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Association between sleep duration and lung function among U.S. adults
BMC Public Health volume 24, Article number: 3530 (2024)
Abstract
Background
Sleep’s impact on the human immune system and inflammatory responses makes it a potential risk factor for lung function impairment. However, the relationship between sleep duration and lung function impairment in middle-aged and young adults has been rarely investigated.
Methods
A total of 9,284 aged 20–64 years were categorized into four groups according to sleep duration (≤ 6 h, 7 h, 8 h, and ≥ 9 h), with 7 h as the reference, by using the U.S. NHANES data, 2007–2012. Forced expiratory volume in the 1 s (FEV1), forced vital capacity (FVC), FEV1 to FVC (FEV1/FVC) ratio, peak expiratory flow (PEF), and forced expiratory flow at 25–75% (FEF25 − 75%) were measured by spirometry. Restrictive impairment was defined as baseline FVC < 80% predicted and obstructive impairment as FEV1/FVC < 0.70. Generalized linear regression and logistic regression were performed to estimate the associations between sleep duration and lung function.
Results
Compared with 7 h of sleep duration, shorter and longer sleep duration were associated with decreases in FEV1 (≤ 6 h: β=-0.010, 95% CI=-0.014 to -0.006; 8 h: β=-0.005, 95% CI=-0.009 to -0.001), FVC (≤ 6 h: β=-0.018, 95% CI=-0.014 to -0.007; 8 h: β=-0.005, 95% CI=-0.009 to -0.002), and PEF (≤ 6 h: β=-0.006, 95% CI=-0.010 to -0.002; 8 h: β=-0.007, 95% CI=-0.011 to -0.002; ≥ 9 h: β=-0.012, 95% CI=-0.020 to -0.004). Similarly, shorter (≤ 6 h: OR = 1.346, 95% CI = 1.065 to 1.700) and longer (≥ 9 h: OR = 1.827, 95% CI = 1.236 to 2.700) sleep duration were associated with increased risks of restrictive impairment. Moreover, the aforementioned associations were more pronounced among male participants.
Conclusions
Compared with 7 h of sleep duration, shorter and longer sleep duration were associated with impaired lung function among adults aged 20–64 years, and these associations were stronger among males.
Background
Chronic lung disease is a significant contributor to the global mortality and a key factor in the rising burden of non-communicable diseases [1]. There is a growing focus on exploring risk factors for impaired lung function and the lung diseases, as well as enhancing primary prevention strategies for chronic lung diseases. Lung function is influenced by various factors, including genetics, lifestyle factors, and chronic respiratory disorders [2,3,4,5]. It is also closely associated with adult cognitive levels [6], mental health [7], incidence of chronic obstructive pulmonary disease and other chronic diseases [8, 9]. Several public health initiatives have been proposed to improve the preservation of lung function, such as promoting optimal diet quality [10] and encouraging physical activity [11]. Therefore, exploring modifiable lifestyle risk factors and engaging in proactive primary healthcare services are crucial for maintaining normal lung function.
The important of sleep in physical, social and mental health of both adults and children has been widely recognized [12], and the relationship between sleep and respiratory health has been attracting attention. Research has revealed links between sleep and various allergic and metabolic diseases, such as obesity [13], allergic rhinitis [14], dermatitis [15], and asthma [16]. Previous studies on sleep and lung function have primarily focused on the consequences of inadequate sleep [17, 18], and have mostly been conducted in populations with a history of lung diseases such as asthma. Reports on the correlation in general population are still vacant. Furthermore, young and middle-aged adults face more stress factors from comprising the main workforce in society [19, 20]. The social stress faced by these populations has been reported to affect sleep quality and may impair lung function. Given the pivotal role of young and middle-aged adults in shaping societal values, it is of paramount importance to explore the relationship between changes in lung function and sleep duration.
Therefore, in this context, this study aimed to investigate the associations between sleep duration and lung function, using data from the U.S. National Health and Nutrition Examination Survey (NHANES) from 2007 to 2012. To examine the consistency of the association, further subgroup analyses were performed to examine whether sex and age differences modified these associations.
