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Global increased demand for seafood and its products has been associated with a concomitant rise in fishing, aquaculture, and processing activities. This increased harvesting of seafood is associated with more frequent reporting of allergic health problems among seafood processors. This review outlines the high-risk working populations, work processes, as well as host and environmental exposure risk factors for occupational respiratory and skin allergies. It also provides insights into the major and minor allergens as well as the pathophysiological mechanisms implicated. Diagnostic and preventive approaches are outlined in managing work-related allergy associated with seafood processing., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Allergic lung diseases present with either lung diseases developed as a result of inhalation of allergens (bronchial asthma) and antigens (hypersensitivity pneumonitis) of as a manifestation of systemic diseases including sarcoidosis and collagen vascular diseases. A limited space is available, therefore only hypersensitivity pneumonitis. bronchial asthma, sarcoidosis. and eosinophilic pneumonia were briefly summarized although a list of the allergic lung diseases is extensive. As a video-assisted lung biopsy has presently been popular, thoracic surgeons should perform surgery with a correct understanding of the pathophysiology of the disease.

Despite considerable advances in identifying the environmental agents that trigger allergy and the immunological mechanisms involved, progress in developing effective treatments remains frustratingly slow. Is it time to rethink some of the paradigms guiding this research?

Asthma has become a very common disease and despite new treatments continues to cause very large numbers of hospital admissions, school absences and so on. Recent evidence from many parts of the world has established that the single most important risk factor for perennial asthma is sensitization to one of the major indoor allergens: dust mite, cat, dog, or cockroach. However, there is also striking evidence about the role of rhinoviruses and ozone as enhancers of the immune response. Over the past 2 years, the ways in which these enhancers interact with the primary immune response both to cause asthma and to influence the severity of the disease have started to become clear.

We examined the effect of a newly synthesized pyridazinone derivative, NIP-502 [4-chloro-5-(3-ethoxy)-4-phenoxybenzamine)-3(2H)-pyridazinone], on antigen-induced bronchial responses and allergic reactions in several animal models. NIP-502 (10 mg/kg, p.o.) inhibited the antigen-induced immediate asthmatic response in passively sensitized guinea pigs. The inhibitory effect was also observed in metyrapone (an inhibitor of 11 beta-hydroxylase)-pretreated guinea pigs. NIP-502 improved ovalbumin (OA)-induced airway hyperresponsiveness to acetylcholine and inhibited the OA-induced increase in the number of inflammatory leukocytes in the bronchoalveolar lavage fluid. These inhibitory effects on OA-induced responses were similar to those of prednisolone. NIP-502 also showed an inhibitory effect on the passive cutaneous anaphylactic reaction in rats but did not inhibit the reversed cutaneous anaphylactic reaction, reversed Arthus reaction or delayed type hypersensitivity reaction. On the other hand, prednisolone showed broad inhibitory effects except for the reversed cutaneous anaphylactic reaction. In the in vitro study, NIP-502 (30 microM) significantly inhibited Formyl-Met-Leu-Phe-induced superoxide anion production by the guinea pig alveolar macrophages. These results indicate that the inhibitory effects of NIP-502 on bronchial responses are similar to those of prednisolone, but this compound seemed to act more selectively on the respiratory tract than prednisolone. Because of its effectiveness against a variety of bronchial responses, NIP-502 may be useful in the treatment of bronchial asthma.