# Sex and Gender in Chronic Obstructive Pulmonary Disease: Does It Matter?

**Authors:** Christos Kyriakopoulos, Georgios Hillas, Antonia Assioura, Anastasia Papanikolaou, Vasileios Angelopoulos, Konstantinos Kostikas, Athena Gogali

PMC · DOI: 10.3390/jpm16030152 · Journal of Personalized Medicine · 2026-03-06

## TL;DR

This paper reviews how sex and gender differences affect COPD, highlighting the need for personalized approaches in diagnosis and treatment.

## Contribution

The paper synthesizes sex- and gender-disaggregated data to emphasize the importance of considering these factors in COPD research and clinical practice.

## Key findings

- Women may be more biologically susceptible to tobacco smoke effects and develop COPD at younger ages.
- Clinical manifestations and disease patterns differ between sexes, with women more likely to have airway-predominant disease and underdiagnosis.
- Current COPD guidelines and treatments often overlook sex and gender differences, suggesting a need for personalized strategies.

## Abstract

Chronic obstructive pulmonary disease (COPD) is a major contributor to global respiratory morbidity and exhibits substantial sex- and gender-related differences in incidence, phenotype, pathophysiology, and outcomes across the life course. Historically regarded as a predominantly male disease due to higher smoking rates, COPD is now increasingly recognized among women, reflecting changing exposure patterns and enhanced diagnostic attention. Moreover, evidence indicates that women may be more biologically susceptible to the harmful effects of tobacco smoke and often develop COPD at younger ages. Clinical manifestations also differ, with women more frequently reporting dyspnea, anxiety, and depression, whereas men may exhibit more cough and sputum production. Imaging studies suggest that airway-predominant disease is more common in women, while men are more likely to demonstrate emphysema-predominant patterns. Furthermore, women face an increased risk of exacerbation, yet they are more likely to experience underdiagnosis or misdiagnosis. Treatment responses and comorbidity patterns also show sex- and gender-related variations. Despite these differences, most clinical guidelines and therapeutic strategies do not differentiate by sex and gender, highlighting a gap in personalized COPD management. Overall, growing evidence underscores the importance of incorporating sex and gender as biological and sociocultural variables in COPD research, diagnosis, and treatment. Recognizing sex/gender-specific risk profiles, symptom patterns, and disease phenotypes may improve early detection and enable more targeted, effective interventions. This narrative synthesis, derived from a meticulous search in PubMed and the critical selection of 74 articles from the 448 identified originally, integrates evidence from guideline statements, registry studies, mechanistic and preclinical research, imaging and physiology investigations, systematic reviews, and randomized controlled trials that report sex- and gender-disaggregated data.

## Linked entities

- **Diseases:** Chronic obstructive pulmonary disease (MONDO:0005002), COPD (MONDO:0005002)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CHRM3 (cholinergic receptor muscarinic 3) [NCBI Gene 1131] {aka EGBRS, HM3, PBS, m3AChR}, Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 21803] {aka TGF-beta1, TGFbeta1, Tgfb, Tgfb-1}
- **Diseases:** respiratory (MESH:D012131), COPD (MESH:D029424), testosterone deficiency (MESH:D007153), Anxiety (MESH:D001007), diabetes (MESH:D003920), breathlessness (MESH:D004417), bronchitis (MESH:D001991), dominant (MESH:C566739), rheumatoid arthritis (MESH:D001172), fractures (MESH:D050723), nicotine dependence (MESH:D014029), Th2 inflammation (MESH:D007249), cardiovascular disease (MESH:D002318), airway damage (MESH:D000402), osteoporosis (MESH:D010024), asthma (MESH:D001249), polycystic ovary syndrome (MESH:D011085), decline in lung function (MESH:D055370), fatigue (MESH:D005221), respiratory disease (MESH:D012140), chronic cough (MESH:D003371), emphysema (MESH:D004646), metabolic syndrome (MESH:D024821), withdrawal symptoms (MESH:D013375), death (MESH:D003643), kidney diseases (MESH:D007674), depression (MESH:D003866), obesity (MESH:D009765), emphysematous (MESH:D041882), small-airway disease (MESH:D056151), obstructive disease (MESH:D001157), ovarian cysts (MESH:D010048), male disease (MESH:D005832), weight gain (MESH:D015430), injury to (MESH:D014947), autoimmune comorbidities (MESH:D001327), infection (MESH:D007239)
- **Chemicals:** indacaterol (MESH:C510790), nicotine (MESH:D009538), Testosterone (MESH:D013739), tamoxifen (MESH:D013629), steroid (MESH:D013256), Progesterone (MESH:D011374), ipratropium (MESH:D009241), COPDGene (-), glycopyrronium (MESH:D006024)
- **Species:** Homo sapiens (human, species) [taxon 9606], Nicotiana tabacum (American tobacco, species) [taxon 4097], Mus musculus (house mouse, species) [taxon 10090]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13028426/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13028426/full.md

## References

73 references — full list in the complete paper: https://tomesphere.com/paper/PMC13028426/full.md

---
Source: https://tomesphere.com/paper/PMC13028426