ABSTRACT
OBJECTIVE: In this study, we explored airway symptoms and exposure to bioaerosols and exhaust gases in seafood industry plants. METHODS: The study details the results from personal and environmental exposure measurements (17 plants), a questionnaire (n = 984), and clinical examinations (n = 225). RESULTS: The workers were exposed to allergens, endotoxins, molds, and exhaust. The 1-year prevalence of work-related airway symptoms was 42.8% for production workers and 25.9% for administrative workers. Mean levels of forced expiratory volume in 1 second and forced vital capacity were less than the predicted values in all exposed nonsmoker groups. A total of 20.5% had increased levels of total IgE (>/=100 kU/L). Specific IgE-mediated reactions seemed to be relevant only in the shrimp industry. CONCLUSIONS: Seafood industry workers showed a high prevalence of work-related airway symptoms. Further research on the relationship between exposure and effects is necessary.
Subject(s)
Food-Processing Industry/statistics & numerical data , Occupational Diseases/epidemiology , Occupational Exposure/statistics & numerical data , Respiratory Tract Diseases/epidemiology , Seafood/toxicity , Adult , Air Pollutants, Occupational/analysis , Female , Health Surveys , Humans , Immunoglobulin E/metabolism , Male , Norway/epidemiology , Occupational Diseases/diagnosis , Occupational Diseases/immunology , Occupational Diseases/metabolism , Prevalence , Respiratory Function Tests , Respiratory Tract Diseases/diagnosis , Respiratory Tract Diseases/immunology , Respiratory Tract Diseases/metabolism , Seafood/statistics & numerical data , Sex DistributionABSTRACT
The potent natural toxins microcystin, nodularin, and okadaic acid act rapidly to induce apoptotic cell death. Here we show that the apoptosis correlates with protein phosphorylation events and can be blocked by protein kinase inhibitors directed against the multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). The inhibitors used comprised a battery of cell-permeable protein kinase antagonists and CaMKII-directed peptide inhibitors introduced by microinjection or enforced expression. Furthermore, apoptosis could be induced by enforced expression of active forms of CaMKII but not with inactive CaMKII. It is concluded that the apoptogenic toxins, presumably through their known ability to inhibit serine/threonine protein phosphatases, can cause CaMKII-dependent phosphorylation events leading to cell death.
