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Objective: Asthma medication adherence is of crucial importance for successful disease management. The aim of this study was to identify and rank factors associated with medication adherence among adults with asthma in the general population., Methods: We used data on physician-diagnosed asthma, medication adherence, and factors associated with asthma medication adherence from the Danish General Suburban Population Study using a cross-sectional study design. We ranked factors associated with asthma medication adherence based on the magnitude of odds ratios, and the population attributable fractions., Results: Among 20,032 individuals from the general population, 1,128 (6%) suffered from asthma and 822 (73%) of these were adherent to asthma medications. Based on odds ratios, the three top-ranked factors associated with asthma medication adherence were asthma attacks within the past year (4.0; 95% CI: 2.9-5.5), allergy medication use (3.8; 2.6-5.6), and age above median (3.4; 2.4-4.7), followed by asthma severity markers like airway obstruction, and coughing with mucus. Based on population attributable fractions, the three top-ranked factors associated with adherence to asthma medications were asthma attacks within the past year (70%), age above median (57%), and use of allergy medication (49%)., Conclusions: The study showed that in the general population recent asthma attacks, higher age, and taking allergy medication were the three most important factors associated with asthma medication adherence. The importance of maintaining adherence to asthma medications even in the absence of severe disease or expressed asthma symptoms should be better communicated to the general population.

Parental asthma or allergy have been linked to higher risk of asthma in a child; this occurs to a variable extent in different study populations. Moreover, it is debated whether maternal more so than paternal asthma history is a stronger predisposing factor: while in some countries/populations the maternal effect was clearly seen over paternal, in others the parental effects were equivalent, and in a few studies paternal effect dominated. Here we aimed to determine parental asthma and allergy effect in the Danish GEneral SUburban population Study (GESUS). This cross-sectional study has involved 21,362 adults aged 20+ years in the suburbs of Copenhagen. We used a combination of questionnaire approach, history of prescribed asthma medications and pulmonary function testing to determine odds ratios for maternal and paternal (and combined) asthma and allergy linked to asthma in the test subjects. We found that the input of maternal vs. paternal asthma effect was approximately equal (age and sex-adjusted OR 2.46, 95% CI: 2.15-2.81 for asthmatic mothers vs. 2.97, 2.58-3.42 for asthmatic fathers), except for the "ever asthma" age and sex-adjusted odds ratios where paternal allergy seems to have conferred a marginally greater effect (age and sex-adj. OR 1.96 for maternal allergy vs. 2.44 for paternal allergy, p = 0.03). Stratifying for gestational tobacco smoking did not affect the maternal results. We conclude that in the GESUS study parental asthma or allergy were strongly linked to higher asthma risk in offspring, without a prominent maternal or paternal effect., Competing Interests: Declaration of competing interest Please find attached our original research article titled “Risk of asthma in offspring of asthmatic fathers versus mothers: A population-based study of 21,000 individuals in Denmark”. The authors declare no conflict of interest., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Background: Cough is a well-recognized symptom in asthma, but the role and impact of chronic cough in individuals with asthma has not been described in the general population., Objective: We hypothesized that among individuals with asthma, those with chronic cough versus those without have a more severe disease phenotype., Methods: We identified individuals with asthma and chronic cough among 14,740 adults from the Copenhagen General Population Study, and investigated respiratory symptoms, health care utilizations, lung function, and biomarkers in blood., Results: A total of 855 (6%) individuals suffered from asthma, and 70 (8%) had chronic cough. Individuals with asthma and chronic cough had a Leicester Cough Questionnaire median total score of 16.8 (25th and 75th percentiles, 14.8-18.9), corresponding to 5.4 (4.6-6.0) for the physical domain, 5.7 (4.6-6.4) for the psychological domain, and 6.0 (5.3-6.8) for the social domain. Among individuals with asthma, those with chronic cough versus those without reported more often wheezing (70% vs 54%), dyspnea (74% vs 49%), night-time dyspnea (27% vs 11%), sputum production (59% vs 14%), chest pain/tightness (14% vs 4%), acute bronchitis/pneumonia episodes, and general practitioner visits. Furthermore, these individuals had more often FEV 1 predicted value of less than 60% (14% vs 7%) and higher levels of neutrophils, leukocytes, and fibrinogen in blood, but there were no differences with regard to levels of high-sensitive C-reactive protein, eosinophils, and IgE in blood., Conclusions: Chronic cough in individuals with asthma is associated with a more severe disease phenotype in terms of worse respiratory symptoms, greater health care utilizations, lower lung function, and higher levels of systemic inflammatory biomarkers in blood., (Copyright © 2019 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Background: Patients with cystic fibrosis (CF) have a higher prevalence of asthma than the background population, however, it is unclear whether heterozygous CF carriers are susceptible to asthma. Given this, a meta-analysis is necessary to determine the veracity of the association of CF heterozygosity with asthma., Methods: We screened the medical literature from 1966 to 2015 and performed a meta-analysis to determine the risk of asthma in CF heterozygotes vs. non-carriers., Results: Aggregating data from 15 studies, the odds ratio for asthma in CF heterozygotes compared with non-carriers was significantly elevated at 1.61 (95% CI: 1.18-2.21). When analyzing the studies considered of high quality in which asthma was diagnosed by a physician, the patients were >18years, or study size was ≥500, the trend remained the same, that heterozygous carriers of CF had elevated risk for asthma., Conclusions: The results show that heterozygous carriers for CF have a higher risk of asthma than non-carriers., (Copyright © 2016 The Authors. Published by Elsevier B.V. All rights reserved.)

