Journal of Pulmonology and Clinical Research

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (202) 780-3397

Short Communication - Journal of Pulmonology and Clinical Research (2025) Volume 8, Issue 1

Emphysema in Non-Smokers: Uncovering Genetic and Environmental Risk Factors

Maria Wei *

Department of Environmental Health, University of Sao Paulo, Brazil

*Corresponding Author:
Maria Wei
Department of Environmental Health, University of Sao Paulo, Brazil
E-mail: m.wei@usp-pulmo.br

Received: 1-Jan-2025, Manuscript No. aajpcr-25-168606; Editor assigned: 4-Jan-2025, PreQC No. aajpcr-25-168606 (PQ) Reviewed:18-Jan-2025, QC No. aajpcr-25-168606 Revised:25-Jan-2025, Manuscript No. aajpcr-25-168606; Published:30-Jan-2025, DOI: 10.35841/ aajpcr - 8.1.188

Citation: Wei M. Emphysema in non-smokers: Uncovering genetic and environmental risk factors. J Pulmonol Clin Res. 2025;8(1):188

Visit for more related articles at Journal of Pulmonology and Clinical Research

Introduction

Emphysema is traditionally associated with long-term cigarette smoking, yet a significant number of cases are found in individuals who have never smoked. This chronic lung condition, characterized by the destruction of alveolar walls and reduced respiratory surface area, leads to breathlessness, chronic cough, and reduced exercise tolerance. The occurrence of emphysema in non-smokers challenges the conventional understanding of the disease and highlights the need to explore genetic and environmental risk factors beyond tobacco exposure [1].

One of the most well-established genetic causes of emphysema in non-smokers is Alpha-1 Antitrypsin Deficiency (AATD). Alpha-1 antitrypsin (AAT) is a protein produced in the liver that protects the lungs from neutrophil elastase, an enzyme that breaks down elastin in the alveolar walls. In individuals with AATD, this protective mechanism is impaired, leading to early-onset emphysema, often in the third or fourth decade of life—even in the absence of smoking. AATD is inherited in an autosomal codominant pattern, and genetic testing is essential for diagnosis, especially in younger patients with unexplained emphysema [2].

Beyond AATD, other genetic factors may play a role. Polymorphisms in genes associated with inflammation, oxidative stress response, and tissue remodeling—such as MMP-12 (matrix metalloproteinase-12) and TGF-β (transforming growth factor-beta)—have been implicated in increased susceptibility to emphysema. While research is ongoing, these genetic variants may explain why some non-smokers develop lung tissue damage similar to that seen in heavy smokers [3].

Environmental exposures also contribute significantly to the development of emphysema in non-smokers. Indoor air pollution, particularly from biomass fuel combustion for cooking and heating, is a major risk factor in developing countries. Prolonged exposure to smoke from wood, charcoal, dung, or crop residue in poorly ventilated homes can lead to chronic lung inflammation and emphysematous changes. Women and children are disproportionately affected due to their higher exposure in domestic settings [4].

Outdoor air pollution is another contributing factor. Long-term exposure to fine particulate matter (PM2.5), nitrogen dioxide, and ozone has been linked to the development and progression of emphysema, even in individuals without a history of smoking. Urban dwellers, traffic workers, and people living near industrial zones are at higher risk due to sustained exposure to harmful airborne pollutants [5].

Conclusion

In conclusion, emphysema in non-smokers is a multifactorial condition influenced by genetic predispositions and environmental exposures. Understanding these risk factors is essential for early diagnosis, personalized treatment, and prevention strategies. As research continues to shed light on the non-smoking pathways to emphysema, greater emphasis must be placed on improving public awareness, expanding genetic screening, and mitigating environmental risks to protect vulnerable populations from this debilitating disease.

References

  1. Di Furia M, Romano L, Salvatorelli A, et al. Giant spigelian hernia presenting as small bowel obstruction: Case report and review of literature. Int J Surg Case Rep. 2019;63:118-21.

    2. Indexed at, Google Scholar, Cross Ref

  2. Chamary SL, Chamary VL. Laparoscopic features and repair of a combined left spigelian hernia and left morgagni diaphragmatic hernia. Ann R Coll Surg Engl. 2015;97(2):e25-6.

    3. Indexed at, Google Scholar, Cross Ref

  3. Tran H, Tran K, Zajkowska M, et al. Single-incision laparoscopic repair of spigelian hernia. JSLS. 2015;19(1):e2015.001644.

    4. Indexed at, Google Scholar, Cross Ref

  4. Szema AM. Work-exacerbated asthma. Clin Chest Med. 2012;33(4):617-24.

    5. Indexed at, Cross Ref

  5. Burge PS, Moore VC, Robertson AS. Sensitization and irritant-induced occupational asthma with latency are clinically indistinguishable. Occup Med (Lond). 2012;62(2):129-33.

    6. Indexed at, Google Scholar, Cross Ref

Get the App