Occupational asthma

Top PDF Occupational asthma:

Factors associated with severity of occupational asthma with a latency period at diagnosis.

Factors associated with severity of occupational asthma with a latency period at diagnosis.

flour persulfate salts isocyanates latex amines quaternary ammoniums aldehydes mites resins & glues isocyanates excluded laboratory animals pollens others bakers and pastry makers hairdr[r]

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Update of an occupational asthma-specific job exposure matrix to assess exposure to 30 specific agents

Update of an occupational asthma-specific job exposure matrix to assess exposure to 30 specific agents

OAsJEM paper _ OEM 9 February 2018 5 M ETHODS The original Asthma-specific JEM Briefly, the original Asthma-specific JEM 19 , is a two dimensional table with a 2- to 4-digit ISCO-88 (International Standard Classification of Occupations, 1988) job codes 25 axis crossed with a second axis of 18 asthmagens and four agents classified at low risk for asthma. Agents were classified into four broad groups: low molecular weight (LMW), high molecular weight (HMW) asthmagens, mixed environments and irritants peaks. In addition, job codes poorly defined and/or with heterogeneous exposures (88 out of all 506 2- to 4-digit ISCO-88 job codes; 17%) were identified and classified as requiring ‘an expert re-evaluation step’ with linked comments and specific recommendations for reviewing each specific exposure (see online supplement Figure E1). When re-evaluation was needed in a study, the exposure attributed by the JEM was checked and modified if necessary by the expert directly, at individual level, according to participant’s job, industry and tasks descriptions.
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Occupational irritants and asthma: an Estonian cross-sectional study of 34,000 adults.

Occupational irritants and asthma: an Estonian cross-sectional study of 34,000 adults.

Occupational asthma is a good model to study asthma in general.[4] More than 400 agents have been recognized to cause occupational asthma, and new agents are reported each year.[5, 6] Occupational asthma is classified into two different types according to the causing agents and the underlying mechanisms. Most occupational asthmagens are low or high molecular weight sensitizers, inducing asthma through immunologic mechanisms.[5, 7] IgE-mediated mechanisms have been proven for most high and some low molecular weight agents.[5, 7] The second type of occupational asthma, referred to as “nonimmunologic occupational asthma”[5] or “irritant induced asthma”,[8] has first been described in relation to a single exposure to high concentrations of irritants. The potential role of repeated low to moderate level of exposure to irritant in occupational asthma is receiving growing attention.[8]
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Asthma heterogeneity: the increasing genetic evidence

Asthma heterogeneity: the increasing genetic evidence

The authors should be commended for the sophisticated analysis conducted to provide biological meaningful interpretation to the genetic loci identified, as well as the sensitivity analysis conducted to address the robustness of the findings to the specificity of the childhood and adult-onset asthma definition. Nevertheless, no study is entirely perfect and this study has weaknesses, many of which have been properly acknowledged by the authors. A further limitation relates to the fact that age at asthma onset is only one dimension of the disease heterogeneity. Indeed, both childhood-onset asthma and, certainly in a greater extent, adult- onset asthma bring together separate syndromes (including obesity-related asthma, occupational asthma, neutrophilic asthma, peri-menstrual asthma, severe and mild asthma,…). The intriguing observation of nearly 2·5-times more adult-onset than childhood-onset cases in the UK Biobank data might partly be related to a recall bias of remittent early-onset asthma (part of the subjects with mild childhood-onset asthma that remits could have been included in controls), which would lead to a more homogeneous moderate-to-severe/persistent asthma among childhood compared to adult-onset asthma. Under the reasonable hypothesis that different asthma phenotypes partly reflect different endotypes and etiologies, as recently illustrated by a genome-wide association study for moderate-to-severe asthma, 6 considering a highly heterogeneous phenotype likely leads to a “dilution effect” of the risk factors. Therefore, the possible stronger phenotypic heterogeneity among adult-onset vs. childhood asthma could have partly biased the results, by contributing to show a greater genetic contribution in childhood vs. adult-onset asthma.
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Update on asthma and cleaners.

Update on asthma and cleaners.