Apolipoprotein E (apoE) is an endogenous negative regulator of airway hyperreactivity (AHR) and mucous cell metaplasia in experimental models of house dust mite (HDM)-induced airway disease. The gene encoding human apoE is polymorphic, with three common alleles (ε2, ε3, and ε4) reflecting single amino acid substitutions at amino acids 112 and 158. The objective of this study was to assess whether the human apoE alleles modify airway responses to repeated nasal HDM challenges. Mice expressing the human apoE ε2 (huApoE2), ε3 (huApoE3), or ε4 (huApoE4) alleles received nasal HDM challenges, and airway responses were compared with mice expressing the endogenous murine apoE gene (muApoE). huApoE3 mice displayed significant reductions in AHR, mucous cell metaplasia, and airway inflammation compared with muApoE mice. The attenuated severity of airway inflammation in huApoE3 mice was associated with reductions in lung mRNA levels of Th2 and Th17 cytokines, as well as chemokines (CCL7, CCL11, CCL24). huApoE4 mice had an intermediate phenotype, with attenuated AHR and IgE production, compared with muApoE mice, whereas airway inflammation and mucous cell metaplasia were not reduced. In contrast, HDM-induced airway responses were not modified in mice expressing the huApoE2 allele. We conclude that the polymorphic huApoE alleles differentially modulate HDM-induced airway disease, which can be stratified, in rank order of increasing disease severity, ε3 < ε4 < ε2. These results raise the possibility that the polymorphic apoE alleles may modify disease severity in human asthma.

Background: Many human epidemiologic studies demonstrate that maternal asthma confers greater risk of asthma to offspring than does paternal disease. However, a handful have shown the opposite. Given this disparity, a meta-analysis is necessary to determine the veracity and magnitude of the "maternal effect.", Methodology/principal Findings: We screened the medical literature from 1966 to 2009 and performed a meta-analysis to compare the effect of maternal asthma vs. paternal asthma on offspring asthma susceptibility. Aggregating data from 33 studies, the odds ratio for asthma in children of asthmatic mothers compared with non-asthmatic mothers was significantly increased at 3.04 (95% confidence interval: 2.59-3.56). The corresponding odds ratio for asthma in children of asthmatic fathers was increased at 2.44 (2.14-2.79). When comparing the odds ratios, maternal asthma conferred greater risk of disease than did paternal asthma (3.04 vs. 2.44, p = 0.037). When analyzing the studies in which asthma was diagnosed by a physician the odds ratios were attenuated and no significant differences were observed (2.85 vs. 2.48, N = 18, p = 0.37). Similarly, no significant differences were observed between maternal and paternal odds ratios when analyzing the studies in which the patient population was 5 years or older (3.15 vs. 2.60, p = 0.14). However, in all cases the trend remained the same, that maternal asthma was a greater risk factor for asthma than paternal., Conclusions/significance: The results show that maternal asthma increases offspring disease risk to a greater extent than paternal disease.

