Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 123, Issue 3, Pages 531-542Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2009.01.057
Keywords
Workplace exposure; asthma; airway hyperresponsiveness; antigen; chemical; genetics; mechanisms; inflammation
Categories
Funding
- Ministry of University and Scientific Research
- University of Padova
- University of Ferrara
- Consorzio Ferrara Ricerche
- Associazione per la Ricerca e Cara dell' Asma, Padova
- Associazione per to Studio dei Tumori e delle Malattie Polmonari, Padova
Ask authors/readers for more resources
Inhalation of agents in the workplace can induce asthma in a relatively small proportion of exposed workers. Like nonoccupational asthma, occupational asthma is probably the result of multiple genetic, environmental, and behavioral influences. It is important that occupational asthma be recognized clinically because it has serious medical and socioeconomic consequences. Environmental factors that can affect the initiation of occupational asthma include the intrinsic characteristics of causative agents as well as the influence of the level and route of exposure at the workplace. The identification of host factors, polymorphisms, and candidate genes associated with occupational asthma may improve our understanding of mechanisms involved in asthma. High-molecular-weight compounds from biological sources and low-molecular-weight chemicals cause occupational asthma after a latent period of exposure. Although the clinical, functional, and pathologic features of occupational asthma caused by low-molecular-weight agents resemble those of allergic asthma, the failure to detect specific IgE antibodies against most low-molecular-weight agents has resulted in a search for alternative or complementary physiopathologic mechanisms leading to airway sensitization. Recent advances have been made in the characterization of the immune response to low-molecular-weight agents. In contrast, the mechanism of the type of occupational asthma that occurs without latency after high-level exposure to irritants remains undetermined. (J Allergy Clin Immunol 2009;123:531-42.)
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available