The role of exhaled 3-nitrotyrosine (3-NT) beyond the severe asthma phenotype remains largely unexplored. Associations of exhaled 3-NT with allergy and with various asthma characteristics were studied in 792 adults from the French Epidemiological study on the Genetics and Environment of Asthma (EGEA, 40% current asthmatics, 56% allergic, 36% adult-onset asthma). Asthma characteristics were defined using questionnaires, and allergy by a positive skin prick test. 3-NT was analyzed as categorical, continuous and ratio (3-NT/tyrosine) variables. Cross-sectional analyses showed that high 3-NT levels were associated with an increased risk of current asthma (adjusted(a)OR [95%CI] = 1.61 [1.09-2.38], particularly in non-allergic asthma (aOR = 2.19 [1.09-4.41]), and no association was found with allergy. Results were consistent across all 3-NT expressions. Longitudinal analyses showed that high 3-NT levels were associated with persistent current asthma at 10-year follow-up. Our results advance understanding of the mechanisms underlying asthma phenotypic heterogeneity, thereby opening new perspectives in its management.

Air pollution is an environmental risk factor associated with lung and cardiovascular disease that may be mediated by physiological pathways such as oxidative stress. Previous studies have identified associations between air pollution and biomarkers of oxidative stress (8-OHdG, 4-HNE, and fluorescent oxidation products (FOPs)), as well as lung health marker CC16, in younger and asthmatic populations. The objective of this study of a large population-based sample of non-smoking adults was to explore the relationship between long-term and short-term atmospheric pollution exposures and plasma or urine levels of these biomarkers. Our study was a post-hoc analysis of the cross-sectional ELISABET study from 2011 to 2013. We included non-smoking inhabitants of Lille, France from the ELISABET study. We assessed mean pluri-annual residential and short-term exposures to atmospheric pollution components (PM10, NO2, and O3) and collected several biomarkers (CC16, 8-OHdG, 4-HNE, and fluorescent oxidation products (FOPs)). We searched for associations between pollutants and biomarkers using log-linear robust multivariate regressions. Our work did not show any association between short- or long-term exposure to air pollution components and CC16, 8-OHdG, 4-HNE or FOP in a large (980 subjects) sample of Lille’s general population, despite having sufficient statistical power to replicate previous findings of associations between air pollution and these biomarkers found in younger or asthmatic populations.

La surveillance des particules dans l’air ambiant ou l’air des lieux de travail, à des fins d’évaluation de l’exposition de la population générale et/ou professionnelle, nécessite des méthodes reproductibles de prélèvement de ces particules au regard des effets sanitaires attendus. Des conventions ont donc été établies pour l’échantillonnage sélectif en taille des particules en suspension dans l’air basées sur des spécifications en termes d’efficacité de prélèvement en fonction du diamètre aérodynamique des particules. Ce diamètre caractérise la sédimentation des particules et permet de déterminer leur pénétration et dépôt dans l’arbre respiratoire.La prise en compte de la taille des particules en lien avec les effets sur la santé de ces particules a commencé au début du XXe siècle. Deux approches distinctes se sont développées dans le domaine de la santé au travail et dans celui de la santé environnementale. Les réflexions se sont poursuivies au fil du temps en parallèle dans les deux domaines. L’approche en santé travail a consisté à considérer et modéliser la pénétration des particules dans l’arbre respiratoire et l’approche en santé environnementale a pris en compte les résultats des études épidémiologiques dépendant des méthodes de mesure développées dans les réseaux de surveillance.Ces approches ont conduit à établir deux référentiels distincts sur lesquels repose l’établissement des valeurs pour la protection de la santé, d’une part, pour la population professionnelle, et d’autre part, pour la population générale : en santé travail les fractions granulométriques inhalable, thoracique et alvéolaire sont prises en compte tandis qu’en santé environnementale ce sont les fractions granulométriques PM10 et PM2,5 qui sont réglementées.Une expertise collective de l’Anses publiée en 2023 décrit les origines scientifiques et réglementaires et analyse la pertinence scientifique de ces deux référentiels distincts utilisés pour l’évaluation des expositions aux particules dans le domaine de la santé au travail et celui de la santé environnementale. Les origines scientifiques et réglementaires de ces référentiels seront présentées plus en détail au cours de cette présentation.