The angiotensin-converting enzyme (ACE) gene is a potential candidate gene for risk of asthma, COPD, and COPD co-morbidity. In 9034 Danish adults, we determined whether individuals homozygous or heterozygous for the ACE D allele are at greater risk of asthma, COPD, or COPD co-morbidity compared with ACE II homozygous individuals. In the general population, serum ACE activity increased with the number of D alleles (Kruskal-Wallis ANOVA: II vs. ID, p<0.001; ID vs. DD, p<0.001); however, this did not translate into altered risk of asthma or COPD. In the general population, the odds ratio (95% confidence interval) for asthma was 1.2 (0.9-1.4) for ID individuals and 1.2 (0.9-1.5) for DD individuals compared with II individuals. In the general population, the odds ratio for COPD was 0.9 (0.8-1.1) for ID individuals and 1.0 (0.8-1.2) for DD individuals compared with II individuals. Among patients with COPD, the odds ratio for ischemic heart disease was 1.1 (0.8-1.6) for ID individuals and 1.2 (0.8-1.7) for DD individuals compared with II individuals; corresponding odds ratios for hypertension were 1.1 (0.7-1.5) and 0.8 (0.5-1.2), and for low physical activity 0.9 (0.5-1.4) and 0.7 (0.4-1.2). The results were similar upon adjustment for sex, age, smoking status, body mass index, total cholesterol, and ACE inhibitor/angiotensin II type 1 receptor blocker use. These data suggest that lifelong genetically elevated ACE activity is not a major risk factor for asthma or COPD, or for ischemic heart disease, hypertension, and low physical activity in COPD patients.

Introduction: New markers of early disease activity and prognosis are needed in asthma and chronic obstructive pulmonary disease (COPD)., Objective: To identify new markers of asthma and COPD to implement in clinical practice, we genotyped for common genetic variants in the cystic fibrosis transmembrane conductance regulator (CFTR), alpha(1)-antitrypsin, and mannose-binding lectin (MBL) genes, and measured baseline fibrinogen and C-reactive protein (CRP) concentrations in up to 9245 adults randomly selected from the Danish general population., Materials and Methods: Information on diagnoses of asthma and COPD was collected from two Danish National Registers covering all hospital discharges and deaths in the country. This data was correlated with genotyping results to determine risk of obstructive lung disease according to the genetic and biochemical markers studied., Results: The genetic marker, F508del, in the cystic fibrosis gene was associated with increased asthma risk, but aggregating this data in a meta-analysis with results from previous reports, the risk of asthma was only marginally elevated [summary odds ratio (95%CI): 1.3 (1.1-1.6)]. The F508del marker was not associated with COPD [odds ratio: 0.9 (0.4-1.6)]. Our data also suggested a significant role of smoking on fertility in cystic fibrosis/F508del heterozygotes. The risk of COPD was marginally elevated for the genetic markers, MS and MZ, in the alpha(1)-antitrypsin gene [summary odds ratio: MS, 1.2 (1.0-1.4) and MZ, 2.3 (1.6-3.4)], whereas the SZ marker was an important risk factor of COPD [summary odds ratio: 3.3 (1.2-8.6)]. The ZZ genotype is already in clinical use as a genetic marker for early-onset COPD. Our data also suggested ZZ and MZ are associated with reduced blood pressure and MZ with reduced risk of ischemic cardiovascular disease. Genetic deficiency of MBL was not a major risk factor for asthma [relative risk: 1.1 (0.8-1.7)] or COPD [1.4 (0.97-2.0)]. We found increased risk of cardiovascular disease with MBL deficiency, but this result could not be confirmed in a matched case-control study using cases with ischemic cardiovascular disease from Copenhagen University Hospital, Denmark. Elevated serum fibrinogen and CRP levels were biochemical markers of future COPD. In the future after further validation, it is possible that these markers, particularly CRP, can be used to categorize individuals with low, medium, or high risk of COPD, and thus point out patients in need of intensified prevention and treatment for COPD. The association between COPD and elevated fibrinogen and CRP levels suggests that either factor or upstream factors regulating fibrinogen and CRP expression are important players in the pathogenesis of COPD., Conclusion: We have set-up an analysis for diagnosing the SZ and ZZ genotypes at the Department of Clinical Biochemistry at Herlev University Hospital, together with measurement of plasma alpha(1)-antitrypsin levels. This will help clinicians to detect alpha(1)-antitrypsin-deficient individuals with a high risk for COPD, and opens up for early smoking prevention counseling and potential therapy for individuals identified with alpha(1)-antitrypsin deficiency. The F508del marker and genetic variants in the MBL-2 gene cannot at present be used as markers for obstructive lung disease in the Danish general population. To determine whether fibrinogen or CRP is causally related to COPD, we are currently investigating whether genetically reduced levels of fibrinogen and CRP are associated with reduced risk of future COPD.

