According to the World Health Organization (WHO), Chronic Obstructive Pulmonary Disease (COPD), a progressive lung disease characterized by airflow limitation that is not fully reversible, stands as the third leading cause of death worldwide due to tobacco smoking, claiming a staggering 3.23 million lives in 2019 alone. This chronic inflammatory lung condition impedes airflow from the lungs, leading to a myriad of debilitating symptoms. Patients often experience persistent breathing difficulties, accompanied by a chronic cough, excessive mucus production, and wheezing. Various risk factors exacerbate COPD’s prevalence. Notably, tobacco smoking, exposure to air pollutants, such as PM2.5, biomass fuel usage, and genetic predispositions take the lead.
Recent research conducted by the esteemed Indian Institute of Technology (IIT) Hyderabad underscores the grave impact of PM2.5 exposure, with an alarming 5.4 lakh premature deaths attributed to it annually. This research further pinpoints the occurrence of approximately one lakh deaths in 53 prominent Indian cities, highlighting the urgent need for effective interventions.
In this interview, we delve deeper into COPD’s multifaceted nature with an exclusive exchange featuring Dr. Astha Ranjan, a distinguished Senior Research Fellow (SRF) under the University Grants Commission (UGC). Dr. Ranjan’s pioneering work explores the intricate interplay between genetic variants and lung volumes, offering a novel perspective on COPD research. Through an insightful dialogue with The Interview World, Dr. Ranjan expounds on her doctoral research findings, providing invaluable insights into the complex mechanisms underlying COPD pathogenesis and potential therapeutic avenues. Below, we present the key highlights gleaned from Dr. Ranjan’s illuminating interview.
Q: How does your doctoral research explore the genetic factors contributing to Chronic Obstructive Pulmonary Disease (COPD)?
A: My doctoral research primarily focused on unravelling the intricate relationship between single nucleotide polymorphisms (SNPs) and their impact on lung function within the population of Ranga Reddy district, Telangana. Environmental factors such as pollution and tobacco smoking exert profound influences on lung-related diseases. However, there remains a notable dearth of research into the genetic predisposition to COPD.
By delving into the genetic nuances of COPD pathogenesis, my study also aimed to bridge this gap in understanding. Such insights hold immense potential in guiding the development of more targeted therapeutic interventions. Armed with a deeper comprehension of the genetic factors at play, healthcare providers can tailor treatments with greater precision, thereby enhancing their effectiveness in managing and combating this debilitating disease.
Q: How can you describe the premise, materials, and methods utilized in your research study?
A: The research study involved 752 samples, comprising 392 males and 360 females, sourced from the Andhra Pradesh Child and Parents Study (APCAPS) cohort. In the third phase of the APCAPS study, I gathered spirometric data on lung function measurements, along with demographic, somatometric, metabolic, and lifestyle data.
Furthermore, DNA was extracted from blood samples, which were subsequently subjected to genotyping using the Sequenom iPLEX Mass Spectrometry platform. This analysis also focused on 7 selected single nucleotide polymorphisms (SNPs).
These SNPs were specifically chosen due to their significant associations with lung function and COPD as established in prior genome-wide association studies conducted on Western populations.
Q: What significant conclusions did you draw from the study’s findings?
A: In our investigation, we unearthed a notable prevalence of potential COPD, impacting a substantial 31.25% of the examined population. A distinct gender disparity emerged, with females showing a heightened vulnerability compared to males. Furthermore, our analysis revealed intriguing associations between single nucleotide polymorphisms and several studied variables, excluding lung function and COPD. Among the identified risk factors, all but pack-years of smoking exhibited significant correlations with lung function. Notably, tobacco smoking stood out as the solitary risk factor linked directly to COPD within our study cohort. Moreover, these findings underscore the multifaceted nature of COPD development and the importance of tailored preventive measures.
Q: What insights do you believe your research study brings to the current understanding of its subject matter?
A: I conducted the research on a limited sample size from the population in Ranga Reddy district, Telangana. To advance future studies on Indian lung function genetics, replication and validation in a larger population are essential. This expansion would bolster the credibility and robustness of such research. Furthermore, it would facilitate pharmaceutical companies in developing innovative drugs for COPD treatment, addressing a significant healthcare need within the Indian population and potentially beyond.
