Effects of Particulate Matter on Obstructive Sleep Apnea and Obesity

Hye Jun Lee

doi:10.18787/jr.2025.00016

J Rhinol > Volume 32(2); 2025

Lee: Effects of Particulate Matter on Obstructive Sleep Apnea and Obesity

Review

Journal of Rhinology 2025;32(2):67-75.

Published online: July 22, 2025

DOI: https://doi.org/10.18787/jr.2025.00016

Effects of Particulate Matter on Obstructive Sleep Apnea and Obesity

Hye Jun Lee, MD

Department of Family Medicine, Chung-Ang University Hospital, College of Medicine, Chung-Ang University, Seoul, Republic of Korea

Address for correspondence: Hye Jun Lee, MD, Department of Family Medicine, Chung-Ang University Hospital, College of Medicine, Chung-Ang University, 102 Heukseok-ro, Dongjak-gu, Seoul 06973, Republic of Korea
Tel: +82-2-6299-1844, Fax: +82-2-6299-2064 E-mail: infiniteme@cau.ac.kr

Received March 19, 2025 Revised April 14, 2025 Accepted April 16, 2025

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

With accelerated global urbanization, understanding the impact of pollutant emissions and air pollution on obstructive sleep apnea (OSA) and obesity has become increasingly important. Particulate matter (PM) is a major component of air pollution. Recent studies have reported that PM influences OSA, obesity, and obesity-related metabolic disorders. The primary mechanisms proposed to underlie the effects of PM on OSA involve chronic inflammation and oxidative stress in the nasal epithelia. Regarding obesity, PM induces chronic inflammation in the hypothalamus, adipose tissue, skeletal muscle, and mitochondria; oxidative stress in white adipose tissue, the lungs, and the thyroid; activation of lipogenesis genes; changes in adipose tissue distribution; dysbiosis of the intestinal microbiome; and disruption of circadian rhythms. Therefore, reducing air pollution, including PM concentrations, represents a potential strategy for treating OSA and obesity and preventing related complications. Further prospective longitudinal studies in human participants are needed to clarify the effects of PM on the risk of OSA and obesity and to elucidate the underlying mechanisms.

KEY WORDS: Particulate matter; Air pollution; Obstructive sleep apnea; Obesity; Metabolic syndrome

INTRODUCTION

Obstructive sleep apnea (OSA) is the most common sleep disorder, characterized by repeated airway obstruction during sleep [1]. This condition is recognized as a risk factor for multiple health complications, including cardiovascular disease (CVD), metabolic syndrome, depression, and impaired cognitive function [2,3].

Risk factors for OSA include craniofacial abnormalities, male sex, obesity, aging, and air pollution [4-6]. Of these, obesity has been rapidly increasing worldwide, becoming a major public health concern [5,6]. Among the factors influencing obesity, air pollution—a physical environmental risk factor—has emerged as a major contributor to the global disease burden [7]. This has prompted growing interest in the health impacts of particulate matter (PM), the primary component of air pollution. Recent studies suggest that PM plays a significant role in overweight, obesity, and obesity-related metabolic diseases. Exposure to PM affects both central and peripheral tissues involved in energy metabolism regulation [8], and these metabolic changes can shift systemic energy balance toward storage [9]. However, some cross-sectional studies have found that exposure to pollutants such as PM does not significantly contribute to obesity [10].

Because the upper respiratory tract—including the nasal passages and upper airway—represents the first entry point for inhaled contaminants [11], air pollution, including PM, has also become recognized as a key risk factor for OSA. The proposed mechanisms by which PM may induce OSA are chronic inflammation and oxidative stress [11].

Both OSA and obesity are risk factors for CVD and share several pathophysiological mechanisms [1]. However, studies on the effects of PM on OSA and obesity have produced inconsistent results, and the underlying mechanisms remain unclear. Therefore, this review aims to comprehensively examine the effects of PM on OSA and obesity and to elucidate the associated mechanisms, aiming to improve awareness and understanding of this issue.

