Other gibberellins, notably GA 4+7, have recently become registered for use in North America, with the major application being maintenance of chlorophyll and increased flower life in Lilium. In commercial flower production, gibberellic acid is used to substitute for cold in dormancy-breaking in plants such as Azalea, Camellia, and hydrangea, to improve flowering uniformity in Cyclamen (although much of this use has now been superseded by more uniformly flowering cultivars), for production of standards (tree-forms) of plants such as Fuchsia, to accelerate and increase flowering ( Spathiphyllum, statice ( Limonium)), altering inflorescence form (chrysanthemum), and reduction of chlorophyll breakdown (maintaining higher-quality foliage) in certain liliaceous crops such as Alstroemeria. Gibberellins find use in a wide range of crops, and differences exist between uses for gibberellic acid (GA 3) and other gibberellins such as GA 4+7. Miller, in Encyclopedia of Applied Plant Sciences, 2003 Gibberellin Unfortunately, despite primary removal of the offending sensitizing agent, asthma symptoms and bronchial hyperresponsiveness induced from multiple causes persist in approximately 70% of individuals with occupational asthma. A longitudinal study demonstrated that powdered latex gloves with high allergen content were the reason for the epidemic of latex allergy and occupational asthma. Atopic individuals are at the highest risk of developing latex allergy. This occurred in the case of latex allergy, where many nonatopic individuals and patients exposed to allergen in their personal healthcare developed occupational allergy to multiple proteins from natural rubber latex. If the allergen exposure is sufficient, these proteins can drive the immune response to a T-lymphocyte type 2 phenotype (Th2), even in patients without prior atopic disposition. Most individuals require a concentration and duration of exposure sufficient to cause IgE antibody sensitization to the offending allergen with development of bronchial hyperresponsiveness and airway inflammatory disease upon reexposure. The pathogenesis of asthma in patients exposed to high molecular weight antigens follows the experience of nonoccupational asthma in patients where atopy, gender, genetics, concentration of antigen, duration of exposure, and other individual factors all contribute to the development of disease. These low molecular weight chemicals appear to act as haptens that bind directly to human proteins, causing an immune response in the human host. These low molecular weight agents are sufficient to induce an immune response, but often not by an IgE-mediated mechanism. Occupational and environmental asthma is also caused by a number of low molecular weight agents including reactive chemicals, transition metals, and wood dusts ( Table 427.6). These include various animals, shellfish, fish, enzymes (e.g., Bacillus subtilis in laundry detergent), and flour or cereals. High molecular weight causes of occupational and environmental asthma can be characterized as allergens, which are normally proteins and enzymes, inhaled from multiple sources ( Table 427.5). The general principles of diagnosis, clinical signs and symptoms, treatment, and causes of asthma are discussed in Chapter 169. Kliegman MD, in Nelson Textbook of Pediatrics, 2020 Occupational and Environmental Asthma
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