Research report in partial fulfillment for the degree of MMed (Occupational Medicine) / Background Occupational asthma is one of the most commonly reported occupational respiratory diseases in industrialized countries. Literature suggests that about 15% of all adult-onset asthma is caused by workplace exposures. It is potentially preventable and the prognosis is good with early diagnosis and adequate treatment. However, occupational asthma is under-diagnosed and under-reported. Identification of common causative agents and employment of preventative measures are necessary for proper management and control. Objectives 1. To characterize occupational asthma cases assessed at NIOH Occupational Medicine Clinic from 1st January 1997 to 31st December 2007 in terms of: • types of industries, occupations and agents • duration of exposure prior to onset of occupational asthma • time from onset of symptoms to diagnosis • nature of exposure e.g. intermittent, daily, etc. 2. To investigate factors influencing latency period in cases of sensitizer-induced asthma 3. To investigate factors influencing lag time to diagnosis in cases of sensitizer-induced asthma Methods A record review of a series of cases of occupational asthma was done. All cases of occupational asthma diagnosed from 1st January 1997 to 31st December 2007 by NIOH doctors were identified from the Clinic’s electronic database. All the records of patients who had a final diagnosis of occupational asthma were assessed using a standard data capture sheet. Doubtful cases were presented at the NIOH Occupational Medicine clinical discussion meeting for a consensus decision as to whether they qualified to be included in the study or not. Ethical approval was granted by the University of the Witwatersrand Human Research Ethics Committee (Medical). vi Results One hundred and forty two cases of occupational asthma were identified. Of these, 131 were sensitizer-induced and 11 were irritant-induced asthma. Low molecular-weight agents were in the majority with isocyanates, welding fumes, vanadium being the most common. Within the high molecular weight category, wheat was the most common. The majority of cases emanated from the Engineering, Chemical, Smelter and Food industries. Latency period from first exposure to development of symptoms was surprisingly long: a mean of 9.8 years and a median of seven years. The time from onset of symptoms to diagnosis was also long (mean of 4.9 years and median of three years). Younger cases had a shorter latency period and a longer delay in diagnosis. Agents and jobs for irritant-induced asthma cases varied widely and some came from unexpected industries. Discussion This review of asthma referrals to the NIOH Occupational Medicine Clinic has highlighted causative industries and identified exposure agents implicated in cases of occupational asthma. The very wide range of industries, occupations and agents associated with these cases is suggestive of a wide-spread occupational asthma problem in the region referring cases to the Clinic. The long latency period and delay in diagnosis are of concern since prompt diagnosis and removal from exposure is associated with a better prognosis. Irritant-induced asthma is infrequently reported in the local literature, but the range of agents and jobs is possibly indicative of under-diagnosis. Conclusion Occupational asthma is potentially preventable. New cases still arise particularly in poorly controlled workplaces which are capable of employing basic measures to control exposures. Medical surveillance, prompt diagnosis, proper medical management and application of workplace preventative measures are essential in decreasing the burden of disease and impairment

PhD, Faculty of Health Sciences, University of the Witwatersrand / Background: Dental procedures associated with dental unit waterlines (DUWLs) in dental health care settings generate aerosolised droplets that have the potential to cause adverse health effects in exposed workers. Aim: The aim of this study was to evaluate the risk of work-related asthma associated with endotoxin exposure in dental health care workers. Materials and methods: The study population included dental personnel (n = 454) from 5 academic dental institutions in South Africa. Personal air samples (n = 413) in various dental jobs as well as airborne area and water samples from dental handpieces and basin taps were collected. A self-administered modified European Community Respiratory Health Survey questionnaire was used to obtain information on respiratory symptoms and the occupational history. Serum samples were collected to determine atopic status, specific IgE to composite latex (k82) extract and 8 recombinant latex proteins, myeloperoxidase (MPO), eosinophilic cationic protein (ECP), inflammatory cytokines, and endotoxin levels. Spirometry including pre- and post-bronchodilator testing was conducted according to ATS/ERS guidelines. Multivariate linear and logistic regression and factor analysis was used in the data analysis. Results: