PMID- 9351595
OWN - NLM
STAT- MEDLINE
DCOM- 19971106
LR  - 20061115
IS  - 1073-449X (Print)
IS  - 1073-449X (Linking)
VI  - 156
IP  - 4 Pt 2
DP  - 1997 Oct
TI  - Human leukocyte antigen associations in occupational asthma induced by 
      isocyanates.
PG  - S139-43
AB  - Exposure to diisocyanates is recognized as a leading cause of occupational 
      asthma. Occupational asthma induced by isocyanates shares many characteristics 
      with immunoglobulin E (IgE)-mediated asthma: in both, the responsible agent is 
      known, and the clinical presentation, response to inhalation challenge in the 
      laboratory, and response to antiasthma drugs are similar. Although asthma 
      mediated by an IgE mechanism occurs in atopic subjects, occupational asthma 
      induced by isocyanates occurs mostly in nonatopic asthmatics, and an IgE-mediated 
      mechanism has not been consistently demonstrated. However, activated T 
      lymphocytes, methacromatic cells, and eosinophils are increased in the bronchial 
      mucosa of allergic and nonallergic asthmatics and subjects with occupational 
      asthma induced by isocyanates, suggesting similar, probably immunologically 
      mediated mechanisms for both nonoccupational and occupational asthma. 
      Occupational asthma occurs in up to 5-10% of the exposed subjects. Evaluation of 
      major histocompatibility complex (MHC) class II genes in exposed subjects who 
      develop toluene diisocyanate (TDI) asthma has shown a negative association with 
      HLA-DQB1*0501 and a positive association with HLA-DQB1*0503 alleles. In addition, 
      a high proportion of TDI asthmatics express the HLA-DQB1*0503-associated aspartic 
      acid at residue 57, suggesting that HLA-DQ may have a key role in conferring 
      susceptibility. Thus, asthma induced by the low-molecular-weight agent TDI may 
      result from an immunologic reaction due to the interaction of genetic 
      susceptibility with exposure in the workplace.
FAU - Mapp, C E
AU  - Mapp CE
AD  - Institute of Occupational Medicine, University of Padova, Italy.
FAU - Balboni, A
AU  - Balboni A
FAU - Baricordi, R
AU  - Baricordi R
FAU - Fabbri, L M
AU  - Fabbri LM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Am J Respir Crit Care Med
JT  - American journal of respiratory and critical care medicine
JID - 9421642
RN  - 0 (Antibodies)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Isocyanates)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Antibodies/immunology
MH  - Asthma/*chemically induced/genetics/immunology
MH  - *Histocompatibility Antigens Class II/immunology
MH  - Humans
MH  - Hypersensitivity, Immediate/*immunology
MH  - Immunoglobulin E/immunology
MH  - Isocyanates/*adverse effects
MH  - Occupational Diseases/*chemically induced/genetics/immunology
RF  - 57
EDAT- 1997/11/14 00:00
MHDA- 1997/11/14 00:01
CRDT- 1997/11/14 00:00
PHST- 1997/11/14 00:00 [pubmed]
PHST- 1997/11/14 00:01 [medline]
PHST- 1997/11/14 00:00 [entrez]
AID - 10.1164/ajrccm.156.4.12-t-12 [doi]
PST - ppublish
SO  - Am J Respir Crit Care Med. 1997 Oct;156(4 Pt 2):S139-43. doi: 
      10.1164/ajrccm.156.4.12-t-12.