Nocturnal polygraphy in public transport drivers in Bucharest – cardiovascular and metabolic comorbidities

Sleep apnoea syndrome (SAS) is a public health problem because of its widespread prevalence (9%–38%) and effects on associated morbidity and mortality (1). In the general population, the symptoms of SAS are increasingly recognisable by the patient or their relatives, leading to a rise in medical referrals.

Starting in 2019, Romania mandated the inclusion of a pulmonology consultation in the annual medical check-up for category II drivers (trucks, public transportation and tractors), aiming to identify the risk of SAS. This retrospective descriptive study aims to analyse the frequency of cardiovascular comorbidities and to correlate them with objective and quantifiable data such as apnoea-hypopnoea index (AHI), time spent with SpO₂ <90%, number of hours slept, presence or absence of symptoms/signs or smoking status.

This study included 47 drivers of the Bucharest Transport Company who presented to the NewMedics Clinic (Bucharest, Romania) for a pulmonologic consultation and a nocturnal cardiorespiratory polygraph examination to assess the risk of sleep apnoea. The result of nocturnal cardiorespiratory polygraph examination was validated manually by a somnology specialist.

Patients were administered the Epworth questionnaire. Other data, such as age, number of hours slept per night, work shift, AHI, time spent with SpO₂ <90%, smoking status and cardiovascular comorbidities, were also recorded. All patients were male. The resulting database was analysed using IBM SPSS Statistics 20 software.

The study group consisted entirely of male patients with a mean age of approximately 52 years (Figure 1).

Figure 1.

Age histogram.

The body mass index (BMI) of the patients was analysed, and a mean score of 38.5 was obtained (Figure 2). All 47 patients were overweight and 2 of them had a BMI >40.

Figure 2.

Body mass index.

Only 2 patients did not meet the criteria for the diagnosis of SAS (AHI >5/hr), while 17 patients had mild SAS (5 < AHI < 15), 13 patients had moderate SAS (15 < AHI < 30) and 15 patients had severe SAS (30 < AHI) (Figure 3). The obtained AHI was, on average, 26.24/hr (Figure 4).

Figure 3.

Classification of enrolled patients.

Figure 4.

AHI histogram. AHI, apnoea-hypopnea index.

Arterial hypertension was reported in 33 patients (70.2%) (Figure 5), and diabetes mellitus was also diagnosed in 15 patients (31.9%) (Figure 6). Other pathologies, such as ischaemic heart disease, dyslipidaemia and stroke, were identified in a smaller proportion.

Figure 5.

Arterial hypertension.

Figure 6.

Diabetes mellitus.

Time spent with oxygen saturation <90%, an important marker for cardiovascular risk assessment in patients with SAS, was analysed. On average, patients included in the study spent 17.5% of their total sleep time (TST) with SpO₂ < 90% (Figure 7).

Figure 7.

Time spent with oxygen saturation <90%.

During the pulmonology consultation, patients completed the Epworth questionnaire, and the results were recorded. The cut-off for the Epworth questionnaire was considered to be 10 points. In contrast to the other results obtained, the mean Epworth score of the patients was 3.45 points, indicating the absence of daytime sleepiness and, by extension, a satisfactory quality of sleep. Only 2 patients had scores of 10 points, and none had a score >10 (Figure 8).

Figure 8.

ESS scores. ESS, Epworth Sleepiness Scale.

The literature establishes a link between BMI and the risk of SAS. In our case, all the patients who presented to the clinic were obese or overweight, and the prevalence of SAS was in accordance with the data available in the literature (95.5%) (2, 3).

Two patients had a BMI >40, which placed them directly in the category of ‘Obesity class III – morbid’. Patients with BMI >35 can be included in the same category, provided they have at least one associated cardiovascular disease or diabetes mellitus (4, 5).

Although we obtained concerning results related to the frequency of hypertension in patients with SAS (70.21%), it is difficult to establish the cause–effect proportionality with SAS due to the presence of well-known individual risk factors such as smoking, obesity and stress.

Historically, the indications for screening for SAS include overweight/obesity, neck circumference >44 cm in men or >37 cm in women, the presence of cardiovascular or metabolic comorbidities, and an Epworth score >8 or 10 points (6).

There have been inconsistencies between Epworth questionnaire scores and other data, suggesting a positive diagnosis of SAS and poor-quality sleep. Hypotheses for this may include accommodation to symptoms, patients’ egos or, most likely, fear of job loss. As professional drivers (public transportation), a positive diagnosis of SAS requires the patient to initiate positive pressure treatment. Epworth sleepiness score was not a reliable indicator for SAS screening in the study population.

Having a small study group (<500 patients), we were unable to find statistically significant correlations (bivariate correlations) between cardiovascular disease and BMI, AHI, age or time spent with SpO₂ < 90%. However, the prevalence of hypertension and diabetes in study patients is higher than in the general population.

Of particular importance is the time spent with SpO₂ < 90% in these patients. In 2019, William G. Kaelin Jr, Sir Peter J. Ratcliffe and Gregg. L. Semenza won the Nobel Prize in Medicine and Physiology for ‘how cells sense and adapt to available oxygen levels’ via hypoxaemia intermittent factor (HIF) (7).

Cheong et al. (8) published a meta-analysis in 2022 showing that patients with obstructive sleep apnoea syndrome (OSAS) have a 30% higher risk of developing neoplasms compared with the general population. This close link between HIF and oncogenic risk is studied and identified by Martinez-Garcia et al. (9). Intermittent hypoxaemia present in patients with OSAS causes overexpression of Hypoxemia intermitent factor – 1a (HIF-1a.) The literature also identifies other molecules involved in carcinogenesis, such as Programmed death – 1 (PD1) and Programmed death ligand – 1 (PD-L1) (checkpoint proteins), Midkine (MDK) and Tumor Growth Factor – Beta 1 (TGF-beta1), and postulates that intermittent hypoxia caused by OSAS promotes tumour cell proliferation and invasion in both in vitro and in vivo animal models (10, 11).

This study has several limitations that should be considered when interpreting the results. First, the sample size is relatively small (47 participants), which may limit the generalisability of the findings to a broader population of public transport drivers. A larger cohort would provide more statistically significant correlations between sleep apnoea severity and cardiovascular comorbidities.

Second, all participants were male, preventing an analysis of potential gender differences in the prevalence and impact of OSAS. Including female drivers in future studies would enhance the study’s applicability.

Third, the reliance on self-reported data, such as the Epworth Sleepiness Scale (ESS), may introduce bias. Some participants may have underreported symptoms due to concerns about job security, potentially affecting the accuracy of subjective sleepiness assessments.

Finally, this study is observational and cross-sectional, limiting the ability to establish causal relationships between OSAS, cardiovascular conditions and potential oncological risks. Longitudinal studies are needed for stronger conclusions.

In our experience, patients with SAS frequently associate cardiovascular pathologies and diabetes in a higher proportion than the general population. The latest data in the literature draw attention to the high oncogenic risk that SAS, through intermittent hypoxaemia, has. This raises public health concerns in terms of frequency, risks and associated costs and should receive more attention, including screening programmes for SAS in the overweight/obese population or people performing work requiring vigilance.