Methods
Study population
The National Health and Nutrition Examination Survey (NHANES) is a cross-sectional data source made publicly available by the Centers for Disease Control and Prevention (CDC). A detailed description of the NHANES study and its data can be accessed online at http://www.cdc.gov/nchs/nhanes.htm. Our study examined data from the NHANES which designed to evaluate the health and nutritional indicators among the U.S. nationwide. Data from three consecutive NHANES cycles (2007–2008, 2009–2010, and 2011–2012) were merged and analyze for this analysis, and 13,384 participants aged 20–64 years were included. Individuals missing data on sleep duration (n = 23) and spirometry examination (n = 2,251) were excluded. We further limited our research subjects without malignancy (n = 533), pregnancy (n = 146), cardiovascular diseases (heart attack, congestive heart failure, angina pectoris, coronary heart disease, and stroke) (n = 447), major depression (n = 85), and unreliable (D, F) assessment of lung function (n = 533). Of these, data on BMI (n = 29), smoking status (n = 8), and chronic pulmonary diseases (asthma, chronic bronchitis, emphysema, and wheezing/whistling in the past 12 months) (n = 15) were missing and further excluded. Finally, a sample of 9,284 adults with completely data on the covariates and outcomes was analyzed (Fig. 1). Because publicly available, anonymized data were used, the institutional review board of Xinhua Hospital, Shanghai Jiao Tong University School of Medicine deemed the study exempt from review.
Sleep duration
Information on sleep duration was created from the self–reported question: “How much sleep do you get (hours)?” This question was asked by trained interviewers who were equipped with Computer–Assisted Personal Interviewing system in the home. For this study, sleep duration was grouped into four groups: ≤ 6 h, 7 h, 8 h, and ≥ 9 h, with 7 h used as a reference group, based on the recommendations of the American Academy of Sleep Medicine [21].
Spirometry measure
For NHANES 2007–2012, participants aged 6–79 years were invited to perform spirometry test. Exclusion criteria such as recent thoracic surgery are detailed in the NHANES spirometry procedure manual [22]. Spirometry was conducted using Ohio 822/827 dry–rolling seal volume spirometers and similar protocols according to the American Thoracic Society (ATS) guidelines during three periods [23]. The FVC and FEV1were tested, and we restricted our analysis on data graded A or B according to ATS quality. Also, FEV1: FVC ratio, FEF25 − 75%, and PEF were included to evaluate pulmonary function. FVC% predicted is calculated by FVC/predicted FVC × 100 [24], while the predicted FVC value is calculated based on NHANES materials such as age, gender, height, and race/ethnicity using previously published equations [24]. The obstructive impairment was defined by an FEV1/FVC < 0.70 and the restrictive impairment by an FVC < 80% predicted [25, 26].
Demographic covariates
Covariate data were obtained from self-reported demographics questionnaires. We categorized age into 20–44 years (young adults) and 45 to 64 years (middle–aged adults) [27]. Race/ethnicity was divided into four categories, including non-Hispanic white, Mexican American, non-Hispanic black, and others. Body mass index (BMI) was categorized as underweight (< 18.5 kg/cm2), normal weight (18.5 to ≤ 24.9 kg/cm2), overweight (25.0 to ≤ 29.9 kg/cm2), or obese (≥ 30.0 kg/cm2). Participants were divided (≥ 1.85 and<1.85) based on the poverty income ratio (PIR), which was determined by dividing the household income by a poverty threshold specific to the family size and geographic location [28]. Participants had not smoked > 100 cigarettes in entire life were considered non–smokers. For subjects who had smoked more than 100 cigarettes during whole life, those who still smoke during the survey period were viewed as current smokers, while those reported quit smoking currently were defined as form smokers [29].
Statistical analysis
Characteristics of the study population were presented by the mean (standard deviation, SD), and percentage, as appropriate. Mann–Whitney U test or Chi–square test was employed to analyze differences in socio-demographic factors between study population and baseline population.
The associations between sleep duration (≤ 6 h, 7 h, 8 h and ≥ 9 h) with lung function, treated as a continuous variable, were analyzed using a generalized linear model (GLM) with the reference group set as 7 h of sleep. Due to the skewed distributions of lung function parameters, analyses were conducted on log10–transformed values of continuous variables. Furthermore, logistic regression model was used to examine odd ratios (OR) and 95% confidence intervals (CI) for association between sleep duration and pulmonary function, treated as binary variable, including restrictive (yes/no) and obstructive impairment (yes/no). To explore whether the associations between lung function and sleep duration differed by demographic factors, we examined potential effect modification by sex (male and female) and age (20–44 and 45–64 years). Obesity can cause sleep disorders like obstructive sleep apnea, further impairing sleep duration. Therefore, stratified analyses were stratified by obesity to examine associations with restrictive impairment in obese and non-obese participants. In addition, restrictive cubic splines (RCS) were performed to depict the potential nonlinear relationship between sleep duration and lung function.