Maternal immune responses can promote allergy development in offspring, as shown in a model of increased susceptibility to asthma in babies of ovalbumin (OVA)-sensitized and -challenged mother mice. We investigated whether inflammatory responses to air pollution particles (diesel exhaust particles, DEP) or control "inert" titanium dioxide (TiO(2)) particles are enhanced during pregnancy and whether exposure to particles can cause increased neonatal susceptibility to asthma. Pregnant BALB/c mice (or nonpregnant controls) received particle suspensions intranasally at Day 14 of pregnancy. Lung inflammatory responses were evaluated 48 hours after exposure. Offspring of particle- or buffer-treated mothers were sensitized and aerosolized with OVA, followed by assays of airway hyperresponsiveness (AHR) and allergic inflammation (AI). Nonpregnant females had the expected minimal response to "inert" TiO(2). In contrast, pregnant mice showed robust and persistent acute inflammation after both TiO(2) and DEP. Genomic profiling identified genes differentially expressed in pregnant lungs exposed to TiO(2). Neonates of mothers exposed to TiO(2) (and DEP, but not PBS) developed AHR and AI, indicating that pregnancy exposure to both "inert" TiO(2) and DEP caused increased asthma susceptibility in offspring. We conclude that (1) pregnancy enhances lung inflammatory responses to otherwise relatively innocuous inert particles; and (2) exposures of nonallergic pregnant females to inert or toxic environmental air particles can cause increased allergic susceptibility in offspring.

Background: Carriers of cystic fibrosis intron-8 5T alleles with high exon-9 skipping could have increased annual lung function decline and increased risk for asthma or chronic obstructive pulmonary disease (COPD)., Methods: We genotyped 9131 individuals from the adult Danish population for cystic fibrosis 5T, 7T, 9T, and F508del alleles, and examined associations between 11 different genotype combinations, and annual FEV1 decline and risk of asthma or COPD., Results: 5T heterozygotes vs. 7T homozygous controls had no increase in annual FEV1 decline, self-reported asthma, spirometry-defined COPD, or incidence of hospitalization from asthma or COPD. In 5T/7T heterozygotes vs. 7T homozygous controls we had 90% power to detect an increase in FEV1 decline of 8 ml, an odds ratio for self-reported asthma and spirometry-defined COPD of 1.9 and 1.7, and a hazard ratio for asthma and COPD hospitalization of 1.8 and 1.6, respectively. Both 5T homozygotes identified in the study showed evidence of asthma, while none of four 5T/F508del compound heterozygotes had severe pulmonary disease. 7T/9T individuals had annual decline in FEV1 of 19 ml compared with 21 ml in 7T homozygous controls (t-test: P = 0.03). 6.7% of 7T homozygotes without an F508del allele in the cystic fibrosis transmembrane conductance regulator gene reported asthma vs. 11% of 7T/9T individuals with an F508del allele (chi2: P = 0.01) and 40% of 7T homozygotes with an F508del allele (P = 0.04). 7T homozygotes with vs. without an F508del allele also had higher incidence of asthma hospitalization (log-rank: P = 0.003); unadjusted and adjusted equivalent hazard ratios for asthma hospitalization were 11 (95%CI: 1.5-78) and 6.3 (0.84-47) in 7T homozygotes with vs. without an F508del allele., Conclusion: Polythymidine 5T heterozygosity is not associated with pulmonary dysfunction or disease in the adult Caucasian population. Furthermore, our results support that F508del heterozygosity is associated with increased asthma risk independently of the 5T allele.

Background: Several risk factors for asthma have been proposed; however, the causality of these associations is sometimes unclear. Mendelian randomization is a powerful epidemiological approach that can help elucidate the causality of risk factors. The aim of the present study was to identify causal risk factors for asthma through Mendelian Randomization studies. Methods: A systematic search of PubMed and EMBASE was conducted, to identify studies investigating risk factors for asthma or respiratory allergies through Mendelian Randomization. When two or more studies investigated the same risk factor a meta‐analysis was conducted. Of 239 studies initially identified, 41 were included. Results: A causal association between adiposity and adult asthma risk was found in 10 out of 12 studies with a summary risk ratio of 1.05 per kg/m2 increase in BMI (95% CI: 1.03–1.07). Puberty timing (n = 3), alcohol (n = 2), and linoleic acid (n = 1) had causal effects on asthma risk, while vitamins/minerals (n = 6) showed no consistent effect on asthma. The effect of smoking on adult asthma conflicted between studies. Several of the significant associations of asthma with immune related proteins (n = 5) and depression (n = 2) investigated through multiple traits analyses could generally benefit from replications in independent datasets. Conclusion: This systematic review and meta‐analysis found evidence for causal effects of adiposity, puberty timing, linoleic acid, alcohol, immune related proteins, and depression on risk of asthma. [ABSTRACT FROM AUTHOR]

