Genetic Variability in Susceptibility to Occupational Respiratory Sensitization

Abstract

Respiratory sensitization can be caused by a variety of substances at workplaces, and the health and economic burden linked to allergic respiratory diseases continues to increase. Although the main factors that affect the onset of the symptoms are the types and intensity of allergen exposure, there is a wide range of interindividual variation in susceptibility to occupational/environmental sensitizers. A number of gene variants have been reported to be associated with various occupational allergic respiratory diseases. Examples of genes include, but are not limited to, genes involved in immune/inflammatory regulation, antioxidant defenses, and fibrotic processes. Most of these variants act in combination with other genes and environmental factors to modify disease progression, severity, or resolution after exposure to allergens. Therefore, understanding the role of genetic variability and the interaction between genetic and environmental/occupational factors provides new insights into disease etiology and may lead to the development of novel preventive and therapeutic strategies. This paper will focus on the current state of knowledge regarding genetic influences on allergic respiratory diseases, with specific emphasis on diisocyanate-induced asthma and chronic beryllium disease.

Identifying Genetic Susceptibility to Sensitization to Cephalosporins in Health Care Workers

“…In recent years, cephalosporins have become the most commonly prescribed antibiotics in most hospitals. These agents cause IgE-mediated reactions such as urticaria, angioedema, and anaphylaxis after sensitization.The early detection of sensitized workers may be critical for preventing the development of occupational allergies due to digestive enzymes and antibiotics ( 4 ). Although the pathogenic role of IgE in cephalosporin allergy is well known, about 30%-50% of patients with cephalosporin allergy show normal IgE levels ( 5 ).…”

“…HMW allergens such as digestive enzymes cause allergic sensitization via an IgE-mediated mechanism ( 7 ), whereas LMW allergens such as antibiotics act as haptens and can cause sensitization that may or may not be associated with specific IgE ( 8 ). The main factors that affect the onset of symptoms are the type, duration, and intensity of allergen exposure ( 4 ).…”