PM

Definition and characteristics

PM, the main component of air pollutants, is composed of inorganic substances (e.g., metals, non-metals, transition metals), organic compounds (e.g., carbon, polycyclic aromatic hydrocarbons, quinones), and aqueous components [10]. PM is classified based on its diameter into PM_0.1, PM_2.5, PM₁₀, and PM₁₀₀ [12]. Among these, PM_2.5—particles with a diameter of 2.5 μm or less—constitutes the majority of ambient PM [13]. Due to its large surface area relative to particle size and high chemical reactivity, PM_2.5 readily carries toxic substances and remains suspended in air for extended periods [14]. Furthermore, once inhaled, PM_2.5 deposits efficiently in the alveoli and can penetrate capillaries to enter the systemic circulation [15]. Reflecting these harmful properties, the US Environmental Protection Agency and the European Union use PM concentrations as key indicators when assessing the health risks of air pollution [16], and the World Health Organization includes PM in its revised guidelines on air pollutants [17]. Moreover, in 2013, the International Agency for Research on Cancer classified outdoor air pollution and PM as Group 1 carcinogens [18].

Human inhalation process

During inspiration, inhaled PM enters the lungs and activates alveolar macrophages [19], inducing an inflammatory response [8]. These particles can then traverse the epithelial-capillary barrier to enter systemic circulation and reach peripheral tissues via endocytosis [20]. Quantifying and clearing PM deposition in the respiratory tract is crucial for assessing health risks [21]. A previous study reported PM_2.5 deposition rates of 80% in the head and nasal region, 7% in the tracheobronchial region, and 13% in the alveolar region [22]. Thus, the relatively high deposition of PM_2.5 in the nasal passages has been suggested to correlate with OSA.

PM AND OSA

Impact of PM on OSA

PM exposure has been linked to an increased risk of sleep-breathing disorders, including OSA [23], although findings remain inconsistent [1]. For instance, one study found that long-term exposure to PM_2.5 was significantly associated with increased time spent with arterial oxygen saturation (SpO₂) below 90% (T<90; Δ%=10.2, p=0.04) and a lower nadir SpO₂ (Δ%=-0.9, p=0.03) [1]. In a large US cohort, an interquartile range increase of 14.5 μg/m³ in mean PM₁₀ exposure corresponded to a 13% rise in the respiratory disturbance index [24]. Another study reported that short-term (1 month) exposure to PM_2.5 and PM₁₀ was significantly associated with greater odds of OSA manifestation, with odds ratios (ORs) of 1.47 (95% confidence interval [CI], 1.34–1.62) for PM_2.5 and 1.17 (95% CI, 1.02–1.34) for PM₁₀ [25]. Moreover, several investigations have suggested that air pollutants aggravate OSA severity. A review found that nitrogen dioxide (NO₂), ozone, and PM were each associated with elevated apnea-hypopnea index (AHI) and oxygen desaturation index [26]. In another analysis, each 1-μg/m³ increase in average PM_2.5 level was linked to a 1.04–1.08-fold increase in the OR for AHI—across 1-, 7-, and 30-day exposure windows—in both mild-to-moderate and severe OSA cases [27]. However, heterogeneity in exposure duration, season, climate, and nation of study (as indicated in a systematic review covering various air pollutants, such as PM_2.5, PM₁₀, and NO₂), likely contributes to the conflicting results observed among studies [28]. Another systematic review and meta-analysis concluded that the effects of PM_2.5 and NO₂ on the risk of OSA are ambiguous [3]. Moreover, studies that have shown correlations between PM and OSA exhibit limitations, including the use of univariable analyses or inadequate adjustment for confounders. These potential confounders include seasonal variations in temperature and humidity, which can impact air pollution levels; differences between developing and developed countries, indoor air quality, and exposure to other pollutants [1,24,29,30]. Additionally, upper airway irritants and seasonal allergic reactions may both exert effects [16]. Diseases such as allergic rhinosinusitis can modulate the severity of sleep apnea, a factor that should be considered in future examinations of the relationship between air pollution and OSA [16]. Future time-series analyses with multiple follow-up points are required to clarify the impact of PM on OSA.

Mechanisms by which PM affects OSA

Long-term exposure to environmental pollutants has cumulative adverse effects that contribute to the development of chronic diseases, including obesity and OSA [31]. Although the exact mechanisms linking PM exposure to OSA remain to be fully defined, evidence points to two principal mechanisms: chronic inflammation and oxidative stress.

