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Exposure to pollen and fungal spores can trigger asthma/allergic symptoms and affect health. Rising temperatures from climate change have been associated with earlier seasons and increasing intensity for some pollen, with weaker evidence for fungal spores. It is unclear whether climate change has resulted in changes in the exposure-response function between temperature and pollen/fungal spore concentrations over time. This study examined associations between temperature and pollen/fungal spores in different time periods and assessed potential adaptation using the longest pollen/fungal spore dataset in existence (52 years). Daily concentrations of pollen (birch and grass) and fungal spores (Cladosporium, Alternaria, Sporobolomyces and Tilletiopsis) collected between April and October from Derby (1970-2005) and Leicester (2006-2021), UK, were analysed. Cumulative seasonal concentrations (seasonal integral) and start-of-season were calculated and linked to seasonal mean temperatures (Tmeans) using generalized additive models. Daily concentrations were evaluated against daily Tmean with distributed lagged nonlinear models. Models were adjusted for precipitation, relative humidity, long-term trend and location. Seasonal and daily analyses were respectively stratified into two periods (1970-1995, 1997-2021) and five decades. Warmer seasonal Tmeans were associated with higher seasonal integral for birch, Cladosporium and Alternaria, as well as earlier start-of-season for birch, grass and Cladosporium. There were indications of changing associations with temperature in the recent decades. A warmer January was associated with higher seasonal integral for grass in 1997-2021, but not in 1970-1995. In 2000-2021, daily concentrations of birch pollen tended to remain at higher levels, vs. decrease during 1990s, when Tmean was between 13 and 15 °C. Our study suggests higher temperatures experienced in recent decades are associated with higher overall abundance of some pollen/fungal spores, which may increase future disease burdens of allergies. The changing responses of some pollen to higher temperatures over time may indicate adaptation to increasing temperatures and should be considered in climate change mitigation and adaptation planning., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)

Background: Exposure to environmental noise is associated with adverse health effects, but there is potential for confounding and interaction with air pollution, particularly where both exposures arise from the same source, such as transport., Objectives: To review evidence on confounding and interaction of air pollution in relation to associations between environmental noise and cardiovascular outcomes., Methods: Papers were identified from similar reviews published in 2013 and 2015, from the systematic reviews supporting the WHO 2018 noise guidelines, and from a literature search covering the period 2016-2022 using Medline and PubMed databases. Additional papers were identified from colleagues. Study selection was according to PECO inclusion criteria. Studies were evaluated against the WHO checklist for risk of bias., Results: 52 publications, 36 published after 2015, were identified that assessed associations between transportation noise and cardiovascular outcomes, that also considered potential confounding (49 studies) or interaction (23 studies) by air pollution. Most, but not all studies, suggested that the associations between traffic noise and cardiovascular outcomes are independent of air pollution. NO 2 or PM 2.5 were the most commonly included air pollutants and we observed no clear differences across air pollutants in terms of the potential confounding role. Most papers did not appear to suggest an interaction between noise and air pollution. Eight studies found the largest noise effect estimates occurring within the higher noise and air pollution exposure categories, but were not often statistically significant., Conclusion: Whilst air pollution does not appear to confound associations of noise and cardiovascular health, more studies on potential interactions are needed. Current methods to assess quality of evidence are not optimal when evaluating evidence on confounding or interaction., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier Inc.)

