Gareth Walters

An outbreak of occupational asthma due to chromium and cobalt

BACKGROUND Five metal turners employed by an aerospace manufacturer presented to the Birmingham Chest Clinic occupational lung disease unit. Four cases of occupational asthma (OA) due to chromium salt (3) and cobalt (1) were diagnosed by serial peak-expiratory flow measurements and specific inhalation challenge testing. AIMS To measure the extent of the outbreak and to provide epidemiological data to ascertain the aetiology. METHODS Participants answered a detailed, self-administered questionnaire, designed to detect occupational lung disease. Urine chromium and cobalt excretion, spirometry and exhaled nitric oxide measurements were taken. Those with possible, probable or definite non-OA or OA, after questionnaire, were invited to undertake two-hourly peak flow measurements and received specialist follow-up. RESULTS A total of 62 workers (95% of workforce) participated. Sixty-one per cent of employees were working in higher metalworking fluid (MWF) exposure areas. Ninety per cent of workers had urinary chromium excretion indicating occupational exposure. Sixty-six per cent of workers reported active respiratory symptoms, although there were no significant differences between exposure groups. Two further workers with probable OA were identified and had significantly higher urinary chromium and cobalt concentration than asymptomatic controls. Eighteen cases of occupational rhinitis (OR) were identified, with significantly raised urinary chromium concentration compared with asymptomatic controls. CONCLUSIONS Chromium salt and cobalt can be responsible for OA and OR in workers exposed to MWF aerosols. Onset of symptoms in those with positive specific challenges followed change in MWF brand. Workers with OA had increased urinary concentrations of chromium and cobalt, and those with OR had increased urinary concentrations of chromium.

Audit of the recording of occupational asthma in primary care

BACKGROUND Occupational asthma (OA) remains common; 1 in 10 cases of adult-onset asthma is due to work. Health outcomes are better with early diagnosis, but there is considerable delay, largely due to lack of enquiry about work effect in primary care. National guidelines (2008) recommend asking two screening questions, which together have a high sensitivity in identifying OA. AIMS To audit how working-age asthmatics are currently screened for OA in a local primary care population. METHODS An audit of the electronic patient records of working-age asthmatics, from four Birmingham primary care practices was undertaken. Practice-level data (list size, gender, prevalence of asthma and OA and socio-economic status) and patient-level data (gender, age, onset, occupation and work-effect enquiry and lung function) were collected. RESULTS The total practice population was 27,295 of which 17,564 (64%) were of working age. The audit sample was 396 of whom 49% were male. The prevalence of asthma in working-age adults was 12% (8-15%) and the prevalence of OA in working-age asthmatics was 0.3% (0-0.8%). Occupation was recorded in only 55/396 (14%) cases with very few (2) documented within the asthma-review template. Occupation was only recorded in 13/55 adult-onset asthmatics in high-risk occupations. Of 396, 9 (2%) had any work-effect enquiry and 4 patients had work-effect enquiry at diagnosis in those with traceable notes (n = 117). CONCLUSIONS The prevalence of OA was low, suggesting under-diagnosis plus under-reporting in primary care. Occupation and work-effect enquiry is lacking despite guidelines for identifying OA. Existing electronic templates for recording asthma review could be modified to include these elements.

Agents and trends in health care workers' occupational asthma.

BACKGROUND There is a disproportionately high number of cases of work-related asthma occurring in health care occupations due to agents such as glutaraldehyde, latex and cleaning products. AIMS To understand the causes and measure trends over time of occupational asthma (OA) in health care workers (HCWs). METHODS We reviewed OA notifications from the Midland Thoracic Societys Surveillance Scheme of Occupational Asthma (SHIELD) database in the West Midlands, UK, from 1991 to 2011 and gathered data on occupation, causative agent and annual number of notifications. RESULTS There were 182 cases of OA in HCWs (median annual notifications = 7; interquartile range [IQR] = 5-11), representing 5-19% of annual SHIELD notifications. The modal annual notification was 20 (in 1996); notifications have declined since then, in line with total SHIELD notifications. The majority of cases (136; 75%) occurred in nursing, operating theatre, endoscopy and radiology staff. The most frequently implicated agents were glutaraldehyde (n = 69), latex (n = 47) and cleaning products (n = 27), accounting for 79% of the 182 cases. Cleaning product-related OA was an emerging cause with 22 cases after 2001 and only 5 cases between 1991 and 2000. CONCLUSIONS Control measures within the UK National Health Service have seen a decline in OA in HCWs due to latex and glutaraldehyde, though OA remains a problem amongst HCWs exposed to cleaning products. Continuing efforts are required to limit the number of cases in this employment sector.

