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Context: Epidemiological studies involving patients with acromegaly have yielded conflicting results regarding cancer incidence and causes of mortality in relation to control of growth hormone (GH) excess. Objective: The objective of this retrospective cohort study is to clarify these questions and identify goals for treatment and monitoring patients. Methods: We studied 1845 subjects from the UK Acromegaly Register (1970–2016), obtaining cancer standardised incidence rates (SIR) and all causes standardised mortality rates (SMR) from UK Office for National Statistics, to determine the relationship between causes of mortality—age at diagnosis, duration of disease, post‐treatment and mean GH levels. Results: We found an increased incidence of all cancers (SIR, 1.38; 95% CI: 1.06–1.33, p <.001), but no increase in incidence of female breast, thyroid, colon cancer or any measure of cancer mortality. All‐cause mortality rates were increased (SMR, 1.35; 95% CI: 1.24–1.46, p <.001), as were those due to vascular and respiratory diseases. All‐cause, all cancer and cardiovascular deaths were highest in the first 5 years following diagnosis. We found a positive association between post‐treatment and mean treatment GH levels and all‐cause mortality (p <.001 and p <.001), which normalised with posttreatment GH levels of <1.0 µg/L or meantreatment GH levels of <2.5 µg/L. Conclusion: Acromegaly is associated with increased incidence of all cancers but not thyroid or colon cancer and no increase in cancer mortality. Excess mortality is due to vascular and respiratory disease. The risk is highest in the first 5 years following diagnosis and is mitigated by normalising GH levels. [ABSTRACT FROM AUTHOR]

The article focuses on the findings of GINA 2024, the latest update to the Global Initiative for Asthma report, for the management of patients with respiratory illness. GINA defines the level of asthma control as the extent to which the features of asthma can be observed in the patient, or have been reduced or removed by treatment. It is suggested that control should be assessed in two parts: symptom control and the risk of adverse outcomes.

Objectives. To quantify past reductions in cold-related mortality attributable to anthropogenic climate change. Methods. We performed a daily time-series regression analysis employing distributed lag nonlinear models of 1 203 981 deaths in Greater London, United Kingdom, in winter months (November–March) during 1976 to 2019. We made attribution assessment by comparing differential cold-related mortality impacts associated with observed temperatures to those using counterfactual temperatures representing no climate change. Results. Over the past decade, the average number of cold days (below 8 °C) per year was 120 in the observed series and 158 in the counterfactual series. Since 1976, we estimate 447 (95% confidence interval = 330, 559) annual cold-related all-cause deaths have been avoided because of milder temperatures associated with climate change. Annually, 241 cardiovascular and 73 respiratory disease deaths have been avoided. Conclusions. Anthropogenic climate change made some contribution to reducing previous cold-related deaths in London; however, cold remains an important public health risk factor. Public Health Implications. Better adaptation to both heat and cold should be promoted in public health measures to protect against climate change. In England, this has been addressed by the development of a new year-round Adverse Weather and Health Plan. (Am J Public Health. 2024;114(4):398–402. https://doi.org/10.2105/AJPH.2023.307552) [ABSTRACT FROM AUTHOR]

Background: Previous studies have shown that respiratory diseases are associated with an increased risk of rheumatoid arthritis (RA). However, whether there is a correlation between chronic rhinosinusitis (CRS) and RA is not known. Due to the high incidence of CRS, it remains to be clarified whether we should pay additional attention to RA risk in the huge population of CRS. Methods: We used a 2-sample Mendelian randomization (MR) analysis to explore the causal effects of CRS on the incidence of RA. The inverse variance weighted (IVW) approach was used as the main analysis in the MR randomization study. Then, we used the data from the U.K. Biobank to examine the association between RA and CRS at the individual level in a prospective cohort. We identified patients with CRS at the time of recruitment and further followed the incidence of RA until 2021. The risk of developing RA in patients with CRS was determined by a multivariate Cox regression model. We used 3 multivariate Cox models to adjust for individual characteristics, lifestyle factors and concomitant diseases, respectively. Results: The MR analysis by the IVW model suggested that the odds ratio of RA associated with genetically predicted CRS was 2.39 (95% CI [1.08-5.30]; p =.032). In the first multivariate model adjusting for individual characteristics, CRS was associated with a 47% increase of risk of developing RA (hazard ratio [HR] = 1.47; 95% CI [1.12-1.90]). In the second multivariate model adjusting for lifestyle factors, the HR of RA associated with CRS was 1.48 (95% CI [1.15-1.90]). In the third multivariate model, chronic sinusitis was associated with a 32% increase in RA risk (HR = 1.32; 95% CI [1.03-1.70]). Conclusion: CRS has a genetically causal effect on the incidence of RA, and the risk of RA is greatly higher in CRS at the individual level. This is the first study to reveal an association between CRS and RA. Due to the high incidence of CRS, it is recommended that additional attention should be paid to the increased RA risk in patients with CRS compared to that in common people. [ABSTRACT FROM AUTHOR]

While rare, the likelihood of encountering a case of a pulmonary endemic mycosis (PEM) in the UK is increasing. Diagnosis may be challenging, often leading to considerable delay to appropriate treatment. Clinical suspicion must be present for respiratory disease, particularly in the immunocompromised or in those not responding to empiric treatment approaches, and an extended travel history should be obtained. This article summarises the epidemiology of PEM, key clinical features, diagnostic strategies and management. [ABSTRACT FROM AUTHOR]

People failing to give a specimen of breath at a police station are assumed to be deliberately obstructive and are charged with Failure to Provide under the Road Traffic Act 1988. However, spirometry records of 281,210 healthy individuals from UK BioBank showed that a significant minority cannot use existing evidential breath analysis machines. Women were three times more likely to be unable to use them than men (1.64% vs 0.54%) with the risk rising with age six-fold from those in their 40s (0.43%) to 2.7% in their 70s, with women more affected (0.65% to 3.8%). Short stature was a further risk factor: 2.6% of men and 3.8% of women below the 2nd percentile of height could not use the current machines, with almost one in ten elderly, short women unable to do so, while smokers aged 50+ were twice as likely as non-smokers of the same age to be unable to provide breath specimens. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic led to unparalleled pressure on healthcare services. Improved healthcare planning in relation to diseases affecting the respiratory system has consequently become a key concern. We investigated the value of integrating sales of non-prescription medications commonly bought for managing respiratory symptoms, to improve forecasting of weekly registered deaths from respiratory disease at local levels across England, by using over 2 billion transactions logged by a UK high street retailer from March 2016 to March 2020. We report the results from the novel AI (Artificial Intelligence) explainability variable importance tool Model Class Reliance implemented on the PADRUS model (Prediction of Amount of Deaths by Respiratory disease Using Sales). PADRUS is a machine learning model optimised to predict registered deaths from respiratory disease in 314 local authority areas across England through the integration of shopping sales data and focused on purchases of non-prescription medications. We found strong evidence that models incorporating sales data significantly out-perform other models that solely use variables traditionally associated with respiratory disease (e.g. sociodemographics and weather data). Accuracy gains are highest (increases in R2 (coefficient of determination) between 0.09 to 0.11) in periods of maximum risk to the general public. Results demonstrate the potential to utilise sales data to monitor population health with information at a high level of geographic granularity. Novel indicators of infectious disease prevalence could improve real-time surveillance and support healthcare planning. Here, the authors show that sales data for non-prescription medications from a UK high street retailer can improve the accuracy of models forecasting mortality from respiratory infections. [ABSTRACT FROM AUTHOR]

