Exposure to Bioaerosols During Fish Processing on Board Norwegian Fishing Trawlers.

OBJECTIVES: The main objective was to gain more knowledge on exposure to bioaerosols in the processing area on board fishing trawlers. METHODS: Exposure sampling was carried out during the work shifts when processing fish in the processing area on board five deep-sea fishing trawlers (trawlers 1-5). Exposure samples were collected from 64 fishermen breathing zone and from stationary sampling stations on board five deep-sea fishing trawlers (1-5). Trawlers 2, 3, and 4 were old ships, not originally built for on board processing of the catch. Trawlers 1 and 5 were relatively new and built to accommodate processing machineries. On trawlers 1-4 round fish was produced; the head and entrails were removed before the fishes were frozen in blocks. Trawler 5 had the most extensive processing, producing fish fillets. Samples were analysed for total protein, trypsin activity, parvalbumin, and endotoxin. One side analysis of variance and Kruskal-Wallis H test were used to compare levels of exposure on the different trawlers. RESULTS: Personal exposure to total protein were higher on the three oldest trawlers (2, 3, and 4) compared with the two new trawlers (1 and 5). Highest activity of trypsin was detected on the four trawlers producing round fish (1-4). Parvalbumin was detected in 58% of samples from the fillet-trawler (5) compared with 13% of samples from the four trawlers producing round fish. The highest level of endotoxin was detected when using high-pressure water during cleaning machines and floors in the processing area. CONCLUSIONS: Fishermen in the processing area on board Norwegian trawlers are exposed to airborne bioaerosols as proteins, trypsin, fish allergen parvalbumin, and endotoxin. Levels varied between trawlers and type of production.

Change in airway inflammatory markers in Danish energy plant workers during a working week.

INTRODUCTION: It is well known that exposure to organic dust can cause adverse respiratory effect. The pathogen-associated molecular patterns (PAMPS) in the organic dust, such as endotoxin from Gram-negative bacteria cell wall and fungal components, can trigger the release of cytokine (e.g. Interleukin 1ß (IL-1ß)) and chemokine (e.g. Interleukin 8 (IL-8)) from the immune cells in the airways. OBJECTIVE: To evaluate the potential inflammatory effects of organic dust exposure in energy plants in Denmark. MATERIALS AND METHODS: Nasal lavage (NAL) and exhaled breath condensate (EBC) were sampled at Monday morning (referred to as before work) and again at Thursday afternoon (referred to as after work). NAL IL-8, EBC pH, IL-1ß concentration were measured. Personal exposure to endotoxin and dust was calculated from time spent on different tasks and measured average work area exposures. RESULTS: Before work, workers from biofuel plants had a higher IL-1ß and IL-8 concentration compared to conventional fuel plants (control group). Specifically, the IL-1ß level of moderately and most exposed group, and IL-8 level of the least exposed group were higher compared to the control group. The changes of IL-1ß, pH and IL-8 during a work week were not significant. Workers with rhinitis had a lower percentage change of IL-8 compared to healthy workers. CONCLUSIONS: An increased level of EBC IL-1ß in biofuel energy plant workers before work indicated a chronic or sub-chronic inflammation. The percentage change of IL-8 was lower in workers with rhinitis compared to healthy workers.

Organic dust toxic syndrome at a grass seed plant caused by exposure to high concentrations of bioaerosols.

