Assessment of public health impact of work-related asthma

<p>Abstract</p> <p>Background</p> <p>Asthma is among the most common chronic diseases in working-aged populations and occupational exposures are important causal agents. Our aims were to evaluate the best methods to assess occurrence, public health impact, and burden to society related to occupational or work-related asthma and to achieve comparable estimates for different populations.</p> <p>Methods</p> <p>We addressed three central questions: <b>1: What is the best method to assess the occurrence of occupational asthma? </b>We evaluated: 1) assessment of the occurrence of occupational asthma <it>per se</it>, and 2) assessment of adult-onset asthma and the population attributable fractions due to specific occupational exposures. <b>2: What are the best methods to assess public health impact and burden to society related to occupational or work-related asthma? </b>We evaluated methods based on assessment of excess burden of disease due to specific occupational exposures. <b>3: How to achieve comparable estimates for different populations? </b>We evaluated comparability of estimates of occurrence and burden attributable to occupational asthma based on different methods.</p> <p>Results</p> <p>Assessment of the occurrence of occupational asthma <it>per se </it>can be used in countries with good coverage of the identification system for occupational asthma, i.e. countries with well-functioning occupational health services. Assessment based on adult-onset asthma and population attributable fractions due to specific occupational exposures is a good approach to estimate the occurrence of occupational asthma at the population level. For assessment of public health impact from work-related asthma we recommend assessing excess burden of disease due to specific occupational exposures, including excess incidence of asthma complemented by an assessment of disability from it. International comparability of estimates can be best achieved by methods based on population attributable fractions.</p> <p>Conclusions</p> <p>Public health impact assessment for occupational asthma is central in prevention and health policy planning and could be improved by purposeful development of methods for assessing health benefits from preventive actions. Registry-based methods are suitable for evaluating time-trends of occurrence at a given population but for international comparisons they face serious limitations. Assessment of excess burden of disease due to specific occupational exposure is a useful measure, when there is valid information on population exposure and attributable fractions.</p

Detection of fish antigens aerosolized during fish processing using newly developed immunoassays

Background: Aerosolization of fish proteins during seafood processing has been identified as a potential route for allergic sensitization and occupational asthma among workers involved in high-risk activities. The aim of this study was to develop immunological assays for the quantification of aerosolized fish antigens in a fish-processing factory. \ud \ud Methods: Polyclonal antibodies to the main fish species processed in the factory (anchovy and pilchard) were generated in rabbits and compared by ELISA inhibition assay and immunoblotting. These antisera were utilized to develop ELISA assays for the detection of fish antigens. The ELISA inhibition assays were evaluated by analyzing environmental air samples collected from three areas in a fish-processing factory: pilchard canning, fish meal production and lobster processing. \ud \ud Results: By immunoblotting, the rabbit polyclonal antibodies demonstrated IgG antibody binding patterns comparable with IgE antibodies of fish-sensitized patients, particularly in regard to the major fish allergens parvalbumins. The sensitivity of the fish-specific ELISA assays developed was 0.5 μg/ml. The ELISA inhibition assays were able to differentiate between the two different fish species of interest but did not recognize a crustacean species. Notable differences in exposure levels to canned pilchard and anchovy antigens were demonstrated in the three different working areas of the factory, with assays having a detection limit as low as 105 ng/m3. \ud \ud Conclusion: These ELISA-based assays are sensitive and specific to quantify differential exposure levels to fish antigens produced during fish processing, making it possible to investigate exposure-disease response relationships among workers in this industry

Review of diagnostic challenges in occupational asthma

Occupational asthma (OA) is one of the most frequent occupational diseases and its diagnosis is often difficult. This review summarizes its current diagnostic challenges. OA is associated with significant health and socio-economic burden. It is underdiagnosed and physicians need to adopt a stepwise approach to confirm the diagnosis. Although early removal from exposure to the offending agent is associated with a better prognosis, physicians should try to confirm the diagnosis of work-related asthma before taking a worker off work. A proper occupational and medical history is very important but is not enough to make the diagnosis of OA. Objective evidence of work-related asthma is required and this represents a serious challenge to most physicians. Measurement of non-specific bronchial responsiveness (NSBR) and spirometry may confirm the diagnosis of asthma but do not confirm the diagnosis of OA. Serial monitoring of peak expiratory flows (PEF), NSBR, and airway inflammation at and off work may confirm the diagnosis of OA but are often difficult to perform. Confirming sensitization by skin prick tests or specific IgE may help to support the diagnosis of OA. Specific inhalation challenges (SIC) in the lab or at work are considered the reference standard but are of limited access. Medical surveillance programs along with primary prevention (reducing exposure) may help to reduce the burden of OA, but the ideal program has yet to be defined. The diagnostic workup of OA remains a challenge and needs a rigorous stepwise evaluation

Chitin-Induced Airway Epithelial Cell Innate Immune Responses Are Inhibited by Carvacrol/Thymol

Chitin is produced in large amounts by fungi, insects, and other organisms and has been implicated in the pathogenesis of asthma. Airway epithelial cells are in direct contact with environmental particles and serve as the first line of defense against inhaled allergens and pathogens. The potential contributions of airway epithelial cells to chitin-induced asthma remain poorly understood. We hypothesized that chitin directly stimulates airway epithelial cells to release cytokines that promote type 2 immune responses and to induce expression of molecules which are important in innate immune responses. We found that chitin exposure rapidly induced the expression of three key type 2-promoting cytokines, IL-25, IL-33 and TSLP, in BEAS-2B transformed human bronchial epithelial cells and in A549 and H292 lung carcinoma cells. Chitin also induced the expression of the key pattern recognition receptors TLR2 and TLR4. Chitin induced the expression of miR-155, miR-146a and miR-21, each of which is known to up-regulate the expression of pro-inflammatory cytokines. Also the expression of SOCS1 and SHIP1 which are known targets of miR-155 was repressed by chitin treatment. The monoterpene phenol carvacrol (Car) and its isomer thymol (Thy) are found in herbal essential oils and have been shown to inhibit allergic inflammation in asthma models. We found that Car/Thy inhibited the effects of chitin on type 2-promoting cytokine release and on the expression of TLRs, SOCS1, SHIP1, and miRNAs. Car/Thy could also efficiently reduce the protein levels of TLR4, inhibit the increase in TLR2 protein levels in chitin plus Car/Thy-treated cells and increase the protein levels of SHIP1 and SOCS1, which are negative regulators of TLR-mediated inflammatory responses. We conclude that direct effects of chitin on airway epithelial cells are likely to contribute to allergic airway diseases like asthma, and that Car/Thy directly inhibits epithelial cell pro-inflammatory responses to chitin