Elite rugby union players face numerous physiological and psychological stressors which can increase upper respiratory and gastrointestinal illness risk, and in turn can compromise training and competitive performance. This study aimed to investigate the effect of daily prebiotic supplementation on upper respiratory symptoms, gastrointestinal symptoms, and markers of immune function in elite rugby union players. Thirty-three elite rugby union players were randomly assigned to consume a prebiotic (2.8 g/day galactooligosaccharide) or placebo (2.8 g/day maltodextrin), daily for 168 days under double-blind conditions. Participants completed daily and weekly questionnaires for self-reported upper respiratory and gastrointestinal symptoms respectively. Blood and saliva samples were collected at 0, 84, and 168 days for assessment of plasma TNF-α and CRP, and saliva IgA respectively. The prebiotic group experienced a 2-day reduction in upper respiratory symptom duration (P = 0.045). Gastrointestinal symptom severity and incidence were lower in the prebiotic group compared to the placebo group (P < 0.001, P = 0.041) respectively. Salivary immunoglobulin A secretion rate was 42% greater in the prebiotic group compared to the placebo group at day 168 (P = 0.004), no differences in CRP and TNF-α were found (P > 0.05). A 168-day dietary prebiotic intervention reduced the duration of upper respiratory symptoms and reduced the incidence and severity of gastrointestinal symptoms in elite rugby union players. These findings suggest that seasonal prebiotic interventions may be beneficial for reducing illness in elite rugby union players, improving their availability to train and compete. Key points Elite athletes are susceptible to upper respiratory symptoms and gastrointestinal symptoms which may impact upon training availability and competition performance. For the first time, this study shows that a dietary prebiotic intervention can reduce the duration of upper respiratory symptoms by 2 days in elite rugby union players. Dietary prebiotic supplementation can improve the incidence and severity of gastrointestinal symptoms experienced by elite rugby union players. Prebiotic supplementation was able to increase salivary IgA secretion after 168 days. These findings can inform practice suggesting that seasonal prebiotic use has the potential to modulate immune function and reduce illness in elite rugby union, which may improve a player's availability to train and compete. The mechanisms by which prebiotics reduce URS and GIS require further research exploration. [ABSTRACT FROM AUTHOR]

While some evidence of an effect of radiation exposure on respiratory disease at low dose levels has now emerged, there is heterogeneity in the risks between different studies and countries. In this paper, we aim to show the effect of radiation on three different sub-types of respiratory disease mortality through the analysis of the NRRW cohort in UK. The NRRW cohort consisted of 174,541 radiation workers. Doses to the surface of the body were monitored using individual film badges. Most of the doses are associated with X-rays and gamma rays and to a less extent of beta and neutron particles. The overall mean 10-year lagged lifetime external dose was 23.2 mSv. Some workers were potentially exposed to alpha particles. However, doses from internal emitters were not available for the NRRW cohort. 25% of male workers and 17% of female workers were identified as being monitored for internal exposure. The Poisson regression methods for grouped survival data with a stratified baseline hazard function were used to describe the dependence of the risk on cumulative external radiation dose. The disease was analyzed by the following subgroups: Pneumonia (1066 cases including 17 cases of influenza), COPD and allied disease (1517 cases) and other remaining respiratory diseases (479 cases). There was very little radiation effect on pneumonia mortality, but evidence of a reduction in mortality risk for COPD and allied disease (ERR/Sv= −0.56, 95%CI: −0.94, −0.06; p =.02) and an increase in risk for other respiratory disease mortality (ERR/Sv = 2.30, 95%CI: 0.67, 4.62; p =.01) with increasing cumulative external dose were observed. The effects of radiation were more prominent amongst workers monitored for internal exposure. The reduction in mortality risk of COPD and allied disease per cumulative external dose was statistically significant for the radiation workers monitored for internal exposure (ERR/Sv= −0.59, 95%CI: −0.99, −0.05; p =.017) but not significant among the workers who were not monitored (ERR/Sv= −0.43, 95%CI: −1.20, 0.74; p =.42). A statistically significant increased risk was observed for other respiratory diseases among monitored radiation workers (ERR/Sv = 2.46, 95%CI: 0.69, 5.08; p =.019), but not among unmonitored workers (ERR/Sv = 1.70, 95%CI: −0.82, 5.65; p =.25). The effects of radiation exposure can be different depending on the type of respiratory disease. No effect was seen in pneumonia; a reduction in mortality risk of COPD, and increased mortality risk of other respiratory diseases were observed with cumulative external radiation dose. More studies are needed to verify these findings. [ABSTRACT FROM AUTHOR]

Objectives: To test the hypotheses that: (1) Prevalence of periodontal disease would be higher in people with a history of psychosis when compared to the general population and (2) Demographic, life‐style related factors and co‐morbid medical conditions would predict periodontal disease in people experiencing psychosis. Methods: The authors performed cross‐sectional analysis of baseline data from the UK Biobank study (2007–2010), identifying cases with psychosis using clinical diagnosis, antipsychotic medication, and self‐report. Demographic (age, gender, ethnicity, socioeconomic status), lifestyle‐related(BMI, blood pressure, smoking and alcohol intake, physical activity) and physical co‐morbidities (cancer, cardiovascular, respiratory, inflammatory disease and metabolic conditions) were included as potential risk factors for periodontal disease among people with a history of psychosis using logistic regression analyses. The analysis sample included 502,505 participants. Results: Risk of periodontal disease was higher in people with psychosis, regardless of how cases were identified. Patients with a clinical diagnosis had the highest proportion of periodontal disease compared to the general population (21.3% vs. 14.8%, prevalence ratio 1.40, 95% CI: 1.26–1.56). Older and female cases were more likely to experience periodontal disease. Lifestyle factors (smoking) and comorbidities (cardiovascular, cancer or respiratory disease) were associated with periodontal disease among people with a history of psychosis. Conclusions: The findings suggest that periodontal disease is more common in people with a history of psychosis, compared to the general population. Prevention and early diagnosis of periodontal disease should be a priority for oral health promotion programmes, which should also address modifiable risk factors like smoking which also contribute to co‐morbid systemic disease. [ABSTRACT FROM AUTHOR]

Background: No existing comprehensive Mendelian randomization studies have focused on how obesity affects respiratory diseases. Methods: BMI and waist circumference, mainly from the UK Biobank, and 35 respiratory diseases from the FinnGen Biobank were subjected to Mendelian randomization analyses. In this study, the inverse variance weightingmethod was used as the predominant analysis method and was complemented by MR-Egger and weightedmedianmethods. Horizontal pleiotropy and potential outliers were detected by employing the MR-PRESSO method. Results:: This study indicated that obesity rises the possibility of acute upper respiratory infections (BMI: OR=1.131, p<0.0001; WC: OR=1.097, p=0.00406), acute sinusitis (BMI: OR=1.161, p=0.000262; WC: OR=1.209, p=0.000263), acute pharyngitis (WC: OR=1.238, p=0.0258), acute laryngitis and tracheitis (BMI: OR=1.202, p=0.0288; WC: OR=1.381, p=0.00192), all influenza (BMI: OR=1.243, p=0.000235; WC: OR=1.206, p=0.0119), viral pneumonia (WC: OR=1.446, p=0.000870), all pneumoniae (BMI: OR=1.174, p <0.0001; WC: OR=1.272, p <0.0001), bacterial pneumoniae (BMI: OR=1.183, p=0.000290; WC: OR=1.274, p<0.0001), acute bronchitis (BMI: OR=1.252, p <0.0001; WC: OR=1.237, p=0.000268), acute unspecified lower respiratory infection (BMI: OR=1.303, p=0.000403), chronic tonsils and adenoids diseases (BMI: OR=1.236, p <0.0001; WC: OR=1.178, p=0.000157), chronic laryngotracheitis and laryngitis (WC: OR=1.300, p=0.00785), COPD (BMI: OR=1.429, p <0.0001; WC: OR=1.591, p <0.0001), asthma (BMI: OR=1.358, p <0.0001; WC: OR=1.515, p <0.0001), necrotic and suppurative conditions of lower respiratory tract (WC: OR=1.405, p=0.0427), pleural effusion (BMI: OR=1.277, p=0.00225; WC: OR=1.561, p<0.0001), pleural plaque (BMI: OR=1.245, p=0.0312), other diseases of the respiratory system (BMI: OR=1.448, p <0.0001; WC: OR=1.590, p <0.0001), and non-small cell lung cancer (BMI: OR=1.262, p=0.00576; WC: OR=1.398, p=0.00181). This study also indicated that obesity decreases the possibility of bronchiectasis (BMI: OR=0.705; p=0.00200). Conclusion:: This study revealed that obesity increases the risk of the majority of respiratory diseases (including 20 of all 35 respiratory diseases) and that obesity decreases the risk of bronchiectasis. [ABSTRACT FROM AUTHOR]