Airborne endotoxin levels were variable across departments with administration having the lowest and laboratories the highest mean exposures (geometric mean: 2.38 versus 5.63 EU/m3). Job status as a student (compared to staff member) and dental unit characteristics (age, model type, number of units) were important predictors of airborne endotoxin. The most common asthma phenotypes were atopic asthma (6.9%), non-atopic asthma (5.9%) and work-aggravated asthma (4%). Four inflammatory groups related to eosinophilic versus neutrophilic inflammation and chronicity of the response were identified. Acute neutrophilic response was associated with work-related chest symptoms (OR = 4.99, 95% CI: 1.32 - 18.92). Cumulative endotoxin exposures (>51.12 EU/m3-year) was an important predictor of work-related ocular-nasal symptoms (OR = 3.82, 95% CI: 1.01 – 14.41) in non-atopic workers. Borderline significant associations were also observed between current airborne endotoxin concentrations (>5.83 EU/m3) and asthma-related symptoms (OR = 2.24, 95% CI: 0.97 – 5.17) as well as suboptimal lung function (FEV1<80% predicted) (OR = 8.02, 95% CI: 0.94 – 68.35) in non-atopic workers. Dental workers using latex gloves and concurrently exposed to low-grade (> 5.83 EU/m3) elevated endotoxin levels were at increased risk (OR = 2.59, 95% CI: 1.20 – 5.60) of presenting with latex sensitisation. Conclusion: This study demonstrated that endotoxin exposures from DUWLs play an important role in the manifestation of non-atopic asthma through the neutrophilic-response mechanism. Neutrophilic inflammatory cell asthma phenotypes coexist with eosinophilic inflammatory cell asthma phenotypes in this group of workers. Furthermore, low-grade elevated endotoxin levels increase the risk of sensitisation to latex among dental workers using latex gloves. This is the first study to demonstrate airway effects associated with low-grade elevated endotoxin exposures in dental settings.

The thesis gives examples of analysing time series data while being employed as statistician at the Industrial and Community Health Research Centre, North Staffordshire Medical Institute, Hartshill Road, Stoke-on-Trent for the period 1988-1997. Topics include:(a) the analysis of asthma data with a view to aid detection and confirmation of occupational asthma. This project highlights possible approaches for modelling regularly and unequally spaced observations (b) modelling bleeding and behavioural patterns of handicapped people using binary valued time series (c) a repeated measures analysis following a surgical intervention (d) a study relating mood scores to progesterone levels

Work-related asthma surveillance is needed to improve management of occupational exposures, clinical recognition/diagnosis, and worker compensation policies. This work investigated asthma in relation to work by evaluating the utility of existing Canadian surveillance data in providing useful information about the burden of work-related asthma; estimating the burden of work-related asthma among Canada's adult population; and evaluating the effect of job risk on asthma after considering other potential risk factors for asthma. The working population formed samples from two Statistics Canada surveillance programs: Canadian Community Health Survey (CCHS), 2002/03 Cycle 2.1 and National Population Health Survey (NPHS), Longitudinal Component (1994/95-2002/03). Both surveys enquired about health professional-diagnosed asthma; NPHS additionally asked age at time of diagnosis, so adult-onset versus childhood-onset asthma was determined. Both surveys enquired about current job held; corresponding job codes were linked to an asthma-specific job exposure matrix to judge job risk for occupational asthma. CCHS only provided current job information, in contrast, NPHS longitudinal data was used to determine job held at time of asthma-onset. Statistical measures for asthma in relation to job risk were estimated. CCHS results were likely biased by the healthy worker effect, as it showed the opposite effect of job risk on asthma than the NPHS; higher asthma prevalence was shown for NPHS men and women in high risk jobs. NPHS results indicated a large burden of adult-onset asthma among men (19,000) and childhood-onset asthma among women (17,000) attributed to working in high risk jobs for occupational asthma. Using NPHS, adjusted and crude prevalence odds ratio estimates were compared to further assess effect of job risk on asthma. For adult-onset asthma, there was no difference between estimates (men: 1.8, women: 1.1); for childhood-onset asthma, adjusted estimates were larger than crude, respectively (men: 1.3 v 1.2, women: 2.0 v 1.7). Age of asthma-onset and job held at time of asthma-onset is necessary surveillance information for estimating work-related asthma. There may be increased risk of work" caused" asthma among men and work "exacerbated" asthma among women in high risk jobs. Considering other risk factors for asthma did not reduce effect of job risk on asthma.

