Nitrous oxide and cytokines as markers of occupational exposure to flour dust

Baker’s asthma is one of the most common occupational disease in Europe. It is worth notion that flour dust is strongly pro-inflammatory and can cause non-allergic airway inflammation and can enhance allergen-mediated airway. In addition, exposure to flour can play a role in the development of rhinitis and asthma in occupationally exposed workers. Aim of the study was to evaluate inflammatory response to flour dust in workers matched for age, sex and time of exposure, but different in the development of respiratory symptoms. Methods. Three groups of subjects for a total of 84 bakery workers including 24 healthy subjects, 22 atopic and 38 occupational asthma ones, who had been submitted to clinical investigation for rhinitis or baker’s asthma, have been included in this study. The clinical assessment was performed in all subjects and included skin prick tests and specific IgE (environmental allergens and occupational ones such as wheat, rye, oat grain and barley grain, α- amylase), spirometry, methacholine challenge and specific bronchial challenge was also included if needed. Evaluation of nitrous oxide (NIOXMINO Aerocrine AB Sweeden) and serum cytokines, such as IL6 and IL8 which are involved in exposure, was also performed. Results. IL6 and IL8 were significantly increased in healthy and atopic subjects, although a slight not significant increase of both cytokines was also observed in baker’s asthma (p < 0.001 for IL6 and p < 0.02 for IL8). Il- 6 mean values ± SD were 16.8 ± 20.4 pg/ml in healthy workers, 4.3 ± 7.6 pg/ml in atopic workers and 4.3± 7.6 pg/ml in subjects with professional respiratory symptoms. IL-8 resulted respectively 65 ± 149.8, 88.4 ± 224.5 pg/ml and 43.9 ± 21.8 pg/ml. A slight increase of TNF-α was also observed in all analysed groups. Expired nitrous oxide was significantly increased in subjects with respiratory symptoms only (occupational asthma and atopic subjects). In addition, a statistically significant correlation was observed between the level of IL8 and nitrous oxide (r = 0.05). Conclusions The increase of cytokines to an inflammatory stimulus is probably due to a defense response in atopic and healthy workers, but not in advanced status of the disease thus suggesting that these cytokines can be a marker of the exposure. Nitrous oxide can be also used as a monitoring parameter of inflammation and it seems to be strictly related to IL8, which is responsible for neutrophil recruitment into the lung after exposure to endotoxin.