Background and Aims: To describe sociodemographic, lifestyle, environmental and traditional clinical risk factor differences between ethnic groups and to investigate the extent to which such differences confound the association between ethnic groups and the risk of cardiovascular disease (CVD) METHODS AND RESULTS: A total of 440,693 white European (55.9% women), 7305 South Asian (48.6%) and 7628 black African or Caribbean (57.7%) people were included from UK Biobank. Associations between ethnicity and cardiovascular outcomes (composite of non-fatal stroke, non-fatal myocardial infarction and CVD death) were explored using Cox-proportional hazard models. Models were adjusted for sociodemographic, lifestyle, environmental and clinical risk factors. Over a median (IQR) of 12.6 (11.8, 13.3) follow-up years, there were 22,711 (5.15%) cardiovascular events in white European, 463 (6.34%) in South Asian and 302 (3.96%) in black African or Caribbean individuals. For South Asian people, the cardiovascular hazard ratio (HR) compared to white European people was 1.28 (99% CI [1.16, 1.43]). For black African or Caribbean people, the HR was 0.80 (0.66, 0.97). The elevated risk of CVD in South Asians remained after adjusting for differences in sociodemographic, lifestyle, environmental and clinical factors, whereas the lower risk in black African or Caribbean was largely attenuated., Conclusions: South Asian, but not black African or Caribbean individuals, have a higher risk of CVD compared to white European individuals. This higher risk in South Asians was independent of sociodemographic, lifestyle, environmental and clinical factors., Competing Interests: Declaration of competing interest TY, MJD are supported by the National Institute for Health Research (NIHR) Leicester Biomedical Research Centre (BRC). KK is Director for the University of Leicester Centre for Ethnic Health Research, Trustee of the South Asian Health Foundation, national NIHR Applied Research Collaborations – East Midlands (ARC-EM) lead for Ethnicity and Diversity and a member of SAGE and Chair of the SAGE subgroup on ethnicity and COVID-19. AH acknowledges funding from the NIHR Health Protection Research Unit in Environmental Exposures and Health Development Award at University of Leicester. Other authors declare no conflicts of interests., (Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.)

Fungal spores make up a significant proportion of organic matter within the air. Allergic sensitisation to fungi is associated with conditions including allergic fungal airway disease. This systematic review analyses outdoor fungal spore seasonality across Europe and considers the implications for health. Seventy-four studies met the inclusion criteria, the majority of which (n = 64) were observational sampling studies published between 1978 and 2020. The most commonly reported genera were the known allergens Alternaria and Cladosporium, measured in 52 and 49 studies, respectively. Both displayed statistically significant increased season length in south-westerly (Mediterranean) versus north-easterly (Atlantic and Continental) regions. Although there was a trend for reduced peak or annual Alternaria and Cladosporium spore concentrations in more northernly locations, this was not statistically significant. Peak spore concentrations of Alternaria and Cladosporium exceeded clinical thresholds in nearly all locations, with median peak concentrations of 665 and 18,827 per m 3 , respectively. Meteorological variables, predominantly temperature, precipitation and relative humidity, were the main factors associated with fungal seasonality. Land-use was identified as another important factor, particularly proximity to agricultural and coastal areas. While correlations of increased season length or decreased annual spore concentrations with increasing average temperatures were reported in multi-decade sampling studies, the number of such studies was too small to make any definitive conclusions. Further, up-to-date studies covering underrepresented geographical regions and fungal taxa (including the use of modern molecular techniques), and the impact of land-use and climate change will help address remaining knowledge gaps. Such knowledge will help to better understand fungal allergy, develop improved fungal spore calendars and forecasts with greater geographical coverage, and promote increased awareness and management strategies for those with allergic fungal disease., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.)

Introduction: Many studies, including the HYENA and the DEBATS studies, showed a significant association between aircraft noise exposure and the risk of hypertension. Few studies have considered aircraft noise annoyance and noise sensitivity as factors of interest, especially in relation to hypertension risk, or as mediating or modifying factors. The present study aims 1) to investigate the risk of hypertension in relation to aircraft noise annoyance or noise sensitivity; and 2) to examine the role of modifier or mediator of these two factors in the association between aircraft noise levels and the risk of hypertension., Methods: This study included 6,105 residents of ten European airports from the HYENA and DEBATS studies. Information on aircraft noise annoyance, noise sensitivity, and demographic, socioeconomic and lifestyle factors was collected during an interview performed at home. Participants were classified as hypertensive if they had either blood pressure levels above the WHO cut-off points or physician-diagnosed hypertension in conjunction with the use of antihypertensive medication. Outdoor aircraft noise exposure was estimated for each participant's home address. Poisson regression models with adjustment for potential confounders were used. Interactions between noise exposure and country were tested to consider possible differences between countries., Results: An increase in aircraft noise levels at night was weekly but significantly associated with an increased risk of hypertension (RR = 1.03, 95% CI 1.01-1.06 for a 10-dB(A) increase in L night ). A significant association was found between aircraft noise annoyance and hypertension risk (RR = 1.06, 95%CI 1.00-1.13 for highly annoyed people compared to those who were not highly annoyed). The risk of hypertension was slightly higher for people highly sensitive to noise compared to people with low sensitivity in the UK (RR = 1.29, 95%CI 1.05-1.59) and in France (RR = 1.11, 95%CI 0.68-1.82), but not in the other countries. The association between aircraft noise levels and the risk of hypertension was higher among highly sensitive participants (RR = 1.00, 95%CI 0.96-1.04; RR = 1.03, 95%CI 0.90-1.11; RR = 1.12, 95%CI 1.01-1.24, with a 10-dB(A) increase in L night for low, medium, and high sensitive people respectively) or, to a lesser extent, among highly annoyed participants (RR = 1.06, 95%CI 0.95-1.18 for a 10-dB(A) increase in L night among highly annoyed participants, and RR = 1.02, 95%CI 0.99-1.06 among those not highly annoyed)., Conclusions: The present study confirms findings in the small number of available studies to date suggesting adverse health effects associated with aircraft noise annoyance and noise sensitivity. The findings also indicate possible modifier effects of aircraft noise annoyance and noise sensitivity in the relationship between aircraft noise levels and the risk of hypertension. However, further investigations are needed to better understand this role using specific methodology and tools related to mediation analysis and causal inference., (Copyright © 2020. Published by Elsevier Inc.)

