Article Text

Ethnic variation in asthma phenotypic presentation and outcomes: a cross-sectional analysis of the UK Biobank
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  1. John Busby1,
  2. P Jane McDowell2,3,
  3. Paul E Pfeffer4,
  4. Adel Hasan Mansur5,
  5. Liam G Heaney2,3
  1. 1 Centre for Public Health, Queen's University Belfast School of Medicine Dentistry and Biomedical Sciences, Belfast, UK
  2. 2 Centre for Experimental Medicine, Queen's University Belfast School of Medicine Dentistry and Biomedical Sciences, Belfast, UK
  3. 3 Belfast Health & Social Care NHS Trust, Belfast, UK
  4. 4 Barts Health NHS Trust, London, UK
  5. 5 University of Birmingham & Heartlands Hospital, University Hospitals Birmingham, Birmingham, UK
  1. Correspondence to Dr John Busby, Centre for Public Health, Queen's University Belfast School of Medicine Dentistry and Biomedical Sciences, Belfast, UK; john.busby{at}qub.ac.uk

Abstract

Ethnic disparities exist within asthma; however, country of birth is rarely investigated. We described demographic and clinical characteristics by ethnicity and country of birth within the UK Biobank. Lung function and asthma hospitalisations were similar for white, black and North-East Asian participants, however, South-East (SE) Asians more commonly had an FEV1 below the lower limits of normal (LLN; 53.8% vs 32.3%, p<0.001), blood eosinophilia (38.6% vs 23.8%, p<0.001) and asthma hospitalisation (12.5% vs 8.3%, p<0.001) than white participants. First-generation SE Asian immigrants had poorer lung function (57.7% vs 27.7% FEV1 below LLN, p<0.001) than UK/Ireland born participants. These data demonstrate inter-ethnic and intra-ethnic disparities.

  • Asthma
  • Ethnicity
  • Inequalities

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Introduction

Several studies have highlighted potential ethnic disparities in asthma, including within the UK where patients from ethnic minority groups (EMGs) report higher emergency department (ED) attendances and hospitalisations.1 2 The mechanisms underlying this are debated; however, socioeconomic status (SES), health literacy and structural racism have been proposed. Previous studies have failed to consider disparities by country of birth, and if first-generation immigrants have a specific unmet need due to cultural factors and childhood exposures. In this study, we report on ethnic differences in asthma characteristics and outcomes, including stratification by country of birth.

Methods

Full details of our methods are provided in online supplemental files 1 and 2. In brief, participants from the UK Biobank were included if they reported doctor-diagnosed asthma and were receiving an asthma medication (short-acting beta agonist, inhaled corticosteroid or oral corticosteroid) at their baseline visit. Participants were excluded if they were mixed or other ethnicity, or their ethnicity or country of birth was missing. Self-reported ethnicity was categorised into white, South-East (SE) Asian, black and North-East (NE) Asian and country of birth was categorised into UK/Ireland born or elsewhere. We used ethnicity-adjusted equations from the Global Lung Initiative to calculate predicted forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC) and FEV1/FVC alongside lower limits of normal (LLN). A cut-off of 300 cells/µL was used to define blood eosinophilia. We used the Hospital Episode Statistics to identify asthma hospitalisations. We explored mediating pathways using logistic regression adjusting for demographics, lifestyle, SES and air pollution. We re-ran our analysis including all participants with doctor-diagnosed asthma and restricted to those in the most deprived index of multiple deprivation (IMD) quintile. Analyses were conducted using STATA V.16.

Supplemental material

Results

A total of 31 875 participants met study inclusion criteria including 30 731 (96.4%) of white, 623 (2.0%) SE Asian, 466 (1.5%) black and 55 (0.2%) NE Asian ethnicity (table 1). Lung function and asthma hospitalisations were similar for white, black and NE Asian participants. However, a substantially larger proportion of SE Asians had an FEV1 below the LLN (53.8% vs 32.3%, p<0.001), blood eosinophilia (38.6% vs 23.8%, p<0.001) and asthma hospitalisation (12.5% vs 8.3%, p<0.001) than white participants.

Table 1

Comparison of participant characteristics and asthma outcomes by ethnicity*

There was little evidence of differences in lung function, blood eosinophilia and asthma hospitalisation between white first-generation immigrants and UK/Ireland born participants (online supplemental file 3, figure 1). Among SE Asians, first-generation immigrants were more likely to have an FEV1 below LLN (57.7% vs 27.7%, p<0.001; table 2, figure 1). Although there was a trend for higher asthma hospitalisations among SE Asian first-generation immigrants, this did not reach statistical significance (13.2% vs 7.7%, p=0.168). Black first-generation immigrants were more likely to have had an asthma hospitalisation (12.2% vs 6.4%, p=0.046; table 2, figure 1). A fuller description of inter-ethnicity and intra-ethnicity differences is provided in online supplemental file 4.

Figure 1

Comparison of study outcomes by immigrant generation status. FEV1, forced expiratory volume in 1 second; LLN, lower limits of normal.