Objectives: Feline herpesvirus (FHV), feline calicivirus (FCV) and Chlamydia felis are common causes of upper respiratory tract disease (URTD) in cats. Their prevalence in the UK pet cat population has not been reported and little is known regarding the risk factors for their oral carriage. Methods: Total nucleic acid was extracted from owner‐collected buccal swabs (n=600) from cats enrolled in a self‐selected longitudinal cohort study. Duplex quantitative PCRs for the detection of FHV and C. felis genomic DNA and reverse‐transcriptase quantitative PCRs for the detection of FCV genomic RNA were performed. Duplicates, swabs with insufficient host DNA/RNA, and cats with missing data were excluded. Selected epidemiological data were interrogated using univariable and multi‐variable logistic regression modelling to identify risk factors. Results: Data from 430 cats were included in the final statistical model. Of these, 2.1% (n=9/430; 95% CI 1.0% to 3.9%) were positive for FHV, 13.3% (n=57/430; 95% CI 10.2% to 16.8%) positive for FCV and 1.2% (n=5/430; 95% CI 0.4% to 2.7%) positive for C. felis. FCV co‐infection was present in five (44%) FHV‐positive cats and three (60%) C. felis‐positive cats. FCV carriage was more frequent in purebred cats (odds ratio 2.48; 95% CI 1.37 to 4.49) and in cats with current or historical clinical signs compatible with URTD (odds ratio 2.98; 95% CI 1.22 to 7.27). Clinical Significance: FCV was the most frequently encountered URTD pathogen in this sample of cats; this should be noted for disinfectant choice. In cats suspected of having FHV or C. felis infection, assessment for co‐infection with FCV is recommended. [ABSTRACT FROM AUTHOR]

Early detection of highly infectious respiratory diseases, such as COVID-19, can help curb their transmission. Consequently, there is demand for easy-to-use population-based screening tools, such as mobile health applications. Here, we describe a proof-of-concept development of a machine learning classifier for the prediction of a symptomatic respiratory disease, such as COVID-19, using smartphone-collected vital sign measurements. The Fenland App study followed 2199 UK participants that provided measurements of blood oxygen saturation, body temperature, and resting heart rate. Total of 77 positive and 6339 negative SARS-CoV-2 PCR tests were recorded. An optimal classifier to identify these positive cases was selected using an automated hyperparameter optimisation. The optimised model achieved an ROC AUC of 0.695 ± 0.045. The data collection window for determining each participant's vital sign baseline was increased from 4 to 8 or 12 weeks with no significant difference in model performance (F(2) = 0.80, p = 0.472). We demonstrate that 4 weeks of intermittently collected vital sign measurements could be used to predict SARS-CoV-2 PCR positivity, with applicability to other diseases causing similar vital sign changes. This is the first example of an accessible, smartphone-based remote monitoring tool deployable in a public health setting to screen for potential infections. [ABSTRACT FROM AUTHOR]

The previous acute respiratory diseases caused by viruses originating from China or the middle east (e.g., SARS, MERS) remained fast developing short diseases without major sequalae or any long-lasting complications. The new COVID-19, on the other hand, not only that it rapidly spread over the world, but some patients never fully recovered or even if they did, a few weeks later started to complain not only of shortness of breath, if any, but general weakness, muscle pains and 'brain fog', i.e., fuzzy memories. Thus, these signs and symptoms were eventually labelled 'long COVID', for which the most widely used definition is 'new signs and symptoms occurring 4–8 weeks after recovering from acute stage of COVID-19'. The other most frequent manifestations associated with long COVID include headache, loss of memory, smell and of hair, nausea, and vomiting. Thus, long COVID is not a simple disease, but complex disorder of several organ systems malfunctioning; hence, it is probably more appropriate to call this a syndrome. The pathogenesis of long COVID syndrome is poorly understood, but initial and persistent vascular endothelial injury that often triggers the formation of microthrombi that if dislodged as emboli, damage several organs, especially in the brain, heart and kidney, by creating microinfarcts. The other major contributory mechanistic factor is the persistent cytokine storm that may last longer in long COVID patients than in others, probably triggered by aggregates of SARS-Co-2 discovered recently in the adrenal cortex, kidney and brain. The prevalence of long COVID is relatively high, e.g., initially varied 3–30%, and recent data indicate that 2.5% of UK population suffers from this syndrome, while in the US 14.7% of acute COVID-19 patients continued to have symptoms longer than 2 months. Thus, the long COVID syndrome deserves to be further investigated, both from clinical and basic research perspectives. [ABSTRACT FROM AUTHOR]

Introduction: Pertussis, a highly infectious respiratory disease caused by Bordetella pertussis, affects people of all ages. Older adults are particularly susceptible to its severe outcomes and complications. Methods: In this retrospective cohort study, the incidence rate of pertussis among individuals aged ≥ 50 years was assessed during 2009–2018 using Clinical Practice Research Datalink and Hospital Episode Statistics databases, United Kingdom. Health care resource utilisation (HCRU) and direct medical costs (DMCs) were compared between patients with a pertussis diagnosis and propensity score-matched controls (matched on demographic and clinical variables). Results: Among 5,222,860 individuals, 1638 had a pertussis diagnosis (incidence rate: 5.8 per 100,000 person-years; 95% confidence interval 5.5–6.0). Baseline (– 18 to – 6 months) HCRU and DMC were similar among 1480 pertussis patients and 1480 matched controls. However, there were increases in HCRU in the pertussis vs. matched cohort around the pertussis diagnosis (from months – 6 to – 1 to 5–11). The most notable increases (pertussis vs. controls) were in the rates of general practitioner (GP)/nurse visits (4.7-fold), clinical assessments (4.1-fold), and accident and emergency visits (3.0-fold) during the month before diagnosis and GP/nurse visits during the 2 months after diagnosis (2.5-fold) (all p < 0.001). DMCs were significantly higher in the pertussis cohort (p < 0.001). Total excess DMC in the pertussis cohort during months – 1 to + 11 was £318 per patient. Conclusion: A pertussis diagnosis among adults aged ≥ 50 years resulted in significant increases in HCRU and DMC across several months around diagnosis. These results highlight the need for increased awareness of pertussis infection among adults aged ≥ 50 years and suggest that pertussis booster doses among this population should be considered. [ABSTRACT FROM AUTHOR]

Simple Summary: (Multi-)Morbidity shares common biological mechanisms or risk factors with breast cancer. However, the risk of breast cancer among women with (multi-)morbidity remains unclear. In this study, using data of 239,436 female participants aged 40–69 of the UK Biobank cohort, we identified five chronic disease patterns: no-predominant morbidity, psychiatric morbidities, respiratory/immunological morbidities, cardiovascular/metabolic morbidities, and unspecific morbidities. After a median follow-up of 7 years, 5326 women developed breast cancer. We found no association between breast cancer risk and either the number of chronic diseases or chronic disease patterns, apart from an increased risk among women aged younger than 50 with a psychiatric pattern. Women with any multi-morbidity were more likely to die or to be diagnosed with other cancers. Our findings suggest that multi-morbidity may not be a key factor to help identify patients at an increased risk of breast cancer. (Multi-)Morbidity shares common biological mechanisms or risk factors with breast cancer. This study aimed to investigate the association between the number of morbidities and patterns of morbidity and the risk of female breast cancer. Among 239,436 women (40–69 years) enrolled in the UK Biobank cohort who had no cancer history at baseline, we identified 35 self-reported chronic diseases at baseline. We assigned individuals into morbidity patterns using agglomerative hierarchical clustering analysis. We fitted Cox models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for breast cancer risk. In total, 58.4% of women had at least one morbidity, and the prevalence of multi-morbidity was 25.8%. During a median 7-year follow-up, there was no association between breast cancer risk (5326 cases) and either the number of morbidities or the identified clinically relevant morbidity patterns: no-predominant morbidity (reference), psychiatric morbidities (HR = 1.04, 95%CI 0.94–1.16), respiratory/immunological morbidities (HR = 0.98, 95%CI 0.90–1.07), cardiovascular/metabolic morbidities (HR = 0.93, 95%CI 0.81–1.06), and unspecific morbidities (HR = 0.98, 95%CI 0.89–1.07), overall. Among women younger than 50 years of age only, however, there was a significant association with psychiatric morbidity patterns compared to the no-predominant morbidity pattern (HR = 1.25, 95%CI 1.02–1.52). The other associations did not vary when stratifying by age at baseline and adherence to mammography recommendations. In conclusion, multi-morbidity was not a key factor to help identify patients at an increased risk of breast cancer. [ABSTRACT FROM AUTHOR]