Background: Environmental stressors such as transport noise may contribute to development of obesity through increased levels of stress hormones, sleep deprivation and endocrine disruption. Epidemiological evidence supporting an association of road traffic noise with obesity markers is still relatively scant and confined to certain geographical regions. We aimed to examine the cross-sectional associations between road traffic noise and obesity markers in three large European cohorts involving nearly 500,000 individuals., Methods: Three population-based cohorts (UK Biobank, Lifelines, HUNT3) were established between 2006 and 2013 in the UK, the Netherlands and Norway respectively. For all three cohorts, residential 24-h road traffic noise (Lden) for 2009 was modelled from a standardised European noise assessment framework. Residential exposures to NO2 for 2007 and PM2.5 for 2010 were estimated from Europe-wide land use regression models. Obesity markers including body mass index and waist circumference were measured at recruitment. Obesity and central obesity status were subsequently derived. Regression models were fitted in each cohort, adjusting for a harmonised set of demographic and lifestyle covariates, with further adjustments for air pollution in the main model., Results: The main analyses included 412,934 participants of UK Biobank, 61,032 of Lifelines and 30,305 of HUNT3, with a mean age of 43-56 years and Lden ranging 42-89 dB(A) across cohorts. In UK Biobank, per 10 dB(A) higher of Lden: BMI was higher by 0.14kg/m2 (95%CI: 0.11-0.18), waist circumference higher by 0.27 cm (95%CI: 0.19-0.35), odds of obesity was 1.06 (95%CI: 1.04-1.08) and of central obesity was 1.05 (95%CI: 1.04-1.07). These associations were robust to most other sensitivity analyses but attenuated by further adjustment of PM2.5 or area-level socioeconomic status. Associations were more pronounced among women, those with low physical activity, higher household income or hearing impairment. In HUNT3, associations were observed for obesity or central obesity status among those exposed to Lden greater than 55 dB(A). In contrast, no or negative associations were observed in the Lifelines cohort., Conclusions: This largest study to date providing mixed findings on impacts of long-term exposure to road traffic noise on obesity, which necessitates future analyses using longitudinal data to further investigate this potentially important epidemiological link., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Bioaerosols have been associated with adverse respiratory-related health effects and are emitted in elevated concentrations from composting facilities. We used modelled Aspergillus fumigatus concentrations, a good indicator for bioaerosol emissions, to assess associations with respiratory-related hospital admissions. Mean daily Aspergillus fumigatus concentrations were estimated for each composting site for first full year of permit issue from 2005 onwards to 2014 for Census Output Areas (COAs) within 4 km of 76 composting facilities in England, as previously described (Williams et al., 2019). We fitted a hierarchical generalized mixed model to examine the risk of hospital admission with a primary diagnosis of (i) any respiratory condition, (ii) respiratory infections, (iii) asthma, (iv) COPD, (v) diseases due to organic dust, and (vi) Cystic Fibrosis, in relation to quartiles of Aspergillus fumigatus concentrations. Models included a random intercept for each COA to account for over-dispersion, nested within composting facility, on which a random intercept was fitted to account for clustering of the data, with adjustments for age, sex, ethnicity, deprivation, tobacco sales (smoking proxy) and traffic load (as a proxy for traffic-related air pollution). We included 249,748 respiratory-related and 3163 Cystic Fibrosis hospital admissions in 9606 COAs with a population-weighted centroid within 4 