The proceedings of the Third Jack Pepys Workshop on Asthma in the Workplace [2] recognised a role of irritant exposures in asthma among cleaners. The relevance of accidental exposures was also noted, hypothesising that some cleaners may have had an initial accidental exposure and following that may have work-exacerbated asthma. A recent review of agents that can cause occupational asthma [3] included several cleaning agents, mostly disinfectants. Although the issue of multiple exposures in cleaning workers was stressed, the main focus was put on sensitising properties of cleaning agents and hence on asthma with a latency period. Nevertheless, it was recognised that many cleaning agents are respiratory irritants and could interact with sensitisers in the development of occupational asthma. Overall, authors considered that not much was known about the risk factors, exposure levels, clinical features, and pathogenetic mechanisms of asthma related to cleaning agents. A review focusing on mechanisms in occupational asthma considered only one form of irritant-induced occupational asthma: that without a latency period after acute exposures to high concentrations [4]. Cleaning agents associated with occupational asthma were classified as low molecular weight agents, inducing asthma following a non-IgE mediated mechanism.
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Cleaning and asthma characteristics in women.

Cleaning and asthma characteristics in women.

15 agents in general (including some cleaning or disinfecting products), non-eosinophilic asthma predominated [Anees et al. 2002], and eosinophilia was lower than in workers with occupational asthma caused by high molecular weight agents [Talini et al. 2011]. In a study of asthma-related biological characteristics in cleaning workers, eosinophilic inflammation (evaluated using the fraction of exhaled nitric oxide) did not appear to play a major role [Vizcaya et al. 2013]. Overall, these results are in line with our findings regarding eosinophils. The role of neutrophilic inflammation in asthma is less well-known, but could be related to irritant exposures [Wenzel 2006]. In addition, non allergic mechanisms have been suggested for neutrophilic asthma [Nadif et al. 2009]. Larger studies, with precise phenotypic characterization, are needed to further understand asthma related to cleaning products.
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Influence of Childhood Asthma and Allergies on Occupational Exposure in Early Adulthood: A Prospective Cohort Study

Influence of Childhood Asthma and Allergies on Occupational Exposure in Early Adulthood: A Prospective Cohort Study

questionnaires at ages 6–7 and 12 years, based on parental reports of episode(s) of asthma, hay fever or eczema in the past 12 months. The 18-year follow-up survey collected information on current job (“if you are currently working, what is your current job?”), which was coded according to the International Standard Classification of Occupations 1988. Occupational exposures were evaluated using the updated version of the occupational asthma specific job-exposure matrix (OAsJEM) [ 4 ]. This method has been described in detail elsewhere. Briefly, the OAsJEM assessments are based on consensus from a working group of international experts, using a standardized procedure. OAsJEM classified exposures to 30 asthmagens/irritants, into three categories: “high” (high probability of exposure and moderate-to-high intensity), “medium” (low-to-moderate probability or low intensity) and “unexposed”. Medium or high exposure to at least one of the 30 asthmagens/irritants was considered in the analyses. The reference group included participants who did not work or worked in jobs without exposure. We examined the association of history of asthma/allergies in childhood with occupational exposures in early adulthood, using logistic regression adjusting for age, sex and parental education. Analyses were conducted among participants with information on asthma/allergies during childhood (n = 499) who completed the 18-year follow-up survey (n = 369). After excluding six participants with imprecise job descriptions, the analytic sample included 363 participants (51% male).
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Clinically relevant subgroups in COPD and asthma.

Clinically relevant subgroups in COPD and asthma.

The constancy of asthma phenotypes over time, or after therapy implementation, is not as clear in COPD. Asthma is variable, thus phenotypes ought to change over time, but few published data exist. Those that appear to remain constant are occupational asthma and ASA. Occupational asthma progresses faster if exposure continues [124], implying that the underlying disease process is unchanged. The risk of precipitating severe exacerbations means that testing whether patients remain aspirin sensitive long-term has rarely been performed. Case reports demonstrate that aspirin sensitivity can develop in patients who have previously taken it without respiratory problems [168], but studies which have challenged known ASA patients have shown that most remain sensitive [169, 170]. Asthma subgroups that clearly change with treatment include ABPA, SAFS and Churg –Strauss syndrome. Atopy and allergy may also remit, usually over time but occasionally with treatment, such as desensitisation [171]. For example, 21% of children aged <2 years with severe peanut allergy will be tolerant by 5 years of age [172]. Remission of asthma was equally common in allergic/atopic and nonatopic patients in a large prospective cohort study of childhood-onset asthma, averaging 65% of patients [173]. Even in adults, allergic responses vary over time, as demonstrated by the fact that 39% of patients have different results on serial skin-prick testing (mostly gaining new allergies), but in 13% of cases allergies were lost and in 4% allergies were gained and lost [174].
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Do young adults with childhood asthma avoid occupational exposures at first hire?