Background: Trauma is a well-known risk factor for many disease, but the effect of trauma on respiratory disease is unclarified. In the present study, we aimed to evaluate the association between trauma and respiratory disease. Method: Using both United Kingdom biobank and Finnish biobank genomewide association study data (GWAS), we performed a two-sample Mendelian randomization (MR) analysis to evaluate the relationship between trauma and respiratory disease. We used four methods including inverse-variance weighted (IVW), weighted median, Maximum likelihood, and MR-Egger in this MR analysis. The IVW MR was selected as the main method. We also performed multivariable Mendelian randomization (MVMR) to simultaneously assess the independent impact of trauma exposure on respiratory disease. Results: In the main two-sample MR analysis, trauma exposure was significantly associated with increased risk of respiratory disease (OR 1.15, 95%CI: 1.05-1.25). Besides, there was no heterogeneity and horizontal pleiotropy observed in the sensitivity analysis. After adjusting for pack years of smoking and body mass index (BMI), trauma exposure retained its association with respiratory disease (OR, 1.13, 95%CI, 1.04-1.23 adjusted by pack years of smoking; and OR, 1.11, 95%CI, 1.04-1.18 adjusted by BMI). Conclusion: Our study discovered the association between trauma exposure and the increased risk of respiratory disease, suggesting the prevention and treatment with trauma to reduce the risk of respiratory disease. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to find out if patients can travel safely on a plane 48 hours after open septo-rhinoplasty (SRP) surgery. Also, to compare analgesic need, mobilization time, readmission rate, side effects, time out of work and routine life between travelling and nontravellingpatients. Materials and Methods: This study was conducted at Istanbul Florence Nightingale Hospitals in Istanbul/Turkey and Group Florence Hospitals in London/United Kingdom. A total of 120 patients who had SRP were included in the study. Sixty patients who traveled from London to Istanbul by plane (approximately 3 hours 40 minutes, 2520 km) for SRP surgery and returned home 48 hours after surgery were compared with 60 local patients. All patients were observed at 8, 12, 24, 36, and 48 hour intervals after surgery. Additionally, all patients who travelled from London to Istanbul were reviewed after 6 days, 14 days, 1 month, 3 months, 6 months and 1 year. The analgesia need, mobilization time, readmission rate, early and late complications patterns and incidence, time out of work and daily routine was compared between the two groups. Early onset side effects include pain, discomfort, bruising, ecchymosis, edema, oozing, bleeding, septal haematoma, and late onset complications like delayed septal haematoma, delayed bleeding, infection, excess edema, breathing problems were compared between travelling and nontravelling patients. Results: The hospital stay was 24 hours for all patients. No further analgesia was needed in both groups during their hospital stay, Mobilization time was in 8 hours in both groups and none of the patients needed readmission in both groups. Common early complications in travelling patients like pain, edema, bruising, ecchymosis, minor oozing, blocked nose, and pain after 48 hours were similar to the local patients and all travelling patients felt confident and strong enough to travel after 48 hours without additional medication or treatment during or after the surgery. Conclusion: People with no underlying medical conditions, who want to travel abroad for surgery and cannot or do not want to stay longer than 48 hours due to their personal or business lives, can consider travelling back to their countries, following SRP surgery, which is as safe as having the surgery locally without travelling abroad. [ABSTRACT FROM AUTHOR]

Linguatula serrata, also known as tongue worm, is a zoonotic parasite that lives in the nasal airways of dogs where it is responsible for mild to severe rhinosinusitis. In recent years, the number of pets entering the United Kingdom from abroad has increased, with a coinciding increase in the number of L. serrata infections diagnosed in UK veterinary clinics. Here, we report a case of linguatulosis in a 10‐month‐old rescued dog imported from Romania. Two weeks post‐arrival, the dog showed coughing, nasal discharge, epiphora and respiratory distress. Two worm‐like parasites were expelled by sneezing and they were morphologically identified as L. serrata. L. serrata eggs were also detected. A macrocyclic lactone treatment was administered, and clinical signs resolved. L. serrata should be included in the differential diagnosis of respiratory disease in imported dogs. Due to the zoonotic potential of this parasite, rapid diagnosis and correct treatment is essential. [ABSTRACT FROM AUTHOR]

(1) Background: Coronavirus disease 2019 (COVID-19) is a dominant, rapidly spreading respiratory disease. However, the factors influencing COVID-19 mortality still have not been confirmed. The pathogenesis of COVID-19 is unknown, and relevant mortality predictors are lacking. This study aimed to investigate COVID-19 mortality in patients with pre-existing health conditions and to examine the association between COVID-19 mortality and other morbidities. (2) Methods: De-identified data from 113,882, including 14,877 COVID-19 patients, were collected from the UK Biobank. Different types of data, such as disease history and lifestyle factors, from the COVID-19 patients, were input into the following three machine learning models: Deep Neural Networks (DNN), Random Forest Classifier (RF), eXtreme Gradient Boosting classifier (XGB) and Support Vector Machine (SVM). The Area under the Curve (AUC) was used to measure the experiment result as a performance metric. (3) Results: Data from 14,876 COVID-19 patients were input into the machine learning model for risk-level mortality prediction, with the predicted risk level ranging from 0 to 1. Of the three models used in the experiment, the RF model achieved the best result, with an AUC value of 0.86 (95% CI 0.84–0.88). (4) Conclusions: A risk-level prediction model for COVID-19 mortality was developed. Age, lifestyle, illness, income, and family disease history were identified as important predictors of COVID-19 mortality. The identified factors were related to COVID-19 mortality. [ABSTRACT FROM AUTHOR]

Background: Electronic health record (EHR) databases provide rich, longitudinal data on interactions with healthcare providers and can be used to advance research into respiratory conditions. However, since these data are primarily collected to support health care delivery, clinical coding can be inconsistent, resulting in inherent challenges in using these data for research purposes. Methods: We systematically searched existing international literature and UK code repositories to find respiratory disease codelists for asthma from January 2018, and chronic obstructive pulmonary disease and respiratory tract infections from January 2020, based on prior searches. Medline searches using key terms provided in article lists. Full-text articles, supplementary files, and reference lists were examined for codelists, and codelists repositories were searched. A reproducible methodology for codelists creation was developed with recommended lists for each disease created based on multidisciplinary expert opinion and previously published literature. Results: Medline searches returned 1126 asthma articles, 70 COPD articles, and 90 respiratory infection articles, with 3%, 22% and 5% including codelists, respectively. Repository searching returned 12 asthma, 23 COPD, and 64 respiratory infection codelists. We have systematically compiled respiratory disease codelists and from these derived recommended lists for use by researchers to find the most up-to-date and relevant respiratory disease codelists that can be tailored to individual research questions. Conclusion: Few published papers include codelists, and where published diverse codelists were used, even when answering similar research questions. Whilst some advances have been made, greater consistency and transparency across studies using routine data to study respiratory diseases are needed. [ABSTRACT FROM AUTHOR]

