Hypersensitivity pneumonitis in fish processing workers diagnosed by inhalation challenge.

Hypersensitivity pneumonitis may be caused by occupational exposure in the fish processing industry http://ow.ly/GbEf30lFnyk.

Pulmonary illness as a consequence of occupational exposure to shrimp shell powder.

OBJECTIVES: An employee with no prior history of allergy or asthma, experienced respiratory and flu-like symptoms during production of shrimp shell powder in a seafood savory factory in Norway. We aimed to clarify the diagnosis and to identify the cause of the symptoms by specific inhalation challenge (SIC) and by characterizing the powder's biocontaminants, particle size fractions and inflammatory potential. METHODS: Respiratory and immunological responses were measured the day before and after each of four challenges with 20-150g shrimp shell powder during three consecutive days. The powder was analyzed for endotoxin, microorganisms and particle size fractions by standardized laboratory methods. Total inflammatory potential was quantified by reactive oxygen species (ROS) production in a granulocyte assay. RESULTS: The patient had elevated IgG, but not IgE, towards shrimp shell powder. 20min challenge with 150g shrimp shell powder induced 15% decrease in FVC, 23% decrease in FEV1 and increased unspecific bronchial reactivity by methacholine. Neutrophils and monocytes increased 84% and 59%, respectively, and the patient experienced temperature increase and flu-like symptoms. The shrimp shell powder contained 1118 endotoxin units/g and bacteria including Bacillus cereus, and 57% respirable size fraction when aerosolized. The ROS production was higher for shrimp shell powder than for endotoxin alone. CONCLUSIONS: Endotoxin and other bacterial components combined with a high fraction of respirable dust might be the cause of the symptoms. The patient's characteristics and response to SIC were best compatible with occupational asthma and organic dust toxic syndrome, while hypersensitivity pneumonitis could not be excluded.

Respiratory Health in Cleaners in Northern Europe: Is Susceptibility Established in Early Life?

RATIONALE: There is some evidence that maternal smoking increases susceptibility to personal smoking's detrimental effects. One might question whether early life disadvantage might influence susceptibility to occupational exposure. OBJECTIVES: In this cross-sectional study we investigated respiratory symptoms, asthma and self-reported chronic obstructive pulmonary disease (COPD) as related to working as a cleaner in Northern European populations, and whether early life factors influenced susceptibility to occupational cleaning's unhealthy effects. METHODS: The RHINE III questionnaire study assessed occupational cleaning in 13,499 participants. Associations with respiratory symptoms, asthma and self-reported COPD were analysed with multiple logistic regressions, adjusting for sex, age, smoking, educational level, parent´s educational level, BMI and participating centre. Interaction of occupational cleaning with early life disadvantage (maternal smoking, severe respiratory infection <5 years, born during winter months, maternal age at birth >35 years) was investigated. MAIN RESULTS: Among 2138 ever-cleaners the risks of wheeze (OR 1.4, 95% CI 1.3-1.6), adult-onset asthma (1.5 [1.2-1.8]) and self-reported COPD (1.7 [1.3-2.2]) were increased. The risk increased with years in occupational cleaning (adult-onset asthma: ≤1 year 0.9 [0.7-1.3]; 1-4 years 1.5 [1.1-2.0]; ≥4 years 1.6 [1.2-2.1]). The association of wheeze with cleaning activity ≥4 years was significantly stronger for those with early life disadvantage than in those without (1.8 [1.5-2.3] vs. 1.3 [0.96-1.8]; pinteraction 0.035). CONCLUSIONS: Occupational cleaners had increased risk of asthma and self-reported COPD. Respiratory symptom risk was particularly increased in persons with factors suggestive of early life disadvantage. We hypothesize that early life disadvantage may increase airway vulnerability to harmful exposure from cleaning agents later in life.

[Work-related COPD]. / Arbeidsrelatert kols.