Occupational asthma caused by sensitization to a cleaning product containing triclosan

A recent consensus statement has highlighted the increased risk of developing asthma after exposure to workplace and domestic cleaning products.1 Specific cleaning agents, such as benzylalkonium chloride, have been recognized as causes of occupational asthma by sensitization and now comprise a significant burden of work-related asthma. European Respiratory Society guidelines recommend that sensitizer-induced occupational asthma should be diagnosed by identifying the workplace as the cause and confirming sensitization to an asthmagen by specific inhalation challenge (SIC) in the absence of any available specific IgE tests.2 We present the first case of occupational asthma caused by the biocide triclosan, commonly used in cleaning and personal care products. A 26-year-old woman presented with a 7-month history of cough, wheeze, and chest tightness that became progressively worse throughout the working week and better on days away from work. She required treatment with a budesonideformoterol inhaler, 400/12 mg twice a day. She had childhood eczema and asthma and previous anaphylaxis caused by peanuts at the age of 16 years. She had been employed as a nursery nurse for 12 months, caring for 30 children aged 2 to 3 years. Her work tasks involved mopping using 5% trisodium nitrilotriacetate (Versatile) cleaner daily and cleaning tables using liquid cleaner containing 0.05% triclosan (Antibac; pH 7.0). She used latex gloves and a gel containing 70% ethanol for hand cleaning (Proform, Gompels Healthcare Ltd, Melksham, United Kingdom). Clinical examination and chest radiographic findings were unremarkable, and spirometry results were normal (forced expiratory volume in 1 second [FEV1], 3.55 L [103% predicted]; forced vital capacity [FVC], 4.05 L [103% predicted]). Total IgE level was less than 2 kU/L, the results of testing for serum specific IgE to latex were negative, and the eosinophil count was 0.02 109/L. Two-hourly peak flow measurements made at home and work for 4 weeks were analyzed using the OASYS computer program.3 The OASYS score was 3.5 and the area between the curves score was 27 L/min per hour, both confirming a significant work effect. The patient underwent SIC testing, with negative control challenges to both the hand gel and 5% trisodium nitrilotriacetate cleaner (diluted to 1:100). She was subsequently exposed to triclosan surface cleaner diluted to 1:60 with water by painting on cardboard for a total of 30 minutes and experienced a sustained, immediate decrease in FEV1 by 24% from a baseline of 3.42 L (Fig 1), consistent with sensitization.4 There was no clinically significant change in fractional exhaled nitric oxide (FeNO) (pre-SIC, 9 ppb; 24 hours

Pulmonary Alveolar Microlithiasis

A 28-year-old Iranian man who had lived in the United Kingdom for 3 years came to the outpatient clinic with a 3-year history of frequent cough, which occasionally produced a little sputum. He had never smoked and did not describe any other respiratory symptoms. Examination revealed sparse fine crepitations over all lung zones. Spirometry revealed a forced expiratory volume in 1 second of 2.85 L (73%) and a forced vital capacity of 4.01 L (86%). A roentgenogram of the chest revealed diffuse micronodular opacities resembling miliary tuberculosis (Fig 1A). His tuberculin test gave a Heaf grade I reaction, and his sputum samples were negative for tuberculosis. The results of laboratory tests for blood count, biochemical profile, C-reactive protein, and erythrocyte sedimentation rate were all normal. An autoantibody screen produced negative results. Computed tomography of the thorax revealed extensive fine centrilobular nodularity throughout both lungs (Fig 1B), associated with ground-glass changes and septal thickening. There were small areas of subpleural calcification, particularly at both lung bases. He underwent bronchoscopy with transbronchial biopsy, which demonstrated

Cleaning agent occupational asthma in the West Midlands, UK: 2000–16

Background Cleaning agents are now a common cause of occupational asthma (OA) worldwide. Irritant airway and sensitization mechanisms are implicated for a variety of old and new agents. Aims To describe the exposures responsible for cleaning agent OA diagnosed within a UK specialist occupational lung disease service between 2000 and 2016. Methods The Birmingham NHS Occupational Lung Disease Service clinical database was searched for cases of OA caused by cleaning agents, and data were gathered on age, gender, atopic status, smoking history, symptom onset, diagnostic investigations (including Occupational Asthma SYStem analysis of workplace serial peak expiratory flow measurements and specific inhalational challenge), proposed mechanism, industry, occupation and causative agent. Results Eighty patients with cleaning agent OA (77% female, 76% arising de novo) were identified. The median annual number of cases was 4 (interquartile range = 2-7). The commonest cleaning agents causing OA were chloramines (31%), glutaraldehyde (26%) and quaternary ammonium compounds (11%) and frequently implicated industries were healthcare (55%), education (18%) and leisure (8%). Conclusions Certain cleaning agents in common usage, such as chlorine-releasing agents, quaternary ammonium compounds and aldehydes, are associated with sensitization and asthma. Their use alters over time, and this is particularly evident in UK healthcare where cleaning and decontamination practice and policy have changed. Vigilance for OA in workplaces such as hospitals, nursing homes, leisure centres and swimming pools, where these cleaning agents are regularly used, is therefore essential.

