Phenotyping Occupational Asthma Caused by Acrylates in a Multicenter Cohort Study.
Acrylate
Cyanoacrylate
Fractional exhaled nitric oxide
Low-molecular-weight agent
Methacrylate
Occupational asthma
Journal
The journal of allergy and clinical immunology. In practice
ISSN: 2213-2201
Titre abrégé: J Allergy Clin Immunol Pract
Pays: United States
ID NLM: 101597220
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
27
09
2019
revised:
11
10
2019
accepted:
15
10
2019
pubmed:
5
11
2019
medline:
15
5
2021
entrez:
4
11
2019
Statut:
ppublish
Résumé
While acrylates are well-known skin sensitizers, they are not classified as respiratory sensitizers although several cases of acrylate-induced occupational asthma (OA) have been reported. To evaluate the characteristics of acrylate-induced OA in a large series of cases and compare those with OA induced by other low-molecular-weight (LMW) agents. Jobs and exposures, 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 to acrylates (n = 55) or other LMW agents (n = 418) including isocyanates (n = 125). Acrylate-containing glues were the most prevalent products, and industrial manufacturing, dental work, and beauty care were typical occupations causing OA. Work-related rhinitis was more common in acrylate-than in isocyanate-induced asthma (P < .001). The increase in postchallenge fractional exhaled nitric oxide was significantly greater in acrylate-induced OA (26.0; 8.2 to 38.0 parts per billion [ppb]) than in OA induced by other LMW agents (3.0; -1.0 to 10.0 ppb; P < .001) or isocyanates (5.0; 2.0 to 16.0 ppb; P = .010). Multivariable models confirmed that OA induced by acrylates was significantly and independently associated with a postchallenge increase in fractional exhaled nitric oxide (≥17.5 ppb). Acrylate-induced OA shows specific characteristics, concomitant work-related rhinitis, and exposure-related increases in fractional exhaled nitric oxide, suggesting that acrylates may induce asthma through different immunologic mechanisms compared with mechanisms through which other LMW agents may induce asthma. Our findings reinforce the need for a reevaluation of the hazard classification of acrylates, and further investigation of the pathophysiological mechanisms underlying their respiratory sensitizing potential.
Sections du résumé
BACKGROUND
While acrylates are well-known skin sensitizers, they are not classified as respiratory sensitizers although several cases of acrylate-induced occupational asthma (OA) have been reported.
OBJECTIVE
To evaluate the characteristics of acrylate-induced OA in a large series of cases and compare those with OA induced by other low-molecular-weight (LMW) agents.
METHODS
Jobs and exposures, 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 to acrylates (n = 55) or other LMW agents (n = 418) including isocyanates (n = 125).
RESULTS
Acrylate-containing glues were the most prevalent products, and industrial manufacturing, dental work, and beauty care were typical occupations causing OA. Work-related rhinitis was more common in acrylate-than in isocyanate-induced asthma (P < .001). The increase in postchallenge fractional exhaled nitric oxide was significantly greater in acrylate-induced OA (26.0; 8.2 to 38.0 parts per billion [ppb]) than in OA induced by other LMW agents (3.0; -1.0 to 10.0 ppb; P < .001) or isocyanates (5.0; 2.0 to 16.0 ppb; P = .010). Multivariable models confirmed that OA induced by acrylates was significantly and independently associated with a postchallenge increase in fractional exhaled nitric oxide (≥17.5 ppb).
CONCLUSIONS
Acrylate-induced OA shows specific characteristics, concomitant work-related rhinitis, and exposure-related increases in fractional exhaled nitric oxide, suggesting that acrylates may induce asthma through different immunologic mechanisms compared with mechanisms through which other LMW agents may induce asthma. Our findings reinforce the need for a reevaluation of the hazard classification of acrylates, and further investigation of the pathophysiological mechanisms underlying their respiratory sensitizing potential.
Identifiants
pubmed: 31678289
pii: S2213-2198(19)30908-0
doi: 10.1016/j.jaip.2019.10.017
pii:
doi:
Substances chimiques
Acrylates
0
Nitric Oxide
31C4KY9ESH
Types de publication
Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
971-979.e1Subventions
Organisme : Medical Research Council
ID : MR/S019669/1
Pays : United Kingdom
Investigateurs
None Vandenplas
Catherine Rifflart
(C)
Pavlina Klusackova
(P)
David Sherson
(D)
Hille Suojalehto
(H)
Irmeli Lindström
(I)
Pirjo Hölttä
(P)
Paula Kauppi
(P)
Frédéric de Blay
(F)
Laura Hurdubaea
(L)
Rolf Merget
(R)
Alexandra M Preisser
(AM)
Volker Harth
(V)
Piero Maestrelli
(P)
Paola Mason
(P)
Gianna Moscato
(G)
Patrizia Pignatti
(P)
Pierluigi Paggiaro
(P)
Donatella Talini
(D)
Marco dell'Omo
(M)
Ilenia Foletti
(I)
Cecilie Svanes
(C)
Jorunn Kirkeleit
(J)
Jolanta Walusiak-Skorupa
(J)
Marta Wiszniewska
(M)
Xavier Munoz
(X)
Christian Romero-Mesones
(C)
Joaquin Sastre
(J)
Mar Fernandez-Nieto
(M)
Santiago Quirce
(S)
Marta Sanchez-Jareno
(M)
Paul Cullinan
(P)
Julie Cannon
(J)
Sherwood Burge
(S)
Vicky Moore
(V)
Jennifer Hoyle
(J)
Commentaires et corrections
Type : ErratumIn
Informations de copyright
Copyright © 2019 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.