Background Risk factors for chronic cough in the general population have not been described systematically. We identified and ranked chronic cough risk factors at the individual and community level using data from 14,669 individuals from the Copenhagen General Population Study. Methods Severity of chronic cough was assessed using the Leicester Cough Questionnaire (LCQ). We ranked chronic cough risk factors based on magnitude of age-adjusted ORs at the individual level and of the population attributable risks (PARs) at the community level. Results Prevalence of chronic cough in the general population was 4% overall and 3% in never smokers, 4% in former smokers, and 8% in current smokers. Median score of the LCQ was 5.8 (25th-75th percentile, 5.0-6.3) for physical domain, 5.6 (25th-75th percentile, 4.6-6.3) for psychologic domain, 6.3 (25th-75th percentile, 5.5-6.8) for social domain, and 17.3 (25th- 75th percentile, 15.4-18.9) in total. At the level of the individual, age-adjusted ORs for the three top-ranked risk factors were 5.0 (95% CI, 1.4-18) for bronchiectasis, 2.6 (95% CI, 1.7-3.9) for asthma and 2.3 (95% CI, 1.5-3.4) for gastroesophageal reflux disease in never smokers, 7.1 (95% CI, 2.6-20) for bronchiectasis, 3.1 (95% CI, 2.2-4.4) for asthma and 2.2 (95% CI, 1.5-3.2) for occupational exposure to dust/fumes in former smokers, and 1.9 (95% CI, 1.3-2.9) for airflow limitation in current smokers. At the level of the community, the three top-ranked risk factors were female sex (PAR, 19%), asthma (PAR, 10%), and gastroesophageal reflux disease (PAR, 8%) in never smokers; abdominal obesity (PAR, 20%), low income (PAR, 20%), and asthma (PAR, 13%) in former smokers; and airflow limitation (PAR, 23%) in current smokers. Conclusions Risk factors for chronic cough differ at the level of the individual and community, and by smoking status. Strategies to prevent and treat modifiable chronic cough risk factors should be tailored accordingly. [ABSTRACT FROM AUTHOR]

Background: MARCO (macrophage receptor with collagenous structure) is a dominant receptor for unopsonized particles and bacteria in the lungs. Reduced function of this receptor due to genetic variation may be associated with susceptibility to chronic obstructive pulmonary disease (COPD) and lung infection. Objectives: To identify novel genetic variants in MARCO that are associated with reduced lung function, or increased risk of COPD or lung infection. Methods: We first screened 760 individuals with extreme lung phenotypes in a large general population study to identify novel variants in the MARCO gene. We next genotyped the entire cohort consisting of 10,604 individuals to assess the clinical relevance of these variants. Results: We identified 4 novel (R124H, K201N, P303L and G340W) and 5 previously described (H101Q, F2825, G319V, K387Q and E511D) non-synonymous variants. When screening the entire cohort for these variants, we found low minor allele frequencies ranging from 0.005 to 5%. None of the individual MARCO genotypes were associated with reduced lung function, or risk of COPD or lung infection. H101Q heterozygotes had an increased odds ratio for sepsis of 2.2 (95% CI: 1.1-4.4) compared to non-carriers, but none of the other MARCO genotypes were associated with the risk of sepsis. Conclusions: We identified 9 non-synonymous variants in the MARCO gene and showed that these variants are not major risk factors for COPD or lung infection in the Danish population. H101Q heterozygotes had increased sepsis risk, but further research is required to confirm this finding. This study is the first to examine genetic variants in MARCO and the risk of COPD and infections in humans. [ABSTRACT FROM AUTHOR]