Work-related asthma surveillance is needed to improve management of occupational exposures, clinical recognition/diagnosis, and worker compensation policies. This work investigated asthma in relation to work by evaluating the utility of existing Canadian surveillance data in providing useful information about the burden of work-related asthma; estimating the burden of work-related asthma among Canada's adult population; and evaluating the effect of job risk on asthma after considering other potential risk factors for asthma. The working population formed samples from two Statistics Canada surveillance programs: Canadian Community Health Survey (CCHS), 2002/03 Cycle 2.1 and National Population Health Survey (NPHS), Longitudinal Component (1994/95-2002/03). Both surveys enquired about health professional-diagnosed asthma; NPHS additionally asked age at time of diagnosis, so adult-onset versus childhood-onset asthma was determined. Both surveys enquired about current job held; corresponding job codes were linked to an asthma-specific job exposure matrix to judge job risk for occupational asthma. CCHS only provided current job information, in contrast, NPHS longitudinal data was used to determine job held at time of asthma-onset. Statistical measures for asthma in relation to job risk were estimated. CCHS results were likely biased by the healthy worker effect, as it showed the opposite effect of job risk on asthma than the NPHS; higher asthma prevalence was shown for NPHS men and women in high risk jobs. NPHS results indicated a large burden of adult-onset asthma among men (19,000) and childhood-onset asthma among women (17,000) attributed to working in high risk jobs for occupational asthma. Using NPHS, adjusted and crude prevalence odds ratio estimates were compared to further assess effect of job risk on asthma. For adult-onset asthma, there was no difference between estimates (men: 1.8, women: 1.1); for childhood-onset asthma, adjusted estimates were larger than crude, respectively (men: 1.3 v 1.2, women: 2.0 v 1.7). Age of asthma-onset and job held at time of asthma-onset is necessary surveillance information for estimating work-related asthma. There may be increased risk of work" caused" asthma among men and work "exacerbated" asthma among women in high risk jobs. Considering other risk factors for asthma did not reduce effect of job risk on asthma.

Work-related asthma surveillance is needed to improve management of occupational exposures, clinical recognition/diagnosis, and worker compensation policies. This work investigated asthma in relation to work by evaluating the utility of existing Canadian surveillance data in providing useful information about the burden of work-related asthma; estimating the burden of work-related asthma among Canada's adult population; and evaluating the effect of job risk on asthma after considering other potential risk factors for asthma. The working population formed samples from two Statistics Canada surveillance programs: Canadian Community Health Survey (CCHS), 2002/03 Cycle 2.1 and National Population Health Survey (NPHS), Longitudinal Component (1994/95-2002/03). Both surveys enquired about health professional-diagnosed asthma; NPHS additionally asked age at time of diagnosis, so adult-onset versus childhood-onset asthma was determined. Both surveys enquired about current job held; corresponding job codes were linked to an asthma-specific job exposure matrix to judge job risk for occupational asthma. CCHS only provided current job information, in contrast, NPHS longitudinal data was used to determine job held at time of asthma-onset. Statistical measures for asthma in relation to job risk were estimated. CCHS results were likely biased by the healthy worker effect, as it showed the opposite effect of job risk on asthma than the NPHS; higher asthma prevalence was shown for NPHS men and women in high risk jobs. NPHS results indicated a large burden of adult-onset asthma among men (19,000) and childhood-onset asthma among women (17,000) attributed to working in high risk jobs for occupational asthma. Using NPHS, adjusted and crude prevalence odds ratio estimates were compared to further assess effect of job risk on asthma. For adult-onset asthma, there was no difference between estimates (men: 1.8, women: 1.1); for childhood-onset asthma, adjusted estimates were larger than crude, respectively (men: 1.3 v 1.2, women: 2.0 v 1.7). Age of asthma-onset and job held at time of asthma-onset is necessary surveillance information for estimating work-related asthma. There may be increased risk of work" caused" asthma among men and work "exacerbated" asthma among women in high risk jobs. Considering other risk factors for asthma did not reduce effect of job risk on asthma. / Medicine, Faculty of / Population and Public Health (SPPH), School of / Graduate

