eLetters

323 e-Letters

  • Is Telerehabilitation a Realistic Alternative to Centre-based Pulmonary Rehabilitation?

    The benefits of pulmonary rehabilitation for individuals with chronic respiratory diseases are well-documented1, but referral practices and programme completion have remained challenging. This has been exacerbated by the COVID-19 pandemic and shielding practices. Thus, highlighting the usefulness of developing a robust telerehabilitation programme as a substitute for centre-based programmes. The data gained from Cox et al addresses this area and demonstrates clinically meaningful advantages of telerehabilitation and is warmly welcomed. A detailed breakdown of the costs involved between both arms would be very helpful in assessing an overall equivalence of the two arms.

    The CRQ is a validated tool for use in research; however, the use of its dyspnoea domain specifically has been shown to be less reliable in comparative research2. Other tools which may be a useful substitute for this study would be ‘incremental shuttle walking test’3 and ‘St George’s respiratory questionnaire’4.

    The number of participants presenting to community healthcare services, and/or those requiring rescue therapy for a mild exacerbation (e.g., antibiotics and/or a short course of corticosteroids) not requiring presentation to a hospital, during the study and follow-up period, may be useful for further assessment of the equivalence of telerehabilitation versus centre-based programmes.

    This study provides useful data regarding the potential benefits of incorporating telerehabilita...

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  • Response to “Letter to the Editor on Thomsen, et al. by Moolgavkar and Attanoos”

    We agree with Drs. Moolgavkar and Attanoos that our observation of increased risk of asbestosis unaccompanied by increased risk of mesothelioma among motor vehicle mechanics (Thomsen, 2021) is inconsistent with other studies of chrysotile exposed populations. As we discussed in our paper, mesothelioma ascertainment is highly reliable in Denmark and our mesothelioma findings are consistent with previous studies (DeBono, 2021; Garabrant, 2016; Hessel, 2021; Tomasallo, 2018; Van den Borre, 2015). Thus, we believe our findings are reliable. Conversely, the asbestosis findings raise important questions. A diagnosis of asbestosis can only be made when a clinician believes the patient has been exposed to asbestos. Pulmonary fibrosis in a vehicle mechanic might readily be diagnosed as asbestosis if the clinician was aware of the occupational history and possible presence of asbestos in brakes, clutches, gaskets, or other vehicle parts. Since our comparison subjects held jobs that did not involve obvious asbestos exposure, it is less likely that pulmonary fibrosis would be diagnosed as asbestosis in this group. Moolgavkar and Attanoos suggest that our comparison selection could have led to diagnostic bias if the vehicle mechanics and the comparisons did not have equal probabilities of exposure to asbestos from sources other than friction products. We agree - we reported that the abrupt increase in outpatient clinic diagnosed asbestosis beginning in the mid-2000s is consistent with...

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  • Letter To The Editor on Thomsen et al

    Thomsen et al’s. (2021)1 suggestion that “asbestosis occurs at cumulative chrysotile exposure levels where mesotheliomas are rare or none were observed…”.to explain the increased risk of asbestosis in the absence of an increased risk of mesothelioma among vehicle mechanics appears implausible for many reasons:
    a. Scientific literature shows that when there is a risk of asbestosis there is also an increased risk of pleural mesothelioma2;
    b. Cumulative exposures to chrysotile asbestos sustained by career vehicle mechanics are far below the cumulative asbestos exposures traditionally associated with asbestosis (25 fibre/cc-years) as cited by Thomsen et al.1,3;
    c. That chrysotile asbestos, with much shorter biopersistence than amphibole asbestos, is more fibrogenic is biologically implausible, and inconsistent with the studies that show that the degree of lung fibrosis/asbestosis correlates with retained amphibole asbestos content, not chrysotile 3,4.
    d. Fibre counts amongst vehicle mechanics with mesothelioma have been found to be either within control reference limits or show increased commercial amphibole asbestos, unrelated to friction exposures 2.
    e. Animal studies do not report asbestosis or mesothelioma following high-dose inhalation exposures to brake dust with and without added chrysotile 5.
    We consider, as Thomsen et al 1 did, that the most plausible explanation is diagnostic bias based on control selection.
    In Thomsen et al...

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  • Response to Raja and colleagues

    We thank A. Raja and colleagues for their interest in our article on risk factors for fibrotic-like changes after severe COVID-19 infection (1). We agree that identification and management of post-COVID fibrosis continues to be impeded by the lack of consensus definitions and we look forward to further studies that help describe the natural history of post-COVID pulmonary manifestations.