Do young adults with childhood asthma avoid occupational exposures at first hire?

was shown in our study. We did not evidence gender differences in selection (in agreement with the study of Olivieri et al. [6]), nor difference between smokers and non-smokers. Work-related asthma has an important individual socioeconomic impact [31, 32], that might be reduced by health-based selection in the early period of the working life, but career choices also depend on socioeconomic conditions. Selection might have arisen from a personal choice, an advice from a physician or another person, or from the employer’s choice. However, no health-based pre-employment selection policy exists in France. Very few asthmatics declared to have received advice regarding job choice, and this advice concerned very specific occupational fields. Considering public health surveillance, this study raises the importance of taking into account this selection bias in studies of occupational asthma. Further research is needed to better understand how current estimates of the effect of specific exposures on respiratory health may be affected by the healthy worker effect.
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Do chronic workplace irritant exposures cause asthma?

Do chronic workplace irritant exposures cause asthma?

Other work environments with high likelihood of irritant exposures IIA is also likely to occur among workers in the metal industry. While there is substantial evidence of a higher risk of occupational asthma associated with work in the aluminium production, and in particular with fluorides and dust exposure, no specific immunologic mechanism has been shown 39 . An effect of chronic, moderate level exposures is suggested especially because episodes of accidental peak exposure are unlikely in the aluminium industry 39 . In a longitudinal study of Norwegian smelters, Soyseth et al. found associations between dust exposure, mostly composed of nonspecific airway irritants, and the incidence of work-related asthma symptoms as well as an increased decline in pulmonary function 40,41 . However, it remains difficult to distinguish occupational asthma from work exacerbated asthma symptoms or occupational COPD among smelters 39,41 . In a recent longitudinal study in Northern Europe (RHINE), incidence of asthma and rhinitis were associated with welding 42 . Welding fumes also contain irritants, and non-specific irritating mechanisms may partly explain associations with asthma or rhinitis.
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Occupational exposure to disinfectants and asthma control in US nurses

Occupational exposure to disinfectants and asthma control in US nurses

combinations of exposures associated with greater risk of poor asthma control. We found particularly increased risk among nurses with exposure to aldehydes (formaldehyde or glutaraldehyde), hypochlorite bleach or hydrogen peroxide, and enzymatic cleaners, based on JTEM estimates. Formaldehyde has been known as an asthmagen for long [31]. Glutaraldehyde and hydrogen peroxide also have been suggested as agents implicated in occupational asthma among healthcare workers in a smaller study in Canada [32] or case reports in France and in the U.S. [33, 34]. Associations between the use of hypochlorite bleach and asthma outcomes have been reported in European studies [11]. Enzymatic products are used to clean items before high level disinfection or sterilization. A role of enzymatic cleaners in asthma among healthcare workers was suspected based on case reports in healthcare settings [35], and earlier reports in the detergent industry [36] in the U.K. We believe this is the first time these agents have been implicated in an epidemiological study. Finally, a strong association between exposure to quats and physician-diagnosed asthma has been reported in a study of 543 French healthcare workers [12], in contrast with our results. Exposure to quats is particularly difficult to evaluate [21]. In our study, although we integrated information collected on products’ brand names and review of the corresponding safety date sheets, as recommended [12], when creating the JTEM, exposure to quats may still be under-estimated. However, any trend for an association between exposure to quats and poor asthma control disappeared after controlling for exposure to other products.
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COVID-19 and biologics in severe asthma: data from the Belgian Severe Asthma Registry.

COVID-19 and biologics in severe asthma: data from the Belgian Severe Asthma Registry.

