BACKGROUND:The absence of nonspecific bronchial hyperresponsiveness (NSBH) has been documented in a substantial proportion of workers with occupational asthma (OA). OBJECTIVE:To investigate the clinical and inflammatory characteristics associated with the absence of baseline NSBH in a cohort of subjects with OA ascertained by a positive specific inhalation challenge (SIC). METHODS:A retrospective study was conducted among 1068 subjects who completed an SIC with various occupational agents at 3 tertiary centers. RESULTS:Among 377 subjects with a positive SIC, 63 (16.7%) did not exhibit baseline NSBH. On postchallenge assessment of these 63 subjects, 45 developed NSBH, whereas 18 still lacked demonstrable NSBH. Multivariate analysis revealed that quiescent asthma-defined by untreated asthma associated with the absence of airway obstruction-was the predominant clinical feature associated with undetectable NSBH at baseline (odds ratio, 3.59; 95% CI, 1.86-6.93). Subjects with and without baseline NSBH exhibited similar rates of postchallenge increases greater than or equal to 13 parts per billion in fractional exhaled nitric oxide (47.8% and 43.6%, respectively) and 2% or higher in sputum eosinophil count (72.2% and 74.2%, respectively). Baseline NSBH assessment identified positive SICs with a substantially lower sensitivity (68%) and negative predictive value (71%) among subjects with quiescent asthma (n = 211) than among those (n = 857) with active disease (87% and 88%, respectively). CONCLUSIONS:The absence of NSBH does not allow OA to be ruled out without further investigation in subjects with quiescent asthma. However, a negative NSBH test result has a high negative predictive value for OA among subjects with active disease.

Objective and design:The objective of the present study was to assess the discriminative accuracy of artificial intelligence (AI) software to identify COPD and other chronic respiratory diseases from primary care spirometry. This was a diagnostic study with blinded analysis. Methods:Retrospective hand-held spirometry data from consecutive patients attending primary care clinics in Hillingdon (London, UK) between September 2015 and March 2019 were used. The index diagnosis was the "preferred" diagnosis determined by AI software (highest probability) using supervised random-forest machine learning to interpret raw spirometry data and basic demographics. The reference diagnosis was based on the consensus of expert pulmonologists with access to primary and secondary care medical notes and results of relevant investigations. Cross-tabulation of the index test results by the results of the reference standard for COPD and other respiratory disease categories provided the main outcome measures. Results:In this primary care spirometry dataset from 1113 patients, 543 (48.8%) had a reference diagnosis of COPD. AI preferred diagnosis detected 456, achieving a sensitivity of 84.0% (95% CI 80.6-87.0%), specificity of 86.8% (83.8-89.5%), accuracy of 85.4% (83.2-87.5%) with area under curve (AUC) of 0.914 (0.896-0.930). AI preferred diagnosis identified 187 out of 249 patients with reference diagnosis of interstitial lung disease and 59 out of 107 patients with asthma, with AUCs of 0.900 (0.880-0.916) and 0.814 (0.790-0.836), respectively. Conclusion:AI software achieved high sensitivity and specificity in identifying COPD using spirometry and basic demographic data and may support accurate diagnosis of COPD in primary care. AI software performed less well for other chronic respiratory disease categories.

We report the management of a 64-year-old male with newly diagnosed bulbar-onset myasthenia gravis (MG) who was hospitalized with acute neuromuscular respiratory insufficiency. This case highlights the challenges in monitoring respiratory function in MG patients, especially in the presence of bulbar and nuchal weakness, and emphasizes the potential utility of single breath-hold time (SBHT) over forced vital capacity (FVC) as a reliable bedside monitoring tool. Despite initial stabilization with intravenous immunoglobulin (IVIG), the patient deteriorated, requiring escalation to the intensive care unit (ICU), and the clinical worsening corresponded with the SBHT rather than with FVC.

BACKGROUND:Exposure-related changes in exhaled nitric oxide (FeNO) and sputum eosinophils have not been thoroughly compared in the investigation of occupational asthma. OBJECTIVE:This study aimed at comparing the accuracies of the changes in FeNO concentrations and sputum eosinophil counts in identifying asthmatic reactions induced by occupational agents during specific inhalation challenges (SICs). METHODS:This retrospective multicenter study included 321 subjects who completed an assessment of FeNO and sputum eosinophils before and 24 h after SICs with various occupational agents, of whom 156 showed a positive result. RESULTS:Post-challenge changes in FeNO and sputum eosinophils showed similar accuracies, with areas under the receiver operating characteristics curve of 0.78 (95% confidence interval [95% CI], 0.72-0.83) and 0.81 (95% CI, 0.76-0.86), respectively. Increases in FeNO level ≥ 13 ppb and sputum eosinophils ≥ 1.25% were identified as the optimal threshold values for differentiating positive from negative SICs. Using these thresholds, the changes in FeNO and sputum eosinophils each achieved a ≥ 95% specificity but a low sensitivity (55% and 62%, respectively). FeNO and sputum eosinophils showed discordant increases in 38% of subjects with a positive SIC. Combining either a rise in FeNO ≥ 13 ppb or an increase in sputum eosinophils ≥ 1.25% increased the sensitivity to 77%. CONCLUSIONS:Increases in FeNO concentration and/or sputum eosinophils after exposure to occupational agents strongly support a diagnosis of occupational asthma. The assessment of both markers of airway inflammation should be regarded as a reliable complementary tool to spirometry for identifying bronchial responses to occupational agents.

