As a condition characterized by a complex interplay of respiratory abnormalities, Chronic Obstructive Pulmonary Disease (COPD) primarily manifests as persistent airflow obstruction and heightened inflammation within the lung tissue (1, 2). It predominantly affects middle-aged and elderly populations (3, 4). In recent decades, COPD prevalence has been on an upward trend, largely driven by factors such as escalating environmental pollution and an aging global population, thereby creating a substantial economic strain on society (5, 6). The World Health Organization (WHO) forecasts that COPD prevalence will keep rising over the coming four decades, with annual deaths potentially exceeding 5.4 million by 2060 due to COPD and its associated complications (7, 8). Despite being a preventable and treatable major public health concern, there remain numerous shortcomings in the clinical management of COPD, including inadequate patient education and follow-up (9–12). These factors significantly impact the stability of the disease, leading to frequent exacerbations and disease progression. Additionally, symptom exacerbations not only affect patients’ daily activities and sleep quality but can also contribute to mental health issues (13, 14). The high prevalence, recurrent exacerbations, and protracted course of COPD place a heavy economic burden on patients, their families, and society (15, 16). Therefore, accelerating the standardization of COPD diagnosis, treatment, and prevention, while improving the precision and efficacy of clinical management, is of critical importance (17).

In the last 40 years, obesity rates have been on a consistent rise worldwide (18, 19). Numerous epidemiological studies have shown that obesity significantly enhances susceptibility to pulmonary diseases, suggesting that lipid accumulation or abnormal distribution resulting from obesity is a critical factor contributing to the development of respiratory conditions, including COPD (20, 21). Traditionally, obesity assessment relies on indicators such as Body Mass Index (BMI) to gauge overall body fat and Waist Circumference (WC) to measure abdominal fat (22–24). However, both methods present specific limitations (25). While BMI serves as a general indicator of obesity, it does not effectively differentiate between various body components, such as lean mass, water content, or visceral fat, which limits its accuracy in assessing the risk linked to specific health conditions (26). While WC can indicate abdominal obesity, it cannot accurately distinguish between visceral and subcutaneous fat, with visceral fat being closely linked to metabolic disorders (27). To better reflect the health impact of excessive fat accumulation, the Lipid Accumulation Product (LAP) was introduced. LAP combines WC and fasting triglyceride (TG) concentration, offering a more accurate assessment of changes in lipid accumulation (28).

Lipid Accumulation Product (LAP) is a cost-effective anthropometric measure that is easy to calculate and obtain, providing a novel perspective for understanding the impact of obesity on respiratory health (29, 30). Studies have demonstrated that LAP outperforms traditional indicators in predicting various health conditions, including heart-related diseases, type 2 diabetes, and metabolic abnormalities (31, 32). As a marker of lipid accumulation abnormalities, LAP can more effectively quantify the accumulation of visceral fat and its associated health risks (33). Therefore, exploring the association between LAP and COPD risk can provide a more comprehensive understanding of how lipid accumulation abnormalities may contribute to COPD progression.

Given this context, this study seeks to investigate how variations in lipid accumulation might relate to the occurrence of COPD, delving deeper into their potential connection. Using data from the National Health and Nutrition Examination Survey (NHANES), a nationally representative dataset, allows us to comprehensively explore this association within a diverse U.S. population. Our research focuses on examining how LAP is related to COPD risk, highlighting the interactions among lipid accumulation, obesity, and COPD. Our hypothesis posits that elevated LAP could increase the risk of developing COPD.

In this study, we investigated the link between the LAP index and COPD prevalence, utilizing data sourced from the NHANES database. The findings indicated a significant positive link between higher LAP levels and a greater risk of COPD, reinforcing the potential involvement of lipid accumulation abnormalities in the development of COPD.

Firstly, the model analysis showed that with every one-unit increment in ln LAP, the odds of developing COPD rose by approximately 16%, as indicated by an OR of 1.16 (95% CI: 1.04–1.30, p < 0.01). This result points to a distinct positive association between LAP levels and COPD risk. Additionally, the quartile-based assessment supported this observation, indicating that participants in the highest ln LAP quartile had a substantially elevated likelihood of COPD relative to those in the lowest quartile. These outcomes imply that lipid accumulation is closely linked to COPD risk, suggesting that monitoring and managing LAP could be crucial in the prevention and treatment strategies for COPD.

Additionally, the study found that the relationship between LAP and COPD may exhibit a non-linear positive correlation. The analysis using smooth curve fitting indicated that the relationship between ln LAP levels and COPD risk is non-linear, showing a marked increase in COPD risk, especially when ln LAP levels reach the higher range. This further emphasizes the importance of controlling lipid accumulation in reducing COPD risk. Moreover, findings derived from subgroup analyses and interaction tests indicated that this association remains fairly consistent across various populations, showing no significant impact from factors such as gender, age, race, or other typical covariates. This finding suggests that lipid accumulation abnormalities may exhibit a consistent association with COPD incidence across diverse groups.

To our knowledge, this is the first study based on NHANES data from 2017 to 2020 that assesses the association between LAP index and COPD risk. Previous studies primarily relied on earlier NHANES data to explore the relationships between other common indicators or specific nutrients and COPD (35).

Research indicates that obesity significantly impacts lung function, with obesity-related indicators showing a negative correlation with pulmonary function (36–38). This effect stems from how adipose tissue impacts the mechanical behavior of the respiratory system; for instance, abdominal obesity can reduce lung compliance and substantially decrease lung volume, while visceral fat may alter diaphragmatic structure and restrict its movement, thereby impairing lung function (39, 40).

