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Background: Air pollution is associated with asthma development in children and adults, but the impact on asthma development during the transition from adolescence to adulthood is unclear. Adult studies lack historical exposures and consequently cannot assess the relevance of exposure during different periods of life. We assessed the relevance of early-life and more recent air pollution exposure for asthma development from birth until early adulthood., Methods: We used data of 3687 participants of the prospective Dutch PIAMA (Prevention and Incidence of Asthma and Mite Allergy) birth cohort and linked asthma incidence until age 20 years to estimated concentrations of nitrogen dioxide (NO 2 ), particulate matter with a diameter <2.5 μm (PM 2.5 ), <10 μm (PM 10 ), and 2.5-10 μm, and PM 2.5 absorbance ("soot") at the residential address. We assessed overall and age-specific associations with air pollution exposure with discrete time-hazard models, adjusting for potential confounders., Results: Overall, we found higher incidence of asthma until the age of 20 years with higher exposure to all pollutants at the birth address (adjusted odds ratio (95% CI) ranging from 1.09 (1.01-1.18) for PM 10 to 1.20 (1.10-1.32) for NO 2 ) per interquartile range increase) that were rather persistent with age. Similar associations were observed with more recent exposure defined as exposure at the current home address. In two-pollutant models with particulate matter, associations with NO 2 persisted., Conclusions: Exposure to air pollution, especially from motorised traffic, early in life may have long-term consequences for asthma development, as it is associated with an increased risk of developing asthma through childhood and adolescence into early adulthood., Competing Interests: Conflict of interest: U. Gehring has nothing to disclose. Conflict of interest: A.H. Wijga has nothing to disclose. Conflict of interest: G.H. Koppelman reports grants from Lung Foundation of the Netherlands, during the conduct of the study; grants from Tetri Foundation, Ubbo Emmius Foundation, TEVA the Netherlands, Vertex and GSK, institutional fees from GSK, outside the submitted work. Conflict of interest: J.M. Vonk has nothing to disclose. Conflict of interest: H.A. Smit has nothing to disclose. Conflict of interest: B. Brunekreef has nothing to disclose., (Copyright ©ERS 2020.)

Evidence for the effects of air pollution exposure on lung function growth into adolescence is scarce. We investigated associations of air pollution exposure with lung function and lung function growth until age 16.We conducted both longitudinal (n=915) and cross-sectional (n=721) analyses of associations of air pollution exposure with forced expiratory volume in 1 s (FEV 1 ) and forced vital capacity (FVC) growth from ages eight to 16 and FEV 1 and FVC at age 16. We estimated residential concentrations of nitrogen dioxide (NO 2 ), "soot" and particulate matter (PM x , where x is the 50% cut-off aerodynamic diameter in µm) with diameters of <2.5 µm (PM 2.5 ), <10 µm (PM 10 ) and 2.5-10 µm (PM coarse ) during the preschool, primary school and secondary school time windows by land use regression models. Associations with (growth in) FEV 1 and FVC were analysed by linear (mixed effects) regression.Higher air pollution exposure was associated with reduced FEV 1 growth ( e.g. adjusted difference -0.26% (95% CI -0.49 to -0.03%) per interquartile range increase in secondary school PM 2.5 ) and lower FEV 1 (adjusted difference -2.36% (95% CI -3.76 to -0.94%)), but was not adversely associated with FVC. Associations with FEV 1 were stronger in boys than girls and were not modified by asthma status.Higher air pollution exposure may lead to increased airway obstruction, but not reduced lung volume in adolescence., Competing Interests: Conflict of interest: G.H. Koppelman reports grants from the Lung Foundation of the Netherlands, during the conduct of the study; grants from the Lung Foundation of the Netherlands, the Ubbo Emmius Foundation, the TETRI Foundation and TEVA Netherlands, outside the submitted work. All funds were paid to G.H. Koppelman's institution., (Copyright ©ERS 2018.)