Summary: Dominant mutations in the surfactant protein-C(SFTPC) gene have been linked with interstitial lung disease. The frequency of lung disease due to SFTPC mutations in the general population is unknown. The aim of this study was to identify novel SFTPC mutations that are associated with lung function or disease in the general population. We resequenced the SFTPC gene in 760 individuals and identified 18 genetic variants, of which 5 were novel. Of the five novel mutations, two were situated in highly conserved areas of the SFTPC gene: A53T and Y106X. We genotyped the Copenhagen City Heart Study(n =10,604) and the Copenhagen General Population Study(n =37,337) to assess the clinical relevance of these mutations. Genotyping identified 36 individuals heterozygous for A53T and 3 individuals heterozygous for Y106X. A53T heterozygotes and Y106X heterozygotes did not differ from non-carriers in FEV1% predicted, FVC% predicted or FEV1/FVC. A53T heterozygotes had a two-fold increased risk for asthma in the Copenhagen City Heart Study and Copenhagen General Population Study combined (adjusted odds ratio 2.2(1.0–4.9)). A53T heterozygotes did not differ consistently from non-carriers in risk of chronic obstructive pulmonary disease or interstitial lung disease. No Y106X heterozygotes suffered from asthma, chronic obstructive pulmonary disease (COPD), or interstitial lung disease. We identified two novel mutations in highly conserved areas of the SFTPC gene, and show that heterozygotes for the mutations have normal lung function and are unaffected by COPD and interstitial lung disease. A53T heterozygotes had increased asthma risk, but further research is required to conclusively determine whether this mutation is associated with asthma. [Copyright &y& Elsevier]

Abstract: Ischemic cardiovascular disease and obstructive pulmonary disease involve inflammation. Leukotrienes may be important pro-inflammatory mediators. We tested the hypothesis that the (-1072)G>A and (-444)A>C promoter polymorphisms of leukotriene C4 synthase confer risk of transient ischemic attack (TIA), ischemic stroke, ischemic heart disease (IHD), asthma, and chronic obstructive pulmonary disease (COPD). We genotyped individuals from the Danish general population, the Copenhagen City Heart Study, and Danish patients with IHD/coronary atherosclerosis, the Copenhagen Ischemic Heart Disease Study. We used prospective (n =10,386), cross-sectional (n =10,386), and case-control (n =2392+5012) designs. Allele frequency was 0.07 for (-1072)A and 0.29 for (-444)C. Cumulative incidence for TIA was higher for (-1072)AA versus GG genotype (log-rank: p <0.001), and lower for (-444)CC versus AA genotype (log-rank: p =0.03). Cumulative incidence for ischemic stroke was also lower for (-444)CC versus AA genotype (log-rank: p =0.04). Multifactorially adjusted hazard ratios for TIA were 5.2(95% CI:1.9–14) for (-1072)AA versus GG genotype, and 0.4(0.2–1.0) for (-444)CC versus AA genotype. Corresponding values were 1.9 (0.7–5.2) and 0.7 (0.5–1.0) for ischemic stroke, and 0.8 (0.4–1.6) and 1.0 (0.9–1.2) for IHD. In the case-control study, corresponding multifactorially adjusted odds ratios for IHD/coronary atherosclerosis were 0.5 (0.2–1.3) and 1.2 (1.0–1.5). These genotypes were not associated with risk of asthma or COPD. Leukotriene C4 synthase promoter genotypes influence risk of TIA and ischemic stroke, but not risk of IHD/coronary atherosclerosis, asthma, or COPD. [Copyright &y& Elsevier]

Background: Cystic fibrosis is a recessive disorder mainly characterised by lung disease. We tested the hypothesis that individuals heterozygous for the common cystic fibrosis deltaF508 mutation are at risk of obstructive pulmonary disease.Methods: We studied a cross-sectional sample from the general population of Copenhagen, Denmark, aged 20 years and older. We did spirometry to measure forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC), and did genotyping on blood samples of 9141 individuals. We asked all participants whether they had asthma, and asked for information on smoking and other factors that could have contributed to obstructive pulmonary disease.Findings: We identified 250 carriers of the deltaF508 mutation (2.7% [95% CI 2.5-3.1]). 9% of carriers reported having asthma compared with 6% of non-carriers (p=0.04). The odds ratio for asthma in participants heterozygous for deltaF508 mutation was 2.0 (1.2-3.5, p=0.02). Furthermore, among individuals with airway obstruction, the percentage predicted FEV1 and FVC were significantly lower in participants heterozygous for deltaF508 than in non-carriers (49 vs 58%, p=0.004; and 70 vs 82%, p<0.001, respectively), mainly due to an effect in those with self-reported asthma.Interpretation: Cystic fibrosis deltaF508 heterozygosity may be over-represented among people with asthma and seems to be associated with decreased pulmonary function in people with airway obstruction who also have asthma. [ABSTRACT FROM AUTHOR]