km of the 76 included composting facilities. After adjustment for confounders, no statistically significant effect was observed for any respiratory-related (Relative Risk (RR) = 0.99; 95% Confidence Interval (CI) 0.96-1.01) or for Cystic Fibrosis (RR = 1.01; 95% CI 0.56-1.83) hospital admissions for COAs in the highest quartile of exposure. Similar results were observed across all respiratory disease sub-groups. This study does not provide evidence for increased risks of respiratory-related hospitalisations for those living near composting facilities. However, given the limitations in the dispersion modelling, risks cannot be completely ruled out. Hospital admissions represent severe respiratory episodes, so further study would be needed to investigate whether bioaerosols emitted from composting facilities have impacts on less severe episodes or respiratory symptoms., Competing Interests: Declaration of competing interest None., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Methods for estimating air pollutant exposures for epidemiological studies are becoming more complex in an effort to minimise exposure error and its associated bias. While land use regression (LUR) modelling is now an established method, there has been little comparison between LUR and other recent, more complex estimation methods. Our aim was to develop a LUR model to estimate intra-city exposures to nitrogen dioxide (NO 2 ) for a Sydney cohort, and to compare those with estimates from a national satellite-based LUR model (Sat-LUR) and a regional Bayesian Maximum Entropy (BME) model., Methods: Satellite-based LUR and BME estimates were obtained using existing models. We used methods consistent with the European Study of Cohorts for Air Pollution Effects (ESCAPE) methodology to develop LUR models for NO 2 and NOx. We deployed 46 Ogawa passive samplers across western Sydney during 2013/2014 and acquired data on land use, population density, and traffic volumes for the study area. Annual average NO 2 concentrations for 2013 were estimated for 947 addresses in the study area using the three models: standard LUR, Sat-LUR and a BME model. Agreement between the estimates from the three models was assessed using interclass correlation coefficient (ICC), Bland-Altman methods and correlation analysis (CC)., Results: The NO 2 LUR model predicted 84% of spatial variability in annual mean NO 2 (RMSE: 1.2 ppb; cross-validated R 2 : 0.82) with predictors of major roads, population and dwelling density, heavy traffic and commercial land use. A separate model was developed that captured 92% of variability in NOx (RMSE 2.3 ppb; cross-validated R 2 : 0.90). The annual average NO 2 concentrations were 7.31 ppb (SD: 1.91), 7.01 ppb (SD: 1.92) and 7.90 ppb (SD: 1.85), for the LUR, Sat-LUR and BME models respectively. Comparing the standard LUR with Sat-LUR NO 2 cohort estimates, the mean estimates from the LUR were 4% higher than the Sat-LUR estimates, and the ICC was 0.73. The Pearson's correlation coefficients (CC) for the LUR vs Sat-LUR values were r = 0.73 (log-transformed data) and r = 0.69 (untransformed data). Comparison of the NO 2 cohort estimates from the LUR model with the BME blended model indicated that the LUR mean estimates were 8% lower than the BME estimates. The ICC for the LUR vs BME estimates was 0.73. The CC for the logged LUR vs BME estimates was r = 0.73 and for the unlogged estimates was r = 0.69., Conclusions: Our LUR models explained a high degree of spatial variability in annual mean NO 2 and NOx in western Sydney. The results indicate very good agreement between the intra-city LUR, national-scale sat-LUR, and regional BME models for estimating NO 2 for a cohort of children residing in Sydney, despite the different data inputs and differences in spatial scales of the models, providing confidence in their use in epidemiological studies., (Copyright © 2019 Elsevier Inc. All rights reserved.)

