Occupational asthma (OA) represents one of the major public health problems due to its high prevalence, important social and economic burden. The aim of this review is to summarize current data about clinical phenotypes, biomarkers, diagnosis and management of OA, a subtype of work-related asthma. Most studies have identified two phenotypes of OA. One is sensitizer-induced asthma, occuring after a latency period and caused by hypersensitivity to high- or low-molecular weight agents. The other is irritant-induced asthma, which can occur after one or more exposures to high concentrations of irritants without latency period. More than 400 agents causing OA have been identified and its list is growing fast. The best diagnostic approach for OA is a combination of clinical history and objective tests. An important tool is a specific inhalation challenge. Additional tests include assessments of bronchial hyperresponsiveness to methacholine/histamine in patients without airflow limitations, monitoring peak expiratory flow at- and off-work, sputum eosinophil count, exhaled nitric oxide measurement, skin prick tests with occupational allergens and serum specific IgE. Treatment of OA implies avoidance of exposure, pharmacotherapy and education. OA is a heterogeneous disease. Mechanisms of its different phenotypes, their diagnosis, role of new biomarkers and treatment require further investigation.

The large amount of evidence and the renewed interest on upper and lower airways involvement in infectious and inflammatory diseases has led Interasma (Global Asthma Association) to take a position on United Airways Diseases (UAD). Starting from an extensive literature review, Interasma excecutive committee discussed and approved this Manifesto developed by Interasma scientific network (INES) members. The manifesto describes the evidence gathered to date and defines, states, advocates, and proposes issues on UAD (rhinitis, rhinosinusitis and nasal polyposis), and concomitant/comorbid lower airways disorders (asthma, chronic obstructive pulmonary disease, bronchiectasis, cystic fibrosis, obstructive sleep apnoea) with the aim of challenging assumptions, fostering commitment, and bringing about change. UAD refer to clinical pictures characterized by the coexistence of upper and lower airways involvement, driven by a common pathophysiological mechanism, leading to a greater burden on patient’s health status and requiring an integrated diagnostic and therapeutic plan. The high prevalence of UAD must be taken into account. Upper and lower airways diseases influence disease control and patient’s quality of life. Patients with UAD need to have a timely and adequate diagnosis, treatment, and, when recommended, referral for management in a specialized center. Diagnostic testing including skin prick or serum specific IgE, lung function, fractional exhaled nitric oxide (FeNO), polysomnography, allergen-specific immunotherapies, biological therapies and homebased continuous positive airway pressure (CPAP) whenever these are recommended, should be part of the management plan for UAD. Education of medical students, physicians, health professionals, patients and caregivers on the UAD is needed.

Introduction: The COVID-19 pandemic has challenged health care across the world, not just by the severity of the disease and the high mortality rate but also by the consequences on the management of the patients with chronic diseases.Areas covered: This review summarizes the most up-to-date published data regarding the impact of COVID-19 on the management and outcomes of patients with chronic noninfectious respiratory illnesses including obstructive sleep apnea, asthma, chronic obstructive pulmonary disease, bronchiectasis, interstitial and pulmonary vascular diseases, and lung cancer.Expert opinion: Most of chronic respiratory diseases (except asthma and cystic fibrosis) are associated with more severe COVID-19 and poor outcomes but the mechanisms involved are not yet identified. The therapeutic management of the patients with chronic respiratory diseases and COVID-19 is similar to the other patients but the post-recovery course could be worse in this population and followed by the development of pulmonary fibrosis, bronchiectasis, and pulmonary hypertension. The pandemic highly impacted our usual medical activities by limiting the access to several diagnosis procedures, the necessity to develop new methods for the monitoring of the disease and adapt the therapeutic strategies. The long-term consequences of all these changes are still unknown.