The parallel epidemics of childhood asthma and obesity over the past few decades have spurred research into obesity as a risk factor for asthma. However, little is known regarding the role of asthma in obesity incidence. We examined whether early-onset asthma and related phenotypes are associated with the risk of developing obesity in childhood.This study includes 21 130 children born from 1990 to 2008 in Denmark, France, Germany, Greece, Italy, The Netherlands, Spain, Sweden and the UK. We followed non-obese children at 3-4 years of age for incident obesity up to 8 years of age. Physician-diagnosed asthma, wheezing and allergic rhinitis were assessed up to 3-4 years of age.Children with physician-diagnosed asthma had a higher risk for incident obesity than those without asthma (adjusted hazard ratio (aHR) 1.66, 95% CI 1.18-2.33). Children with active asthma (wheeze in the last 12 months and physician-diagnosed asthma) exhibited a higher risk for obesity (aHR 1.98, 95% CI 1.31-3.00) than those without wheeze and asthma. Persistent wheezing was associated with increased risk for incident obesity compared to never wheezers (aHR 1.51, 95% CI 1.08-2.09).Early-onset asthma and wheezing may contribute to an increased risk of developing obesity in later childhood., Competing Interests: Conflict of interest: L. Duijts reports grants from European Union's Horizon 2020 co-funded programme ERA-Net on Biomarkers for Nutrition and Health (ERA HDHL) (the ALPHABET project (number 696295; 2017) and ZonMW The Netherlands (number 529051014; 2017)) and grants from the European Union's Horizon 2020 programme (the LIFECYCLE project, grant agreement number 733206; 2016), during the conduct of the study. Conflict of interest: B. Gerhard reports grants from the EU FP7, during the conduct of the study. Conflict of interest: H. Inskip reports grants (salary) from the UK Medical Research Council, grants from the British Heart Foundation, the UK Food Standards Agency, the British Lung Foundation, Arthritis Research UK, the NIHR Southampton Biomedical Research Centre and the European Union's Seventh Framework Programme (FP7/2007-2013, project EarlyNutrition under grant agreement number 289346), during the conduct of the study; and members of H. Inskip's team have received funding from Nestec, Abbott Nutrition and Danone Nutricia for various projects to which she is linked, but she has received no direct funding herself. Conflict of interest: S. Lau reports grants and personal fees (honoraria) from Symbiopharm and Allergopharma, personal fees (honoraria) and non-financial support (advisory board work) from DBV, personal fees from ALK, and non-financial support (advisory board work) from Boehringer and Merck, outside the submitted work. Conflict of interest: D. Maier reports grants from the European Commission (FP7 MeDALL, 261357), during the conduct of the study., (Copyright ©ERS 2018.)

Outdoor air pollution has been associated with decrements in lung function and growth of lung function in school-age children. Lung function effects have not been examined in preschoolers, with the exception of one study on minute ventilation in newborns. Our goal was to assess the relationship between long- and short-term exposure to traffic-related air pollution and interrupter resistance in 4-year-old children. Lung function was measured using the interrupter resistance method in children participating in a Dutch birth cohort study. Long-term average air pollution concentrations of fine particulate matter, nitrogen dioxide and soot at the residential address at birth were assessed using land-use regression models. Daily average air pollution concentrations on the day of clinical examination were obtained from the Dutch National Air Quality Monitoring Network. Significant associations were found between long-term average air pollution concentrations and interrupter resistance. Interrupter resistance increased by 0.04 kPa·s·L(-1) (95% CI 0.01-0.07) per interquartile range increase (3.3 μg·m(-3)) in fine particle concentration. Short-term exposure was not associated with interrupter resistance. Long-term exposure to traffic-related air pollution was associated with increased interrupter resistance in 4-year-old children, supporting previous birth cohort studies reporting effects of air pollution on subjectively reported respiratory symptoms in preschool children.