This paper investigates trends in asthma and COPD by using multiple data sources to help understanding the relationships between disease prevalence, morbidity and mortality. GP drug prescriptions, hospital admissions, and deaths are analysed at clinical commissioning group (CCG) level in England from August 2010 to March 2011. A Bayesian hierarchical model is used for the analysis, which takes into account the complex space and time dependencies of asthma and COPD, while it is also able to detect unusual areas. Main findings show important discrepancies across the different data sources, reflecting the different groups of patients that are represented. In addition, the detection mechanism that is provided by the model, together with inference on the spatial, and temporal variation, provide a better picture of the respiratory health problem., (Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Introduction: Exposure to road traffic noise may increase blood pressure and heart rate. It is unclear to what extent exposure to air pollution may influence this relationship. We investigated associations between noise, blood pressure and heart rate, with harmonized data from three European cohorts, while taking into account exposure to air pollution., Methods: Road traffic noise exposure was assessed using a European noise model based on the Common Noise Assessment Methods in Europe framework (CNOSSOS-EU). Exposure to air pollution was estimated using a European-wide land use regression model. Blood pressure and heart rate were obtained by trained clinical professionals. Pooled cross-sectional analyses of harmonized data were conducted at the individual level and with random-effects meta-analyses., Results: We analyzed data from 88,336 participants, across the three participating cohorts (mean age 47.0 (±13.9) years). Each 10dB(A) increase in noise was associated with a 0.93 (95% CI 0.76;1.11) bpm increase in heart rate, but with a decrease in blood pressure of 0.01 (95% CI -0.24;0.23) mmHg for systolic and 0.38 (95% CI -0.53; -0.24) mmHg for diastolic blood pressure. Adjustments for PM 10 or NO 2 attenuated the associations, but remained significant for DBP and HR. Results for BP differed by cohort, with negative associations with noise in LifeLines, no significant associations in EPIC-Oxford, and positive associations with noise >60dB(A) in HUNT3., Conclusions: Our study suggests that road traffic noise may be related to increased heart rate. No consistent evidence for a relation between noise and blood pressure was found., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: Understanding the genetic basis of airflow obstruction and smoking behaviour is key to determining the pathophysiology of chronic obstructive pulmonary disease (COPD). We used UK Biobank data to study the genetic causes of smoking behaviour and lung health., Methods: We sampled individuals of European ancestry from UK Biobank, from the middle and extremes of the forced expiratory volume in 1 s (FEV1) distribution among heavy smokers (mean 35 pack-years) and never smokers. We developed a custom array for UK Biobank to provide optimum genome-wide coverage of common and low-frequency variants, dense coverage of genomic regions already implicated in lung health and disease, and to assay rare coding variants relevant to the UK population. We investigated whether there were shared genetic causes between different phenotypes defined by extremes of FEV1. We also looked for novel variants associated with extremes of FEV1 and smoking behaviour and assessed regions of the genome that had already shown evidence for a role in lung health and disease. We set genome-wide significance at p<5 × 10(-8)., Findings: UK Biobank participants were recruited from March 15, 2006, to July 7, 2010. Sample selection for the UK BiLEVE study started on Nov 22, 2012, and was completed on Dec 20, 2012. We selected 50,008 unique samples: 10,002 individuals with low FEV1, 10,000 with average FEV1, and 5002 with high FEV1 from each of the heavy smoker and never smoker groups. We noted a substantial sharing of genetic causes of low FEV1 between heavy smokers and never smokers (p=2.29 × 10(-16)) and between individuals with and without doctor-diagnosed asthma (p=6.06 × 10(-11)). We discovered six novel genome-wide significant signals of association with extremes of FEV1, including signals at four novel loci (KANSL1, TSEN54, TET2, and RBM19/TBX5) and independent signals at two previously reported loci (NPNT and HLA-DQB1/HLA-DQA2). These variants also showed association with COPD, including in individuals with no history of smoking. The number of copies of a 150 kb region containing the 5' end of KANSL1, a gene that is important for epigenetic gene regulation, was associated with extremes of FEV1. We also discovered five new genome-wide significant signals for smoking behaviour, including a variant in NCAM1 (chromosome 11) and a variant on chromosome 2 (between TEX41 and PABPC1P2) that has a trans effect on expression of NCAM1 in brain tissue., Interpretation: By sampling from the extremes of the lung function distribution in UK Biobank, we identified novel genetic causes of lung function and smoking behaviour. These results provide new insight into the specific mechanisms underlying airflow obstruction, COPD, and tobacco addiction, and show substantial shared genetic architecture underlying airflow obstruction across individuals, irrespective of smoking behaviour and other airway disease., Funding: Medical Research Council., (Copyright © 2015 Wain et al. Open Access article distributed under the terms of CC BY. Published by Elsevier Ltd.. All rights reserved.)