Background: Mannheimia haemolytica is commonly associated with respiratory disease in cattle worldwide as a cause of fibrinous pneumonia, bronchopneumonia and pleuritis. M. haemolytica is further subdivided into 12 serovars, however not all are considered to be pathogenic in cattle. The study aim was to determine the most common serovars of M. haemolytica associated with respiratory disease in cattle in Great Britain, which is currently unknown and could be useful information for clinicians when considering preventative strategies. Results: One hundred four M. haemolytica isolates isolated from bovine clinical pathology and post-mortem samples from pneumonia cases between 2016 and 2018 were tested using a multiplex PCR assay to identify M. haemolytica serovars A1, A2 and A6. 46 isolates (44.2%) typed as M. haemolytica serovar A1, 31 (29.8%) as M. haemolytica serovar A2 and 18 isolates (17.3%) as M. haemolytica serovar A6. Nine isolates (8.7%) were not A1, A2 or A6 so were considered to belong to other serovars or were not typable. Conclusion: This study highlights the importance of M. haemolytica serovars other than A1 which may be responsible for respiratory disease in cattle and could help guide the veterinarian when making choices on preventative vaccination programmes. [ABSTRACT FROM AUTHOR]

Background: COVID-19 is characterized by strikingly large, mostly unexplained, interindividual variation in symptom severity: while some individuals remain nearly asymptomatic, others suffer from severe respiratory failure. Previous vaccinations for other pathogens, in particular tetanus, may partly explain this variation, possibly by readying the immune system. Methods: We made use of data on COVID-19 testing from 103,049 participants of the UK Biobank (mean age 71.5 years, 54.2% female), coupled to immunization records of the last ten years. Using logistic regression, covarying for age, sex, respiratory disease diagnosis, and socioeconomic status, we tested whether individuals vaccinated for tetanus, diphtheria or pertussis, differed from individuals that had only received other vaccinations on 1) undergoing a COVID-19 test, 2) being diagnosed with COVID-19, and 3) whether they developed severe COVID-19 symptoms. Results: We found that individuals with registered diphtheria or tetanus vaccinations are less likely to develop severe COVID-19 than people who had only received other vaccinations (diphtheria odds ratio (OR)=0.47, p-value=5.3*10-5; tetanus OR=0.52, p-value=1.2*10-4). Discussion: These results indicate that a history of diphtheria or tetanus vaccinations is associated with less severe manifestations of COVID-19. These vaccinations may protect against severe COVID-19 symptoms by stimulating the immune system. We note the correlational nature of these results, yet the possibility that these vaccinations may influence the severity of COVID-19 warrants follow-up investigations. [ABSTRACT FROM AUTHOR]

Background: Non-communicable diseases (NCDs) have been highlighted as important risk factors for COVID-19 mortality. However, insufficient data exist on the wider context of infectious diseases in people with NCDs. We aimed to investigate the association between NCDs and the risk of death from any infection before the COVID-19 pandemic (up to Dec 31, 2019).Methods: For this observational study, we used data from the UK Biobank observational cohort study to explore factors associated with infection death. We excluded participants if data were missing for comorbidities, body-mass index, smoking status, ethnicity, and socioeconomic deprivation, and if they were lost to follow-up or withdrew consent. Deaths were censored up to Dec 31, 2019. We used Poisson regression models including NCDs present at recruitment to the UK Biobank (obesity [defined by use of body-mass index] and self-reported hypertension, chronic heart disease, chronic respiratory disease, diabetes, cancer, chronic liver disease, chronic kidney disease, previous stroke or transient ischaemic attack, other neurological disease, psychiatric disorder, and chronic inflammatory and autoimmune rheumatological disease), age, sex, ethnicity, smoking status, and socioeconomic deprivation. Separate models were constructed with individual NCDs replaced by the total number of prevalent NCDs to define associations with multimorbidity. All analyses were repeated with non-infection-related death as an alternate outcome measure to establish differential associations of infection death and non-infection death. Associations are reported as incidence rate ratios (IRR) accompanied by 95% CIs.Findings: After exclusion of 9210 (1·8%) of the 502 505 participants in the UK Biobank cohort, our study sample comprised 493 295 individuals. During 5 273 731 person-years of follow-up (median 10·9 years [IQR 10·1-11·6] per participant), 27 729 deaths occurred, of which 1385 (5%) were related to infection. Advancing age, male sex, smoking, socioeconomic deprivation, and all studied NCDs were independently associated with the rate of both infection death and non-infection death. Compared with White ethnicity, a pooled Black, Asian, and minority ethnicity group was associated with a reduced risk of infection death (IRR 0·64, 95% CI 0·46-0·87) and non-infection death (0·80, 0·75-0·86). Stronger associations with infection death than with non-infection death were observed for advancing age (age 65 years vs 45 years: 7·59, 95% CI 5·92-9·73, for infection death vs 5·21, 4·97-5·48, for non-infection death), current smoking (vs never smoking: 3·69, 3·19-4·26, vs 2·52, 2·44-2·61), socioeconomic deprivation (most vs least deprived quintile: 2·13, 1·78-2·56, vs 1·38, 1·33-1·43), class 3 obesity (vs non-obese: 2·21, 1·74-2·82, vs 1·55, 1·44-1·66), hypertension (1·36, 1·22-1·53, vs 1·15, 1·12-1·18), respiratory disease (2·21, 1·96-2·50, vs 1·28, 1·24-1·32), chronic kidney disease (5·04, 4·28-7·31, vs 2·50, 2·20-2·84), psychiatric disease (1·56, 1·30-1·86, vs 1·23, 1·18-1·29), and chronic inflammatory and autoimmune rheumatological disease (2·45, 1·99-3·02, vs 1·41, 1·32-1·51). Accrual of multimorbidity was also more strongly associated with risk of infection death (five or more comorbidities vs none: 9·53, 6·97-13·03) than of non-infection death (5·26, 4·84-5·72).Interpretation: Several NCDs are associated with an increased risk of infection death, suggesting that some of the reported associations with COVID-19 mortality might be non-specific. Only a subset of NCDs, together with the accrual of multimorbidity, advancing age, smoking, and socioeconomic deprivation, were associated with a greater IRR for infection death than for other causes of death. Further research is needed to define why these risk factors are more strongly associated with infection death, so that more effective preventive strategies can be targeted to high-risk groups.Funding: British Heart Foundation. [ABSTRACT FROM AUTHOR]

Asthma is a common, chronic respiratory disease which affects 1 in 11 children within the UK. The National Review of Asthma Deaths (NRAD) highlighted common and avoidable factors contributing to the deaths and made recommendations for care. The team at the Great North Children's Hospital (GNCH) recognized a need for change, which led to the development of a new educational programme. BeatAsthma was co-designed with stakeholders. It comprises over 170 resources available for use in primary, secondary and tertiary care. This article briefly describes our experience and some of the materials available and the early results of this intervention. [ABSTRACT FROM AUTHOR]

Background: It is unclear whether late-effect risks among childhood cancer survivors vary internationally. We compared late mortality in the North American Childhood Cancer Survivor Study (CCSS) and British Childhood Cancer Survivor Study (BCCSS).Methods: Late mortality was assessed among 49 822 5-year survivors of childhood cancer diagnosed before 15 years of age from 1970 to 1999 (CCSS, n = 31 596; BCCSS, n = 18 226) using cumulative mortality probabilities (CM%) and adjusted ratios of the standardized mortality ratio.Results: The all-cause CM% at 10 years from diagnosis was statistically significantly lower in the CCSS (4.7%, 95% confidence interval [CI] = 4.5% to 5.0%) compared with the BCCSS (6.9%, 95% CI = 6.5% to 7.2%), attributable to a lower probability of death from recurrence or progression of the primary cancer, with statistically significant differences observed in survivors of leukemia, lymphoma, central nervous system tumors, and sarcoma. However, at 40 years from diagnosis, the CCSS had a greater CM% (22.3% vs 19.3%), attributable to a twofold higher risk of mortality from subsequent malignant neoplasms, cardiac and respiratory diseases, and other health-related causes. Differences increased when assessed by follow-up interval, with the CCSS faring worse as time-since-diagnosis increased. Finally, the gap in all-cause mortality widened more recently, with CCSS survivors diagnosed in 1990-1999 experiencing one-half the excess deaths observed in the BCCSS (ratios of the standardized mortality ratio = 0.5, 95% CI = 0.5 to 0.6).Conclusions: Our findings suggest that US survivors may have received more intensive regimens to achieve sustainable remission and cure, but the cost of this approach was a higher risk of death from late effects. Although the clinical impact of these differences is unclear, our results provide important evidence to aid the discussion of late effects management. [ABSTRACT FROM AUTHOR]