    The authors propose that lung fibrosis be classified into different ILDs by the pattern of lung parenchymal abnormalities six months after the initial COVID illness has resolved. We agree with the authors that persistent radiographic abnormalities are an adverse outcome of COVID that deserve future study, but we disagree with their proposed classification of patterns. We believe that recognition of fibrotic interstitial lung abnormalities (ILAs), as opposed to non-fibrotic ILAs, help prognosticate which abnormalities are less likely to resolve over time (2). Han et al (3) recently demonstrated that individuals with post-COVID fibrotic ILAs at six months had persistent fibrosis at 1-year, suggesting that fibrotic ILAs rarely resolve completely. Ultimately, serial imaging, quantitative measures of fibrosis (4), and assessment of pharmaceutical interventions (5), will be key to fully understanding the trajectory of post-COVID fibrosis.

    Secondly, the authors report that disease severity did not significantly impact the development of particular parenchymal abnormalities on CT...

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  • Response to Priyadarshi

    We thank Nimmo et al for their comments on our paper, and for recognising that this work
    addresses an important gap in high quality data on aerosol generation and also the technical
    challenges associated with measuring aerosol from the respiratory tract.
    We agree that interparticipant variability in aerosol emission is significant (spanning several orders
    of magnitude) and acknowledge in the paper that interpretation of the data on patients with COVID-
    19 is limited due to the small cohort size. The AERATOR study was the first group to collect detailed
    aerosol measures from patients with active SARS-CoV-2, the aim of this exploratory sub group
    analysis was to consider if active infection had a meaningful impact on the use of healthy controls as
    proxies in the main analysis.
    Measuring aerosol emission from patients with COVID-19 is very challenging in the acute clinical
    setting because of both the very low aerosol background concentration required to make a
    measurement and infection control precautions. We therefore chose to report the raw data while
    acknowledging the difficulties in interpretation.
    In this analysis, we did not perform a sample size calculation; as we were limited by both
    epidemiological (level of COVID-19 infection in the community) and practical challenges, detailed
    below.
    Future studies could consider the collection of detailed aerosol measures from patients a...

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  • ENVIRONMENTAL CONTAMINATION WITH AEROSOLS FROM HOSPITALISED COVID-19 PATIENTS RECEIVING AEROSOL GENERATING PROCEDURES

    The AERATOR study (Hamilton et al) compares and quantifies the risk of aerosol generation in both healthy patients and those infected with COVID-19 in a variety of contexts, including normal respiration, speaking and coughing, and the same activities whilst receiving therapy with continuous positive airway pressure (CPAP) and high-flow nasal oxygen (HFNO), and also whilst wearing a fluid-resistant surgical mask (FSRM)1. This study is particularly welcome as it is an area where data are scarce, yet the theoretical risks have major implications for both patients and health care professionals and influence recommendations that guide patient care, such as the use of side rooms and personal protective equipment, both of which are limited resources2. However, we have some questions about the study design.

    Hamilton et al demonstrated that the size of aerosols generated by healthy individuals and those infected with COVID-19 were comparable, thereby validating the use of healthy volunteers for aerosol characterisation, though the sample sizes involved within the COVID-19 cohort were relatively small (n=6). Furthermore, the study highlights that aerosolisation was lower in healthy volunteers with non-humidified CPAP, whilst it was increased in those receiving HFNO (though it was shown to originate mostly from the device), compared to baseline for breathing, speaking, and coughing. Given the study also mentions a considerable degree of inter- and intra-individual variability...

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  • View from South East Asia on Post-COVID Fibrotic Lung Disease

    Dear Editor,

    We read with interest McGroder et al’s study on the radiographic findings of patients four months after severe COVID-19 and the associated risk factors. Hürsoy and colleagues’ comment (1) on the paper was equally thought-provoking. We would like to further this discussion by contributing some of our observations from the pulmonology clinic at a major academic medical center in South East Asia.

    It has been tremendously challenging globally to achieve precision in the diagnosis of Interstitial Lung Disease (ILD) post-COVID as invasive testing such as lung biopsies are performed sparingly. Histopathological pulmonary findings have largely remained inaccessible since COVID survivors are hypoxic so biopsies pose a high risk for the patient, and healthcare personnels are reluctant to perform such high-risk procedures. Hence, we are left to derive our diagnosis from radiological data and pulmonary function tests (PFTs) of the patient.