Introduction: MicroRNAs are epigenetic regulatory factors capable of silencing the expression of target genes and might mediate the effects of air pollution on health. The objective of the present population-based study was to investigate the association between microRNA expression and long-term, residential exposure to atmospheric PM10 and NO2.Method: We included 998 non-smoking adult participants from the cross-sectional ELISABET survey (2010-2014) in the Lille urban area of France. The mean residential annual pollution levels were estimated with an atmo-spheric dispersion modelling system. Ten microRNAs were selected on the basis of the literature data, together with two housekeeping microRNAs (miR-93-5p and miR-191-5p) and were quantified with RT-qPCRs. Multi-variate linear regression models were used to study the association between microRNAs and air pollution. The threshold for statistical significance (after correction for the FDR) was set to p < 0.1.Results: The mean annual exposure between 2011 and the year of inclusion was 26.4 +/- 2.0 mu g/m3 for PM10 and 24.7 +/- 5.1 mu g/m3 for NO2. Each 2 mu g/m3 increment in PM10 exposure was associated with an 8.6% increment (95%CI [3.1; 14.3]; pFDR = 0.019) in miR-451a expression. A 5 mu g/m3 increment in NO2 exposure was associated with a 5.3% increment ([0.7; 10]; pFDR = 0.056) in miR451a expression, a 3.6% decrement (95%CI [-6.1;-1.1]; pFDR = 0.052) in miR-223-3p expression, a 3.8% decrement (95%CI[-6.8;-0.7]; pFDR = 0.079) in miR-28-3p expression, a 4.3% decrement (95%CI [-7.7;-0.8]; pFDR = 0.055) in miR-146a-5p expression, and a 4.0% decrement (95% CI[-7.4;-0.4]; pFDR = 0.059) in miR-23a-5p expression. The difference between the two housekeeping microRNAs miR-93-5p and miR-191-5p was also associated with PM10 and NO2 exposure. Conclusion: Our results suggest that circulating miRNAs are potentially valuable biomarkers of the effects of air pollution.

Aims: Type 1 diabetes is associated with a substantially increased risk of impaired lung function, which may impair aerobic fitness. We therefore aimed to examine the ventilatory response during maximal exercise and the pulmonary diffusion capacity function at rest in individuals with uncomplicated type 1 diabetes.Methods: In all, 17 adults with type 1 diabetes free from micro-macrovascular complications (glycated haemoglobin: 8.0 +/- 1.3%), and 17 non-diabetic adults, carefully matched to the type 1 diabetes group according to gender, age, level of physical activity and body composition, participated in our study. Lung function was assessed by spirometry and measurements of the combined diffusing capacity for nitric oxide (DLNO) and carbon monoxide (DLCO) at rest. Subjects performed a maximal exercise test during which the respiratory parameters were measured.Results: At rest, DLCO (30.4 +/- 6.1 ml min(-1) mmHg(-1) vs. 31.4 +/- 5.7 ml min(-1) mmHg(-1), respectively, p = 0.2), its determinants Dm (membrane diffusion capacity) and Vc (pulmonary capillary volume) were comparable among type 1 diabetes and control groups, respectively. Nevertheless, spirometry parameters (forced vital capacity = 4.9 +/- 1.0 L vs. 5.5 +/- 1.0 L, p < 0.05; forced expiratory volume 1 = 4.0 +/- 0.7 L vs. 4.3 +/- 0.7 L, p < 0.05) were lower in individuals with type 1 diabetes, although in the predicted normal range. During exercise, ventilatory response to exercise was different between the two groups: tidal volume was lower in type 1 diabetes vs. individuals without diabetes (p < 0.05). Type 1 diabetes showed a reduced VO2max (34.7 +/- 6.8 vs. 37.9 +/- 6.3, respectively, p = 0.04) in comparison to healthy subjects.Conclusions: Individuals with uncomplicated type 1 diabetes display normal alveolar-capillary diffusion capacity and at rest, while their forced vital capacity, tidal volumes and VO2 are reduced during maximal exercise.

