Job exposure matrices for occupational respiratory disease: a narrative review.

BACKGROUND: Job exposure matrices (JEMs) are epidemiological tools used to provide estimations of occupational exposures when it is not feasible to complete detailed individual occupational histories. AIMS: To identify and summarize the characteristics of published general population JEMs (GPJEM) of inhalable occupational exposures applied in studies of respiratory disease. METHODS: MEDLINE and EMBASE databases were searched using pre-defined search terms, with screening performed by two independent reviewers to identify studies reporting the use of a GPJEM. JEM creation papers were subsequently identified and reviewed for each individual GPJEM, noting its characteristics in terms of occupational classification system and exposure estimates. RESULTS: From 728 studies identified in initial searches, 33 GPJEMs of inhalable occupational exposures were identified. Versions of the International Standards Classification of Occupations were the most used occupational classification system. Binary, probability and intensity-based exposure estimates were most frequently reported in GPJEMs. CONCLUSIONS: Selection of a GPJEM to apply in epidemiological research should be based on the exposure(s) of interest, time period of occupations under review, geographical region for intended use, occupation classification system used and the exposure estimate outcome.

Occupational asthma in office workers.

BACKGROUND: Office work has a relative perception of safety for the worker. Data from surveillance schemes and population-based epidemiological studies suggest that office work carries a low risk of occupational asthma (OA). Office workers are frequently used as comparators in studies of occupational exposure and respiratory disease. AIMS: We aimed to describe and illustrate our tertiary clinical experience of diagnosing OA in office workers. METHODS: We searched the Birmingham NHS Occupational Lung Disease Service clinical database for cases of occupational respiratory disease diagnosed between 2002 and 2020, caused by office work or in office workers. For patients with OA, we gathered existing data on demographics, diagnostic tests including Occupational Asthma SYStem (OASYS) analysis of serial peak expiratory flow and specific inhalational challenge, and employment outcome. We summarised data and displayed them alongside illustrative cases. RESULTS: There were 47 cases of OA (5% of all asthma) confirmed using OASYS analysis of PEFs in the majority. Sixty percent of cases occurred in healthcare, education and government sectors. The most frequently implicated causative exposures or agents were: indoor air (9), printing, copying and laminating (7), cleaning chemicals (4), mould and damp (4), and acrylic flooring and adhesives (4). Exposures were grouped into internal office environment, office ventilation-related and adjacent environment. CONCLUSIONS: Clinicians should be vigilant for exposures associated with OA in office workers who present with work-related symptoms, where respiratory sensitizing agents may be present. A structured approach to assessment of the workplace is recommended.

Occupational causes of hypersensitivity pneumonitis: a systematic review and compendium.

BACKGROUND: Hypersensitivity pneumonitis (HP) is caused by a variety of antigens and low-molecular-weight chemicals, often through occupational exposure. Making a diagnosis of HP and identifying a cause are challenging. Cryptogenic cases are frequently reported, and missing or incomplete exposure histories can cause misclassification. AIMS: To provide an evidence-based compendium of sources of exposure and causes of HP for the clinician, through systematic review of medical literature. METHODS: Articles related to HP causative agents and occupational exposure were searched from the databases OVID Medline (1946 to October 2020) and EMBASE (1974 to October 2020). Abstracts and full texts of articles were screened by two reviewers. Data on causative antigens, occupational source of exposure and any associated eponymous name were extracted and grouped according to source of exposure. RESULTS: A total of 1790 articles were identified, from which 305 articles met the inclusion criteria. An additional 22 articles were identified from citation lists of the selected review articles. Sources of exposure identified for HP were sorted into 14 categories of work (agricultural, plant matter processing, wood, animal-related, foodstuff, food processing, metal processing, polymers, other manufacturing, chemicals, aerosolized water, service, waste and sewage and wind instruments). CONCLUSIONS: This work is a comprehensive list of occupational causative agents and exposures causing HP. Cases are grouped by source of exposure, allowing an immediately accessible compendium of causes for use during occupational exposure assessment, which could also form the basis for a clinical questionnaire.

