Skin Exposure Contributes to Chemical-Induced Asthma: What is the Evidence? A Systematic Review of Animal Models

Bang

Allergy Asthma Immunol Res

et al. 2021

The spectrum of allergic diseases includes atopic dermatitis (AD), allergic rhinitis (AR), and asthma. To date, the association between allergic diseases and psoriasis has not yet been completely evaluated. This study was conducted to determine the risk of psoriasis in patients with allergic diseases. A health screening database, a sub-dataset of the Korean National Health Insurance Service database, was used. All 9,718,722 subjects who underwent health examination in 2009 at age over 20 were included. Subjects with allergic diseases including AD (n = 35,685), AR (n = 1,362,713), asthma (n = 279,451) and control subjects without all three allergic diseases (n = 8,210,042), without AD (n = 9,683,037), without AR (n = 8,356,009) and without asthma group (n = 9,439,271) were analyzed. The subjects were tracked using their medical records during the 8-year period from 2010 to 2017 to identify those who developed psoriasis. Multivariate Cox regression models were used to assess the risk of psoriasis. The incidence probability of psoriasis was analyzed through the Kaplan–Meier method. The incidence of psoriasis per 1,000 person-years was 9.57, 3.78, and 4.28 in the AD, AR, and asthma groups, respectively. The AD group exhibited a significantly increased risk of developing psoriasis compared to subjects without AD (hazard ratio [HR], 3.18; 95% confidence interval [95% CI], 3.05–3.31; P < 0.001) after adjustment for confounding factors. The risk of psoriasis was significantly increased in the AR group compared to subjects without AR (HR, 1.32; 95% CI, 1.31–1.34; P < 0.001) and asthma group compared to subjects without asthma (HR, 1.30; 95% CI, 1.27–1.33; P < 0.001). Allergic diseases, particularly AD, may be a risk factor for psoriasis.

Section: Discussionmentioning

confidence: 55%

The Risk of Psoriasis in Patients With Allergic Diseases: A Nationwide Population-based Cohort Study

Bang

Allergy Asthma Immunol Res

et al. 2021

Annals of Work Exposures and Health

“…In addition to inhalation exposure, there is an obligation to assess dermal exposures in the worker exposure scenarios under REACH. The dermal route is of particular relevance when assessing the overall exposure to diisocyanates, as the role of skin exposure to diisocyanates for development of respiratory sensitization and occupational asthma is discussed ( Fent et al , 2009 ; Tsui et al , 2020 ). Cowie et al conducted a comprehensive study on where diisocyanates were used in the UK and found that the airborne diisocyanate exposure were minimal in almost all of the investigated workplaces, but ‘there was nearly always potential for skin contact’ ( Cowie et al , 2005 ).…”

Section: Scope and Methods Of The Assessmentmentioning

confidence: 99%

Occupational Exposure to Diisocyanates in the European Union

Rother

Schlüter

2021

Objectives Diisocyanates are a chemical group that are widely used at workplaces in many sectors. They are also potent skin- and respiratory sensitizers. Exposure to diisocyanates is a main cause of occupational asthma in the European Union. To reduce occupational exposure to diisocyanates and consequently the cases of diisocyanate-induced asthma, a restriction on diisocyanates was recently adopted under the REACH Regulation in the European Union. Methods A comprehensive evaluation of the data on occupational exposure to the most important diisocyanates at workplaces was made and is reported here. The diisocyanates considered are methylene diphenyl diisocyanate (MDI), toluene diisocyanate (TDI), and hexamethylene diisocyanate (HDI), accounting for more than 95% of the market volume in the EU. The exposure assessment is based on data from Chemical Safety Reports (CSRs) of REACH Registration Dossiers, workplace air monitoring data from Germany, from the UK Health and Safety Executive (HSE), and literature data relevant for the EU, and the USA. Results Occupational exposure to diisocyanates is particularly relevant in: (i) C.A.S.E. applications (Coatings, Adhesives, Sealants, Elastomers), (ii) production of polyurethanes (PUs) (e.g. slab-stock foam), (iii) handling of partly uncured PU products (e.g. cutting, demoulding, spray application of foam), and (iv) when diisocyanates/PUs are heated (e.g. hot lamination, foundry applications/casting forms). Ranking of the reported data on inhalation to diisocyanate exposure at workplaces (maximum values) leads to following order: (i) HDI and its oligomers in coatings, (ii) MDI in spray foam applications, (iii) TDI in manufacture of foam, (iv) TDI in manufacture of PUs and PU composite materials, (v) TDI in adhesives, (vi) MDI in adhesives, (vii) MDI in manufacture of PUs and PU composite materials, (viii) TDI in coatings, (ix) MDI in manufacture of foam, and (x) HDI in adhesives.

Allergy Asthma Immunol Res

“…We and other groups already emphasized the importance of previous skin exposure in inducing a pronounced airway response. 43 44 45 46 …”

Section: Discussionmentioning

confidence: 99%

Involvement of Innate Lymphoid Cells and Dendritic Cells in a Mouse Model of Chemical-induced Asthma

Pollaris

Decaesteker

Broucke

et al. 2021

Self Cite

Purpose Exposure to low concentrations of toluene diisocyanate (TDI) leads to immune-mediated chemical-induced asthma. The role of the adaptive immune system has already been thoroughly investigated; nevertheless, the involvement of innate immune cells in the pathophysiology of chemical-induced asthma is still unresolved. The aim of the study is to investigate the role of innate lymphoid cells (ILCs) and dendritic cells (DCs) in a mouse model for chemical-induced asthma. Methods On days 1 and 8, BALB/c mice were dermally treated (20 µL/ear) with 0.5% TDI or the vehicle acetone olive oil (AOO; 2:3). On days 15, 17, 19, 22 and 24, the mice received an oropharyngeal challenge with 0.01% TDI or AOO (1:4). One day after the last challenge, airway hyperreactivity (AHR) to methacholine was assessed, followed by an evaluation of pulmonary inflammation and immune-related parameters, including the cytokine pattern in bronchoalveolar lavage fluid, lymphocyte subpopulations of the lymph nodes and their ex vivo cytokine production profile, blood immunoglobulins and DC and ILC subpopulations in the lungs. Results Both DC and ILC2 were recruited to the lungs after multiple airway exposures to TDI, regardless of the prior dermal sensitization. However, prior dermal sensitization with TDI alone results in AHR and predominant eosinophilic airway inflammation, accompanied by a typical type 2 helper T (Th2) cytokine profile. Conclusions TDI-induced asthma is mediated by a predominant type 2 immune response, with the involvement of adaptive Th2 cells. However, from our study we suggest that the innate ILC2 cells are important additional players in the development of TDI-induced asthma.