Des associations entre marqueurs de stress oxydatif et d'atteinte pulmonaire ont été retrouvées dans des populations vulnérables. L'objectif de ce travail est d'explorer la relation entre les expositions à la pollution atmosphérique résidentielle et à court terme et des marqueurs biologiques d'atteinte pulmonaire et de stress oxydatif chez des adultes non-fumeurs. Nous avons utilisé les données de mesure de stations de pollution et de modélisation d'Atmo-Haut-de-France pour établir l'exposition à court (moyenne de la veille sur la ville) et long terme (moyenne sur l'année glissante précédente au lieu de résidence) à la pollution atmosphérique (PM10, NO2 et O3) d'un échantillon de Lillois de non-fumeurs ayant participé à l'étude transversale ELISABET (2011 à 2013). Nous avons recherché des associations entre les polluants et les biomarqueurs (CC16, 8-OHdG, 4-HNE et produits d'oxydation fluorescents POF) à l'aide de régressions log-linéaires, les pvalues ont été ajustées pour les tests multiples avec la méthode fdr. Pour les modèles dont les résidus étaient mal distribués, des modèles log-linéaires robustes (estimation MM) ont été utilisés comme analyse de sensibilité. Au total, 1004 habitants ont été échantillonnés pour les marqueurs sélectionnés. Une seule association significative entre l'exposition court terme aux PM10 et les POF (320nm) a été trouvée, avec une augmentation de 2,48 % [0,66 %; 4,33 %] (p=0,007) des niveaux de POF pour chaque 10µg/m³ de PM10. Après ajustement pour tests multiples ou en l'analyse de sensibilité robuste l'association étaient non significative. Aucune autre association entre les expositions court ou long-terme et les biomarqueurs n'était significative. Notre travail n'a pas montré d'association significative, malgré une puissance suffisante (99,9 % pour répliquer une étude sur le CC16 chez des adolescents et 99,7 % pour une étude sur les POFs chez des asthmatiques) entre les différents composants de la pollution atmosphérique et le CC16, 8-OHdG, 4-HNE et les produits d'oxydation fluorescents, que ce soit pour une exposition à court ou à long terme dans la population lilloise. Base de données géographiques ; Pollution atmosphérique ; Épidémiologie ; Biomarqueurs ; Biomarqueurs stress oxydatif Les auteurs déclarent ne pas avoir de liens d'intérêts.

Les miARN sont des facteurs de régulation épigénétiques capables de réguler l'expression de gènes cibles. Les miARN peuvent médier les effets de la pollution de l'air sur la santé. L'objectif de cette étude est d'étudier, dans la population générale, l'association entre l'exposition à long terme à l'adresse résidentielle aux PM10 et NO2 atmosphériques et l'expression des microARN. Nous avons utilisé les données des modèles ADMS d'Atmo-Haut-de-France pour établir les niveaux moyens annuels de pollution atmosphérique (PM10, NO2) au domicile des participants d'un échantillon de 998 Lillois de non-fumeurs ayant participé à l'étude transversale ELISABET menée de 2011 à 2013. 12 microARN ont été sélectionnés, puis quantifiés par RT-PCR. Des modèles de régression linéaire multivariée ont été utilisés avec des valeurs de p significatives basées sur un taux de fausses découvertes (FDR) de 10 %. L'exposition annuelle moyenne sur les niveaux annuels de pollution entre 2011 et l'année d'inclusion était de 26,4±2,0 µg/m3 pour les PM10 et de 24,7±5,1 µg/m3 pour NO2. Une augmentation de 2µg/m3 de l'exposition aux PM10 a été associée à une augmentation de 8,6 % ([3,1; 14,3]; pFDR=0,019) de l'expression de miR-451a. Une augmentation de 5µg/m3 de l'exposition au NO2 a été associée à une augmentation de 5,3 % ([0,7; 10]; pFDR=0,056) de l'expression de miR-451a, une diminution de 3,6 % ([-6,1; -1,1]; pFDR=0,052) de l'expression de miR-223-3p, une diminution de 3,8 % ([-6,8; -0,7]; pFDR=0,079)) de l'expression de miR-28-3p, une diminution de 4,3 % ([-7,7; -0,8]; pFDR=0,055) de l'expression de miR-146a-5p et une diminution de 4,0 % ([-7,4; -0,4]; pFDR=0,059) de l'expression de miR-23a-5p. Ces résultats suggèrent l'intérêt des microARN circulants comme biomarqueurs potentiels pour l'évaluation des risques environnementaux. Base de données géographiques ; Pollution atmosphérique ; Epidémiologie ; Epigénétique Les auteurs déclarent ne pas avoir de liens d'intérêts.

