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Abstract
Bronchial asthma is a state of airflow limitation and/or bronchial hyperresponsiveness (BHR) resulting from a persistent inflammatory process in response to a number of stimuli in a genetically susceptible individual. Simple definition of occupational asthma (OA) is asthma due to causes and conditions attributable to a particular working environment and not to stimuli encountered outside the workplace. Exposures that lead to allergic-type OA are called allergens which are either of high or low molecular weight substances. High molecular weight (HMW) allergens are substances of animal origin (such as animal hair, urine or saliva proteins, epidermal squamae, small insects, molds, dander, bacteria, protein dust, and mites) and vegetable origin (such as wood or wood products, cotton, flax, hemp, grain, flour, and latex). Low molecular weight allergens are substances of chemical origin, metals and pharmaceuticals. On the other hand, exposures that lead to irritant-type OA are inhaled irritants. Workers most commonly reported to surveillance programs for OA include paint sprayers, bakers, nurses, animal handlers, welders, farmers, waiters, cleaners, laboratory and dental technicians, forestry workers, and workers in chemical, plastics, rubber, textile, and electrical industries. Several studies revealed a link between IgE and asthma. Some studies demonstrated that elevated pre-employment total serum IgE is a risk factor. In the context of new candidate genes for asthma, the presence of airway inflammation is an important biochemical feature of asthma. There is evidence that a genetic predisposition may alter the capability of the airway to protect itself against inhaled toxic substances from the environment. Oxidative stress, with the formation of reactive oxygen species (ROS), is a key component of inflammation. Although host antioxidant defenses should detoxify ROS, individuals differ in their ability to deal with an oxidant burden, and such differences are in part genetically determined. Inability to detoxify ROS should perpetuate the inflammatory process, activate bronchoconstrictor mechanisms, and precipitate asthma symptoms. Some studies have reported the presence of an association between null alleles in the GSTT1 and GSTM1 genes and asthma. However, other studies reported opposing results. Genetic studies have examined the effect of polymorphism of GST genes on lung function, with a focus on GSTM1. GSTM1 has a null allele, which results in complete lack of the enzyme. The GSTM1 null allele has been associated with diisocyanate-induced asthma. Moreover, GSTM1-null children exposed to environmental tobacco smoke have an increased prevalence of early-onset asthma. The association of GSTM1 deficiency as well as GSTT1 deficiency and asthma has also been shown in German population. These studies suggest an interaction between genetic variants in antioxidant genes and disease expression.Objective assessment of pulmonary function are necessary for the diagnosis of asthma because medical history and physical examination are not reliable means of excluding other diagnoses or of characterizing the status of lung impairment. Although physicians generally seem able to identify a lung abnormality as obstructive, they have a poor ability to assess the degree of airflow obstruction or to predict whether the obstruction is reversible. Spirometry measurements—FEV1, FVC, FEV1/FVC— before and after the patient inhales a short-acting bronchodilator should be done to determine whether there is airflow obstruction, its severity, and whether it is reversible over the short term. A reduced FEV1, and FEV1/FVC relative to references or predicted values indicates airflow obstruction, whereas a proportionately reduced FVC with a normal or increased FEV1/FVC ratio suggests a restrictive pattern. The severity of airflow obstruction is evaluated by comparison of the patient’s results with reference values based on age, height, sex, and race. Many workers in Alexandria are exposed to varieties of occupational and environmental allergens and/or irritants that predispose them to the development of bronchial asthma. In spite of the extent of occupational exposures and the fact that bronchial asthma and work-related asthma are nowadays often preventable by early detection of genetically predisposed individuals and cessation of exposure to the causative agent, yet, little attention has been given to the problem; as the Egyptian national table for prescribed occupational diseases till now does not include occupational asthma, and consequently, pre-placement examination for bronchial asthma is till date not conducted.