As a comprehensive lipid accumulation indicator, LAP incorporates waist circumference and fasting triglyceride (TG), both closely related to lipid accumulation. While WC and TG may individually contribute to COPD risk, LAP could offer a more comprehensive reflection of both abdominal obesity and dyslipidemia. Elevated LAP typically reflects visceral fat accumulation and metabolic dysfunction, with increased TG levels often associated with inflammatory responses and the onset of various chronic diseases (41, 42). In the pathogenesis of COPD, lipid accumulation abnormalities and systemic inflammation are recognized as significant triggering factors (43, 44). Additionally, the higher prevalence of comorbid diabetes within the COPD group suggests that dyslipidemia may interact with metabolic disorders to exacerbate COPD severity (45, 46). Thus, LAP serves as a crucial indicator of lipid accumulation in relation to COPD. Earlier clinical investigations have examined how LAP relates to different disease outcomes, yet research specifically addressing COPD remains limited. Studies have shown that COPD patients often exhibit lipid accumulation abnormalities (47, 48). A study involving a Spanish population found that among 1,500 subjects, 48.3% of COPD patients had dyslipidemia (49). This indicates that disruptions in lipid accumulation could be a key factor in the pathogenesis of COPD.

Chronic inflammation and smoking are recognized as major mechanisms leading to lipid accumulation abnormalities in patients with COPD. TG and other lipids are transported from the liver to the bloodstream via lipoproteins. Once these lipid-rich particles are taken up by macrophages, they can lead to lipid deposition, subsequently triggering inflammatory responses (50). Chronic inflammation and lipid accumulation abnormalities play a dual role in COPD. Pro-inflammatory cytokines can elevate circulating TG levels, while inflammation suppression may lower these levels (51, 52). This phenomenon further underscores the complex interplay between lipid accumulation and inflammation, highlighting their central roles in the pathogenesis of COPD. These mechanisms may partly explain the observed association between elevated LAP and increased COPD risk in this study, as LAP reflects both TG levels and abdominal obesity, which are closely linked to systemic inflammation.

Smoking is recognized as a major risk factor for COPD and has a profound effect on lipid accumulation (53). Research has demonstrated that smoking can increase the levels of circulating lipids in the bloodstream, contributing to an altered lipid profile that may include higher concentrations of harmful fats (54). Earlier research has suggested that exposure to cigarette smoke can trigger the production of fatty acids within epithelial cells of the respiratory tract. This process subsequently impacts autophagy, the release of inflammatory mediators, and cell apoptosis (55, 56). Chronic exposure to cigarette smoke disrupts fatty acid accumulation homeostasis, a factor considered crucial in the onset and progression of COPD (57, 58). Furthermore, the increased fatty acid oxidation (FAO) caused by cigarette smoke exposure may exacerbate cellular damage through mitochondrial injury and the accumulation of reactive oxygen species (ROS), implying that such metabolic changes are crucial for preserving lipid accumulation homeostasis in the body (59, 60).

Daily symptoms experienced by patients with COPD, such as cough and chest tightness, can further impact their exercise tolerance, potentially increasing the risk of lipid accumulation abnormalities (61). Additionally, the use of glucocorticoids, particularly during acute exacerbations, may lead to adverse outcomes such as obesity and lipid accumulation abnormalities due to elevated glucocorticoid levels in the body (62). Evidence from a large-scale population study has revealed that brief, low-dose glucocorticoid treatment can have a notable impact on lipid accumulation levels (63). The prevalence of elevated LAP values among COPD patients is gradually increasing, and these abnormalities may be closely associated with poor prognosis and systemic complications (64). Recent studies have increasingly emphasized that COPD is not solely a pulmonary disease; it often accompanies extrapulmonary manifestations such as cardiovascular disease, malnutrition, and metabolic disorders (65). Dysregulation of lipid accumulation plays a significant role in these processes (49). Furthermore, lipid accumulation abnormalities not only exacerbate the risk of COPD but may also trigger systemic inflammation through increased oxidative stress and chronic inflammatory responses, further worsening the condition (66). Therefore, LAP has the potential to be an effective supplementary indicator for evaluating disease severity in individuals with COPD and may guide early identification of high-risk patients and tailored interventions to mitigate lipid accumulation abnormalities. However, to fully understand the underlying mechanisms, additional research involving larger cohorts and prospective study designs is required.

This study possesses certain strengths. Firstly, it makes use of nationally representative sampling data, allowing the study to effectively examine how LAP relates to COPD risk among diverse population groups. Secondly, the large sample size not only improves the precision of the statistical analysis but also supplies sufficient data to investigate how LAP correlates with COPD across different subgroups, revealing variations in this association according to demographic factors, including gender, age groups, and smoking habits. Nevertheless, this research has its constraints. Primarily, due to the study’s cross-sectional nature, identifying a clear causal link between the variables remains challenging. This means that while an association between LAP and COPD has been observed, we cannot determine whether changes in LAP directly lead to an increased risk of COPD. Second, due to data limitations, we were unable to include all potential covariates, which may result in unmeasured confounding bias. Additionally, the reliance on self-reported COPD diagnosis may introduce recall bias and potential misclassification, further suggesting that our findings should be interpreted with caution.

Therefore, future research should consider adopting longitudinal designs and more comprehensive data collection methods, which would allow for a deeper understanding of how lipid accumulation may influence the development and progression of COPD.

This study’s findings highlight a significant relationship between lipid accumulation levels and the risk of COPD. Notably, elevated LAP is positively correlated with the prevalence of COPD, exhibiting a dose–response relationship. Furthermore, the smooth curve fitting analysis reveals a potential nonlinear positive correlation between LAP and COPD. Overall, this work provides insights into the interplay between LAP and COPD, highlighting the importance of managing lipid accumulation levels as a strategy for the prevention and management of COPD. These findings establish a scientific foundation for formulating public health strategies and set the stage for future research to explore the role of lipid accumulation in COPD pathogenesis.