Objective This study explores whether the prognosis of interstitial lung disease in rheumatoid arthritis (RA-ILD) has improved over time and assesses the potential influence of drug therapy in a large multicentre UK network. Methods We analysed data from 18 UK centres on patients meeting criteria for both RA and ILD diagnosed over a 25-year period. Data included age, disease duration, outcome and cause of death. We compared all cause and respiratory mortality between RA controls and RA-ILD patients, assessing the influence of specific drugs on mortality in four quartiles based on year of diagnosis. Results A total of 290 RA-ILD patients were identified. All cause (respiratory) mortality was increased at 30% (18%) compared with controls 21% (7%) (P  =0.02). Overall, prognosis improved over quartiles with median age at death rising from 63 years to 78 years (P  =0.01). No effect on mortality was detected as a result of DMARD use in RA-ILD. Relative risk (RR) of death from any cause was increased among patients who had received anti-TNF therapy [2.09 (1.1–4.0)] P  =0.03, while RR was lower in those treated with rituximab [0.52(0.1–2.1)] or mycophenolate [0.65 (0.2–2.0)]. Patients receiving rituximab as their first biologic had longer three (92%), five (82%) and seven year (80%) survival than those whose first biologic was an anti-TNF agent (82%, 76% and 64%, respectively) (P  =0.037). Discussion This large retrospective multicentre study demonstrates survival of patients with RA-ILD has improved. This may relate to the increasing use of specific immunosuppressive and biologic agents. [ABSTRACT FROM AUTHOR]

Summary: Background: Coeliac disease arises in genetically susceptible individuals, in particular in carriers of HLA‐DQ2/DQ8 risk alleles and is associated with various comorbidities. Coeliac disease may confer an increased mortality, but the data are conflicting. Aims: We aimed to characterize mortality and morbidity in patients with coeliac disease with a special focus on the role of the number of HLA risk alleles. Methods: We studied coeliac disease‐associated morbidity and mortality in ~500 000 participants of the UK Biobank including 2482 individuals with the diagnosis of coeliac disease. We used an unbiased, multivariable Phenome‐Wide Association Study (PheWAS) method to uncover the coeliac disease‐associated disorders. The tag SNP approach was used to divide the coeliac disease subjects into HLA‐DQ2/DQ8‐based risk categories. Results: We found 225 ICD‐10 codes significantly associated with coeliac disease. During the median follow‐up of 10.7 years, coeliac disease individuals (n = 2482) had higher overall mortality (HR 1.6 [95% CI, 1.4‐1.8]) than controls and both an increased occurrence of and an increased mortality from cancer, respiratory and cardiovascular diseases (HR 1.4‐1.6). Coeliac disease individuals with 2 HLA‐DQ2/8 risk alleles had a similar overall mortality as coeliac disease participants with 0‐1 HLA‐DQ2/8 alleles, but were more likely to die from lymphoproliferative diseases (HR 7.6 [95% CI, 1.01‐57.25]). Conclusions: Our data suggest that the increased mortality from lymphoproliferative diseases is restricted to those coeliac patients with 2 HLADQ2/8 alleles and that a combination of coeliac disease and HLADQ2/8 alleles is needed to increase the susceptibility. Once confirmed, closer monitoring may be warranted in this high‐risk subpopulation. [ABSTRACT FROM AUTHOR]

This population-based study compares U.S. effectiveness with 20 Other Western Countries (OWC) in reducing mortality 1989–1991 and 2013–2015 and, responding to criticisms of Britain's National Health Service, directly compares U.S. with U.K. child (0–4), adult (55–74), and 24 global mortality categories. World Health Organization Age-Standardized Death Rates (ASDR) data are used to compare American and OWC mortality over the period, juxtaposed against national average percentages of Gross Domestic Product (GDP) Expenditure on Health (%GDPEH) drawn from World Bank data. America's average %GDPEH was highest at 13.53% and Britain's the lowest at 7.68%. Every OWC had significantly greater ASDR reductions than America. Current U.S. child and adult mortality rates are 46% and 19% higher than Britain's. Of 24 global diagnostic mortalities, America had 16 higher rates than Britain, notably for Circulatory Disease (24%), Endocrine Disorders (70%), External Deaths (53%), Genitourinary (44%), Infectious Disease (65%), and Perinatal Deaths (34%). Conversely, U.S. rates were lower than Britain's for Neoplasms (11%), Respiratory (12%), and Digestive Disorder Deaths (11%). However, had America matched the United Kingdom's ASDR, there would have been 488,453 fewer U.S. deaths. In view of American %GDPHE and their mortality rates, which were significantly higher than those of the OWC, these results suggests that the U.S. health care system is the least efficient in the Western world. [ABSTRACT FROM AUTHOR]

Background: There is limited understanding on patterns of systemic treatment in adults with moderate-to-severe atopic dermatitis (AD) in the UK. Objective: To characterize treatment patterns in adult AD patients prescribed immunosuppressants (IMMs) in the primary care setting. Results: Six hundred and fifty-six patients with AD (6.6%) were prescribed IMM in the analysis (mean age 52.1 years; 59.1% female; age-adjusted Charlson comorbidity index 1.4). Most prevalent (>5%) conditions at baseline were depression (10.8%), contact dermatitis (10.7%), rheumatological disease (7.9%), skin/subcutaneous tissue disorders (6.4%), upper respiratory disease (5.8%), and psoriasis (5.2%). At baseline, up to 50% of patients were prescribed ≥1 IMM. During follow-up, 42.7% of patients were prescribed oral corticosteroids (OCSs), increasing in line with IMM exposure. The most commonly prescribed IMM was methotrexate (43.3%). Ciclosporin, the only approved IMM for AD, was prescribed to 16.9% of patients. Conclusions: The prevalence of comorbidities and high rate of IMM prescriptions demonstrate the impact of AD on quality of life. The frequency of OCS prescribing in AD patients treated with IMMs suggests a lack of disease control with existing therapies, and an unmet need for safe and effective targeted agents for long-term disease control. [ABSTRACT FROM AUTHOR]

Asthma is a chronic and genetically complex respiratory disease that affects over 300 million people worldwide. Here, we report a genome-wide analysis for asthma using data from the UK Biobank and the Trans-National Asthma Genetic Consortium. We identify 66 previously unknown asthma loci and demonstrate that the susceptibility alleles in these regions are, either individually or as a function of cumulative genetic burden, associated with risk to a greater extent in men than women. Bioinformatics analyses prioritize candidate causal genes at 52 loci, including CD52, and demonstrate that asthma-associated variants are enriched in regions of open chromatin in immune cells. Lastly, we show that a murine anti-CD52 antibody mimics the immune cell-depleting effects of a clinically used human anti-CD52 antibody and reduces allergen-induced airway hyperreactivity in mice. These results further elucidate the genetic architecture of asthma and provide important insight into the immunological and sex-specific relevance of asthma-associated risk variants. Asthma is a common disease of the airways for which numerous genetic loci have been identified. Here, Han et al. carry out a genome-wide analysis for asthma to identify additional loci, report sex-stratified and genetic risk score analyses, and functionally follow-up one locus using a murine model of airway hyperreactivity. [ABSTRACT FROM AUTHOR]

