Atopy is thought to predispose to occupational asthma from high molecular weight agents: in your context, fish protein would qualify as a high molecular weight agent, if occupational asthma is suspected.
The evidence for atopy as a risk factor for occupational asthma in general can be found from the link at the bottom titled "Is atopy a risk factor for developing occupational asthma?".
The link at the bottom titled "Occupational asthma caused by automated salmon processing" gives some information from the BOHRF occupational asthma guidelines on the subject.
The following section is from the HSE report on causative agents of occupational asthma (2001) with particular reference to fish protein allergies in general.
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Exposure to aerosols generated during the cleaning of various species of fish has been shown to induce occupational asthma. Although only one study has included bronchial challenges, the quality of the remaining studies is sufficient to provide further good evidence. The prevalence when using automatic gutting machines was as high as 75% in one study. There is sufficient evidence to conclude that fish protein meets the revised EU criteria (1996) for classification as a respiratory sensitiser (a cause of asthma) and labelling with R42.
Manual gutting of fish has been carried out for centuries, but it has not been until the introduction of automatic machines that cases of occupational asthma have begun to be reported. These machines produce aerosols that certain fish protein and may also be contaminated with bacterial products (Sherson et al., 1989; Douglas et al., 1995). Within three months of the opening of a salmon processing plant with automated machines, 24 out of the 291 workers developed occupational asthma (Douglas et al., 1995). Diagnosis was made on the basis of a new history of asthma, work related symptoms and pulmonary function changes; there were no specific bronchial challenge tests. The latent period for the development of symptoms varied from 2 weeks to 3 months. The original 291 workers, who were exposed to respirable fish aerosol at up to 3.14 mg/m3 were compared with a further 37 who joined after ventilation was improved to achieve levels of 0.09 mg/m3. None of these new workers developed occupational asthma. When the 291 workers were graded according to severity of symptoms, the groups showed a severity related increase in the percentage with specific immunoglobulin E (IgE) to salmon serum; 85% of the group with most severe symptoms had specific IgE compared to 3% in asymptomatic workers. Occurrence or specific immunoglobulin G (IgG) ranged from 28% in exposed workers without symptoms to 62% in the most severely affected group. Salmon serum antigen was identified in the aerosol produced by the machine.
In a case control study at the same factory, 13 affected cases without previous history of asthma were compared with 36 controls (Douglas et al., 1995). Following the improvement in ventilation, the pulmonary function of the cases improved. There was a significant association between the degree (but not the length) of exposure and specific IgE and IgG production. All 8 production workers at a small trout-processing factory complained of rhinitis and/or asthma associated with working near an automatic gutting machine (Sherson et al., 1989). The latent period before the start of symptoms ranged from one week to eleven years. Pulmonary function studies, bronchial responsiveness to histamine and peak flow variation confirmed that 6 of the workers had occupational asthma (a prevalence of 75%), with a further one being a possibility. No specific bronchial challenge tests were carried out. The water from the gutting machine was found to be contaminated with bacterial growth and edoxtoxin, and air collected above the machine grew several species of bacteria. Specific IgE as measured by radioallergosorbent test (RAST) was definitely positive to scraped trout skin in only one person, and to contaminated water fromthe gutting machine in two people. None were definitely positive to salmon. It is not clear how much bacterial contamination played a part in the reactions obtained, but the latent period suggests involvement of an allergic reaction to a protein component in the contaminated water. Two people who cleaned fish in fish factories developed occupational asthma with latent periods of a few weeks and one year (Rodriguez et al., 1997). It is unclear whether automatic gutting machines were in use. Neither subject had a previous history of allergies, although one man (patient 2) developed a food allergy to fish after he had developed occupational asthma. Peak flow measurements were more variable at work than off work, but the differences were generally unconvincing. However, specific bronchial challenge tests, apparently carried out in an open manner, with extracts of a range of fish species were positive in both subjects (patient 1: hake, salmon, plaice, tuna; patient 2: salmon), whereas the control, house dust mite, proved negative. Negative findings were also obtained with the fish extracts in three asthmatic controls who were not allergic to fish. Patient 2 suffered a severe anaphylactic reaction after intradermal injection with trout extract, and so was not challenged by inhalation with this fish. Both patients had specific IgE to a range of fish extracts, which included plaice, salmon, trout, hake, tuna and anchovy, as measured by RAST and skin prick test.
Allergic reactions after eating fish are well recognised, and in one group of patients, 54% suffered wheezing or chest tightness after ingesting fish (Helbling et al., 1996). Specific IgE testing revealed significant cross-reactivity between several species of fish. In another study, 21 out of 197 children with IgE-mediated fish hypersensitivity showed allergic reactions (wheezing and urticaria) after accidental inhalation of fish odours or fumes (Crespo et al., 1995). These studies provide evidence that asthma commonly occurs in people who are allergic to fish. A chef who had developed occupational asthma to lobster also gave a strong skin prick test haddock and cod, suggesting a secondary allergy to these fish, or a cross-reactivity between crustacean and fish protein (Patel et al., 1992). This study does not provide strong evidence that haddock or cod can induce occupational asthma.
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Some publications related to fish industry and occupational asthma have been quoted earlier in a separate post as a reply to your question. A comprehensive review of occupational seafood allergy (MF Jeebhay, Cape Town) is also linked below.
Hope this is of help.
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Rodríguez J, Reaño M, Vives R, Canto G, Daroca P, Crespo JF, Vila C, Villarreal O, Bensabat Z.,
Occupational asthma caused by fish inhalation,
Allergy,
1997;52:866-869,
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