Disease relevance of Desmodur H

• METHODS: We addressed these issues by testing the sera of 13 subjects with asthma (n = 12) and hypersensitivity pneumonitis (n = 1) induced by MDI (n = 4 or 5, see below) by comparing them with sera obtained from subjects with occupational asthma caused by toluene diisocyanate (TDI; n = 5) and hexamethylene diisocyanate (HDI; n = 2) [1].
• We previously developed a novel mouse model of diisocyanate-induced asthma involving epicutaneous sensitization to hexamethylene diisocyanate (HDI) that demonstrates many features of the human disease, including airway eosinophilia and mucus hypersecretion [2].
• RESULTS: HDI sensitization resulted in development of contact hypersensitivity and HDI-specific antibody production [3].
• A worker exposed intermittently to hexamethylene diisocyanate (HDI) developed episodes of dyspnea, wheezing, and fever on working days [4].
• Pulmonary toxicity of polymeric hexamethylene diisocyanate aerosols in mice [5].

Psychiatry related information on Desmodur H

• OBJECTIVES: To study inhalation and dermal exposure to hexamethylene diisocyanate (HDI) and its oligomers as well as personal protection equipment (PPE) use during task performance in conjunction with urinary hexamethylene diamine (HDA) in car body repair shop workers and industrial spray painters [6].

High impact information on Desmodur H

• Vapor HDI-exposed albumin was specifically recognized by the humoral arm of the human immune system, with a strong dependence on albumin as the carrier [7].
• Vapor HDI-exposed albumin was characterized by electrophoresis, chemical substitution analysis, mass spectrometry, and serology studies on auto body shop workers (N=203) and HDI asthmatics (N=11) [7].
• Human gamma/delta T-cell proliferation and IFN-gamma production induced by hexamethylene diisocyanate [8].
• METHODS: Mice were epicutaneously exposed to HDI and then challenged with HDI, either by means of inhalation to induce airway inflammation or on the ear to induce contact hypersensitivity (CHS) [2].
• Studies in mice deficient in either CD4(+) or CD8(+) T cells revealed that CD4(+) T cells were critical for HDI-induced airway eosinophilia, whereas CD8(+) T cells were the major effector cells in CHS [2].

Chemical compound and disease context of Desmodur H

• The inhalation of isocyanates, such as toluene diisocyanate (TDI), diphenylmethane diisocyanate (MDI), and hexamethylene diisocyanate (HDI) can induce hypersensitivity pneumonitis (HP) as well as bronchial asthma in humans, but the precise pathological features and their pathogenetic mechanisms have not been elucidated [9].
• Inhalation toxicity of 1,6-hexamethylene diisocyanate homopolymer (HDI-IC) aerosol: results of single inhalation exposure studies [10].
• In serum, there were specific immunoglobulin (Ig) G (IgG1 and IgG4) and IgE antibodies to 4,4'-MDI-HSA and other isocyanates (phenylisocyanate, toluene diisocyanate, p-toluene monoisocyanate, hexamethylene diisocyanate) conjugated with HSA, a very high total IgE, a raised total IgG, and moderate neutrophilia and eosinophilia [11].
• This article addresses results of two 13-wk inhalation toxicity studies in Wistar rats with aerosolized 1,6-hexamethylene diisocyanate (HDI) homopolymers using either the isocyanurate (HDI-IC) type or biuret (HDI-BT) type [12].
• We propose that the pathogenesis of this case of hemorrhagic pneumonitis is immunologic because of uncontrolled exposure to HDI and TDI, is analogous to the immunologic hemorrhagic pneumonia caused by TMA, and should be considered as a possible cause of a similar acute lung disease after isocyanate exposure [13].

Biological context of Desmodur H

• We conducted a study involving 24 subjects who had undergone specific inhalation challenges to isocyanates (toluene diisocyanate [TDI], n = 8; hexamethylene diisocyanate [HDI], n = 10; and methylene diisocyanate [MDI], n = 6) on three or more consecutive days [14].
• BACKGROUND: Asthma caused by occupational exposure to hexamethylene diisocyanate (HDI) is well known; however, the exact pathogenic mechanisms remain unclear [15].
• We hypothesize that secondary cytotoxicity results from enzymatic release of pendant molecules from hexamethylene-diisocyanate-cross-linked dermal sheep collagen, e.g. formed after reaction of hydrolysis products of hexamethylenediisocyanate with dermal sheep collagen.(ABSTRACT TRUNCATED AT 250 WORDS)[16]
• Gene expression profiling in mouse lung following polymeric hexamethylene diisocyanate exposure [17].
• OBJECTIVES: The clinical features, airway histology, and detection of hexamethylene diisocyanate (HDI) protein adducts in endobronchial biopsies from a patient with HDI asthma are described [18].