COVID-19 related death [11], but in our cohort none of the 58 patients treated with maintenance OCS (median prednisone dose of 5 mg) were diagnosed with COVID-19. To the best of our knowledge, this study is among the first to investigate the risk and severity of COVID-19 in a large cohort of well-characterised patients with severe asthma. The findings indicated a low incidence of COVID-19 infection in severe asthma patients (14 out of 676 patients; 2.1%). Nevertheless, it is difficult to compare the incidence rate of confirmed COVID-19 cases in our BSAR cohort to the figure in the general population. Analysis of blood samples from Belgian blood donors revealed a seroprevalence reaching up to 5.1% [15]. Our study showed that only 2.1% of patients with severe asthma in Belgium had positive PCR or specific IgG to SARS-CoV-2 and that only 5% presented COVID-19-related symptoms. Whether this relatively low incidence is due to those with severe asthma being more cautious than the general population and complying better with social distancing and other hygienic measures, or whether it is due to (patho) physiological features (type 2 inflammation) or beneficial effects of treatments such as ICS (the latter factors being associated with lower angiotensin-converting enzyme 2 expression) [16] remains to be elucidated. Whereas viral respiratory tract infections are the most important cause of asthma exacerbations, none of the patients with confirmed COVID-19 in our BSAR cohort experienced an exacerbation. This is in line with the recent publication by B EURNIER et al. [1] reporting that, among hospitalised patients with severe pneumonia due to SARS-CoV-2 infection, patients with asthma were not overrepresented and did not present with an asthma exacerbation. The national restrictions with regard to PCR testing and the resulting possible underestimation of the true incidence of COVID-19 are a limitation of our study. Also, the participation in the survey of severe asthma patients already participating in a registry might have created some selection bias, limiting the generalisability of our data. On the other hand, the careful characterisation of the patients in our cohort is a strength of this research.
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Asthma rescue treatments, time to reboot

Asthma rescue treatments, time to reboot

L’archive ouverte pluridisciplinaire HAL, est destinée au dépôt et à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d’enseignemen[r]

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Impact of asthma education and/or specialized asthma care on subsequent morbidity in asthmatic children

Impact of asthma education and/or specialized asthma care on subsequent morbidity in asthmatic children

27 1.7 Emergency department-based interventions to prevent subsequent emergency department visits GINA asthma guidelines recommend prompt medical appointment following ED discharge and addressing strategies to improve asthma management, including medications, inhalation skills and a written action plan. 10 Following an ED visit, the 2010 Canadian Asthma Guidelines for 6 year old and older also recommend prompt review of maintenance therapy and addressing the factors that resulted in poor asthma control. 178 Whereas patients should be recommended a medical follow-up at least with their general practitioners for education and management, it is still not clear who should be referred to the AEC, a specialized clinic or both. Indeed, specific criteria for referral to asthma education and/or specialist care following an ED visit are inconsistently mentioned, let alone harmonized, across guidelines. GINA guidelines recommend targeting patients discharged from the emergency department or a hospital admission to an asthma education program, 10 while Canadian guidelines, although they recommend asthma education for all affected patients, do not include any criteria for referral to the AEC for preschoolers 6 or for children aged 6 years and older. 9,178 GINA 10 and Canadian guidelines (for preschoolers 6 and children aged 6 years and older 9,178 ) recommend referral to specialist care when there is failure to achieve proper control (i.e., asthma exacerbations) despite good adherence to controller medications. Additionally, Canadian guidelines have issued specific recommendation for when preschoolers should to be oriented towards specialist care. Indeed, the 2015 Canadian guidelines for preschoolers recommend that in children aged less than 6 years, an specialist referral should be considered if there is diagnostic uncertainty, repeated (≥2) exacerbations requiring rescue oral corticosteroids or hospitalization or frequent symptoms (≥8 days/month) despite moderate (200 µg to 250 µg) daily doses of inhaled corticosteroids, a life-threatening event (e.g., an admission to the intensive care unit), need for allergy testing or other considerations. 6 Otherwise, in pediatrics, referral to AEC, SAC or both services are based on the perception of needs of the emergency physician or on the institution-specific clinical protocols.
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HLA and asthma in the Consortium on Asthma among African-ancestry Populations in the Americas (CAAPA)

HLA and asthma in the Consortium on Asthma among African-ancestry Populations in the Americas (CAAPA)

We identified for the first time an HLA allele associated with asthma severity amongst African Americans. Our report emphasizes that by leveraging powerful computational methods, specific/extreme phenotypes, and population diversity, we can explore HLA gene polymorphisms in depth and reveal the full extent of complex disease associations.

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Using Smart Offices to Predict Occupational Stress

