Occupational asthma due to latex in a hospital administrative employee

A case is described of occupational asthma caused by indirect exposure to airborne latex allergens in an administrative hospital employee who never used latex gloves.     

Occupational asthma due to latex in health care workers

Immediate hypersensitivity reactions ranging from mild urticaria to life threatening anaphylaxis after exposure to natural rubber latex have been reported frequently in health care workers while occupational asthma due to latex exposure is less well studied. The results of specific challenge tests and immunological tests in four health care workers with work related respiratory and skin disorders induced by the use of latex gloves are described. Occupational asthma was confirmed in three subjects by specific challenge tests. All had a positive skin test reaction to the latex extract; specific IgE antibodies were detected in only one subject. The fourth subject had a negative specific inhalation and skin test reaction to the latex extract. Peak expiratory flow monitoring at work and away from work showed a pattern consistent with work related asthma. These findings confirm that latex is a cause of occupational asthma in health care workers.     

Occupational asthma

The definition of occupational asthma is described. Causative agents which may be responsible for the development of occupational asthma are listed. Among factors responsible for the development of occupational asthma, immunological and nonimmunological mechanisms are specially described. The clinical characteristics of the disease, diagnostic methods, differential diagnosis, prognosis and prevention of occupational asthma are described. Procedures for determining exposure, occupations in which most frequently occupational asthma can develop, as well as preventive measures are reported.     

Occupational bronchial asthma

Examination of 400 patients with occupational bronchial asthma helped to identify various clinical and pathogenetic variants of the disease in accordance with independent and combined occupational allergens and irritants. The authors evaluated diagnostic value of endonasal tests with occupational allergen, rhinocytologic tests and some specific allergologic blood tests in vitro.     

Occupational asthma, IgE and IgG

Cyproheptadine is an antihistamine and serotonin antagonist given to children for allergies, migraine headaches, and growth problems. A 5-year-old boy began to have episodes of violent behavior after the initiation of cyproheptadine therapy. After cyproheptadine was discontinued, the aggression ceased over the course of a few weeks. Although there are other causal explanations possible in this case, cyproheptadine seems the most likely cause of the violent behavior, especially in view of the literature on the relation between serotonin and aggression.     

Occupational asthma caused by fish inhalation

Occupational asthma (OA) due to fish inhalation, confirmed by specific bronchial challenge (SBC), has not been described as yet in medical literature, as far as we know. We describe two patients whose asthma was induced by occupational exposure to fish and confirmed by serial measurements of PEFR and SBC. Two fish-processing workers reported asthma symptoms related to their workplace. They were skin tested with fish extracts and their sera assayed for IgE antibodies to various fish species. Nonspecific bronchial reactivity was assessed by methacholine challenge. The occupational relationship was confirmed by PEFR monitoring in working and off-work periods. SBC with fish extracts was carried out to confirm the diagnosis of OA. Skin tests with raw and cooked plaice, salmon, hake, and tuna in patient 1 and anchovy, sardine, trout, salmon, Atlantic pomfret, and sole in patient 2 were positive. Specific IgE serum antibodies were found to salmon in patient 1 and to trout, anchovy, and salmon in patient 2. PEFR measurements differed significantly (P < 0.001) between work and off-work periods for both patients. A bronchial challenge with methacholine was positive in patient 1. SBC with raw hake, salmon, plaice, and tuna extracts in patient 1 and raw salmon extract in patient 2 were all positive with an immediate response. SBC with Dermatophagoides pteronyssinus extract was entirely negative in both patients. In three asthmatic, non-fish-allergic controls, SBC with tuna, hake, salmon, and plaice were all negative. These results suggest that fish inhalation can elicit IgE-mediated occupational asthma.     

Occupational asthma: what have we learned?

Occupational asthma is one of the most frequent work-related diseases and may represent between 2% and 6% of all cases of asthma. It is defined as asthma causally and specifically related to exposure to airborne dusts, gases, vapors, or fumes in the working environment. Because it may cause long-lasting disability, it is important to properly identify affected workers and to withdraw them from exposure to the sensitizing agent as soon as possible. Although the history is the clue to the diagnosis, it is not sensitive or specific. The diagnosis should be confirmed by objective means, essentially by monitoring of peak expiratory flow and nonallergic bronchial responsiveness or by specific inhalation challenges. In this article the author reviews the investigation of occupational asthma.     

Occupational asthma to the slime mold Dictyostelium discoideum

Dictyostelium discoideum is a slime mold that exists in a unicellular amoeboid form under certain nutritional conditions. In this form, it produces unique lysosomal enzymes that are valuable in studying cell-to-cell signaling systems. We report on a research microbiologist who developed rhinoconjunctivitis and asthma after release of D. discoideum from a pressurized canister. Immediate skin test reactivity was demonstrated to whole and lysed organisms. Enzyme-linked immunosorbent assay results revealed IgE antibody against D. discoideum whole organism, lysed organism, and lysosomal enzymes with the strongest response being directed toward lysosomal enzymes. Pulmonary function testing showed a decline in forced expiratory volume in 1 second and forced expiratory flow after modified laboratory exposure to D. discoideum. This case represents the first report of occupational rhinoconjunctivitis and asthma from slime mild.     

Occupational asthma. Practical points for diagnosis and management

Asthma is a common chronic illness characterized by episodes of reversible airflow obstruction. A cornerstone of asthma management is identifying and avoiding agents that cause bronchospasm. The workplace is an important potential source of respirable exposures that can cause or trigger asthma. Identification of an occupational factor in asthma is important: early diagnosis and removal of the worker from the exposure is associated with improved prognosis; the diagnosis of occupational asthma may lead to compensation for work-related impairment and disability; and the diagnosis of occupational asthma is a Sentinel Health Event with implications for public health and prevention. In this article, we review specific causes of occupational asthma and general settings in which an occupational factor should be suspected and explored as part of the management of the worker with asthma. We also review specific and simple elements of history and pulmonary function testing that can be easily assessed by most health care practitioners and may be sufficient to establish a diagnosis of occupational asthma. Finally, we review the medical-legal implications of occupational asthma.     

Occupational asthma: measures of frequency from four countries

Both altered energy metabolism and oxidative stress have been proposed to contribute to tissue damage in neurogenerative diseases. Animal models and cell culture studies provide evidence for a role of these processes in several forms of neuronal death. Reductions in the activities of some key mitochondrial enzymes have been found in autopsied brain in Alzheimer's disease. However, results obtained with biopsied brain tissue as well as assessments of metabolic rates for glucose in vivo indicate that a reduced functional capacity of mitochondria is probably not a general feature in the brain in Alzheimer's disease. These studies do not address the possibility that short-lived changes in energy metabolism affecting a small number of cells at any one time could be contributing to cell death. Several findings point to a moderate increase in oxidative damage in those areas of brain which are most severely affected in this disease, probably resulting from an increase in production of reactive oxygen species. Whether this is a contributor to neurodegeneration or a consequence of it remains unresolved.