Introduction: Air pollution has an impact on health, and low-grade inflammation might be one of the underlying mechanisms. The objective of the present study of adults from northern France was to assess the associations between short-term and residential exposure to air pollution and levels of various inflammatory biomarkers. Methods: The cross-sectional Enquete Littoral Souffle Air Biologie Environnement (ELISABET) study was conducted from 2011 to 2013 in the Lille and Dunkirk urban areas of northern France. Here, we evaluated the associations between PM10, NO2 and O-3 exposure (on the day of the blood sample collection and on the day before, and the mean annual residential level) and levels of the inflammatory biomarkers high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-1 beta, IL-6, IL-8, IL-10, IL-17A, IL-22, and tumor necrosis factor alpha. Results: We assessed 3074 participants for the association with hsCRP and a subsample of 982 non-smokers from Lille for the association with plasma cytokine levels. A 10 mu g/m(3) increment in PM10 and NO2 levels on the day of sample collection and on the day before was associated with a higher hsCRP concentration (3.43% [0.68; 6.25] and 1.75% [-1.96; 5.61], respectively, whereas a 10 mu g/m(3) increment in O-3 was associated with lower hsCRP concentration (-1.2% [-3.95; 1.64]). The associations between mean annual exposure and the hsCRP level were not significant. Likewise, the associations between exposure and plasma cytokine levels were not statistically significant. Conclusion: Short-term exposure to air pollution was associated with higher serum hsCRP levels in adult residents of two urban areas in northern France. Our results suggest that along with other factors, low-grade inflammation might explain the harmful effects of air pollution on health.

Le cancer broncho-pulmonaire (CBP) présente un pronostic défavorable lorsqu’il est diagnostiqué à un stade avancé ou métastatique. Le dépistage par tomodensitométrie thoracique à faible dose montre des résultats encourageants pour les populations à risque mais rapporte des taux de faux positifs encore élevés. Les composés organiques volatils (COVs) de l’air exhalé sont des produits du catabolisme cellulaire ayant diffusé dans le compartiment alvéolaire. L’ensemble des COVs dans l’air expiré d’un sujet est le « volatolome » ; celui-ci se modifie si le métabolisme cellulaire change, notamment au cours de la carcinogenèse. Les études disponibles sur l’utilisation du volatolome dans le diagnostic du CBP présentent de faibles effectifs ainsi que des méthodologies disparates d’identification des COVs. Peu de COVs sont donc formellement identifiés comme biomarqueurs d’intérêt dans la détection précoce du CBP. L’objectif de l’étude CATOCOV est d’identifier les COVs marqueurs de CBP dans une large population de patient atteints de CBP (n = 750). Dans cette étude cas-témoins en cours, les sujets atteints de CBP sont recrutés au sein de plusieurs services de pneumologie-oncologie thoracique et les sujets témoins au sein de l’Institut Pasteur de Lille. Chacun répond à un questionnaire et bénéficie du prélèvement d’air exhalé pendant 10 minutes. Ce recueil s’effectue à l’aide du masque ReCIVA® (Owlstone Medical) qui piège les COVs dans des tubes de sorbants. Ceux-ci sont analysés en chromatographie gazeuse par spectrométrie de masse (GC-MS) par TERA Environnement afin de qualifier et quantifier les COVs piégés. Une collaboration avec le laboratoire ORKAD (Université de Lille) permettra de sélectionner au mieux les COVs marqueurs de CBP grâce à des algorithmes d’optimisation combinatoire multi-objectifs déjà éprouvés (antibiorésistance). A date, plus de 600 sujets témoins et 200 cas ont été recrutés. Une analyse intermédiaire sur 300 témoins et 100 cas définira un nombre restreint de COVs (n = 50) pour les futures interprétations. Le reste de la population permettra d’éprouver le potentiel de détection du panel sélectionné. Ce projet ciblera les COVs les plus pertinents pour détecter précocément le CBP afin d’anticiper le diagnostic et optimiser les chances de prise en charge chirurgicale, à visée curative. Nous espérons ainsi améliorer la survie globale de ces patients.