L'asthme professionnel (AP) est la maladie respiratoire d'origine professionnelle la plus fréquente dans les pays industrialisés. Il s'agit d'une pathologie complexe dite « multifactorielle » mettant en jeu un grand nombre de facteurs de risques génétiques, constitutionnels, comportementaux et environnementaux. Sur le plan génétique, l'asthme professionnel représente un bon modèle pour l'étude de l'asthme chez l'adulte et les mécanismes d'interactions gène-gène-environnement masquant ou modulant l'effet de la génétique restent encore à élucider. Aucune étude épidémiologique sur l'asthme professionnel n'a examiné le rôle des facteurs génétiques à un stade très précoce de l'exposition aux allergènes et aux irritants aéroportés. Nous avons donc cherché dans un premier temps à évaluer le rôle de certains polymorphismes génétiques en rapport avec l'inflammation et l'allergie, à savoir les IL4RA, IL13, TNFa, IL1A et IL5, sur le déclin de la fonction pulmonaire, l'apparition d'une obstruction ou d'une hyperréactivité bronchiques et l'évolution du monoxyde d'azote exhalé (FeNO) chez 441 apprentis boulangers/pâtissiers et coiffeurs (étude MIBAP). Dans cette première partie nous observons des interactions entre IL13 R130Q/IL4RA S478P et IL13 R130Q//IL4RA Q551R et la diminution du volume expiratoire forcé ou de la capacité vitale forcée. Le génotype GG du TNFA-G308A a été trouvé associé à l'hyperréactivité bronchique dans l'ensemble de la population et chez les sujets non atopiques ; nous avons aussi observé que certaines interactions gène-gène étaient associées à une modification du FeNO au cours des deux années d'apprentissage. Dans un deuxième temps, des déterminants nutritionnels de l'asthme ont été explorés dans une population de jeunes travailleurs engagés dans ces métiers à risque depuis 3 à 10 ans (étude ABCD). Les apports en vitamines, principalement les vitamines A, C, E D, et en acides gras polyinsaturés omégas 3 et 6 ont été étudiés par questionnaire de fréquence, le diagnostic d'asthme professionnel étant réalisé au moyen d'une batterie d'outils (examen clinique, spirométrie et test de réversibilité d'une obstruction bronchique, mesure du FeNO et examen des taux sériques d'IgE spécifiques). Les résultats portant sur 31 cas d'asthme professionnel et 196 témoins montrent une différence en fonction de la filière : chez les boulangers-pâtissiers, aucun facteur nutritionnel n'est objectivé, contrairement au groupe des coiffeuses chez qui les asthmatiques présentent des apports plus élevés des vitamines A et D. Un déficit en B12 semble être un facteur de risque de survenue d'asthme professionnel et ce indépendamment de la filière. En revanche, aucune corrélation n'est trouvée avec les taux sériques de l'homocystéine et la vitamine B9. A travers ces études au sein de ces jeunes populations à risque, il ressort que l'expression de certains facteurs de risque de l'asthme professionnel sont modulables en fonction du type d'exposition. Des comportements alimentaires à l'environnement de travail, l'émergence d'une maladie telle que l'asthme professionnel fait appel à des facteurs multiples dont la plupart peuvent être contrôlés et limités par des mesures de prévention efficaces / Occupational asthma (OA) is the occupational respiratory disease most common in industrialized countries. It is a multifactorial disease involving a large number of risk factors genetic, constitutional, behavioral and environmental. At the genetic level, occupational asthma is a good model for the study of adult asthma and the mechanisms of interaction gene-gene-environment masking or modulating effect of genetic remain to be elucidated. None epidemiological studies on occupational asthma have examined the role of genetic factors in a very early exposure to allergens and airborne irritants. We initially assess the role of genetic polymorphisms related to inflammation and allergy, namely IL4RA, IL13, TNF, IL1A and IL5, on the decline of lung function, bronchial hyperresponsiveness and increasing of exhaled nitric oxide (FeNO) in 441 apprentice bakers / pastry-makers and hairdressers (MIBAP study). In this first part we observed interactions between IL13 and IL13 R130Q R130Q/IL4RA S478P / / IL4RA Q551R and decreased forced expiratory volume or forced vital capacity. The GG genotype of TNFA-G308A was found associated with bronchial hyperreactivity in the general population and in non-atopic subjects, we also observed that some gene-gene interactions were associated with a change in the FeNO after two years of training. In a second time, nutritionals determinants of asthma