BACKGROUND: Work-related COPD occurs as a result of exposure to harmful particles and gases/fumes in the workplace, including among non-smokers. The objective of this article is to present more recent findings on the correlation between occupational exposure and COPD. In addition, we review diagnostic and prognostic considerations and the potential for prevention. METHOD: We have undertaken literature searches in Medline and EMBASE for the period May 2009 - July 2014. Studies without any measurements of pulmonary function or references to occupational exposure were excluded. We have also included three prospective studies on pulmonary function and occupational exposure that were not indexed with the search terms used for obstructive pulmonary disease. RESULTS: Three population studies and eight studies that described a specific industry or sector were included. Recent studies detect an association between exposure and an increased risk of COPD in the construction industry, metallurgical smelting, cement production and the textile industry. In other respects, the findings from previous review studies are confirmed. INTERPRETATION: Exposure to a number of organic and inorganic particles and fumes in the workplace may cause COPD even at prevailing levels of exposure. Doctors should inquire about such exposure in cases of suspected and established COPD and should have a low threshold for referral to occupational health assessment.

[Work-related asthma--diagnostics and follow-up]. / Arbeidsrelatert astma--diagnostikk og oppfølging.

BACKGROUND: Approximately 10-15% of all cases of asthma occurring in adults can be ascribed to exposure at work. Work-related asthma (WRA) includes cases that represent an exacerbation of pre-existing asthma as well as occupational asthma where exposure at work is the cause of the disease. Somewhat more than 350 different sources of exposure are known to be causes of allergic WRA. The purpose of this article is to present an updated review of diagnostics and follow-up of WRA. MATERIAL: In addition to our own searches in PubMed and comprehensive clinical experience with this patient group, the article is based on a number of literature reviews undertaken internationally. RESULTS: Early diagnosis requires attention to occupational asthma and rapid initiation of diagnostics, in which primary doctors play a key role. Further examination requires resources that are available only in departments with special competence in this field. Awareness of the condition and an early and correct diagnosis that leads to cessation of exposure have been shown to improve the patients' prognosis. INTERPRETATION: All doctors who have responsibility for asthma patients need to be aware of this condition and provide adequate diagnostics, so that interventions to halt the exposure can be undertaken. Cooperation between GPs, employers, enterprise health services and specialists are required to achieve this.

Specific inhalation challenge in the diagnosis of occupational asthma: consensus statement.

This consensus statement provides practical recommendations for specific inhalation challenge (SIC) in the diagnosis of occupational asthma. They are derived from a systematic literature search, a census of active European centres, a Delphi conference and expert consensus. This article details each step of a SIC, including safety requirements, techniques for delivering agents, and methods for assessing and interpreting bronchial responses. The limitations of the procedure are also discussed. Testing should only be carried out in hospitals where physicians and healthcare professionals have appropriate expertise. Tests should always include a control challenge, a gradual increase of exposure to the suspected agent, and close monitoring of the patient during the challenge and for at least 6 h afterwards. In expert centres, excessive reactions provoked by SIC are rare. A positive response is defined by a fall in forced expiratory volume in 1 s ≥ 15% from baseline. Equivocal reactions can sometimes be clarified by finding changes in nonspecific bronchial responsiveness, sputum eosinophils or exhaled nitric oxide. The sensitivity and specificity of SIC are high but not easily quantified, as the method is usually used as the reference standard for the diagnosis of occupational asthma.

Occupational chronic obstructive pulmonary disease: a systematic literature review.

OBJECTIVE: Occupational-attributable chronic obstructive pulmonary disease (COPD) presents a substantial health challenge. Focusing on spirometric criteria for airflow obstruction, this review of occupational COPD includes both population-wide and industry-specific exposures. METHODS: We used PubMed and Embase to identify relevant original epidemiological peer-reviewed articles, supplemented with citations identified from references in key review articles. This yielded 4528 citations. Articles were excluded for lack of lung function measurement, insufficient occupational exposure classification, lack of either external or internal referents, non-accounting of age or smoking effect, or major analytic inadequacies preventing interpretation of findings. A structured data extraction sheet was used for the remaining 147 articles. Final inclusion was based on a positive qualitative Scottish Intercollegiate Guidelines Network (SIGN) score (≥2+) for study quality, yielding 25 population-wide and 34 industry/occupation-specific studies, 15 on inorganic and 19 on organic dust exposure, respectively. RESULTS: There was a consistent and predominantly significant association between occupational exposures and COPD in 22 of 25 population-based studies, 12 of 15 studies with an inorganic/mineral dust exposure, and 17 of 19 studies on organic exposure, even though the studies varied in design, populations, and the use of measures of exposure and outcome. A nearly uniform pattern of a dose-response relationship between various exposures and COPD was found, adding to the evidence that occupational exposures from vapors, gas, dust, and fumes are risk factors for COPD. CONCLUSION: There is strong and consistent evidence to support a causal association between multiple categories of occupational exposure and COPD, both within and across industry groups.