Chronic inflammation

High levels of inhaled PM are believed to disrupt the nasal mucociliary clearance system, which normally traps and eliminates particles [16]. Young adults who relocate from rural to urban settings have been shown to exhibit inflammatory changes in their nasal epithelia [32]. In animal models, PM exacerbates pulmonary inflammation and increases mucus secretion, leading to upper airway edema and elevated airway resistance [33]. PM can also induce inflammatory reactions in nasal epithelial cells, contributing to chronic rhinosinusitis and upper airway obstruction [34,35]. Moreover, the patency of the upper airway is influenced by the disruption of the sinonasal epithelial cell barrier [36]. This disruption triggers a persistent inflammatory process through the activation of proinflammatory pathways, further degrading barrier integrity and perpetuating inflammation [37]. Increased nasal resistance from this inflammation has been implicated in the pathogenesis of OSA [37]. Furthermore, the relationship between upper airway inflammation and OSA may be bidirectional, where the oxygen desaturation and altered lung ventilation seen in OSA can themselves sustain a low-grade inflammatory state [38].

Oxidative stress

As one study reported, exposure to PM_2.5 and PM₁₀ can increase oxidative stress, exacerbating nocturnal hypoxia [39]. PM contains pro-oxidant molecules that disrupt mitochondrial respiratory chains, generating reactive oxygen species (ROS) [40] and inducing oxidative damage in nasopharyngeal and other cells. These mechanisms may impact ventilation and perfusion, aggravating the hypoxia associated with OSA.

PM AND OBESITY

Impact of PM on obesity

PM adversely affects both environmental quality and human health. Epidemiological and animal studies indicate that exposure to PM—especially PM_2.5—promotes weight gain, suggesting that PM acts as an obesogen (a substance that promotes obesity) and a risk factor for obesity [41,42]. A meta-analysis found that each 10 μg/m³ increase in PM concentration corresponded to a 1.16-fold higher risk of obesity (95% CI, 1.11–1.21) [43]. In an 8-year longitudinal cohort study of 3.9 million US veterans, every 10 μg/m³ increase in annual average PM concentration was linked to an average weight gain of 10 pounds (approximately 4.54 kg; hazard ratio [HR], 1.07; 95% CI, 1.06–1.08) and an increased clinical risk of obesity (HR, 1.08; 95% CI, 1.06–1.11) [44]. Similarly, a cross-sectional study of over 47,000 Chinese adults reported that each 10 μg/m³ increase in PM concentration was associated with higher odds of general obesity (OR, 1.12; 95% CI, 1.09–1.14) and abdominal obesity (OR, 1.10; 95% CI, 1.07–1.13) [45]. In animal studies, PM-exposed mice developed greater subcutaneous and visceral fat mass than control animals breathing filtered air [42]. However, some cross-sectional analyses have found no significant association between PM exposure and obesity or markers of lipid metabolism [46]. These inconsistencies may reflect limited cumulative PM exposure in younger adults (aged 17–22 years) or methodological constraints, such as the reliance on area-level administrative data on PM concentrations, despite the fact that approximately 70% of the participants were university students, with no verification of whether they lived in dormitories and no data regarding time spent outside of their residence [46].

Mechanisms by which PM affects obesity

Although the precise mechanisms linking PM exposure to obesity remain unclear, considerable research suggests that chronic inflammation and oxidative stress play major roles in this relationship. In addition, several other potential mechanisms have been proposed (Fig. 1) [47].

Chronic inflammation

PM can induce both local and systemic chronic inflammatory responses, contributing to obesity and metabolic disorders. Evidence indicates that PM exposure is associated with a greater increase in markers of systemic inflammation (such as C-reactive protein [CRP] level and white blood cell count) among individuals with obesity than in controls without obesity [48]. Moreover, a study of 52 children (mean age, 8.6±0.1 years) from Mexico City—an area with high PM levels—reported significant elevations in inflammatory mediators compared with Polotitlán, a city with low levels. These mediators included tumor necrosis factor alpha (TNF-α), prostaglandin E2, CRP, interleukin-1 beta, and endothelin-1 [49].

Through various mechanisms, this chronic inflammation impacts the hypothalamus, adipose tissue, skeletal muscles, and mitochondria, causing functional impairments that ultimately lead to obesity.