    We propose that a consensus definition be reached for the diagnosis of post-COVID ILD, one that incorporates well-accepted radiological terms (used to represent any interstitial lung disease). We recommend that lung fibrosis only be classified as ILD if the lung parenchymal abnormalities persist for a minimum of six months after the COVID infection has resolved. Post-COVID ILD should then be further subclassified based on distinct radiological patterns. In our retrospective cohort study, four patterns of post-COV...

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  • Malignant Mesothelioma Among Vehicle Mechanics

    Hessel(1) published an editorial concerning mesothelioma among vehicle mechanics and concluded that ‘with nearly two dozen studies of mesothelioma among vehicle mechanics and no evidence of increased risk, it would appear obvious that vehicle mechanics as an occupational group, are not at increased risk of mesothelioma.’ In my opinion Hessel relies too heavily upon epidemiology for his conclusions. Epidemiology is important if studies reliably address the question at issue, but published epidemiologic studies are generally not helpful to the evaluation of risk among vehicle mechanics. Few were designed to be studies of mesothelioma in mechanics. Most are general studies of the disease Mesothelioma in which some of the subjects happened to be mechanics. Since they were not designed to be studies of vehicle mechanics, none of the information necessary for a study of risk, such as the numbers of brake jobs performed, the use of compressed air, sanding or grinding, was collected. Not a single one of the studies had information adequate to compute a quantitative exposure estimate for any of the subjects. Misclassification of exposures will mask risk among those truly exposed(2,3).
    Hessel suggests that the paper in Thorax by Thomsen (4) supports his opinion. The aim of that paper was to compare risk among men in a cohort of vehicle mechanics with a comparison cohort of men not occupationally exposed to asbestos. When studying risk in a population exposed to a toxic subs...

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  • Response to: Letter to the Editor of Thorax by Drs. Marty S. Kanarek and Henry A. Anderson RE: Risk of asbestosis, mesothelioma, other lung diseases or death among motor vehicle mechanics: a 45-year Danish cohort study

    We appreciate the thoughtful letter from Drs. Kanarek and Anderson. Our study does not address the well-established fact that asbestos exposure is the main causal factor of mesothelioma. The objective of our study was to investigate the risk of mesothelioma (and other asbestos related diseases) in motor vehicle mechanics. The key finding is that Danish motor vehicle mechanics do not on average have an elevated risk of mesothelioma during the studied up to 45 years of follow-up. This does not exclude the possibility that some subpopulations of motor vehicle mechanics with more extreme exposure/latency time are at increased risk – but this occupation as a group is not.

    We agree that exposure misclassification is a potential problem in epidemiology studies based on occupation and industry titles. We also agree that lifetime asbestos exposure histories, if they could be obtained, might reduce exposure misclassification. However, asbestos exposure is often not recognized or recalled by workers, and workers often do not recall jobs in the distant past. Also, experts may misclassify self-reported jobs regarding asbestos exposure, particularly with respect to asbestos fiber type. Thus, while Drs. Kanarek and Anderson claim “obtaining an individual lifetime occupational and environmental exposure history is crucial to understanding individual work-related causes of disease” they offer no practical advice on how reliable asbestos exposure histories can be obtained. They also...

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  • Author response: Eosinophils as covariates

    We thank James R Camp for his response and interest in our study. To answer the question posed directly, we did not use blood eosinophils as a covariate in the model, since leukocyte differential count is not routinely made at every outpatient visit for COPD patients in Denmark.

    The relation between blood eosinophils in COPD and pulmonary infections is not a trivial one. As mentioned by James R Camp, mouse models indicate that eosinophils have antibacterial properties in vitro (1). However, few clinical studies have included blood eosinophil counts as a risk factor of pneumonia in COPD, mostly showing either a weak or no association (2,3).

    Eosinophils from human blood have been demonstrated to have bactericidal effects against S. aureus and E. coli, but noteworthy, this effect was not as potent as the neutrophils (4). Additionally, severe acute bacterial infection like sepsis almost uniformly causes eosinopenia (5,6) and experimental lipopolysaccharide injection in healthy humans and diabetic humans cause profound and long-lasting eosinopenia (7). This is not easily comprehensible if the eosinophils are a needed part of the innate host immune response to bacterial infection.

    An alternative explanation for a possible association could be that eosinophils and neutrophils act in bacterial infection in a complex interplay, while regulating and adjusting the response of each other. To support this, it has been demonstrated that integrin β chain-2 (CD18),...

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