Diagnostic approach in cases with suspected work-related asthma.

BACKGROUND: Work-related asthma (WRA) is a major cause of respiratory disease in modern societies. The diagnosis and consequently an opportunity for prevention are often missed in practice. METHODS: Based on recent studies and systematic reviews of the literature methods for detection of WRA and identification of specific causes of allergic WRA are discussed. RESULTS AND CONCLUSIONS: All workers should be asked whether symptoms improve on days away from work or on holidays. Positive answers should lead to further investigation. Spirometry and non-specific bronchial responsiveness should be measured, but carefully performed and validly analysed serial peak expiratory flow or forced expiratory volume in one second (FEV1) measurements are more specific and confirm occupational asthma in about 82% of those still exposed to the causative agent. Skin prick testing or specific immunoglobulin E assays are useful to document allergy to high molecular weight allergens. Specific inhalational challenge tests come closest to a gold standard test, but lack standardisation, availability and sensitivity. Supervised workplace challenges can be used when specific challenges are unavailable or the results non-diagnostic, but methodology lacks standardisation. Finally, if the diagnosis remains unclear a follow-up with serial measurements of FEV1 and non-specific bronchial hyperresponsiveness should detect those likely to develop permanent impairment from their occupational exposures.

[Occupational exposure for dust and gases is an important risk factor for developing COPD]. / Erhvervseksposition for støv og dampe er en betydende risikofaktor for KOL.

Some patients with chronic obstructive pulmonary disease (COPD) are never-smokers, which suggests that there must be other important risk factors. This paper describes the evidence for an association between occupational exposure and COPD. In several studies a consistent and predominantly significant association between occupational exposures and COPD is found, even though the studies vary in design, enrolled populations and in measures of exposure and outcome. Strong evidence supports a causal association between multiple categories of occupational exposure and COPD, both within and across industry groups.

The management of work-related asthma guidelines: a broader perspective.

The aim of the European Respiratory Society work-related asthma guidelines is to present the management and prevention options of work-related asthma and their effectiveness. Work-related asthma accounts for 5-25% of all adult asthma cases and is responsible for a significant socioeconomic burden. Several hundred occupational agents, mainly allergens but also irritants and substances with unknown pathological mechanisms, have been identified as causing work-related asthma. The essential message of these guidelines is that the management of work-related asthma can be considerably optimised based on the present knowledge of causes, risk factors, pathomechanisms, and realistic and effective interventions. To reach this goal we urgently require greatly intensified primary preventive measures and improved case management. There is now a substantial body of evidence supporting the implementation of comprehensive medical surveillance programmes for workers at risk. Those workers who fail surveillance programmes need to be referred to a clinician who can confirm or exclude an occupational cause. Once work-related asthma is confirmed, a revised risk assessment in the workplace is needed to prevent further cases. These new guidelines confirm and extend already existing statements and recommendations. We hope that these guidelines will initiate the much-needed research that is required to fill the gaps in our knowledge and to initiate substantial improvements in preventative measures.

Occupational allergy to Artemia fish fry feed in aquaculture.