Several sensitivity analyses were conducted to validate the robustness of our findings. Firstly, to exclude the potential influence of wheezing and asthma, we evaluated the associations between sleep duration and restrictive impairment in participants with/without chronic lung diseases. Additionally, we also performed separate stratified analysis for lung function, restricted to participants without chronic lung diseases. Secondly, we separately examined the association in participants who had not used bronchodilators or inhaled corticosteroids, given that these medications can influence the decline of lung function. Finally, we re-ran GLMs for lung function parameters by using z-score values [30].
All statistical analyses were performed using SPSS (version 22.0; IBM SPSS Statistics, NY, USA), and R studio (R Version 4.2.3, The R Foundation of statistical computing, Vienna, Austria) was using to produce graphs. Statistical significance was achieved when P value < 0.05 (two-tailed), and P ≤ 0.10 were defined as bolding line.
Results
Table 1 showed the sociodemographic characteristics of the 9,284 participants aged 20–64 years included in our study. Among them, 5,539 (59.7%) were aged 20–44 years, and 4,756 (51.2%) were male. Individuals with older age, female, non-Hispanic Black, underweight status, current smoking, lower family income, and those with chronic lung diseases tended to have poorer lung function. In comparison to the baseline population, participants in our study tended to have higher household income, to be male, and younger (Table E1).
The distributions of lung function measures were summarized in Table E2. The median values for FEV1, FVC, FEV1 /FVC, FEF25 − 75% and PEF were 3113.5 mL, 4031.0 mL, 80.3%, 3147.0 mL/s, and 8295.0 mL/s, respectively.
Table 2 presented the relationships between sleep duration and lung function, treated as continuous variables by GLM. Compared with 7 h of sleep duration, shorter (≤ 6 h) and longer sleep duration (8 h and ≥ 9 h) were associated with decreases in FEV1 (≤ 6 h: β=-0.010, 95% CI=-0.014 to -0.006; 8 h: β=-0.005, 95% CI=-0.009 to -0.001), FVC (≤ 6 h: β=-0.018, 95% CI=-0.014 to -0.007; 8 h: β=-0.005, 95% CI=-0.009 to -0.002), and PEF (≤ 6 h: β=-0.006, 95% CI=-0.010 to -0.002; 8 h: β=-0.007, 95% CI=-0.011 to -0.002; ≥ 9 h: β=-0.012, 95% CI=-0.020 to -0.004). In the sensitivity analyses, the results were similar when we separately reanalyzed the data by excluding individuals with chronic lung diseases (Table E3), those using bronchodilators (Table E4), or those on inhaled corticosteroid therapy (Table E5). Furthermore, the findings remained robust when lung function parameters were analyzed as z-scores (Table E6). The stratified analyses were further stratified by chronic lung disease (with/without), showing a similar result (Table E7).
The RCS model revealed that lung function parameters were nonlinearly related to sleep duration, with the indication that participants with approached 7 h of sleep duration appeared had the highest values of FEV1, FVC and PEF (Fig. 2A).
We further analyzed the correlation between sleep duration and lung function stratified by age and sex (Table 3) and visually displayed Fig. 2B and C, and the associations were stronger among male participants. Among men aged 20–44 years, compared to those reporting 7 h of sleep, individuals with sleep durations of ≤ 6 h (β=-0.013, 95% CI=-0.018 to -0.007), 8 h (β=-0.007, 95% CI=-0.013 to -0.001) and ≥ 9 h (β=-0.018, 95% CI=-0.029 to -0.007) were associated with decreased FVC. FEV1 values were lower in individuals with either shorter (≤ 6 h: β =-0.010, 95% CI=-0.016 to -0.004) or longer (≥ 9 h: β=-0.016, 95% CI=-0.027 to -0.004) sleep duration. Whatmore, individuals with ≥ 9 h of sleep exhibited decreased PEF (β =-0.022, 95% CI=-0.035 to -0.009). Among men aged 45–64 years, compared to those reporting 7 h of sleep, individuals with sleep durations of ≤ 6 h (β=-0.016, 95% CI=-0.024 to -0.008), 8 h (β=-0.011, 95% CI=-0.020 to -0.002) and ≥ 9 h (β=-0.029, 95% CI=-0.046 to -0.012) were associated with decreased FVC. FEV1 values were lower in individuals with either shorter (≤ 6 h: β =-0.015, 95% CI=-0.024 to -0.006) or longer (≥ 9 h: β=-0.026, 95% CI=-0.046 to -0.007) sleep duration.