Using Smart Offices to Predict Occupational Stress

Physiology A B S T R A C T Occupational stress is increasingly present in our society. Usually, it is detected too late, resulting in physical and mental health problems for the worker, as well as economic losses for the companies due to the consequent absenteeism, presenteeism, reduced motivation or staff turnover. Therefore, the development of early stress detection systems that allow individuals to take timely action and prevent irreversible damage is required. To address this need, we investigate a method to analyze changes in physiological and behavioral patterns using unobtrusively and ubiquitously gathered smart office data. The goal of this paper is to build models that predict self-assessed stress and mental workload scores, as well as models that predict workload conditions based on physiological and behavior data. Regression models were built for the prediction of the self-reported stress and mental workload scores from data based on real office work settings. Similarly, classification models were employed to detect workload conditions and change in these conditions. Specific algorithms to deal with class-imbalance (SMOTEBoost and RUSBoost) were also tested. Results confirm the predictability of behavioral changes for stress and mental workload levels, as well as for change in workload conditions. Results also suggest that computer-use patterns together with body posture and movements are the best predictors for this purpose. Moreover, the importance of self-reported scores' standardization and the suitability of the NASA Task Load Index test for workload assessment is noticed. This work contributes significantly towards the development of an unobtrusive and ubiquitous early stress detection system in smart office environments, whose implementation in the industrial environment would make a great beneficial impact on workers’ health status and on the economy of com-panies.
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Dupuytren's disease: personal factors and occupational exposure.

Dupuytren's disease: personal factors and occupational exposure.

Unité 687 Santé publique et épidémiologie des déterminants professionnels et sociaux de la santé Hôpital National de Saint-Maurice 14 rue du Val d’Osne 94415 SAINT MAURICE CEDEX 01 45 1[r]

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Using Smart Offices to Predict Occupational Stress

Using Smart Offices to Predict Occupational Stress

Physiology A B S T R A C T Occupational stress is increasingly present in our society. Usually, it is detected too late, resulting in physical and mental health problems for the worker, as well as economic losses for the companies due to the consequent absenteeism, presenteeism, reduced motivation or staff turnover. Therefore, the development of early stress detection systems that allow individuals to take timely action and prevent irreversible damage is required. To address this need, we investigate a method to analyze changes in physiological and behavioral patterns using unobtrusively and ubiquitously gathered smart office data. The goal of this paper is to build models that predict self-assessed stress and mental workload scores, as well as models that predict workload conditions based on physiological and behavior data. Regression models were built for the prediction of the self-reported stress and mental workload scores from data based on real office work settings. Similarly, classification models were employed to detect workload conditions and change in these conditions. Specific algorithms to deal with class-imbalance (SMOTEBoost and RUSBoost) were also tested. Results confirm the predictability of behavioral changes for stress and mental workload levels, as well as for change in workload conditions. Results also suggest that computer-use patterns together with body posture and movements are the best predictors for this purpose. Moreover, the importance of self-reported scores' standardization and the suitability of the NASA Task Load Index test for workload assessment is noticed. This work contributes significantly towards the development of an unobtrusive and ubiquitous early stress detection system in smart office environments, whose implementation in the industrial environment would make a great beneficial impact on workers’ health status and on the economy of com-panies.
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Air pollution and asthma control in the Epidemiological study on the Genetics and Environment of Asthma.

Air pollution and asthma control in the Epidemiological study on the Genetics and Environment of Asthma.

All the associations are first reported crude and then followed by the multivariate analysis, for each pollutant separately. Variables taken into account in the multivariate analysis were those known to be associated with asthma control in EGEA 14 (on-line supplement) [ ] and another European cohort (ECRHS) 12 . In order to address the independent effect of each pollutant on asthma control, a two-pollutant [ ] model was performed, including O 3-sum and PM 10 . Finally, analyses were also conducted on the three domains of asthma control (lung function, symptoms, exacerbations), (on-line supplement). The lack of data on activity limitation in our study did not allow including this domain in the asthma control classification. Analyses were performed with Stata 9.
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Does urban asthma exist? How climatic changes and urban air pollution intervene on asthma and respiratory allergy

Does urban asthma exist? How climatic changes and urban air pollution intervene on asthma and respiratory allergy

However, air pollution is not the only culprit for asthma and allergies in individuals living in the cities. Other urban factors associated with asthma include: passive smoking, high exposure to cock- roaches or other pests, damp, indoor air pollution, poor ventilation, inadequate heating or faulty air conditioning, air-borne viral infections, overcrowd- ing, stress and violence as well as, for low social classes of some countries, inadequate access to health care. These “stressors” have been identified thanks to epidemiological investigations among which the study of inner-city asthma in the USA showing that children living in inner cities suffered more from asthma and related diseases than other children from the same city. These other factors are essential to explain why worldwide the geographi- cal distributions of air pollution and asthma and al- lergies do not match with the lowest prevalence of asthma in megalopolis of developing countries where the level of air pollution is very high and the highest prevalence in English-speaking countries, like Australia, New Zealand or UK, in spite of the fact that the levels of air pollution are not exagger- ated there (Figure 1). Indeed, asthma is a multifac- torial condition caused by several environmental and genetic factors. These factors influence the de-
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