Excessive Ca intakes have been proposed to associate with vascular calcification and a higher risk of prostate cancer. We investigated the associations of supplemental and dietary Ca intake with mortality using data from 497 828 UK Biobank participants. The average follow-up was 4·2 years and 14 255 participants died, 8297 from cancer, 2959 from CVD and 572 from respiratory disease. The use of Ca supplements and milk consumption were associated with differences in mortality in younger (≤65 years) but not in older participants (>65 years, P interaction ≤ 0·04 for all comparisons). Among participants <65 years, there was an inverse association between Ca supplementation (OR 0·91, 95 % CI 0·83, 0·99) and milk consumption (OR 0·93, 95 % CI 0·86, 1·00) with respect to all-cause mortality. In the same age group, milk drinkers had lower odds of cancer mortality (OR 0·89, 95 % CI 0·80, 0·98) but Ca supplement use was associated with increased odds of respiratory mortality (OR 1·69, 95 % CI 1·16, 2·74). All associations in participants aged ≥65 years were null after full adjustment. In sensitivity analyses stratified by hormone replacement therapy, Ca supplement use was associated with decreased odds of cancer mortality in users but increased risk in other women (OR 0·81, 95 % CI 0·69, 0·94 v. OR 1·17, 95 % CI 1·01, 1·35, respectively). To conclude, we saw little evidence for harm with dietary or supplemental Ca. Further studies are required to confirm the proposed interaction with hormone replacement therapy and to exclude reverse causation as a determinant in the association between Ca supplements and increased risk of respiratory diseases. [ABSTRACT FROM AUTHOR]

Worldwide exposure to fine atmospheric particles can exasperate the risk of a wide range of heart and respiratory diseases, due to their ability to penetrate deep into the lungs and bloodstreams. Epidemiological studies in Europe and elsewhere have established the evidence base pointing to the important role of PM2.5 (fine particles with a diameter of 2.5 microns or less) in causing over 4 million deaths per year. Traditional approaches to model atmospheric transportation of particles suffer from high dimensionality from both transport and chemical reaction processes, making multi-sale causal inference challenging. We apply alternative model reduction methods - a data-driven directed graph representation to infer spatial embeddedness and causal directionality. Using PM2.5 concentrations in 14 UK cities over a 12-month period, we construct an undirected correlation and a directed Granger causality network. We show for both reduced-order cases, the UK is divided into two northern and southern connected city communities, with greater spatial embedding in spring and summer. We go on to infer stability to disturbances via the network trophic coherence parameter, whereby we found that winter had the greatest vulnerability. As a result of our novel graph-based reduced modeling, we are able to represent high-dimensional knowledge into a causal inference and stability framework. [ABSTRACT FROM AUTHOR]

Introduction recently, the European Working Group on Sarcopenia in Older People (EWGSOP) established a new operational definition and cut-off points for sarcopenia. The aim of this study was, therefore, to compare the prevalence of sarcopenia and its associations with different health outcomes using the old (EWGSOP1) and new (EWGSOP2) definitions of sarcopenia in the UK Biobank cohort. Methods sarcopenia was defined as low grip strength plus low muscle mass. Using both EWGSOP cut-off points, we created specific sarcopenia variables. Prevalence of sarcopenia derived using both EWGSOP definitions was calculated and compared as well as prospective health outcomes including all-cause mortality as well as incidence and mortality from cardiovascular disease (CVD), respiratory disease and chronic obstructive pulmonary disease (COPD). Results the prevalence of sarcopenia based on the EWGSOP1 and EWGSOP2 classifications were 8.14 and 0.36%, respectively. Sarcopenia defined by EWGSOP1 was associated with a higher risk of respiratory disease and COPD as well as mortality from all-cause, CVD and respiratory diseases. However, only respiratory incidence remained associated with sarcopenia when EWGSOP2 was used (HR: 1.32 [95% CI: 1.05–1.66]). Moreover, although individuals classified as sarcopenic using both classifications had the highest risk of all-cause mortality and respiratory disease, those with sarcopenia based on EWGSOP1 only experienced a more extensive range of poorer health outcomes. Conclusion in comparison with EWGSOP1, the new classification (EWGSOP2) produced a lower estimate of sarcopenia prevalence and fewer associations with adverse health outcomes. Although these associations were higher, many become non-significant. [ABSTRACT FROM AUTHOR]

Background The world of work is continually changing, and this could result in new and emerging risks being introduced, including those that may cause work-related respiratory diseases (WRRD). Aims To describe recently emerging and new cases of WRRD and the relevant methodology using data in a national occupational respiratory disease surveillance scheme in the UK. Methods Incident cases of respiratory diseases reported by physicians to the Surveillance of Work-related and Occupational Respiratory Disease (SWORD) between January 2015 and December 2017 were included. Potentially emerging respiratory hazards manifesting in SWORD data were identified with the following hierarchical approach: (i) new respiratory disease not previously associated with work, (ii) specific exposure/agent not previously associated with WRRD and (iii) industry and/or occupation not previously associated with WRRD. Results A total of 1215 cases of WRRD were reported to SWORD between January 2015 and December 2017. No new WRRD were identified. Thirteen potentially emerging causes of occupational asthma were identified, including exposures to agents such as ninhydrin. Four potential new causes were identified for interstitial pneumonia, which included wood and brass dust. Two potentially emerging causes of WRRD were identified for inhalational accidents (green coffee and nitrocellulose), hypersensitivity pneumonitis (diphenylmethane diisocyanate and salami mould), rhinitis (morphine and Amaranthus quitensis) and sarcoidosis (prions and horses). Conclusions Continuous monitoring and reporting of any new work-related disease is a critical function of any occupational disease reporting scheme. Potential emerging causes of work-related health risks have been identified by using a simple and systematic way of detecting emerging causes of WRRDs. [ABSTRACT FROM AUTHOR]

Asthma, the most common chronic respiratory disease, is frequently misdiagnosed, and accounts for a significant proportion of healthcare expenditure. This has driven the National Institute for Health and Care Excellence (NICE) in the United Kingdom (UK) to produce recent guidance; in places, this contrasts to that of the British Thoracic Society/Scottish Intercollegiate Guideline Network (BTS/SIGN), which have been producing their own guidance since 2003. Here we review the history of asthma diagnostic guidelines, and compare and review the evidence behind them, in adults and in children. We discuss the definitions of asthma and how these drive the concepts behind diagnostic strategies. We anticipate future directions in asthma diagnosis which will take into account the concepts of personalised medicine and disease endotypes. We also consider the utility of tests in use now and in the future, in particular novel tests relating to small airway inflammation and obstruction. [ABSTRACT FROM AUTHOR]

Background: Smoking is an important cause of mortality and recent studies have suggested that even low-intensity smoking might be associated with increased mortality. Still, smoking is associated with lower socio-economic status as well as other potential risk factors, and disease onset might motivate smoking cessation, thus residual confounding and reverse causality might bias results. We aimed to assess the evidence of a causal relationship between smoking intensity and cause-specific as well as all-cause-mortality using Mendelian randomization analyses.Methods: We included 56 019 participants from the Norwegian HUNT2 Study and 337 103 participants from UK Biobank, linked to national registry data on causes of death. We estimated associations of self-reported smoking as well as the genetic variant rs1051730 as an instrument for smoking intensity with all-cause and cause-specific mortality. We subsequently meta-analysed the results from the two cohorts.Results: Each effect allele of the rs1051730 was associated with a 9% increased hazard of all-cause mortality [95% confidence interval (CI) 6-11] among ever smokers. Effect alleles were also associated with death by neoplasms [hazard ratio (HR) 1.11, 95% CI 1.06-1.15], circulatory diseases (HR 1.06, 95% CI 1.01-1.11) and respiratory diseases (HR 1.15, 95% CI 1.05-1.26) among ever smokers. The association was stronger among ever than never smokers for all-cause mortality (p < 0.001), neoplasms (p = 0.001) and respiratory diseases (p = 0.038).Conclusions: Our results indicate a causal effect of smoking intensity on all-cause mortality and death by neoplasms and respiratory diseases. There was weaker evidence of a causal effect of smoking intensity on death by circulatory diseases. [ABSTRACT FROM AUTHOR]