Interstitial lung diseases (ILDs) are a diverse group of lung parenchymal diseases. They cover a spectrum of inflammatory to fibrotic pathologies. Many ILDs are labelled idiopathic, meaning there is no recognized cause, but many can be triggered by environmental and occupational exposures. Occupational ILD can present as many different ILD subtypes, including hypersensitivity pneumonitis, granulomatous disease (e.g. chronic beryllium disease), pneumoconiosis (silicosis) and usual interstitial pneumonia (typically asbestosis). Traditionally, there have been few available treatments; however, increasing emphasis is now placed on identifying causative agents, with a subsequent reduction or removal of exposure. Furthermore, the recognition of a progressive fibrosing ILD phenotype has enabled the use of antifibrotic therapy.

Background: Zintec is a cold rolled mild steel electrolytically coated with a thin layer of zinc used in vehicle manufacture to limit rust (different to galvanized steel). We report the first case series of occupational asthma in workers exposed to the fumes of spot welding through Zintec-coated steel. Methods: All workers with possible occupational asthma referred to our clinic since 2001 were asked to record PEF 2-hourly for 4 weeks at home and work. Those with confirmed occupational asthma with a positive Oasys score were included. Results: Fifteen workers with work-related PEFs were included. Seven showed late reactions, 7 immediate reactions and one was unclassifiable. Figure 1 shows a late reaction ABC plot from the Oasys program. Twenty percent had pre-existing asthma, 33% has non-specific bronchial reactivity, 77% were atopic and 54% had either a FeNO >25ppb or blood eosinophils >0.15 x 10-9. The mean latency from first exposure to first symptom was 7 years (SD 7.5). 3/5 had immediate reactions following specific challenge (SIC) with Zinc sulphate or Zinc Chloride. Figure 1. Discussion Fumes from Zintec-coated steel welding are a cause of occupational asthma probably related to zinc in the fume. SIC with zinc salts may not reproduce real life exposures, which are difficult to replicate in the challenge chamber. The replacement of steel with aluminium for car bodies can overcome the problem.

Introduction: Breathlessness persists in about 50% patients following acute PE despite anticoagulation. Chronic thromboembolic pulmonary hypertension (CTEPH) occurs in only a small proportion of cases, but early diagnosis is critically important. Aims: Utility of CPET in identifying CTEPH. Methods: CPET was performed in 57 patients with persisting symptoms >6 months of anticoagulation. RV strain and PE size were assessed from original imaging. Retrospective analysis was undertaken to identify whether any indices could distinguish patients with subsequent CTEPH diagnosis using one way ANOVA of 3 groups; Gp 1 (No CTED/CTEPH), Gp 2 (Chronic thromboembolic disease), Gp 3 (CTEPH). Results: Sex, age, BMI and smoking history did not differ but ANOVA identified significant CPET differences between groups: post-hoc multiple comparisons identified several indices differentiating Group 3 from Group 2 and Group 1, tabulated as mean (sd). There was no significant difference between groups for AT, AT %VO2, VO2/WR, BR%, Peak HR, Peak HR%, SPO2 peak, RV strain. Conclusions: CPET differentiates Gp 3 from Gp 1 and 2, but cannot differentiate Gp 2 from Gp 1.

Introduction: Early identification of chronic thromboembolic pulmonary disease/pulmonary hypertension (CTED/CTEPH) is of clinical importance. VQ imaging is reliable for detection of chronic disease but poorly distinguishes CTEPH from CTED. Aims: Utility of CPET in distinguishing CTED from CTEPH. Methods: 57 patients with persisting symptoms after ≥6 months of anticoagulation underwent CPET as part of investigations prior to referral to a tertiary PH centre. Retrospective analysis was undertaken to identify indices predictive of subsequent confirmatory CTEPH diagnosis. ROC analysis was used to assess CPET indices (identified by one way ANOVA and post hoc multiple comparisons) for discriminating CTEPH from CTED. Results: ROCs for indices with AUC >0.8 are shown in the figure. VE/VCO2 slope was the only parameter able to differentiate between CTEPH and CTED with an AUC 0.809 p=0.002. Sensitivity and specificity values of VE/VCO2 slope for identification of CTEPH are shown in the table. Conclusions: In this patient population, VE/VCO2 slope identified ventilatory inefficiency arising from CTEPH.