BACKGROUND: Artemia (brine shrimp) is used as feed for fish fry and shrimp in aquaculture. Two employees in a Norwegian aquaculture research farm reported having chest symptoms when working in an Artemia hatch room. AIMS: To determine the presence and prevalence of Artemia sensitization at the farm and the extent of any Artemia-related respiratory and hand skin symptoms and to identify the allergens involved. METHODS: Participants completed a questionnaire and structured interview. Skin prick tests (SPTs) were performed, and immunoglobulin E (IgE) antibodies to Artemia, shrimp and recombinant tropomyosin were determined. Gel electrophoresis and immunoblots of Artemia extracts were also carried out. RESULTS: Thirty of 42 employees (71%) participated. Among the 24 subjects exposed to Artemia, four (17%) reported chest and/or hand skin symptoms during exposure and three of them were IgE sensitized to Artemia. Five (21%) of those exposed demonstrated IgE antibodies to Artemia and four (17%) had immediate-positive SPTs. A serum pool from these subjects exhibited IgE binding to a protein of approximately 97 kDa in the Artemia extract. CONCLUSIONS: Occupational exposure to the Artemia fish fry feed can cause IgE sensitization and allergic symptoms affecting airways and skin.

Bronchial responsiveness in bakery workers: relation to airway symptoms, IgE sensitization, nasal indices of inflammation, flour dust exposure and smoking.

BACKGROUND: Bronchial hyperresponsiveness (BHR) is common in bakery workers. The relation between bronchial responsiveness measured with a tidal breathing method and smoking, airway symptoms, IgE-sensitization, nasal indices of inflammation and flour dust exposure have been studied with bronchial responsiveness expressed as a continuous outcome. MATERIAL AND METHODS: Bakery workers (n = 197) were subjected to interviews, questionnaires, allergy tests, workplace dust measurements and bronchial metacholine provocation. Eosinophil cationic protein (ECP) and alpha(2)-macroglobulin were measured in nasal lavage. Bronchial responsiveness was expressed as slope(conc), a measurement based on regressing the per cent reduction in FEV(1) at each provocation step. RESULTS: BHR expressed as slope(conc) was associated with smoking (P = 0.009), asthma symptoms at work (P = 0.001), and occupational IgE sensitization (P = 0.048). After adjusting for baseline lung function the association between BHR and IgE sensitization was no longer present. We demonstrated an association between nasal ECP and BHR (slope(conc) < 3: P = 0.012), but not to alpha(2)-macroglobulin in nasal lavage. No association was seen between BHR and current exposure level of flour dust, number of working years in a bakery or a history of dough-making. CONCLUSION: BHR is related to baseline lung function, work-related asthma symptoms, smoking and nasal eosinophil activity, but not to occupational IgE sensitization and current flour dust exposure when measured with metacholine provocation. The slope(conc) expression seems to be a useful continuous outcome in bronchial responsiveness testing.

Nasal indices of eosinophilic and exudative inflammation in bakery-workers.

AIMS: Rhinitis symptoms frequently occur in bakery-workers. Yet, little is known about the pathophysiology of this condition. The objective of the present study was to examine nasal indices of inflammation in relation to occupational dust exposure, occupational rhinitis according to defined criteria, rhinitis symptoms associated to the workplace, and occupational sensitization in bakery-workers. METHODS: Bakery-workers (n = 197) were subjected to interviews, questionnaires, workplace dust measurements, allergy tests, and nasal lavages with and without histamine. alpha(2)-Macroglobulin and eosinophil cationic protein (ECP) were measured in saline lavages as indices of plasma exudation and eosinophilic activity, respectively. Histamine lavages were employed to explore the nasal exudative responsiveness. RESULTS: alpha(2)-Macroglobulin and ECP increased significantly by increased workplace dust exposure (P< or =0.035). Furthermore, the exudative responsiveness to histamine increased significantly by such exposure (P< or =0.016). Similar patterns were seen in workers with occupational rhinitis and in subjects with rhinitis symptoms associated to the workplace, but not in workers with occupational sensitization. CONCLUSIONS: We conclude that occupational dust exposure in bakery-workers is associated with nasal eosinophilic exudative inflammation. In contrast, occupational sensitization is not a discriminating factor with regard to indices of eosinophilic, exudative inflammation in the present material.