Furthermore, we investigated the association between sleep duration and risk of restrictive and obstructive impairment. Compared to 7 h of sleep, sleep duration of ≤ 6 h (OR = 1.346, 95% CI = 1.065 to 1.700) or ≥ 9 h (OR = 1.827, 95% CI = 1.236 to 2.700) was associated with higher odds of restrictive impairment (Table 4). No associations were observed between sleep duration and obstructive impairment. The aforementioned associations of sleep duration with restrictive impairment were further sex- or age-stratified analyzed in Table 5, and the associations were stronger among males. Compared with men reporting 7 h of sleep, those reporting shorter (≤ 6 h: OR = 1.531, 95% CI = 1.085 to 2.161) and longer (8 h: OR = 1.560, 95% CI = 1.061 to 2.293; ≥ 9 h: OR = 2.530, 95% CI = 1.436 to 4.457) hours of sleep were more likely have higher risks of restrictive impairment. No differences were found between two age groups. Among non-obese participants, individuals sleeping 9 h or more (OR = 2.127, 95% CI = 1.266 to 3.571) exhibited an increased likelihood of restrictive impairment compared to those sleeping 7 h, whereas no differences were found in obese individuals. RCS curve revealed that sleep duration was nonlinearly related to restrictive impairment, with the indication that participants with approximate 7 h of sleep duration appeared had the lowest risk of restrictive impairment (Fig. 3).
Discussion
In this study, we investigated the associations between sleep duration and lung function among the U.S. general population aged 20–64 years, using U.S. NHANES data, 2007–2012. Compared with 7 h of sleep duration, both shorter and longer sleep duration was associated with decreased lung function. Likewise, shorter and longer sleep duration was associated with higher risks of restrictive impairment. Moreover, these associations were more pronounced among male participants.
Our findings were parallel to the findings of previous studies indicating that insufficient sleep was associated with decreased lung function. Evidence from the NHANES study analyzed 558 individuals with current asthma suggested that short (≤ 6 h) sleep duration were associated with worser lung function than those with healthy (7–8 h) sleep duration [31]. Another study using NHANES data and involving 15,442 general adults aged 20–79 years had reported that ≤ 5 h of sleep duration was associated with lower percent predicted FEV1, FVC, and FEV1/FVC, while a U-shaped relationship existed between sleep duration and lung function measures [32]. Similarly, a 3-week randomized controlled study, of 10 adolescents with asthma reported that short sleep duration reduced the levels of morning FEV1 and morning PEF by 14% and 6%, respectively [33]. However, Project Nocturnal Asthma and Performance in School (NAPS) found no associations between sleep duration and FEV1 change in 216 asthma children aged 7–9 years living in Northeast American cities [18]. Our research corroborates and broadens the association between limited sleep duration and lung function, and differences between the aforementioned studies and our research may be attributed to variation in age of the participants, division of sleep duration, and control of confounders.
Relationship between excessive sleep duration and lung function is understudied, with several studies having investigated the association with respiratory symptoms. In a cross-sectional Korean National Health and Nutrition Examination Survey analyzed 10,148 subjects aged 19–39 years and reported that sleep duration ≥ 9 h was associated with higher risk of asthma in female adults [15]. Furthermore, a prospective cohort study in UK Biobank included 469,691 individuals free of lung cancer reported that long (> 8 h) sleepers had a 17% higher risk of lung cancer than normal (7 to 8 h) sleepers [34]. To understand why the effects of sleep duration on lung function, it is important to discuss the influence of sleep on the degree of airway inflammation. Both reduced sleep [35, 36] and excessive sleep duration [37] have been associated with increased level of Interleukin-6 (IL-6). Notably, IL-6 is a cytokine has been negatively correlated with post-bronchodilator FEV1 [38] and FEV1 levels in COPD patients [39]. In addition, certain sleep-related respiratory disorders, such as obstructive sleep apnea (OSA), may induce airway inflammation and constriction due to chronic intermittent hypoxia [40] and vibration trauma resulting from upper airway obstruction [41]. These may partially account for observed relationship between lung function impairment and inappropriate sleep duration in our study.