Do laboratory challenge tests for occupational asthma represent what happens in the workplace

Specific inhalation challenge (SIC) is the diagnostic reference standard for occupational asthma; however, a positive test cannot be considered truly significant unless it can be reproduced by usual work exposures. We have compared the timing and responses during SIC in hospital to Oasys analysis of serial peak expiratory flow (PEF) during usual work exposures. All workers with a positive SIC to occupational agents between 2006 and 2015 were asked to measure PEF every 2 h from waking to sleeping for 4 weeks during usual occupational exposures. Responses were compared between the laboratory challenge and the real-world exposures at work. All 53 workers with positive SIC were included. 49 out of 53 had records suitable for Oasys analysis, 14 required more than one attempt and all confirmed occupational work-related changes in PEF. Immediate SIC reactors and deterioration within the first 2 h of starting work were significantly correlated with early recovery, and late SIC reactors and a delayed start to workplace deterioration were significantly correlated with delayed recovery. Dual SIC reactions had features of immediate or late SIC reactions at work rather than dual reactions. The concordance of timings of reactions during SIC and at work provides further validation for the clinical significance of each test. Positive specific challenge tests with occupational agents in the laboratory and real-life work exposures monitored with PEF show similar reactions http://ow.ly/lNuv30jWDtQ

Respiratory failure caused by lipoid pneumonia from vaping e-cigarettes

A young female vaper presented with insidious onset cough, progressive dyspnoea on exertion, fever, night sweats and was in respiratory failure when admitted to hospital. Clinical examination was unremarkable. Haematological tests revealed only thrombocytopenia, which was long standing, and her biochemical and inflammatory markers were normal. Chest radiograph and high-resolution CT showed diffuse ground-glass infiltrates with reticulation. She was initially treated with empirical steroids and there was improvement in her oxygenation, which facilitated further tests. Since the bronchoscopy and high-volume lavage was unyielding, a video-assisted thoracoscopicsurgical biopsy was done later and was suggestive of lipoid pneumonia. The only source of lipid was the vegetable glycerine found in e-cigarette (EC). Despite our advice to quit vaping, she continued to use EC with different flavours and there is not much improvement in her clinical and spirometric parameters.

Biopsy-proven hypersensitivity pneumonitis caused by a fluorocarbon waterproofing spray.

Background We present the case of a 35-year-old male who developed a chronic hypersensitivity pneumonitis (HP) following inhalational exposure to a fluorocarbon waterproofing aerosol spray, caused by his work for an upholstery and soft furnishings retailer. This is the first case report from inhalational fluorocarbon exposure with histological evidence of chronic HP. This is then discussed in the context of previous reports of interstitial lung disease and lung injury, caused by similar occupational and non-occupational exposures.

Occupational asthma caused by acrylic compounds from SHIELD surveillance (1989–2014)

Background Acrylic monomers (acrylates), methacrylates and cyanoacrylates all cause asthma by respiratory sensitization. Occupational inhalation exposures occur across a variety of industries including health care and dental work, beauty, laboratory science, assembly and plastic moulding. Aims To examine notifications of occupational asthma caused by acrylic compounds from a UK-based regional surveillance scheme, in order to highlight prevalent exposures and trends in presentation. Methods Retrospective review of all cases reported to the SHIELD surveillance scheme for occupational asthma, West Midlands, UK between 1989 and 2014. Patient data were gathered on demographics, employment, asthma symptoms and diagnostic investigations including serum immunological testing, serial peak flow analysis and specific inhalation challenge tests. Descriptive statistics were used to illustrate worker characteristics and evidence for sensitization to acrylic compounds. Results There were 20 affected patients out of 1790 total cases of occupational asthma (1%); all cases were confirmed by OASYS (Occupational Asthma SYStem) analysis of serial peak flow measurements, with three additional positive specific inhalation challenge tests. Three out of 20 (15%) patients were current smokers and 11/20 (55%) were atopic. A variety of exposures and industries were implicated including: manufacturing, health care, beauty and printing and a novel presentation seen in teachers exposed to floor adhesives. Conclusions This is the largest reported series of occupational asthma caused by acrylic compounds, which remain an important aetiological factor in this disease. Exposure occurs in a variety of industries, particularly in manufacturing and is seen with other, perhaps better recognized sensitizing agents such as isocyanates and epoxy resins.