were investigated in a population of young workers employed in these occupations at risk from 3 to 10 years (ABCD study). Intake of vitamins, especially vitamins A, C, E,D, and polyunsaturated fatty acids omega 3 and 6 were studied by frequency questionnaire, the diagnosis of occupational asthma is achieved through a battery of tools (review clinical spirometry and reversibility of bronchial obstruction, FeNO measurement and examination of serum specific IgE). The results on 31 cases of occupational asthma and 196 controls showed a difference in terms of the sector: among bakers, no nutritional factor is objectified, unlike the hairdresser's asthmatics that have higher intakes vitamins A and D. B12 deficiency appears to be a risk factor for onset of occupational asthma regardless of the sector. In contrast, no correlation was found with serum levels of homocysteine and vitamin B9. Through studies in these young people at risk, it appears that the expression of certain risk factors of occupational asthma is flexible, depending on the type of exposure. The emergence of a disease such as occupational asthma involves multiple factors, most of which can be controlled and limited by effective preventive measures

Please read the abstract in the section 00front of this document / Thesis (PhD (Medical Immunology))--University of Pretoria, 2008. / Immunology / unrestricted

L’asthme professionnel est une maladie fréquente, qui coûte cher, qui touche des travailleurs jeunes, dont le diagnostic est difficile et avec d’importantes conséquences socio-économiques. La prévention occupe une place centrale dans la gestion de l’asthme professionnel, d’un point de vue de santé publique. Ce mémoire de maîtrise présente trois articles rapportant des développements récents en matière de prévention de l’asthme professionnel. Tout d’abord, une revue de la littérature sur les agents sensibilisants de bas poids moléculaire dans l’asthme professionnel entre 2000 et 2010 recense 41 nouveaux agents et insiste sur l’importance de mettre à jour régulièrement les bases de données afin d’améliorer la prévention primaire. Ensuite, basé sur un cas clinique, la deuxième publication présente l’utilité potentielle du modèle d’analyse de risque QSAR (Quantitative Structure-Activity Relationship) dans le processus diagnostique de l’asthme professionnel, notamment lors d’une exposition multiple à des agents sensibilisants. Enfin, le troisième article présente la performance en milieu clinique du premier questionnaire de dépistage spécifique à l’asthme professionnel. Un modèle simple associant 8 items du questionnaire, l’âge des travailleurs et leur durée d’exposition professionnelle permet de discriminer 80% des 169 sujets adressés pour suspicion d’asthme professionnel. Un tel modèle pourrait être intégré dans les programmes de surveillance médicale qui constituent la base de la prévention secondaire. Ces trois publications insistent sur les possibilités d’explorer de nouveaux outils préventifs dans le domaine de l’asthme professionnel, outils qui ouvrent des perspectives de développements futurs dont les implications cliniques et socio-économiques peuvent être importantes. / Occupational asthma is a common disease, which affects young workers and is difficult to diagnose. It is a major financial burden and has important socioeconomic consequences. Prevention is central in the management of occupational asthma, in terms of public health. This thesis presents three articles reporting on recent developments in the prevention of occupational asthma. First, a review of the literature on sensitizing low-molecular- weight agents in occupational asthma between 2000 and 2010 reports 41 new agents and emphasizes the importance of regularly updating databases to improve primary prevention. Then, based on a clinical case, the second publication presents the potential utility of the model of risk analysis QSAR (Quantitative Structure-Activity Relationship) in the diagnostic workup for occupational asthma, especially in the case of multiple exposure to sensitizing agents. The third article presents the clinical performance of the first screening questionnaire specific to occupational asthma. A simple model consisting of 8 items of the questionnaire, age and exposure duration could discriminate 80% of the 169 subjects with and without OA in a clinical setting. Such a model could be integrated into medical surveillance programs, which are the basis of secondary prevention. These three publications emphasize the possibilities to explore new prevention tools in the field of occupational asthma, tools that provide opportunities for future developments, which could have major clinical and socio-economic implications.

