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This study generated several novel findings that characterized overnight snoring objectively relative to noise pollution standards. First, snoring severity can be characterized by its frequency and intensity, which are well correlated. Second, more than half of our self-reported habitual snorers produced sound levels that exceeded noise thresholds for sleep disturbance, with some who actually surpassed the noise thresholds associated with adverse cardiovascular events [27, 28]. Third, despite the fact that our habitual snorers were asymptomatic, they still demonstrated a high prevalence of OSA. Fourth, self-reported habitual snoring spans a spectrum from negligible to severe noise production throughout the night. Finally, both snoring frequency and intensity predicted the presence of OSA and accuracy improved even further when age and sex were incorporated in the models. These findings suggest that objective measures of habitual snoring constitute a health risk for both snorers and bed partners alike, and that strategies to reduce the snoring impacts can decrease the risk of adverse health consequences.

Snore exposure as noise pollution

Snoring is a potential form of noise pollution with attendant health consequences. Using accepted methods for quantifying noise exposure, we characterized the intensity and frequency of nocturnal snoring among a group of habitual snorers without overt symptoms of OSA. On a single study night, a substantial proportion of these snorers produced sound levels that exceeded the thresholds for nocturnal noise pollution. Specifically, the World Health Organization (WHO) guidelines and empiric data caution [29] that sleep disruption commonly occurs at sound levels greater than 45 dB(A) [30, 31], which we found in 66% of our cohort. Further increases in sound intensity from road traffic exceeding a 53 dB(A) threshold have been associated with adverse cardiovascular events [27, 28] possibly due to surges in sympathetic activity [10, 32]. We found that measurements of snoring frequency correlated well with calibrated measures of snoring intensity, suggesting that commonly available measures of snoring frequency (i.e. phone applications) may offer reasonable surrogates for bedroom noise pollution. Of note, objective sound recordings in our study indicated little to no snoring in approximately 35% of our cohort (Figure 4B). In those without objective snoring, therapeutic efforts can be redirected to focus on identifying a primary sleep disturbance in the bed partner rather than noise pollution from the putative snorer per se. Nonetheless, our findings indicate that bed partners of habitual snorers are exposed to noise at or above thresholds for a healthy environment, putting them at risk for chronic sleep disturbance and adverse health effects.

Objective snoring and OSA

Even after excluding participants with overt symptoms of OSA, we still found a high prevalence of this disorder in otherwise asymptomatic habitual snorers. This finding is consistent with previous epidemiologic studies that demonstrated a similarly high prevalence in the general population [, 33]. Epidemiologic risk factors for OSA including age, male sex and BMI are known to increase pharyngeal collapsibility in humans and animal models [34, 35]. The present study demonstrates that objective snoring is associated with OSA severity, suggesting that snoring is a surrogate for marked elevations in airway collapsibility during sleep [5, 36]. Nonetheless, we acknowledge that symptomatic OSA confers greater cardiovascular risk than asymptomatic OSA, particularly in those with relatively mild disease. The present study documents strong associations between snoring severity and OSA, suggesting that health risks be taken seriously in loud snorers. Health risks may be due to nocturnal hemodynamic stresses resulting from intermittent hypoxia, recurrent arousals and widening pleural pressure swings [37, 38] during periods of UAO.

Several lines of evidence suggest that snoring can predict the presence of OSA from the data in the present study population. First, we demonstrated that OSA was dependent on snoring severity using the Fischer exact test. Specifically, the Fischer exact tests showed that snoring intensity ≥53 dB(A) and snoring frequency ≥25% were both significantly associated with the presence of OSA in our population. Second, we accounted for potential covariates of this relationship including age and sex by applying a multivariate regression logistic model to predict the presence of OSA based on snoring severity, and found that snoring intensity and frequency were independent predictors of the presence of OSA. Third, having demonstrated significant odds of OSA in logistic models, we generated ROC curves to determine the accuracy in classifying (diagnosing) participants from snoring parameters. The ROC curves discriminated those with and without OSA with a high degree of accuracy. Taken together, multiple lines of evidence offer a compelling case for using snoring to predict OSA.

Limitations

A few limitations should be considered when interpreting our results. First, the decibel meter was placed vertically above the pillow. Participants who slept supine may appear to produce louder snores compared to those who slept on their side, leading to an underestimation of snore intensity in these participants. Second, in calculating snoring intensity, we only used the sound data points associated with inspiration. Sound decay during the ensuing expiratory period or expiratory snoring was not included given our definition of snoring for this project, which has led us to underestimate overall noise pollution. Third, a pertinent factor for the perceived sound level is the distance from the noise source. In this study, sound meters were placed at 25.5 inches (65 cm) above the pillow. Halving the distance would increase perceived sound levels by 6 dB (A) [23] and vice versa. Fourth, although the snoring intensity was related to snore frequency (see Supplementary Figure S1), it does not account for the temporal distribution of snore exposure. For example, a snorer with 30% snore breaths would produce approximately 2000 snore sounds over the course of the night. The snores could either be equally spaced or clustered. It remains unclear if the temporal distribution of snoring plays a role finadverse health effects. Fifth, we acknowledge that night to night variability in snoring severity may introduce some inaccuracies in our objective snoring measurement in a single night. Finally, our current semi-automated procedure for detecting inspiration and characterizing breath-by-breath snoring is painstaking and time consuming. To streamline this process, structured development and cross validation of the custom algorithm are required, especially if the process is to become fully automated.

Implications

Objective measurements suggest that snoring is a significant environmental noise pollutant with potential implications for public and personal health in snorers and bed partners alike. First, objective measures of snoring severity constitute a strong predictor for concomitant OSA after adjusting for risk factors such as age and sex. Increased availability of home-based assessments of snoring can facilitate OSA screening strategies in the community at large, although further work will be required to account for ambient domiciliary noise, and to standardize and streamline the process of accurately characterizing inspiratory snoring for the purpose of OSA screening. Second, in those who do not have objective evidence of snoring, self-reported snoring may reflect an underlying discord or a primary sleep disturbance in the bed partner, and offer a cautionary note in snoring management. Finally, sleep disruption leading to intermittent surges in sympathetic activity and elevations in blood pressure has been suggested as a potential mechanism for noise-induced cardiovascular morbidity [32]. Implementing WHO paradigms for examining health consequences of noise pollution, we can envision strategies to elucidate dose–response relationships between snoring and markers of cardiovascular stress, as well as long-term adverse health events.