Little is known about the relationship between sleep duration and obstructive or restrictive impairment, and our research found that both shorter and longer sleep duration increased the risk of restrictive impairment. Specifically, a cross-sectional examination of 6,814 U.S. community-dwelling adults aged 45 to 84 years and were free of clinical cardiovascular disease, a U-shaped relationship was discovered between sleep duration and interstitial lung abnormalities (ILA), where both insufficient (< 6 h) and excessive sleep duration (≥ 9 h) were found to increase the risk of ILA [42]. Similarly, a recent cross-section study conducted among 500,074 participants of the UK Biobank reported that both longer and shorter sleep durations, compared to 7 h, were proved to be associated with pulmonary fibrosis [43]. Typically, patients with interstitial lung disease have reduced pulmonary function as evidenced by a restrictive ventilatory impairment [44]. Changes in sleep duration and the potential accompanying differences in circadian rhythms may influence lipid metabolism processes, such as adipogenesis [45] and lipid homeostasis [46], which could be relevant to the development of interstitial lung disease. This mechanism may offer insights into how sleep duration impacts the incidence of restrictive lung impairment.
Stratified analyses revealed a more pronounced correlation between sleep duration and lung function in males. This finding is consistent with data from the Austrian general population showing the higher prevalence of restrictive lung function in males [47]. Underlying mechanisms for this sex discrepancy are unknown; however, sex hormones in regulating sex-specific physiology probably impacts lung development and pathophysiology through various mechanisms [48]. Several epidemiological studies have shown a positive correlation between total testosterone [49, 50] and free testosterone levels [51] with FEV1 and FVC levels in adult males. In contrast, in the female population, there is no significant association between free testosterone and lung function measures [51]. Moreover, studies on male populations have revealed an inverted U-shaped relationship between sleep duration and testosterone levels [52], aligning with our observed correlation between sleep duration and FEV1. Previous studies have identified a correlation between abdominal obesity and restrictive impairment [26]; however, our stratified analysis by obesity status revealed that the increased incidence of restrictive lung function impairment was confined to non-obese patients. These effects might be attributed to obesity independently altering airway inflammation [41], thereby overshadowing the impact on airway inflammation caused by reduced [35, 36] or excessive [37] sleep duration.
Our study analyzed data from the NHANES survey, employing the same methodology. The substantial sample size and high data quality enhance the reliability of our findings. Moreover, our study focuses on the young and middle-aged adults who comprising the main workforce in society, making our research socially significant. To the best of our knowledge, this is the first study to examine sleep duration and restrictive impairment. However, our study does have several limitations. Firstly, due to our cross-sectional design we cannot draw definite causal conclusions, further assessment in a large prospective study is warranted to confirm these findings. Secondly, we lack relevant results from post-bronchodilator spirometry, which may limit the completeness of our analysis. Finally, the absence of data on sleep onset time and the inability to analyze the impact of OSA on sleep and lung function due to the small sample size are additional limitations.
Conclusions
Compared with 7 h of sleep duration, shorter and longer sleep duration were associated with impaired lung function among participants aged 20–64 years, and these associations were stronger among males. A large longitudinal study is warranted to confirm our findings, while fundamental research to illustrate the mechanistic pathways linking sleep duration and lung function.
Data availability
The datasets generated and/or analyzed during the current study are available from the website (https://www.cdc.gov/nchs/nhanes/index.htm).
Abbreviations
- BMI:
-
Body mass index
- CI:
-
Confidence intervals
- FEF25-75% :
-
Forced expiratory flow at 25–75%
- FEV1:
-
Forced expiratory volume in the 1 s, FVC = forced vital capacity
- GLM:
-
Generalized linear model
- NHANES:
-
National Health and Nutrition Examination Survey
- OR:
-
Odd ratios
- OSA:
-
Obstructive sleep apnea
- PEF:
-
Peak expiratory flow
- PIR:
-
Poverty income ratio
- RCS:
-
Restrictive cubic splines
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Acknowledgements
The NHANES team and all participants involved in our study are acknowledged.
Funding
This study was partly funded by the National Natural Science Foundation of China (Grant No. 82300028 and 81972991) and the Interdisciplinary Program of Shanghai Jiao Tong University (Grant No. YG2022QN038).
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GD and JL conceived the study. JL and XQ wrote the first draft that was revised and formatted for publication by GD and YZ. YZ revised the manuscript critically for important intellectual content and provided input for manuscript preparation for publication. All authors reviewed and approved this manuscript.
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Li, J., Qian, X., Ding, G. et al. Association between sleep duration and lung function among U.S. adults. BMC Public Health 24, 3530 (2024). https://doi.org/10.1186/s12889-024-21024-4
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DOI: https://doi.org/10.1186/s12889-024-21024-4