Background An increase in the number of diagnosed cases of silicosis is anticipated in the UK following the introduction of silica workplace respiratory health surveillance. However, upon diagnosing silicosis, the medium and long-term clinical outcomes remain unclear. Aim To describe clinical outcomes, pulmonary function change over time and survival following a diagnosis of silicosis. Methods A retrospective longitudinal study of all types of silicosis diagnosed at the Birmingham Regional NHS Occupational Lung Disease service since 2000. Eligible participants were identified from a local pre-existing clinical database. Clinical data (including pulmonary function tests) were extracted from medical records, as was ongoing silica exposure after despite a diagnosis of silicosis. Physiological decline was assessed applying a GLS random effects model. Kaplan Meier Survival Estimates of all-cause mortality were performed using STATA v17. Results 37 patients were diagnosed with silicosis (1 acute, 32 chronic simple and 4 progressive massive fibrosis). 97.3% were male and mean (SD) age at diagnosis was 61.6 (11.7) years. 32.4% had ongoing silica exposure after receiving a silicosis diagnosis. Further silica exposure after silicosis diagnosis was not predictive of FEV1, FVC or TLco (p>0.05) decline. Percent predicted values of FEV1, FVC and TLco deteriorated annually (all p<0.001) - FEV1 (0.77%/year), FVC (0.52%/year), TLco (1.42%/year). Figure 1 demonstrates all-cause mortality of approximately 40% at 2 years. Connective tissue disease was diagnosed in 2 patients and mycobacterial infection diagnosed in 2 patients after silicosis diagnosis. Discussion Silicosis is a slowly progressive disease – whilst% predicted value annual change was small, often it is diagnosed in patients of working age and is likely to contribute to morbidity and mortality after diagnosis. Approximately 40% of patients died within 2 years of a diagnosis of silicosis.

Introduction and Aims: Occupational asthma from welding fume is often thought to be due to irritant mechanisms rather than hypersensitivity. We have investigated the patterns of response to welding fume in 58 workers with welding-related asthmatic symptoms to see if there are characteristic patterns which are distinct from occupational asthma due to hypersensitivity. Methods: PEF was measured 2-hourly at home and work usually for 4 weeks. Included workers had at least one positive score from the Oasys PEF plotter indicating occupational asthma1. The mean 2-hourly PEF plot was used to identify reactions starting at the first measurement after staring work (immediate reaction compatible with irritant or hypersensitive mechanisms) or later (late reaction, favouring hypersensitivity), and recovery starting at the first time point after leaving work, early recovery) or later, and the patterns of repeated daily exposure (equivalent or progressive deterioration) and recovery by the first day away from exposure or later. Welding exposures were divided into mild steel, stainless steel and spot welding of zintec coated steel. ∗Χ2 NS Conclusion: There was a full range of responses seen in all groups as seen in occupational asthma due to hypersensitivity. Similar responses were seen in the zintec group where exposures were much lower. A purely irritant mechanism for welding asthma is unlikely. 1Thorax 2009;64:1032

Introduction: Clinics are trying to keep face to face capacity to a minimum thereby reducing physiological monitoring of patients undergoing changes in treatment. With the availability of cost-effective, reliable remote spirometers, it is possible to offer remote monitoring. Aim: To assess whether remote spirometry has enabled more efficient patient care. Methods: 8 consecutive patients with either asthma or hypersensitivity pneumonitis (HP) seen at the Birmingham Chest Clinic were included. A virtual appointment was undertaken to perform the 1st spirometry at home after application download. Spirometries were then performed unsupervised and a pdf report of results sent by email. If results did not meet ERS reproducibility criteria or deterioration had occurred, a further virtual spirometry was performed before any action was taken. Results: 6 patients with HP and 2 with asthma were included and monitored by a physiologist. The median weeks of recordings and coefficient of variation (COV) of measurements are shown in Table 1. 7 patients only needed a supervised set up spirometry, one patient had 2 further supervised assessments due to deterioration. Quality criteria was met in all for FEV1, repeat measurements were needed for FVC in 2/7, 1/7 had turbine malfunction. FEV1 decline coupled with a change in symptoms instigated either a change in treatment (2/7), exposures (1/7) or referral for oxygen/transplant (1/7). Conclusion: Remote spirometry produces quality usable data that has enabled intervention in patient care sooner than if seen in a face to face clinic.