Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Nov 17;30(162):210067.
doi: 10.1183/16000617.0067-2021. Print 2021 Dec 31.

Sex and gender in asthma

Affiliations
Review

Sex and gender in asthma

Nowrin U Chowdhury et al. Eur Respir Rev. .

Abstract

Asthma is a heterogenous disease, and its prevalence and severity are different in males versus females through various ages. As children, boys have an increased prevalence of asthma. As adults, women have an increased prevalence and severity of asthma. Sex hormones, genetic and epigenetic variations, social and environmental factors, and responses to asthma therapeutics are important factors in the sex differences observed in asthma incidence, prevalence and severity. For women, fluctuations in sex hormone levels during puberty, the menstrual cycle and pregnancy are associated with asthma pathogenesis. Further, sex differences in gene expression and epigenetic modifications and responses to environmental factors, including SARS-CoV-2 infections, are associated with differences in asthma incidence, prevalence and symptoms. We review the role of sex hormones, genetics and epigenetics, and their interactions with the environment in the clinical manifestations and therapeutic response of asthma.

PubMed Disclaimer

Conflict of interest statement

Conflict of interest: N.U. Chowdhury reports support for the present manuscript from the National Institute of Health, who provided the following funding sources: T32GM007347. Conflict of interest: V.P. Guntur reports receiving support for attending meetings and/or travel from AstraZeneca and CASCADE Investigator meeting, outside the submitted work. Conflict of interest: D.C. Newcomb reports support for the present manuscript from National Institute of Health, who provided the following funding sources: HL122554, HL136664 and DK020593. Conflict of interest: M.E. Wechsler reports support for the present manuscript from the Jin Hua Foundation. Consulting fees were received outside the submitted work from AstraZeneca, Boehringer Ingelheim, Equillium, Genentech, GlaxoSmithKline, Novartis, Regeneron, RestorBio, Sanofi, Teva, Cohero Health and Pulmatrix.

Figures

FIGURE 1
FIGURE 1
Asthma prevalence percentage throughout life in developed countries. Graph based on 2018 data from the Global Health Data Exchange (https://ghdx.healthdata.org).
FIGURE 2
FIGURE 2
Sex and gender differences in asthma are influenced by several factors that vary across the lifespan. As shown by bi-directional arrows, these factors affect the sex and gender differences observed in asthma or are affected by sex hormones. DHEA: dehydroepiandrosterone; GERD: gastro-oesophageal reflux disease; SNP: single nucleotide polymorphism.
FIGURE 3
FIGURE 3
Mechanisms driving airway inflammation in asthma pathogenesis. Type 2 (green) and nontype 2 (yellow) adaptive immune responses associated with asthma pathogenesis. This cartoon shows how increased activation and differentiation of type 2 responses leads to increased IL-4, IL-5, IL-9 and IL-13 production as well as increased eosinophil infiltration, B-cell production of IgE, AHR, FENO and mucus production. Nontype 2 inflammation is more commonly seen in adults than children with asthma. Nontype 2 inflammation results in increased production of IL-17A or IFN-γ from T-cells or increased IL-6, TNF and IL-1β leading to increased neutrophil infiltration, AHR, FENO and mucus production. AHR: airway hyperresponsiveness; FENO: exhaled nitric oxide fraction; IFN: interferon; IL: interleukin; ILC2: type 2 innate lymphoid cell; Th: T-helper cell; TNF: tumour necrosis factor; TSLP: thymic stromal lymphopoietin.

Comment in

  • doi: 10.1183/16000617.0330-2020
  • doi: 10.1183/16000617.0038-2021

References

    1. GBD 2016 Disease and Injury Incidence and Prevalence Collaborators . Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet 2017; 390: 1211–1259. doi:10.1016/S0140-6736(17)32154-2 - DOI - PMC - PubMed
    1. Schatz M, Camargo CA Jr. The relationship of sex to asthma prevalence, health care utilization, and medications in a large managed care organization. Ann Allergy Asthma Immunol 2003; 91: 553–558. doi:10.1016/S1081-1206(10)61533-5 - DOI - PubMed
    1. El-Husseini ZW, Gosens R, Dekker F, et al. . The genetics of asthma and the promise of genomics-guided drug target discovery. Lancet Respir Med 2020; 8: 1045–1056. doi:10.1016/S2213-2600(20)30363-5 - DOI - PubMed
    1. Han YY, Forno E, Celedon JC. Sex steroid hormones and asthma in a nationwide study of U.S. adults. Am J Respir Crit Care Med 2020; 201: 158–166. doi:10.1164/rccm.201905-0996OC - DOI - PMC - PubMed
    1. Gomez JL. Epigenetics in asthma. Curr Allergy Asthma Rep 2019; 19: 56. doi:10.1007/s11882-019-0886-y - DOI - PMC - PubMed

Substances