We describe an outbreak of sudden health problems in workers at a Danish grass seed plant after exposure to a particularly dusty lot of grass seeds. The seeds are called problematic seeds. The association between development of organic dust toxic syndrome (ODTS) and the handling of grass seeds causing exposure was assessed in a four-step model: (i) identification of exposure source, (ii) characterization of the emission of bioaerosols from the problematic and reference seeds, (iii) personal and stationary exposure measurement at the plant and (iv) repeated health examinations. The grass seeds were identified as the exposure source; the emissions of some bioaerosol components were up to 10(7) times higher from the problematic seeds than from reference seeds. Cleaning of the seeds was not enough to sufficiently reduce the high emission from the problematic seeds. Emission in terms of dust was 3.4 times as high from the problematic cleaned seeds as from cleaned reference seeds. The personal exposure reached 3 × 10(5) endotoxin units m(-3), 1 × 10(6) colony-forming units (cfu) of thermophilic actinomycetes m(-3), 8 × 10(5) cfu of Aspergillus fumigatus m(-3) and 9 × 10(6) hyphal fragments m(-3). Several workers working with the problematic seeds had symptoms consistent with ODTS. The most severe symptoms were found for the workers performing the tasks causing highest exposure. Respiratory airway protection proved efficient to avoid development of ODTS. Work with reference seeds did not cause workers to develop ODTS. Exposure was during work with the problematic seeds higher than suggested occupational exposure limits but lower than in studies where researchers for some minutes have repeated a single task expected to cause ODTS. In this study, many different bioaerosol components were measured during a whole working day. We cannot know, whether it is the combination of different bioaerosol components or a single component which is responsible for the development of ODTS. In conclusion, workers developed specific health symptoms due to the high bioaerosol exposure and were diagnosed with ODTS. Exposure to high concentrations of endotoxin, actinomycetes, fungi, hyphal fragments, ß-glucan, and A. fumigatus occurred when working with a dusty lot of grass seed. Suspicion should be elicited by seeds stored without being properly dried and by seeds producing more dust than usually.

Carbon black nanoparticle instillation induces sustained inflammation and genotoxicity in mouse lung and liver.

BACKGROUND: Widespread occupational exposure to carbon black nanoparticles (CBNPs) raises concerns over their safety. CBNPs are genotoxic in vitro but less is known about their genotoxicity in various organs in vivo. METHODS: We investigated inflammatory and acute phase responses, DNA strand breaks (SB) and oxidatively damaged DNA in C57BL/6 mice 1, 3 and 28 days after a single instillation of 0.018, 0.054 or 0.162 mg Printex 90 CBNPs, alongside sham controls. Bronchoalveolar lavage (BAL) fluid was analyzed for cellular composition. SB in BAL cells, whole lung and liver were assessed using the alkaline comet assay. Formamidopyrimidine DNA glycosylase (FPG) sensitive sites were assessed as an indicator of oxidatively damaged DNA. Pulmonary and hepatic acute phase response was evaluated by Saa3 mRNA real-time quantitative PCR. RESULTS: Inflammation was strongest 1 and 3 days post-exposure, and remained elevated for the two highest doses (i.e., 0.054 and 0.162 mg) 28 days post-exposure (P < 0.001). SB were detected in lung at all doses on post-exposure day 1 (P < 0.001) and remained elevated at the two highest doses until day 28 (P < 0.05). BAL cell DNA SB were elevated relative to controls at least at the highest dose on all post-exposure days (P < 0.05). The level of FPG sensitive sites in lung was increased throughout with significant increases occurring on post-exposure days 1 and 3, in comparison to controls (P < 0.001-0.05). SB in liver were detected on post-exposure days 1 (P < 0.001) and 28 (P < 0.001). Polymorphonuclear (PMN) cell counts in BAL correlated strongly with FPG sensitive sites in lung (r = 0.88, P < 0.001), whereas no such correlation was observed with SB (r = 0.52, P = 0.08). CBNP increased the expression of Saa3 mRNA in lung tissue on day 1 (all doses), 3 (all doses) and 28 (0.054 and 0.162 mg), but not in liver. CONCLUSIONS: Deposition of CBNPs in lung induces inflammatory and genotoxic effects in mouse lung that persist considerably after the initial exposure. Our results demonstrate that CBNPs may cause genotoxicity both in the primary exposed tissue, lung and BAL cells, and in a secondary tissue, the liver.