Olivier Vandenplas1, Julien Godet2, Laura Hurdubaea3, Catherine Rifflart1, Hille Suojalehto4, Marta Wiszniewska5, Xavier Munoz6, Joaquin Sastre7, Pavlina Klusackova8, Vicky Moore9, Rolf Merget10, Donatella Talini11, Cecilie Svanes12, Paola Mason13, Marco dell'Omo14, Paul Cullinan15, Gianna Moscato16,17, Santiago Quirce18, Jennifer Hoyle19, David L Sherson20, Paula Kauppi21, Alexandra Preisser22, Nicolas Meyer2, Frédéric de Blay3. 1. Department of Chest Medicine, Centre Hospitalier Universitaire UCL Namur, Université Catholique de Louvain, Yvoir, Belgium. 2. Pôle de Santé Publique, Strasbourg University, Strasbourg, France. 3. Division of Asthma and Allergy, Department of Chest Diseases, University Hospital of Strasbourg and Fédération de Médecine translationnelle, Strasbourg University, Strasbourg, France. 4. Occcupational Medicine, Finnish Institute of Occupational Health, Helsinki, Finland. 5. Department of Occupational Diseases and Environmental Health, Nofer Institute of Occupational Medicine, Lodz, Poland. 6. Servei Pneumologia, Hospital Vall d'Hebron, Universitat Autonoma de Barcelona and CIBER de Enfermedades Respiratorias (CIBERES), Barcelona, Spain. 7. Department of Allergy, Fundacion Jimenez Dıaz and CIBER de Enfermedades Respiratorias (CIBERES), Madrid, Spain. 8. Department of Occupational Medicine, 1st Faculty of Medicine, Charles University, Prague, Czech Republic. 9. Occupational Lung Disease Unit, Birmingham Heartlands Hospital, Birmingham, UK. 10. Institute for Prevention and Occupational Medicine of the German Social Accident Insurance (PA), Ruhr University, Bochum, Germany. 11. Cardio-Thoracic and Vascular Department, University of Pisa, Pisa, Italy. 12. Department of Occupational Medicine, Haukeland University Hospital, Bergen, Norway. 13. Unit of Occupational Medicine and Public Health, University of Padova, Padova, Italy. 14. Department of Medicine, Section of Occupational Medicine, Respiratory Diseases and Occupational and Environmental Toxicology, University of Perugia, Perugia, Italy. 15. Department of Occupational and Environmental Medicine, Royal Brompton Hospital and Imperial College (NHLI), Royal Brompton and Harefield NHS Foundation Trust, London, UK. 16. Department of Public Health, Experimental and Forensic Medicine, University of Pavia, Pavia, Italy. 17. Allergy and Immunology Unit, Istituti Clinici Scientifici Maugeri, IRCCS, Pavia, Italy. 18. Department of Allergy, Hospital La Paz, Institute for Health Research (IdiPAZ) and CIBER de Enfermedades Respiratorias (CIBERES), Madrid, Spain. 19. Department of Respiratory Medicine, North Manchester General Hospital, Manchester, UK. 20. Department of Pulmonary Medicine and Occupational Medicine, Odense University Hospital, Odense, Denmark. 21. Department of Allergy, Skin and Allergy Hospital, Helsinki University Central Hospital, Helsinki, Finland. 22. Institute for Occupational and Maritime Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Abstract
BACKGROUND: High-molecular-weight (HMW) proteins and low-molecular-weight (LMW) chemicals can cause occupational asthma (OA) although few studies have thoroughly compared the clinical, physiological, and inflammatory patterns associated with these different types of agents. The aim of this study was to determine whether OA induced by HMW and LMW agents shows distinct phenotypic profiles. METHODS: Clinical and functional characteristics, and markers of airway inflammation were analyzed in an international, multicenter, retrospective cohort of subjects with OA ascertained by a positive inhalation challenge response to HMW (n = 544) and LMW (n = 635) agents. RESULTS: Multivariate logistic regression analysis showed significant associations between OA caused by HMW agents and work-related rhinitis (OR [95% CI]: 4.79 [3.28-7.12]), conjunctivitis (2.13 [1.52-2.98]), atopy (1.49 [1.09-2.05]), and early asthmatic reactions (2.86 [1.98-4.16]). By contrast, OA due to LMW agents was associated with chest tightness at work (2.22 [1.59-3.03]), daily sputum (1.69 [1.19-2.38]), and late asthmatic reactions (1.52 [1.09-2.08]). Furthermore, OA caused by HMW agents showed a higher risk of airflow limitation (1.76 [1.07-2.91]), whereas OA due to LMW agents exhibited a higher risk of severe exacerbations (1.32 [1.01-1.69]). There were no differences between the two types of agents in the baseline sputum inflammatory profiles, but OA caused by HMW agents showed higher baseline blood eosinophilia and a greater postchallenge increase in fractional nitric oxide. CONCLUSION: This large cohort study describes distinct phenotypic profiles in OA caused by HMW and LMW agents. There is a need to further explore differences in underlying pathophysiological pathways and outcome after environmental interventions.
BACKGROUND: High-molecular-weight (HMW) proteins and low-molecular-weight (LMW) chemicals can cause occupational asthma (OA) although few studies have thoroughly compared the clinical, physiological, and inflammatory patterns associated with these different types of agents. The aim of this study was to determine whether OA induced by HMW and LMW agents shows distinct phenotypic profiles. METHODS: Clinical and functional characteristics, and markers of airway inflammation were analyzed in an international, multicenter, retrospective cohort of subjects with OA ascertained by a positive inhalation challenge response to HMW (n = 544) and LMW (n = 635) agents. RESULTS: Multivariate logistic regression analysis showed significant associations between OA caused by HMW agents and work-related rhinitis (OR [95% CI]: 4.79 [3.28-7.12]), conjunctivitis (2.13 [1.52-2.98]), atopy (1.49 [1.09-2.05]), and early asthmatic reactions (2.86 [1.98-4.16]). By contrast, OA due to LMW agents was associated with chest tightness at work (2.22 [1.59-3.03]), daily sputum (1.69 [1.19-2.38]), and late asthmatic reactions (1.52 [1.09-2.08]). Furthermore, OA caused by HMW agents showed a higher risk of airflow limitation (1.76 [1.07-2.91]), whereas OA due to LMW agents exhibited a higher risk of severe exacerbations (1.32 [1.01-1.69]). There were no differences between the two types of agents in the baseline sputum inflammatory profiles, but OA caused by HMW agents showed higher baseline blood eosinophilia and a greater postchallenge increase in fractional nitric oxide. CONCLUSION: This large cohort study describes distinct phenotypic profiles in OA caused by HMW and LMW agents. There is a need to further explore differences in underlying pathophysiological pathways and outcome after environmental interventions.
Authors: Lavinia Clara Del Roio; Rafael Futoshi Mizutani; Regina Carvalho Pinto; Mário Terra-Filho; Ubiratan Paula Santos Journal: J Bras Pneumol Date: 2021-08-11 Impact factor: 2.624
Authors: Angelica I Tiotiu; Silviya Novakova; Marina Labor; Alexander Emelyanov; Stefan Mihaicuta; Plamena Novakova; Denislava Nedeva Journal: Int J Environ Res Public Health Date: 2020-06-24 Impact factor: 3.390