Oxidative stress (OS) is the main pathophysiological mechanism involved in several chronic diseases, including asthma. Fluorescent oxidation products (FlOPs), a global biomarker of damage due to OS, is of growing interest in epidemiological studies. We conducted a genome-wide association study (GWAS) of the FlOPs level in 1216 adults from the case-control and family-based EGEA study (mean age 43 years old, 51% women, and 23% current smokers) to identify genetic variants associated with FlOPs. The GWAS was first conducted in the whole sample and then stratified according to smoking status, the main exogenous source of reactive oxygen species. Among the top genetic variants identified by the three GWAS, those located in BMP6 (p = 3 × 10−6), near BMPER (p = 9 × 10−6), in GABRG3 (p = 4 × 10−7), and near ATG5 (p = 2 × 10−9) are the most relevant because of both their link to biological pathways related to OS and their association with several chronic diseases for which the role of OS in their pathophysiology has been pointed out. BMP6 and BMPER are of particular interest due to their involvement in the same biological pathways related to OS and their functional interaction. To conclude, this study, which is the first GWAS of FlOPs, provides new insights into the pathophysiology of chronic OS-related diseases.

BACKGROUND:Eosinophils play a key role in the asthma allergic response by releasing cytotoxic molecules such as eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN) that generate epithelium damages. OBJECTIVE:We sought to identify genetic variants influencing ECP and EDN levels in asthma-ascertained families. METHODS:We performed univariate and bivariate genome-wide association analyses of ECP and EDN levels in 1018 subjects from the EGEA study with follow-up in 153 subjects from the Saguenay-Lac-Saint-Jean study and combined the results of these 2 studies through meta-analysis. We then conducted Bayesian statistical fine mapping together with quantitative trait locus and functional annotation analyses to identify the most likely functional genetic variants and candidate genes. RESULTS:We identified 5 genome-wide significant loci (P &amp;lt; 5 × 10&lt;sup&gt;-8&lt;/sup&gt;) including 7 distinct signals associated with ECP and/or EDN levels. The genes targeted by our fine mapping and functional search include RNASE2 and RNASE3 (14q11), which encode EDN and ECP, respectively, and 4 other genes that regulate ECP and EDN levels. These 4 genes were JAK1 (1p31), a transcription factor that plays a key role in the immune response and acts as a potential therapeutic target for eosinophilic asthma; ARHGAP25 (2p13), which is involved in leukocyte recruitment to inflammatory sites; NDUFA4 (7p21), which encodes a component of the mitochondrial respiratory chain and is involved in cellular response to stress; and CTSL (9q22), which is involved in immune response, extracellular remodeling, and allergic inflammation. CONCLUSION:Analysis of specific phenotypes produced by eosinophils allows the identification of genes that play a major role in allergic response and inflammation, and offers potential therapeutic targets for asthma.

Aim The biological mechanisms of work-related asthma induced by irritants remain unclear. We investigated the associations between occupational exposure to irritants and respiratory endotypes previously identified among never asthmatics (NA) and current asthmatics (CA) integrating clinical characteristics and biomarkers related to oxidative stress and inflammation. Methods We used cross-sectional data from 999 adults (mean 45 years old, 46% men) from the case-control and familial Epidemiological study on the Genetics and Environments of Asthma (EGEA) study. Five respiratory endotypes have been identified using a cluster-based approach: NA1 (n=463) asymptomatic, NA2 (n=169) with respiratory symptoms, CA1 (n=50) with active treated adult-onset asthma, poor lung function, high blood neutrophil counts and high fluorescent oxidation products level, CA2 (n=203) with mild middle-age asthma, rhinitis and low immunoglobulin E level, and CA3 (n=114) with inactive/mild untreated allergic childhood-onset asthma. Occupational exposure to irritants during the current or last held job was assessed by the updated occupational asthma-specific job-exposure matrix (levels of exposure: no/medium/high). Associations between irritants and each respiratory endotype (NA1 asymptomatic as reference) were studied using logistic regressions adjusted for age, sex and smoking status. Results Prevalence of high occupational exposure to irritants was 7% in NA1, 6% in NA2, 16% in CA1, 7% in CA2 and 10% in CA3. High exposure to irritants was associated with CA1 (adjusted OR aOR, (95% CI) 2.7 (1.0 to 7.3)). Exposure to irritants was not significantly associated with other endotypes (aOR range: 0.8 to 1.5). Conclusion Occupational exposure to irritants was associated with a distinct respiratory endotype suggesting oxidative stress and neutrophilic inflammation as potential associated biological mechanisms.