Table 2

Comparison of South-East Asian and black participant characteristics and asthma outcomes by country of birth*

High rates of lung function impairment and blood eosinophilia among SE Asians were not explained by differences in demographics (including country of birth), lifestyle, SES or air pollution (online supplemental file 5). In contrast, there was some evidence that differences in asthma hospitalisation were mediated by SES, with this accounting for 24% (95% CI 15% to 58%) of the observed disparity. Nevertheless, when restricting to participants in the lowest IMD quintile SE Asians remained substantially more likely to have an FEV1 below the LLN (61.8% vs 38.3%, p<0.001), blood eosinophilia (38.5% vs 22.3%, p<0.001) and an asthma hospitalisation (17.1% vs 11.2%, p=0.012) than their white counterparts (online supplemental file 6). Our conclusions were unchanged when expanding the cohort to include participants not receiving any asthma medication at study entry (online supplemental file 7).

Discussion

We found substantial differences in asthma characteristics and outcomes between ethnicities. In particular, SE Asians had substantially poorer lung function, higher rates of blood eosinophilia and increased rates of asthma hospitalisation when compared with white participants, which was not substantially attenuated when adjusting for lifestyle factors, comorbidities, SES and air pollution. Lung function impairment was significantly higher among first-generation immigrant SE Asians compared with those who were born in the UK/Ireland. Our findings agree with previous UK-based studies, which have also reported poorer lung function and higher rates of asthma hospitalisation among SE Asians when compared with the white population.2 3

Poorer outcomes among EMG patients could reflect potential disparities within the UK. In particular, SE Asians had substantially worse outcomes, which may be related to higher rates of blood eosinophils potentially driven by a greater propensity for physicians to underestimate disease severity,4 poorer adherence to maintenance medications2 or parasitic infestation.5 EMGs are also known to experience difficulties registering with a primary care physician and report poorer communication once they are registered.6 Cultural factors related to stigma may also lead to reduced preventative therapy use and are likely to be exacerbated among first-generation immigrants.7

Our finding that substantially poorer lung function among SE Asian participants was largely driven by those born outside the UK could suggest that early-life factors, such as exposure to air pollution and lower birth weight, could play an important role.8 Age of diagnosis was substantially later for SE Asian and black first generation immigrants, which may indicate a delayed asthma diagnosis, leading to poor symptom control in early life and airway remodelling. The validity of ethnically corrected lung function reference equations has been debated, and these require validation in the UK population. Our data suggest that interventions which target type 2 biology through improved medication adherence, asthma education and self-management could successfully reduce disparities. Previous evidence suggests that these should be culturally adapted, although UK-based randomised trials of such interventions have shown mixed results.9 10 Future studies should consider the country of birth as a potential driver of asthma outcomes. Our study is limited by an under-representation of EMGs in the UK Biobank, a restriction to patients aged 40–69 years, and lack of data on key asthma outcomes including symptom control, exacerbations and ED visits.

In conclusion, we found substantial ethnic differences in asthma characteristics and outcomes. SE Asians had substantially poorer lung function and increased rates of asthma hospitalisation. This appears partly driven by first-generation immigrant status and not solely by lower SES. Higher type 2 inflammation is likely to be an important mediating pathway.

Ethics statements

Patient consent for publication

Ethics approval

This study involves human participants and the UK Biobank has approval from the North West Multi-centre Research Ethics Committee and the Community Health Index Advisory Group. Participants gave informed consent to participate in the study before taking part.

References

Supplementary materials

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Footnotes

  • Contributors JB conceptualised the research question, performed statistical analyses, interpreted the data and wrote the initial draft of the manuscript. PJM, PEP, AHM and LGH supervised the research, interpreted the data and critically revised the manuscript. The corresponding author attests that all listed authors meet authorship criteria and that no others meeting the criteria have been omitted.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests JB reports grants from Astrazeneca, personal fees from Nuvoair, outside the submitted work. PJM has received speaker’s honoraria from GSK and support for attending meetings from Cheisi, outside the submitted work. PEP reports grants from GSK and participation in clinical trials and consultancy and talks fees and attending conferences sponsorship from AZ, GSK, Chiesi, Novartis, Sanofi. AHM reports payment for talks and advisory board and sponsorships to attend conferences from AZ, GSK, Novartis, Teva, Chiesi, Sanofi and grants from GSK and AZ LGH has received non-financial support from GlaxoSmithKline during the conduct of the study; has received grants from Amgen, AstraZeneca, Medimmune, Janssen, Novartis, Roche/Genentech, GlaxoSmithKline, Boehringer Ingelheim, Aerocrine and Vitalograph; is the lead for the UK MRC Consortium for Stratified Medicine in Severe Asthma in partnership with Novartis, Hoffman la Roche/Genentech, Evelo Biosciences, Sanofi, GlaxoSmithKline, AstraZeneca, Teva, Theravance and Circassia; has received travel funding support for international respiratory meetings (institution remunerated) from AstraZeneca, Boehringer Ingelheim, Chiesi, GlaxoSmithKline and Napp Pharmaceutical; has received project grant funding from Medimmune, Novartis UK, Roche/Genentech and GlaxoSmithKline; and has received funding for clinical trials (institution remunerated) from AstraZeneca, GlaxoSmithKline, Schering Plough, Synairgen, Novartis and Roche/Genentech. These are outside of the submitted work.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.