Extreme geological events, such as earthquakes, are a significant global concern and sometimes their consequences can be devastating. Geographic information plays a critical role in health protection regarding hazards, and there are a range of initiatives using geographic information to communicate risk as well as to support early warning systems operated by geologists. Nevertheless we consider there to remain shortfalls in translating information on extreme geological events into health protection tools, and suggest that social scientists have an important role to play in aiding the development of a new generation of toolkits aimed at public health practitioners. This viewpoint piece reviews the state of the art in this domain and proposes potential contributions different stakeholder groups, including social scientists, could bring to the development of new toolkits., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Objectives: The effect modifying impact of annoyance due to aircraft noise and road traffic noise on the relationships between the aircraft noise level and road traffic noise level on the prevalence of hypertension was investigated in 4861 subjects of the HYENA study (HYpertension and Exposure to Noise near Airports)., Methods: Different models were investigated either including the noise level and noise annoyance variables separately, or simultaneously, or together with an interaction term referring to the same noise source for the noise level and the noise annoyance., Results: Significant effect modification was found with respect to the association between aircraft noise and hypertension. The association was stronger in more annoyed subjects. No clear interaction was found with respect to road traffic noise. The comparison of the magnitude of the main effects (per standard deviation or inter-quartile range) of noise level and noise annoyance variables revealed stronger associations with hypertension for the noise levels., Conclusion: There is some indication that the noise level has a stronger predictive meaning for the relationship between noise exposure and hypertension than the reported noise annoyance (main effects). The results from the Hyena study support the hypothesis that noise annoyance acts as an effect modifier of the relationship between the noise level and hypertension., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Genetic epidemiology is a rapidly expanding research field, but the implications of findings from such studies for individual or population health are unclear. The use of molecular genetic screening currently has some legitimacy in certain monogenic conditions, but no established value with respect to common complex diseases. Personalised medical care based on molecular genetic testing is also as yet undeveloped for common diseases. Genetic epidemiology can contribute to establishing the causal nature of environmentally modifiable risk factors, through the application of mendelian randomisation approaches and thus contribute to appropriate preventive strategies. Technological and other advances will allow the potential of genetic epidemiology to be revealed over the next few years, and the establishment of large population-based resources for such studies (biobanks) should contribute to this endeavour.

Study Objectives: There is increasing interest in the frequency and nature of comorbidities in patients with obstructive lung disease: COPD and asthma. We aimed to quantify baseline rates of comorbidities in COPD and asthma patients and to compare the risks to the general population., Design, Setting, and Participants: Within the UK General Practice Research Database, we compared incident patients with COPD (n = 2,699) and asthma (n = 7,931) physician diagnosed in 1998 with age, gender, time, and practice-matched cohorts. Rates were calculated and relative risks (RRs) were estimated for comorbidities in major organ systems and selected medical events of a priori interest., Measurements and Results: In both COPD and asthma, the total sum of diagnoses related to major organ systems was higher than in their matched population controls. Among incident COPD patients, a frequency > 1% within the first year after diagnosis was observed for angina, cataracts, bone fractures, osteoporosis, pneumonia, and respiratory infections, the highest being angina with 4.0%. Compared to the non-COPD cohort, COPD patients were at increased risk for pneumonia (relative risk [RR] = 16.0), osteoporosis (RR = 3.1), respiratory infection (RR = 2.2), myocardial infarction (RR = 1.7), angina (RR = 1.7), fractures (RR = 1.6), and glaucoma (RR = 1.3) [all p < 0.05]. Of note, 2.0% of COPD patients had cataracts recorded, but this rate was no different than that of the non-COPD cohort (RR = 0.9). Among incident asthma patients, the occurrence of events was generally lower, likely due to the younger age distribution, except for 4.0% with respiratory infection (RR = 1.84) and 1.7% with fractures (RR = 1.5). Angina prevalence was 0.7% in the asthma cohort and 1.4 times more common than in patients without asthma., Conclusion: COPD and asthma are conditions associated with many comorbidities, albeit asthma to a lesser extent than COPD, which had not been systematically reviewed before. Baseline rates of cardiovascular-, bone-, and other smoking-related conditions are high.