INTRODUÇÃO: Há evidências consistentes a partir de estudos epidemiológicos de que os profissionais de limpeza têm um risco elevado de desenvolver asma. Os determinantes deste risco não são totalmente conhecidos. Esses trabalhadores estão expostos a agentes ocupacionais de baixo e alto peso molecular, tanto a agentes sensibilizantes, como a irritantes. É importante produzir evidências de que este risco está relacionado ao trabalho e não às condições sociais ou outros fatores concorrentes, conhecer a anormalidade patológica subjacente, e investigar os possíveis agentes. O acúmulo deste conhecimento permitirá a proposição de medidas para substituição ou controle do uso dos agentes envolvidos e prevenção da ocorrência de novos casos desnecessariamente. Além disso, o uso de novas técnicas não invasivas, como a citologia do escarro e A FeNO, poderá facilitar o diagnóstico precoce dos casos. Desta maneira, este estudo pretende avaliar se o ambiente de trabalho induz inflamação pulmonar em trabalhadores assintomáticos, antes da alteração das provas funcionais e a eficácia do escarro induzido e da FeNO NO como marcadores de inflamação pulmonar precoce entre trabalhadores de limpeza profissional não doméstica. MÉTODO: Os trabalhadores foram avaliados através da comparação da citologia do escarro, valores da FeNO, espirometria e PFE, realizados durante o período de trabalho e após as férias. A amostra foi caracterizada através do questionário de triagem do estudo de saúde respiratória da Comunidade Européia, questionário de sintomas respiratórios e a pontuação no ISAAC. RESULTADOS: Em nosso estudo, encontramos um aumento significativo dos valores do VEF1 após o período de férias, (pré 2,76 ± 0,57 e pós 2,94 ± 0,61; p < 0,05) apesar de estar dentro da normalidade, em ambos os períodos. A média das medidas do PFE também mostrou-se maior durante o período de férias em comparação ao período de trabalho, embora não estatisticamente significante (pré 366,6 ± 54,1 e pós 386,4 ± 62,9 e p > 0,05). Encontramos uma redução dos valores da medida da FeNO após as férias (pré 16,3 ± 9,7 e pós 13,8 ± 7,8 p < 0,05) e redução de eosinófilos (pré 0,019 ± 0,05 e pós 0,003 ± 0,01 p < 0,05), linfócitos (pré 0,16 ± 0,35 e pós 0,01 ± 0,09 p < 0,05) e macrófagos (pré 0,421 ± 0,47 e pós 0,235 ± 0,30 p < 0,05) na citologia do escarro induzido, realizada após o período de férias. CONCLUSÃO: Demonstramos que o ambiente ocupacional ao qual são expostos os trabalhadores de limpeza profissional não doméstica provoca inflamação nas vias aéreas de trabalhadores assintomáticos. Esta inflamação pode ser aferida por métodos não invasivos como escarro induzido e FeNo, antes do aparecimento de alterações nas provas funcionais, embora estes métodos ainda necessitem de padronização. São necessários novos estudos para quantificar a exposição ao cloro e sua relação com inflamação, assim como para padronizar o uso do escarro induzido e da FeNO no diagnóstico de doenças ocupacionais entre trabalhadores de limpeza, além de medidas preventivas e educativas nesta população / There is consistent evidence from epidemiological studies that the cleaning professionals have a high risk of developing asthma. The determinants of this risk are not fully known. These workers are exposed to occupational agents of low and high molecular weight, both the sensitizing agents, such as irritant. It is important to produce evidence that this risk is related to work and not social conditions or other competitive factors, know the underlying pathological abnormality, and investigate possible agents. The accumulation of this knowledge will allow proposing measures to replace or control the use of the agents involved and preventing the occurrence of new cases unnecessarily. In addition, the use of new non-invasive techniques, such as sputum cytology and the FeNO may facilitate early diagnosis of cases. Thus, this study aims to assess if the work environment induces lung inflammation in asymptomatic workers, before the change of functional tests and the effectiveness of induced sputum and exhaled NO as early lung inflammation markers between professional cleaning workers. METHOD: Workers were evaluated by comparing the sputum cytology, FeNO values, spirometry and PEF, made during the work period and after the holidays. The sample was characterized by screening questionnaire of respiratory health study of the European Community, questionnaire of respiratory symptoms and a score in ISAAC. RESULTS: In our study, we found a significant increase in FEV1 values after the vacational period, (pre 2.76 ± 0.57 and 2.94 ± 0.61; post; p < 0.05) despite of being within the normal range in both periods. The average peak flow measurements also was higher during the vacational period compared to the period of work, although not statistically significant (366.6 ± 54.1 pre and post 386.4 ± 62.9; p > 0.05). We found a reduction of the exhaled measured values of NO after the holidays (pre and post 16.3 ± 9.7, 13.8 ± 7.8; p < 0.05), reduction of eosinophils (pre and post 0.05 ± 0.019, 0.003 ± 0.01; p < 0.05), lymphocytes (pre and post 0.16 ± 0.35, 0.01 ± 0.09; p < 0.05) and macrophages (pre and post 0.421 ± 0.47 0.235 ± 0 30 p < 0.05) in induced sputum cytology, performed after the holiday period. CONCLUSION: We demonstrate that the occupational environment to which professional cleaning non-domestic workers are exposed causes inflammation in the airways of asymptomatic workers. This inflammation can be measured by non-invasive methods such as induced sputum and FeNo, before the onset of changes in functional tests, although these methods still require standardization. Further studies are needed to quantify the exposure to chlorine and its relation to inflammation, as well as to standardize the use of induced sputum and exhaled nitric oxide in the diagnosis of occupational diseases among cleaning workers, and preventive and educational measures in this population