49 research outputs found
Early incidence of occupational asthma among young bakers, pastry-makers and hairdressers: design of a retrospective cohort study
<p>Abstract</p> <p>Background</p> <p>Occupational exposures are thought to be responsible for 10-15% of new-onset asthma cases in adults, with disparities across sectors. Because most of the data are derived from registries and cross-sectional studies, little is known about incidence of occupational asthma (OA) during the first years after inception of exposure. This paper describes the design of a study that focuses on this early asthma onset period among young workers in the bakery, pastry making and hairdressing sectors in order to assess early incidence of OA in these "at risk" occupations according to exposure duration, and to identify risk factors of OA incidence.</p> <p>Methods/Design</p> <p>The study population is composed of subjects who graduated between 2001 and 2006 in these sectors where they experience exposure to organic or inorganic allergenic or irritant compounds (with an objective of 150 subjects by year) and 250 young workers with no specific occupational exposure. A phone interview focusing on respiratory and 'Ear-Nose-Throat' (ENT) work-related symptoms screen subjects considered as "possibly OA cases". Subjects are invited to participate in a medical visit to complete clinical and lung function investigations, including fractional exhaled nitric oxide (FE<sub>NO</sub>) and carbon monoxide (CO) measurements, and to collect blood samples for IgE (Immunoglobulin E) measurements (total IgE and IgE for work-related and common allergens). Markers of oxidative stress and genetic polymorphisms exploration are also assessed. A random sample of 200 "non-cases" (controls) is also visited, following a nested case-control design.</p> <p>Discussion</p> <p>This study may allow to describ a latent period between inception of exposure and the rise of the prevalence of asthma symptoms, an information that would be useful for the prevention of OA. Such a time frame would be suited for conducting screening campaigns of this emergent asthma at a stage when occupational hygiene measures and adapted therapeutic interventions might be effective.</p> <p>Trial registration</p> <p>Clinical trial registration number is NCT01096537.</p
EAACI position paper on occupational rhinitis
The present document is the result of a consensus reached by a panel of experts from European and non-European countries on Occupational Rhinitis (OR), a disease of emerging relevance which has received little attention in comparison to occupational asthma. The document covers the main items of OR including epidemiology, diagnosis, management, socio-economic impact, preventive strategies and medicolegal issues. An operational definition and classification of OR tailored on that of occupational asthma, as well as a diagnostic algorithm based on steps allowing for different levels of diagnostic evidence are proposed. The needs for future research are pointed out. Key messages are issued for each item
Computerized respiratory sounds can differentiate smokers and non-smokers
Cigarette smoking is often associated with the development of several respiratory diseases however, if diagnosed early, the changes in the lung tissue caused by smoking may be reversible. Computerised respiratory sounds have shown to be sensitive to detect changes within the lung tissue before any other measure, however it is unknown if it is able to detect changes in the lungs of healthy smokers. This study investigated the differences between computerised respiratory sounds of healthy smokers and non-smokers. Healthy smokers and non-smokers were recruited from a university campus. Respiratory sounds were recorded simultaneously at 6 chest locations (right and left anterior, lateral and posterior) using air-coupled electret microphones. Airflow (1.0–1.5 l/s) was recorded with a pneumotachograph. Breathing phases were detected using airflow signals and respiratory sounds with validated algorithms. Forty-four participants were enrolled: 18 smokers (mean age 26.2, SD = 7 years; mean FEV1 % predicted 104.7, SD = 9) and 26 non-smokers (mean age 25.9, SD = 3.7 years; mean FEV1 % predicted 96.8, SD = 20.2). Smokers presented significantly higher frequency at maximum sound intensity during inspiration [(M = 117, SD = 16.2 Hz vs. M = 106.4, SD = 21.6 Hz; t(43) = −2.62, p = 0.0081, d z = 0.55)], lower expiratory sound intensities (maximum intensity: [(M = 48.2, SD = 3.8 dB vs. M = 50.9, SD = 3.2 dB; t(43) = 2.68, p = 0.001, d z = −0.78)]; mean intensity: [(M = 31.2, SD = 3.6 dB vs. M = 33.7,SD = 3 dB; t(43) = 2.42, p = 0.001, d z = 0.75)] and higher number of inspiratory crackles (median [interquartile range] 2.2 [1.7–3.7] vs. 1.5 [1.2–2.2], p = 0.081, U = 110, r = −0.41) than non-smokers. Significant differences between computerised respiratory sounds of smokers and non-smokers have been found. Changes in respiratory sounds are often the earliest sign of disease. Thus, computerised respiratory sounds might be a promising measure to early detect smoking related respiratory diseases
Methyl methacrylate and respiratory sensitization: A Critical review
Methyl methacrylate (MMA) is a respiratory irritant and dermal sensitizer that has been associated with occupational asthma in a small number of case reports. Those reports have raised concern that it might be a respiratory sensitizer. To better understand that possibility, we reviewed the in silico, in chemico, in vitro, and in vivo toxicology literature, and also epidemiologic and occupational medicine reports related to the respiratory effects of MMA. Numerous in silico and in chemico studies indicate that MMA is unlikely to be a respiratory sensitizer. The few in vitro studies suggest that MMA has generally weak effects. In vivo studies have documented contact skin sensitization, nonspecific cytotoxicity, and weakly positive responses on local lymph node assay; guinea pig and mouse inhalation sensitization tests have not been performed. Cohort and cross-sectional worker studies reported irritation of eyes, nose, and upper respiratory tract associated with short-term peaks exposures, but little evidence for respiratory sensitization or asthma. Nineteen case reports described asthma, laryngitis, or hypersensitivity pneumonitis in MMA-exposed workers; however, exposures were either not well described or involved mixtures containing more reactive respiratory sensitizers and irritants.The weight of evidence, both experimental and observational, argues that MMA is not a respiratory sensitizer
Original waveform of lung sound crackles: a case study of the effect of high-pass filtration
The Influence of “Sputum-Like Gel” Viscosity on Crackle Characteristics in a Mechanically Ventilated Porcine Lung Model
Can serial PEF measurements separate occupational asthma from allergic alveolitis?
BACKGROUND
Occupational asthma commonly results in work-related changes in serial peak expiratory flow (PEF) measurements. Whether alveolitis can result in similar changes is unknown.
AIMS
To identify differences and similarities of serial PEF between workers with occupational alveolitis and asthma seen during an outbreak investigation in a factory with metal-working fluid exposure.
METHODS
Workers with respiratory symptoms and rest-day improvement were identified by questionnaire. Each was asked to measure PEF 8 times daily for 4 weeks at home and work. Alveolitis was subsequently diagnosed from a validated scoring system including radiological changes, carbon monoxide diffusing capacity, bronchoalveolar lavage and biopsy results. Occupational asthma was confirmed with a positive Oasys score >2.5 and a mean rest-work PEF >16 l/min from serial 2-hourly PEF measurements. The Oasys PEF plotter calculated differences between rest and workdays for mean PEF, diurnal variation and the scores were used to confirm an occupational effect (Oasys, area between curve and time point). Records were compared between the alveolitis group and the group with occupational asthma without alveolitis.
RESULTS
Forty workers with occupational asthma and 16 with alveolitis had indistinguishable PEF changes on workdays in terms of magnitude (median reduction 18.5 and 16.1 l/min, respectively) and diurnal variation. Immediate reactions were more common with occupational asthma and late reactions more common with alveolitis.
CONCLUSIONS
PEF responses to metal-working fluid aerosols do not distinguish occupational asthma from alveolitis except in timing. They can be used to identify the workplace as the cause of asthma and also alveolitis