Updated review of reported cases of reactive airways dysfunction syndrome.

BACKGROUND: A previous systematic review of the diagnosis of reactive airways dysfunction syndrome (RADS), undertaken from 1985 to 2004, found a lack of standardization of case reporting, thus misattribution of symptoms can occur. AIMS: We aimed to update the systematic review, update the list of reported causes and see whether a more structured approach to reporting has been adopted. METHODS: We undertook a systematic literature review, using the databases EMBASE and Ovid MEDLINE, with search terms 'reactive airways dysfunction syndrome' or 'asthma AND acute irritant', and reported according to PRISMA guidelines. We included papers and abstracts published from January 2005 to September 2019, and articles were grouped by the presence or absence of diagnostic features: 'definite' RADS (met Brooks' criteria) or 'possible' RADS (Brooks' criteria not met or insufficient data). We collected demographic and diagnostic data for cases, where given. RESULTS: Eleven papers and six conference abstracts met the inclusion criteria, 13 of which were case series or reports, and comprised 752 cases in total; seven articles met Brooks' criteria for RADS diagnosis. A variety of agents were implicated, with chlorine or chlorine-releasing molecules most frequently reported. CONCLUSIONS: A lack of standardized reporting of RADS remains. The majority of published articles and conference abstracts either do not meet, or contain insufficient data to judge against, Brooks' criteria, particularly in relation to onset of symptoms and bronchial hyper-reactivity or variability of airflow obstruction. Some novel agents are described, in keeping with recognized structural taxonomies.

Occupational asthma caused by peracetic acid-hydrogen peroxide mixture.

BACKGROUND: Healthcare practice in the UK has moved away from using aldehyde disinfectants for the decontamination of endoscopes, in part due to the risk of respiratory sensitization. Peracetic acid (PAA) in combination with hydrogen peroxide (HP) is a commonly used alternative. AIM: We describe a case of occupational asthma (OA) diagnosed at our specialist occupational lung disease clinic and caused by occupational exposure to PAA-HP mixture, used as a disinfectant in an endoscope washer-disinfector machine. CASE REPORT: A 48-year-old man employed as a mycologist and environmental microbiologist at a Birmingham city hospital, UK, presented following an acute exposure to PAA-HP mixture causing lacrimation, burning optic pain and headache. He had also experienced symptoms suggestive of OA for the preceding 10 months, and the diagnosis was confirmed through OASYS analysis of serial peak expiratory flow measurements. He had been exposed to PAA-HP mixture whilst working in the endoscopy department for 12 months prior to the acute episode, and a subsequent specific inhalation challenge test was positive with a late asthmatic response to PAA-HP mixture. CONCLUSION: This case provides evidence for a sensitization mechanism in OA caused by PAA-HP mixture.

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.

Asbestosis is prevalent in a variety of construction industry trades.

A diagnosis of asbestosis, which is a long-latency, fibrotic lung disease, has implications for the patient in terms of prognosis, treatment and compensation. Identifying and quantifying asbestos exposure is difficult without a detailed occupational history, and the threshold dose of asbestos required to cause asbestosis is not well understood. We reviewed all cases of asbestosis diagnosed between 2001 and 2016 at the Birmingham Regional NHS Occupational Lung Disease Service to determine the industries and occupations most frequently implicated in causation, in order to help clinicians identify where asbestosis might enter the differential diagnosis for a patient with chronic respiratory symptoms. A variety of construction trades were frequently reported including carpenters and joiners, pipe fitters, laggers, labourers, painters and shop fitters. Traditionally heavily exposed occupations such as shipbuilding were not commonly seen.

Missed opportunities to identify occupational asthma in acute secondary care.