Thymic stromal lymphopoietin (TSLP), a cytokine involved in severe asthma treatment, was never studied in non-severe asthma.Among 969 adults from a large epidemiological study, cross-sectional analyses showed that plasma TSLP levels were associated with increased age and BMI, male sex, smoking and high TSLP levels (one IQR increase) with current asthma and poor lung function. High TSLP levels were also associated with persistence of asthma attacks (aOR=2.14 (95% CI 1.23 to 3.72)) and dyspnoea (aOR=2.71 (95% CI 1.39 to 5.28)) 10 years later.Our results suggest that TSLP could be a cytokine of interest in non-severe asthma, and its determinants of circulating levels could be considered in asthma management.

This study of endotypes responsible for the development of irritant induced occupational asthma raises questions as to what is meant by a respiratory irritant. Classifying an exposure as irritant usually implies that the effect is nonspecific, that is, all similar asthmatics would react to the exposure whether they have had previous exposure to the agent or not. For instance, sulphur dioxide is a respiratory irritant, the exposure needed to provoke asthma is correlated with the degree of preexisting nonspecific reactivity, as measured with methacholine or histamine. The paper by Andrianjafimasy et al uses a job exposure matrix (JEM) whose list of irritants includes the best known lowmolecularweight respiratory sensitisers, such as isocyanates, acrylates, epoxy resins and amines where there is no evidence of airflow obstruction in previously unexposed, or exposed asymptomatic workers induced by exposures that can cause severe reactions in sensitised individuals. Reactive low molecular weight chemicals may act as haptens, binding to body protein creating neoantigens. The action of biocides denaturing proteins may have a similar effect again leading to specificity in the airway response. The mechanisms, and perhaps susceptibility to reactions with specificity is likely to differ from agents which lack specificity. Labelling a chemical as a sensitiser should lead to better control than adding an irritant label, which risks degrading the significance of the exposure, similar to classifying an exposure as a ‘nuisance’ dust. We believe that labelling a substance as an irritant needs as much evidence as labelling a chemical as a sensitiser. The potential for a lowmolecularweight chemical to act as a sensitiser can often be predicted from its chemical structure. We may need an additional category where the mechanism awaits elucidation, such as exhaust fumes and textile dust where there are studies appearing to show some specificity of the airway responses.

Type 1 diabetes is associated with a substantially increased risk of impaired lung function, which may impair aerobic fitness. We therefore aimed to examine the ventilatory response during maximal exercise and the pulmonary diffusion capacity function at rest in individuals with uncomplicated type 1 diabetes.

Abstract Background Long-term pulmonary sequelae, including 1-year thoracic computed tomography (CT) sequelae of paediatric acute respiratory distress syndrome (ARDS) remain unknown. The purpose of the study was to determine pulmonary abnormalities in child survivors of pulmonary (p-ARDS) and extra-pulmonary ARDS (ep-ARDS) 1 year after paediatric intensive care unit discharge (PICUD). Methods Prospective multicentre study in four paediatric academic centres between 2005 and 2014. Patients with ARDS were assessed 1 year after PICUD with respiratory symptom questionnaire, thoracic CT and pulmonary function tests (PFT). Results 39 patients (31 p-ARDS) aged 1.1–16.2 years were assessed. Respiratory symptoms at rest or exercise and/or respiratory maintenance treatment were reported in 23 (74%) of children with p-ARDS but in 1 (13%) of those with ep-ARDS. Thoracic CT abnormalities were observed in 18 (60%) of children with p-ARDS and 4 (50%) of those with ep-ARDS. Diffuse and more important CT abnormalities, such as ground glass opacities or mosaic perfusion patterns, were observed in 5 (13%) of children, all with p-ARDS. PFT abnormalities were observed in 30 (86%) of patients: lung hyperinflation and/or obstructive pattern in 12 (34%) children, restrictive abnormalities in 6 (50%), mild decrease in diffusing capacity in 2 (38%) and 6-min walking distance decrease in 11 (73%). Important PFT abnormalities were observed in 7 (20%) children, all with p-ARDS. Increasing driving pressure (max plateau pressure—max positive end-expiratory pressure) was correlated with increasing CT-scan abnormalities and increasing functional residual capacity (more hyperinflation) (p < 0.005). Conclusions Children surviving ARDS requiring mechanical ventilation present frequent respiratory symptoms, significant CT-scan and PFT abnormalities 1 year after PICUD. This highlights the need for a systematic pulmonary assessment of these children. Trial registration The study was registered on Clinical Trials.gov PRS (ID NCT01435889)