Children with asthma are thought to have impaired sleep quality and quantity. In this study, we investigated which of the many sleep aspects are associated with asthma. Our sample consisted of 2529 children (aged 11 years) who participated in the Prevention and Incidence of Asthma and Mite Allergy (PIAMA) birth cohort study. Parents reported about asthma symptoms (wheezing, dyspnoea, prescription of inhaled corticosteroids and asthma diagnosis) and children reported about different aspects of sleep (bedtime, rise time, sleep quality and daytime sleepiness/tiredness). Results were analysed with (logistic) regression analysis. Children with frequent asthma symptoms significantly more often reported that they felt sleepy or tired during the day (34.4% experienced daytime sleepiness/tiredness at least once a week) than children without asthma symptoms (22.2%) and children with infrequent asthma symptoms (21.9%). This association was not confounded by sex, age of the child, parental educational level or smoking inside the house; the effect was also not modified by sex. There were no associations between asthma and bedtime, time spent in bed or sleep quality. Children with frequent asthma symptoms experienced daytime sleepiness/tiredness more often than children with infrequent or no asthma symptoms. Otherwise, children with asthma did not differ much from children without asthma with regard to sleep.

Previous studies have suggested possible adverse side-effects of maternal use of folic acid-containing supplements (FACSs) during pregnancy on wheeze and asthma in early childhood. We investigated the association between maternal use of FACSs and childhood respiratory health and atopy in the first 8 yrs of life. Data on maternal use of FACSs, collected during pregnancy, were available for 3,786 children participating in the Prevention and Incidence of Asthma and Mite Allergy birth cohort study. Questionnaire data on children's respiratory and allergic symptoms were collected annually and allergic sensitisation and bronchial hyperresponsiveness (BHR) were measured at 8 yrs of age. No overall (from 1 to 8 yrs of age) associations were observed between maternal use of FACSs and (frequent) asthma symptoms, wheeze, lower respiratory tract infection, frequent respiratory tract infection and eczema. Maternal folic acid use was associated with wheeze at 1 yr of age (prevalence ratio 1.20, 95% CI 1.04-1.39), but not with wheeze at later ages. Pre-natal exposure to FACSs was not associated with sensitisation and BHR. Apart from a small increased risk of early wheeze, we observed no adverse respiratory or allergic outcomes associated with pre-natal FACSs exposure in our study population.

Diet may affect the development of asthma. We investigated whether asthma or atopy outcomes at 8 yrs of age were associated with long-term dietary exposure, and whether associations were different for consumption at early or later age. The Prevention and Incidence of Asthma and Mite Allergy (PIAMA) birth cohort enrolled 4,146 participants at baseline, who were followed up to 8 yrs of age. Dietary intakes of interest were fruit, vegetables, brown/wholemeal bread, fish, milk, butter and margarine. Associations between food intake at early (2-3 yrs) and later (7-8 yrs) age, and long-term intake, asthma and atopy at 8 yrs of age were calculated by logistic regression. Complete longitudinal dietary data for at least one of the food groups were available for 2,870 children. Fruit consumption at early age was associated with reduced asthma symptoms (OR per 1 consumption day per week increase 0.93, 95% CI 0.85-1.00). Long-term fruit intake was inversely associated with asthma symptoms (OR 0.90, 95% CI 0.82-0.99) and sensitisation to inhaled allergens (OR 0.90, 95% CI 0.82-0.99). We found no consistent associations between diet and outcomes for other foods. This study indicates no consistent effects of increased early or late consumption, or long-term intake of certain foods on asthma and atopy in 8-yr-olds, with a possible exception for fruit.

Airway inflammation is an early feature of asthma. Early detection and anti-inflammatory treatment may have important therapeutic impact. Exhaled nitric oxide is a noninvasive marker of airway inflammation. The current study investigated the association between exhaled nitric oxide and asthma, wheezing phenotypes, atopy and blood eosinophilia in a large group of 4-yr-old children from the general population. All children participated in the Prevention and Incidence of Asthma and Mite Allergy study, a birth cohort study of high-risk (atopic mother) and low-risk children in the Netherlands. Nitric oxide levels were successfully determined in 429 children. Although there was overlap in the distribution of values of children with and without asthma or atopy, mean values were higher in children with atopy or doctor's diagnosed asthma (geometric mean (ppb) 9.4 and 10.0, respectively) as compared to those without (7.7 and 7.9). Values were highest in atopic symptomatic children. Values were not associated with wheezing phenotype or blood eosinophilia. This study is one of the few large-scale epidemiological studies among 4-yr-old children from the general population showing that children with symptoms of asthma and atopy have higher levels of exhaled nitric oxide than those without.