Background: Occupational asthma (OA) accounts for one in six cases of new-onset adult asthma. Despite this it remains under-recognized in the UK. Delayed and missed diagnoses of OA lead to poor health outcomes for workers at significant cost to the UK economy. The burden of occupational aetiology on hospital admissions with asthma is not known. Aims: To measure how frequently medical professionals consider occupational aetiology in patients presenting to secondary care with acute asthma symptoms. Methods: We reviewed electronic records of working-age patients with asthma symptoms, presenting to three sites at a large West Midlands acute hospital NHS trust. We searched emergency department (ED) and acute medical unit (AMU) admission documents, looking specifically at documentation of employment status, job role and work effect on symptoms. We also examined the effect of using a prompt for enquiry about occupation contained within the clerking pro-forma. Results: We searched 100 ED and 100 AMU admission documents. Employment status was established in only 20-31% of patients and none were asked about the effect of their work on current asthma symptoms. The use of a clerking pro-forma, including a prompt for occupation, increased documentation to 63% from 10 to 14% where an enhanced pro-forma was not used. Conclusions: Enquiry into employment status and work effect in working-age patients with asthma symptoms presenting to the ED and the AMU is poor. These may be missed opportunities to identify OA. We propose medical education about high-risk exposures and the use of pro-formas including prompts about 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.

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.

Twenty years of SHIELD: decreasing incidence of occupational asthma in the West Midlands, UK?

INTRODUCTION: Since 2000 a decline in the incidence of occupational asthma (OA) has been reported in the UK and Europe. We aimed to describe and account for trends in the incidence of OA in the West Midlands, UK using annual notification data from the SHIELD voluntary surveillance scheme over the period 1991-2011. METHODS: All notifications to the SHIELD database between January 1991 and December 2011 were identified, along with patients' demographic data, occupations, causative agents and confirmatory tests. Annual notifications were scaled to give an annual count per million workers, giving a measure of incidence, and also standardised against those of bakers' asthma. Non-parametric analyses were undertaken between annual incidence and time (years) for common causative agents using (1) a negative binomial regression univariate model and (2) a logistic regression model calculating annual reporting ORs. A step-change analysis was used to examine time points at which there were marked reductions in incidence. RESULTS: A decrease in annual incidence of OA was observed over the study period (incident rate ratio=0.945; 95% CI 0.933 to 0.957; p<0.0001), an effect that was lost after standardising for bakers' asthma. Decreases in incidence were seen for most common causative agents, with only cleaning product-related OA increasing over 21 years. Marked fall in incidence was seen in 2004 for isocyanates, and in 1995 for latex. Most notifications came from a regional specialist occupational lung disease unit, with notifications from other sites falling from 16 cases/million workers/annum in 1995 to 0 in 2004. CONCLUSIONS: Reporter fatigue and increasing under-recognition of OA are both factors which contribute to the apparent fall in incidence of OA in the West Midlands. There is a future need for interventions that enable health professionals to identify potential cases of OA in the workplace and in healthcare settings.

Cobalt asthma in metalworkers from an automotive engine valve manufacturer.

BACKGROUND: Cobalt asthma has previously been described in cobalt production workers, diamond polishers and glassware manufacturers. AIMS: To describe a case series of occupational asthma (OA) due to cobalt, identified at the Birmingham Heartlands Occupational Lung Disease Unit, West Midlands, UK. METHODS: Cases of cobalt asthma from a West Midlands' manufacturer of automotive engine valves, diagnosed between 1996 and 2005, were identified from the SHIELD database of OA. Case note data on demographics, employment status, asthma symptoms and diagnostic tests, including spirometry, peak expiratory flow (PEF) measurements, skin prick testing (SPT) and specific inhalational challenge (SIC) tests to cobalt chloride, were gathered, and descriptive statistics used to illustrate the data. RESULTS: The natural history of presentations has been described in detail, as well as a case study of one of the affected workers. Fourteen metalworkers (86% male; mean age 44.9 years) were diagnosed with cobalt asthma between 1996 and 2005. Workers were principally stellite grinders, stellite welders or machine setter-operators. All workers had positive Occupational Asthma SYStem analyses of serial PEF measurements, and sensitization to cobalt chloride was demonstrated in nine workers, by SPT or SIC. CONCLUSIONS: We have described a series of 14 workers with cobalt asthma from the automotive manufacturing industry, with objective evidence for sensitization. Health care workers should remain vigilant for cobalt asthma in the automotive manufacturing industry.

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 Society's 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.

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.

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.