First, PM can induce hypothalamic inflammation. The hypothalamus integrates hormonal, environmental, and neural signals to regulate systemic energy balance and metabolic efficiency [50]. Three pathways have been proposed for PM entry into the central nervous system: 1) translocation via olfactory epithelial neurons; 2) disruption of the gut microbiota and the gut-brain axis; and 3) upregulation of pro-inflammatory mediators in the bloodstream.

The resulting hypothalamic inflammation then increases appetite, reduces energy expenditure, and induces leptin resistance, ultimately contributing to obesity [51]. Hypothalamic inflammation is also linked to insulin resistance [52] and inhibits thermogenesis and energy expenditure in brown adipose tissue [53], promoting weight gain [54]. In one animal study, PM exposure increased the expression of inflammatory markers such as TNF-α, inhibitor of nuclear factor kappa-B kinase-β, and nuclear factor kappa B in the paraventricular nucleus [55].

Second, PM induces inflammation in adipose tissue. As shown in a previous study, PM exposure suppresses the expression of anti-inflammatory M2 genes and promotes pro-inflammatory (M1) gene expression, driving adipose inflammation and metabolic disturbance [42]. It also increases macrophage infiltration into adipose depots, exacerbating local inflammation [42]. Cross-sectional data indicate that people with obesity have higher baseline adipose inflammation and are more susceptible to PM-induced inflammatory responses [56]. Increased levels of pro-inflammatory factors due to PM exposure can lead to inflammation in white adipose tissue, increased fat production, and “whitening” of brown adipose tissue [57]. In particular, the last of these is believed to be caused by inflammation within the tissue [8].

Third, PM-induced inflammation can impair mitochondrial function in endothelial cells [58], cardiomyocytes [40], skeletal myocytes [59], and both white and brown adipocytes [60]. The proposed mechanism involves pro-inflammatory mediators disrupting mitochondrial respiratory chain complexes, leading to mitochondrial dysfunction [61,62]. This phenomenon impairs mitochondrial DNA replication [63] and alters fusion/fission dynamics [64]. Through inflammation, chronic PM exposure significantly reduces the number and size of mitochondria in both white and brown adipose tissue [61], impairing glucose and lipid oxidation, leading to triglyceride accumulation and adipocyte hypertrophy, and ultimately causing obesity [61,65].

Fourth, skeletal muscle plays a key role in energy metabolism [66]. Chronic PM-induced inflammation drives muscle protein degradation and mitochondrial dysfunction in these tissues [67,68]. Additionally, pro-inflammatory factors and dysfunction in white adipose tissue can increase insulin resistance in muscles, contributing to muscle atrophy [69,70]. Recent human studies have demonstrated that chronic PM exposure adversely affects muscle mass and physical function [71,72]. Moreover, PM-related cardiopulmonary and neurophysiological effects increase sedentary behavior and discourage physical activity, furthering the deterioration of muscle mass and function [9]. A separate study similarly shows that increased PM concentrations can discourage outdoor activity, potentially leading to weight gain [73]. Animal studies also suggest that PM exposure induces inflammatory changes in the muscle microvasculature, causing functional impairment [74,75]. Specifically, PM exposure promotes inflammation in the microvascular endothelium and surrounding smooth muscle, impairing vasodilation, inducing mitochondrial dysfunction, and promoting muscle atrophy [76,77].