A large body of literature has shown marked differences in the average levels of resources and child well-being across different family structures. Studies have examined cognitive, educational and behavioural outcomes; less is known about differentials in physical health, and about dynamics in early childhood. Furthermore, up to the present time, less emphasis has been placed on describing the underlying mechanisms relating childhood experiences of family structure to health. In this paper, we hypothesize that socio-economic characteristics and family structure trajectories will affect every-day, more proximal processes (material, behavioural and family stress pathways) directly experienced by the child, which will in turn affect child health. Using the UK Millennium Cohort Study, a nationally representative cohort of over 19 000 children born in 2001 and living in the UK shortly thereafter, we employ Graphical Chain Models to map the processes linking family structure trajectories to three physical health outcomes at age 5: overweight/obesity, respiratory health, and accidental injury. We construct family trajectories to highlight two components: status (distinguishing between married, cohabiting and single parents), and (in)stability. We show that both status, the (in)stability of that status, and their interplay, are important components of family structure trajectories which correlate to children's early physical health. Analyses highlight the relative importance of distinct pathways across different health outcomes. As well as some outcome-specific paths, we find that "family stress" variables appeared to underscore the relationship between family structure and child physical health, pointing to the importance of such variables in understanding how family structure relates to early child health. • Family structure trajectories are correlated to early child physical health. • Both status (married, cohabiting, single) and instability were important features. • We know little about the mechanisms relating family structure to early child health. • Family stress appeared to be an important mechanisms across all family trajectories. • Housing quality was important for cohabitors; daily routines for separating parents. [ABSTRACT FROM AUTHOR]

We determined the change in seroprevalence of enterovirus D68 (EV-D68) in the United Kingdom in age-stratified cohorts from 2006 to 2016, the period during which EV-D68 emerged as a cause of severe respiratory disease occasionally leading to paralysis. Infections were acquired primarily in infants and young children, and incidence was markedly higher in 2016. [ABSTRACT FROM AUTHOR]

Supplemental digital content is available in the text. Purpose: Walking pace is associated with all-cause and cardiovascular disease (CVD) mortality. Whether this association extends to other health outcomes and whether it is independent of total amount of time walked are currently unknown. Therefore, the aim of this study was to investigate whether usual walking pace is associated with a range of health outcomes. Methods: UK Biobank participants (318,185 [54%] women) age 40 to 69 yr were included. Walking pace and total walking time were self-reported. The outcomes comprised: all-cause mortality as well as incidence and mortality from CVD, respiratory disease and cancer. The associations were investigated using Cox proportional hazard models. Results: Over a mean of 5.0 yr [ranging from 3.3 to 7.8], 5890 participants died, 18,568 developed CVD, 5430 respiratory disease and 19,234 cancer. In a fully adjusted model, compared to slow pace walkers, men and women, respectively, with a brisk pace having lower risk of mortality from all-causes (hazard ratio [HR], 0.79; 95% confidence interval [CI], 0.69–0.90 and HR, 0.73; 95% CI, 0.62–0.85), CVD (HR, 0.62; 95% CI, 0.50–0.76 and HR, 0.80; 95% CI, 0.73–0.88), respiratory disease (HR, 0.58; 95% CI, 0.43–0.78 and HR, 0.66; 95% CI, 0.57–0.77), chronic obstructive pulmonary disease (HR, 0.26; 95% CI, 0.12–0.56 and HR, 0.28; 95% CI, 0.16–0.49). No associations were found for all-cause cancer, colorectal, and breast cancer. However, brisk walking was associated with a higher risk of prostate cancer. Conclusions: Walking pace is associated with lower risk of a wide range of important health conditions, independently of overall time spent walking. [ABSTRACT FROM AUTHOR]

Study Objectives: Our cohort study aimed to study the association between sleep duration and risk of mortality due to respiratory diseases., Methods: We included 498,200 participants from UK Biobank (2006-2021). We classified sleep duration as short sleep duration (< 7 hours), long sleep duration (> 9 hours for adults, > 8 hours for older adults), and midrange sleep duration (7-9 hours). We used the Cox proportional hazards model and restricted cubic spline analysis to explore the association between sleep duration and respiratory diseases mortality., Results: During a median follow-up of 12.49 years, 2,477 deaths due to respiratory diseases were recorded, of which 1,099 were deaths due to chronic lower respiratory diseases. Cox models with penalized splines showed U-shaped associations of sleep duration with mortality due to total respiratory diseases and chronic lower respiratory diseases. Compared with midrange sleep duration, short sleep duration was associated with 14% higher risk of total respiratory diseases mortality (hazard ratio = 1.14; 95% confidence interval: 1.04, 1.25), and long sleep duration was associated with 35% higher risk of total respiratory diseases mortality (hazard ratio = 1.35; 95% confidence interval: 1.19, 1.55), after adjustment of baseline characteristics, health status, and lifestyle habits. Similarly, the hazard ratios for chronic lower respiratory diseases mortality were 1.20 (95% confidence interval: 1.04, 1.38) and 1.44 (95% confidence interval: 1.19, 1.74), respectively., Conclusions: There was a U-shaped association between sleep duration and respiratory diseases mortality. Appropriate sleep duration may improve the progress of respiratory diseases., Citation: Du M, Liu M, Liu J. U-shaped association between sleep duration and the risk of respiratory diseases mortality: a large prospective cohort study from UK Biobank. J Clin Sleep Med . 2023;19(11):1923-1932., (© 2023 American Academy of Sleep Medicine.)

Objective: The study set out to investigate socio-economic, biomedical, health and behavioural and psychological factors in childhood and adulthood associated with the prevalence of asthma in adulthood, drawing data from The National Child Development Studies (NCDS), a birth cohort in the UK. Design: The National Child Development Study, a nationally representative sample of 17,415 babies born in Great Britain in 1958 and followed up at 7, 11, 33 and 50 years was used. Main Outcome Measure: The prevalence of asthma at age 50 was the outcome measure. The analytic sample consists of 5118 participants with complete data on a set of measures at birth, at ages 7, 11, 33 and 50 years. Results: Using logistic regression analyses, results showed that childhood asthma (OR = 6.77: 4.38-10.48, p < .001) and respiratory symptoms (OR = 1.83: 1.18-2.86, p < .01), maternal smoking during pregnancy (OR = 1.26: 1.00-1.59, p < .05), Body and Mass Index (BMI) (OR = 1.03: 1.02-1.05, p < .001), traits Neuroticism (OR = 1.13: 1.01-1.21, p < .05) and Conscientiousness (OR = 0.76: 0.76-0.96, p < .01), as well as sex (OR = 1.49: 1.15-1.94, p < .001) were all significantly associated with the prevalence of asthma in adulthood. Conclusion: The study shows that both childhood and adulthood psychological and sociological factors are significantly associated with the prevalence of asthma in adulthood, though more work need to be done in this area. [ABSTRACT FROM AUTHOR]

An estimated 1.9 million animals are affected by bovine respiratory disease (BRD) each year in the UK cattle industry with costs estimated at around £60 million annually. The principal pathogens assumed to be implicated in BRD have been identified and their epidemiology and pathogenesis generally understood. A range of effective therapeutic (anti-inflammatory and anti-microbial products) and preventative tools (vaccines) have been developed and offer positive opportunities for control. However, BRD is complex, multi-factorial and despite the available tools continues to represent a threat to cattle health, welfare and farm profitability. A fundamental appreciation of animal–pathogen–environment interactions is necessary to understand the success and failure of current control measures. This article explores whether some current control strategies are actually unsuccessful, is knowledge exchange inadequate, are recommendations generally being ignored or are there new developments, pathogens or approaches that merit investigation? [ABSTRACT FROM AUTHOR]