Recognition of the huge economic burden chronic respiratory diseases pose for society motivated fundamental and clinical research leading to insight into the role of airway inflammation in various disease entities and their phenotypes. However, no easy, cheap and patient-friendly methods to assess it have found a place in routine clinical practice. Measurement of exhaled breath temperature (EBT) has been suggested as a non-invasive method to detect inflammatory processes in the airways as a result of increased blood flow within the airway walls. As EBT values are within a narrow range, the thermometers designed for the purpose of assessing it need to be precise and very sensitive. EBT increases linearly over the pediatric age range and seems to be influenced by gender, but not by height and body weight. In non-smoking individuals with no history of respiratory disease EBT has a natural circadian peak about noon and increases with food intake and physical exercise. When interpreting EBT in subjects with alleged airway pathology, the possibilities of tissue destruction (chronic obstructive pulmonary disease, cystic fibrosis) or excessive bronchial obstruction and air trapping (severe asthma) need to be considered, as these conditions drive (force) EBT down. A prominent advantage of the method is to assess EBT when patients are in a steady state of their disease and to use this ‘personal best’ to monitor them and guide their treatment. Individual devices outfitted with microprocessors and memory have been created, which can be used for personalized monitoring and disease management by telemedicine.

Introduction: Patients with asthma often have important co-morbidities which reduce the likelihood of gaining optimal asthma control. Beta2-blockers are commonly prescribed for the treatment of different clinical indications, including coronary artery disease, cardiac arrhythmia, arterial hypertension, heart failure and glaucoma. Areas covered: The aim of this reviw is to summarize current evidence on the effect of systemic and local β-blockers on asthma outcomes based on their pharmacologic properties,and to help clinicians when prescribing for patients with asthma and co-morbidities. Current data suggest that risk of asthma worsening from systemic and local use of non-selective β-blockers outweighs any potential benefits for their clinical indications. Recent studies confirm that topical and systemic prescription of cardio-selective β-blockers is not associated with a significant increased risk of moderate or severe asthma exacerbations. Expert opinion: Non-selective β-blockers should not be prescribed for the management of comorbidities in patients with asthma while cardio-selective β-blockers, preferably in low doses, may be used when strongly indicated and other therapeutic options are not available. More prospective real-life studies are needed to evaluate the risk of long-term use of β-blockers in patients with asthma.

COPD-6™ is a lung function testing device for a rapid pre-spirometry testing to screen-out at-risk individuals not having COPD and indicating those at risk. The aim of this study was to validate COPD-6™ lung function testing (index test) in general practice in discriminating patients with COPD out of the population at risk - smokers/ex-smokers with no previous diagnosis of COPD, using measurements at tertiary care as reference standard. Consecutive 227 subjects (115 women, 185 smokers/42 ex-smokers, ≥20 pack-years) with no previous diagnosis of COPD, aged 52.5 (SD 6.8) years from 26 general practitioners (GPs) were recruited, lung function tested with COPD-6™, referred to the tertiary institution for repeated COPD-6™ testing followed by spirometry with a bronchodilator (salbutamol), examination, and pulmonologist consultation for the diagnosis and severity of COPD. COPD was diagnosed in 43 subjects (18.9 %), with an AUC of 0.827 (95 % CI 0.769-0.875, P < 0.001) for the diagnosis of COPD when lung function was measured using COPD-6™ in GP’s office with a specificity of 100 % (95 % CI, 97.95–100 %) but a very low sensitivity of 32.56 % (95 % CI, 20.49–47.48 %). Significant agreement for forced expiratory volume in 1 s measured at GP’s office and at lung function lab was found (mean difference 0.01 L, p = 0.667) but not for other measured parameters (p < 0.001 for all). Our study results point out that active case finding in a population at risk for COPD should be instituted (almost 20 % of undiagnosed COPD). Based on our results lung function testing with COPD-6™ can substitute spirometry testing in cases where it is not readily available to the patient/physician taken into account that the traditional FEV1/FEV6 cutoff value of <0.7 is not the only criterion for diagnosis and/or further referral. ClinicalTrials.gov Identifier NCT01550679 Registered 28 September 2014, retrospectively registered