Anatomical context of Desmodur H

• We have previously shown that human lung epithelial cell proteins can become conjugated with hexamethylene diisocyanate (HDI) and may be biologically important in diisocyanate-induced asthma [19].
• OBJECTIVE: To determine what factors are critical for the development of HDI-induced airway inflammation, we investigated the strain distribution of this response and the roles of CD4(+) and CD8(+) T cells [2].
• CONCLUSIONS: The data demonstrate that epithelial cell proteins readily react with HDI and that HDI-conjugated epithelial cell proteins can stimulate lymphocyte proliferation [20].
• HDI-specific antibodies and lymph node IL-5 and IL-13 production were also diminished in non-BALB/c strains [2].
• Hexamethylene diisocyanate causes contraction of canine tracheal smooth muscles through activation of muscarinic receptors [15].

Associations of Desmodur H with other chemical compounds

• Although increased levels of specific IgE and/or IgG antibodies have been documented in individual cases of occupational asthma caused by common types of isocyanates (hexamethylene diisocyanate [HDI] and diphenylmethane diisocyanate [MDI]), the frequency among workers with occupational asthma is still unknown [21].
• OBJECTIVE: The purpose of this investigation was to characterize human T cells that respond to hexamethylene diisocyanate (HDI), an aliphatic isocyanate routinely used in the automobile body industry [8].
• Different diisocyanates were used for making SPUs: 4,4-diphenylmethane diisocyanate (MDI), 4,4-dicyclohexylmethane diisocyanate (MDCI), hexamethylene diisocyanate (HMDI) and isophorone diisocyanate (IPDI) [22].
• In an effort to make composites from hydroxyapatite and a PEG/PBT copolymer (Polyactive 70/30), chemical linkages were introduced between the filler particles and polymer matrix using hexamethylene diisocyanate as a coupling agent [23].
• Double bonds were introduced to the surface of HA via the coupling reaction of isocyanateoethyl methacrylate (ICEM) with HA, or through hexamethylene diisocyanate (HMDI) with hydroxyethyl methacrylate (HEMA) and HA, followed by radical polymerization in MMA, BMA, or HEMA [24].

Gene context of Desmodur H

• When stratified according to specific diisocyanate exposure, a significant association was found between IL4RA (I50V) II and DA among individuals exposed to hexamethylene diisocyanate (HDI) (odds ratio [OR], 3.29; 95% confidence interval [CI], 1.33-8.14; P = .01) only [25].
• RESULTS: Specific IgG antibodies that recognize MDI-HSA conjugates were detected in all but 1 of the MDI-exposed workers and could not be found in TDI-exposed and HDI-exposed workers [1].
• Nearest neighbor analysis of D1 and D2 subunits in the photosystem II reaction center using a bifunctional cross-linker, hexamethylene diisocyanate [26].
• A cross-linked product between the D1 and D2 subunits was generated by treating isolated spinach PS II reaction center with a bifunctional cross-linker, 1,6-hexamethylene diisocyanate [26].
• Determination of hexamethylene diisocyanate-based isocyanates in spray-painting operations. Part 2. Comparison of high performance liquid chromatography with capillary zone electrophoresis [27].

Analytical, diagnostic and therapeutic context of Desmodur H

• METHODS: Human lung epithelial cell lines were exposed to vapor- and liquid-phase HDI, and the cellular proteins were analyzed for HDI conjugation by Western blotting and tested for the ability to induce lymphocyte proliferation in vitro [20].
• Determination of airborne 1,6-hexamethylene diisocyanate by gas chromatography [28].
• Development of immunoassays for biomonitoring of hexamethylene diisocyanate exposure [29].
• In the second approach, prior to immobilization, hydrophobic modification of DFPase was achieved through its conjugation with a dimer/trimer mixture of a uretdione based on 1,6-diisocyanatohexane [30].
• METHODS: Serum samples from 139 anonymous donors without known diisocyanate exposure were assayed by means of enzyme-linked immunosorbent assay for IgG or IgE specific for TDI-HSA, diphenylmethane diisocyanate (MOI)-HSA, and hexamethylene diisocyanate (HDI)-HSA [31].

References