overall odds ratio was 2.0 (95% confidence interval = 1.1-3.5), and for nonallergic asthma, the odds ratio was 3.8 (0.9-16.2) for a 5th to 95th percentile increase in time-weighted average exposure to PM₁₀ (corresponding to 7.2 μg/m³). Results were similar using exposure to traffic-NO x . Conclusions: We found modest positive associations between air pollution exposure from traffic during infancy and asthma in children during the first 12 years of life, with stronger effects suggested for nonallergic asthma.
•This genome-wide study investigated the association of gene expression with PM2.5.•Two differentially expressed transcripts were associated with PM2.5 exposure at birth.•Integration of gene ...expression and DNA methylation identified hubs linked to PM2.5.•Our study shows the added value of integrating environmental and multi-omics data.
Air pollution has been associated with adverse health effects across the life-course. Although underlying mechanisms are unclear, several studies suggested pollutant-induced changes in transcriptomic profiles. In this meta-analysis of transcriptome-wide association studies of 656 children and adolescents from three European cohorts participating in the MeDALL Consortium, we found two differentially expressed transcript clusters (FDR p < 0.05) associated with exposure to particulate matter < 2.5 µm in diameter (PM2.5) at birth, one of them mapping to the MIR1296 gene. Further, by integrating gene expression with DNA methylation using Functional Epigenetic Modules algorithms, we identified 9 and 6 modules in relation to PM2.5 exposure at birth and at current address, respectively (including NR1I2, MAPK6, TAF8 and SCARA3). In conclusion, PM2.5 exposure at birth was linked to differential gene expression in children and adolescents. Importantly, we identified several significant interactome hotspots of gene modules of relevance for complex diseases in relation to PM2.5 exposure.
Epidemiologic studies on health effects of air pollution usually rely on time-series of ambient monitoring data or on spatially modelled levels. Little is known how well these estimate residential ...outdoor and indoor levels. We investigated the agreement of measured residential black carbon (BC) levels outdoors and indoors with fixed-site monitoring data and with levels calculated using a Gaussian dispersion model. One-week residential outdoor and indoor BC measurements were conducted for 15 families living in central Stockholm. Time-series from urban background and street-level monitors were compared to these measurements. The observed weekly concentrations were also standardized to reflect annual averages, using urban background levels, and compared spatially to long-term levels as estimated by dispersion modelling. Weekly average outdoor BC level was 472 ng/m
3
(range 261–797 ng/m
3
). The corresponding fixed-site urban background and street levels were 313 and 1039 ng/m
3
, respectively. Urban background variation explained 50% of the temporal variation in residential outdoor levels averaged over 24 h. Modelled residential long-term outdoor levels were on average comparable with the standardized measured home outdoor levels, and explained 49% of the spatial variability. The median indoor/outdoor ratio across all addresses was 0.79, with no difference between day and night time. Common exposure estimation approaches in the epidemiology of health effects related to BC displayed high validity for residencies in central Stockholm. Urban background monitored levels explained half of the outdoor day-to-day variability at residential addresses. Long-term dispersion modelling explained half of the spatial differences in outdoor levels. Indoor BC concentrations tended to be somewhat lower than outdoor levels.
PDF