Oxidative stress

Oxidative stress plays a key mediating role in the development of PM-induced obesity [78]. PM contains various prooxidant molecules that disrupt mitochondrial respiratory chains, generating ROS [61] and causing oxidative injury in various tissues and cells, including white adipose tissue, the lungs, and the thyroid [79]. Elevated ROS levels in white adipose tissue promote triglyceride accumulation and inhibit breakdown, resulting in expansion of white fat depots and reduction of brown adipose tissue. These changes impair metabolism, decrease insulin sensitivity, and contribute to obesity [80]. In fact, exposure to air pollution has been associated with abnormalities in signaling pathways related to insulin resistance [42,80]. In an animal study, PM exposure reduced Akt (protein kinase B) levels, increased endothelial nitric oxide synthase phosphorylation, and upregulated protein kinase C in endothelial cells [42]. Recent research also indicated that PM exposure elevates xanthine concentrations in murine white adipose tissue, further driving oxidative stress [80]. Furthermore, interventions that reduce pulmonary oxidative stress—such as antioxidant treatments or overexpression of extracellular superoxide dismutase—have been shown to alleviate PM-induced insulin resistance in mice, further suggesting that oxidative stress contributes to insulin resistance [76]. Additionally, PM-driven oxidative injury can impact thyroid function and reduce circulating levels of thyroid hormones [81,82]. The thyroid plays a central role in energy metabolism, and dysfunction in thyroid hormone synthesis and secretion can lead to obesity [50]. Epidemiological studies have linked chronic exposure to high levels of PM with thyroid dysfunction and reduced serum thyroid hormone levels [81,82]. In rodents, PM exposure induces oxidative stress in thyroid follicles, diminishing follicular epithelial cells and enlarging follicular cavities; consequently, thyroid hormone synthesis and secretion are impaired [83]. Moreover, thyroid dysfunction induced by PM exposure leads to the “whitening” of brown adipose tissue [84].

Activation of adipogenesis-related genes and changes in adipose tissue distribution

PM exposure activates genes involved in adipogenesis and alters adipose tissue distribution [85-87]. Animal studies have demonstrated that long-term exposure to PM upregulates genes governing lipogenesis, adipocyte differentiation, and lipid droplet formation in adipose tissue [85], resulting in larger adipocytes, increased visceral fat mass, and obesity [85,86]. In particular, PM exposure increases the expression of key adipogenic markers, such as acetyl-CoA carboxylase and diglyceride acyltransferase-2, in white adipose tissue [87]. It also increases the expression of pro-adipogenic transcription factors, including peroxisome proliferator-activated receptor-γ and cyclic adenosine monophosphate response element-binding protein-α, in murine models [87].

Gut microbiota imbalance

Imbalances in the gut microbiota may play a mediating role in the relationship between PM and obesity, as well as other metabolic diseases [88-91]. Previous studies have shown that inhalation of air pollutants, including PM, can alter microbial diversity and relative abundance, compromise intestinal barrier integrity, and trigger increased gastrointestinal inflammation via chronic endotoxemia [88]. Moreover, certain gut microbiota patterns have been observed in patients with obesity and disorders of glucose and lipid metabolism, implicating the gut microbiome in metabolic processes [89]. Population-based analyses further indicate that the gut microbiota partially mediates the association between PM exposure and obesity or metabolic diseases, such as disorders of glucose and lipid metabolism [90,91].

Disruption of circadian rhythms

PM exposure can influence circadian rhythms, indirectly leading to obesity [92,93]. Recent data have shown that circadian rhythm disruption leads to metabolic syndrome, including the dysregulation of energy homeostasis and insulin resistance, and is linked to PM exposure [92]. Another study reported that 10 weeks of PM exposure disrupted the oscillations of clock genes in both white and brown adipose tissues [92]. A separate investigation also observed changes in major clock genes (Per1-3, Rev-erbα, and Bmal1), accompanied by increased inflammation and oxidative stress in the plasma and lungs [93].

Factors affecting exposure to PM

When analyzing the effects of PM on obesity, it is important to consider factors such as the age of exposure, cumulative effects, and regional variations.

Age of exposure and cumulative effects

Multiple studies indicate that the obesogenic impact of PM varies by age, with children and adolescents being especially vulnerable [43,46]. A meta-analysis reported that the risk of obesity from PM exposure was higher among those under 18 years (relative risk [RR], 1.24; 95% CI, 1.09–1.38) than in adults (RR, 1.10; 95% CI, 1.09–1.20) [43]. This heightened susceptibility in youth likely reflects incomplete lung development and greater time spent engaging in outdoor activities [43,46]. However, research has indicated that older adults may be more adversely affected by aspects of PM exposure [44], potentially from the cumulative effects of heavy metals in these pollutants [94]. Most human studies on the impact of PM on obesity have focused on short-term PM exposure (<1 month), and although long-term exposure is hypothesized to exert a stronger obesogenic influence [95], reports on the cumulative effects of long-term exposure are rare. One cross-sectional study indicated a correlation between 1 year of PM exposure and higher blood insulin and total cholesterol levels, although no significant correlation with obesity was found [96].

Regional variations

The health impact of PM exposure varies by region. A meta-analysis found a statistically significant association between PM and obesity in Asia (RR, 1.09; 95% CI, 1.06–1.12), whereas results for Europe (RR, 1.12; 95% CI, 0.99–1.27) and the United States (RR, 1.36; 95% CI, 0.85–2.18) did not reach significance [43]. Additionally, the effects of PM were stronger in developing countries (RR, 1.17; 95% CI, 1.12–1.23) than in developed nations (RR, 1.10; 95% CI, 1.03–1.18) [43]. These regional differences likely stem from the impacts of industrialization and development.

Interaction between PM and obesity

Although PM exposure promotes obesity, obesity may also magnify the harmful effects of PM. Epidemiological evidence suggests that individuals with obesity exhibit greater sensitivity to PM-related health risks [46]. In this population, PM exposure shows stronger associations with chronic obstructive pulmonary disease [97], hypertension [98], CVDs [99,100], and coronavirus disease 2019 severity [101]. This increased vulnerability may stem from elevated baseline proinflammatory cytokine levels in those with obesity following PM exposure, making them particularly vulnerable to PM-induced inflammation [102].

Table 1 summarizes key findings from human studies regarding the effects of PM on OSA and obesity.

CONCLUSION

With accelerated global urbanization, growing industrial and vehicular emissions have contributed to air pollution, which is increasingly impacting OSA and obesity [12]. Current evidence details PM exposure as a newly identified risk factor for these conditions. Discrepancies among studies likely stem from differences in research design; methods of measuring and quantifying PM, OSA, and obesity; regional and participant characteristics; sample size biases; and residual confounding.

Accordingly, strategies to tackle the global burden of OSA and obesity must consider exposure to air pollution, including PM, and incorporate measures to reduce PM concentrations. Improving air quality could become a key strategy in the treatment of OSA and obesity and in the prevention of related complications. At a policy level, national public health initiatives and preventive measures that lower human exposure to PM—and thus its associated health risks—are urgently needed to lessen the socioeconomic and medical impact of these disorders. However, most current research relies on animal models. Large-scale, long-term human studies are necessary to clarify the impact of PM on the risk of OSA and obesity and to elucidate the underlying mechanisms. Future work should also examine whole-body impacts, extending beyond individual organs, and explore how PM interacts with energy metabolism pathways and hormonal regulation.

Ultimately, however, as indicated by the maxim “you are where you live,” one’s risk of OSA or obesity is likely shaped by their surrounding environment.

Notes

Ethics Statement

Not applicable

Availability of Data and Material

Data sharing not applicable to this article as no datasets were generated or analyzed during the study.

Conflicts of Interest

The author has no potential conflicts of interest to disclose.

Funding Statement

This research was supported by the Chung-Ang University Research Grant in 2025.

Acknowledgments

None

Fig. 1.

Schematic diagram showing the mechanism by which PM affects obesity. The mechanisms by which PM impacts obesity appear to include chronic inflammation in organs associated with energy metabolism, oxidative stress, activation of adipogenic genes, changes in adipose tissue distribution, gut microbiota imbalance, and disruption of circadian rhythms. Adapted from Della Guardia L, Wang L. Fine particulate matter induces adipose tissue expansion and weight gain: pathophysiology. Obes Rev 2023;24(4):e13552 [47] under the terms of the Creative Commons License. BAT, brown adipose tissue; PM, particulate matter; T3, triiodothyronine; T4, thyroxine; WAT, white adipose tissue.

Table 1.

Key findings from human studies on the effects of particulate matter on OSA and obesity

OSA	OSA manifestations ↑ [25]
	OSA symptoms and severity ↑ [26]
	- Time spent with SpO₂<90% (T<90) ↑ [1]
	- Lowest SpO₂ (Δ%=-0.9, p=0.03) ↑ [1]
	- Respiratory disturbance index ↑ [24]
	- Apnea-hypopnea index ↑ [26]
	- Oxygen desaturation index ↑ [26]
Obesity	Risk of obesity ↑ [43]
	Increased risk of weight gain (10 lb, approximately 4.54 kg) ↑ [44]
	Abdominal obesity ↑ [45]

OSA, obstructive sleep apnea; SpO₂, arterial oxygen saturation

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