Obstructive sleep apnoea (OSA) is a condition characterised by repetitive occlusions of the upper airway during sleep, resulting in arousals and sleep fragmentation. It impacts on daytime vigilance1and contributes to cognitive dysfunction2and mood disorders.3 It is a source of lost productivity in the workplace4 and increases motor vehicle accident risk.5 OSA has also been implicated as a cause of hypertension,6 with studies showing small but consistent falls in blood pressure following continuous positive airway pressure (CPAP) treatment.7 Epidemiological studies have also shown OSA to be independently associated with an increased risk of diabetes8 and cardiovascular disease,9,10 although definitive evidence for a causal link with these diseases awaits the results of large-scale randomised controlled trials of OSA treatment. In the early 1990s, the prevalence of OSA in the community in the United States, determined by polysomnography (PSG), was shown to be 24% of adult men and 9% of women,11 with recent evidence suggesting a further increase due to the obesity epidemic and an ageing population.12 OSA is now recognised as a major public health and economic burden, with an estimated cost to the Australian community of more than $5.1 billion a year in health care and indirect costs.4

The purpose of this article is to describe the key issues in evaluation and management of OSA, to assist health care professionals to better engage in OSA management. We outline several evidence-based models of care that could be scaled up to allow the primary care physician to have a greater role in addressing the high burden of OSA in the community. To do this, primary care health professionals must be skilled in identifying those at high risk of OSA who are likely to benefit from treatment and must know which investigation to order, what treatments to recommend, and when specialist referral is needed.

Despite the high prevalence of OSA, most patients are minimally symptomatic. About 15% of patients have moderate to severe sleep apnoea.13 The vital issue in clinical practice is to identify those with OSA who have clinically important disease. Lack of clarity around goals of treatment can lead to excessive investigation, inappropriate treatment and patient disengagement. We believe the major goals of management of OSA should be:

• to identify and offer treatment to symptomatic patients, regardless of disease severity, whose safety and quality of life is affected;

• to identify and offer treatment to patients with severe OSA determined by PSG, regardless of symptoms, who may be at risk of adverse health outcomes; and

• to modify adverse lifestyle factors that contribute to OSA pathogenesis and other poor health outcomes. This may include advice on diet and exercise to lose weight, and encouragement to reduce alcohol intake and stop smoking.

Optimal outcomes are usually achieved through an initial identification of the presenting clinical triggers, an evaluation of the symptom profile, and an exploration of the patient’s treatment preferences and capacity to afford or comply with the range of treatment options. The workup for OSA must start with a careful clinical assessment to identify patients who are likely to benefit from treatment. Clinicians must then select an investigation: either in-laboratory PSG, home-based PSG or simplified limited channel sleep testing. The test result must then be coupled closely with the clinical assessment to inform a personalised treatment plan. This plan should identify adverse lifestyle factors, overlapping sleep disorders and medical comorbidities (eg, hypertension, diabetes, depression, dyslipidaemia), and consider these when advising on OSA-specific treatments.14 Box 1 depicts an algorithm that may assist the primary care practitioner with this process. There is no one preferred treatment for OSA but rather a range of options of proven effectiveness that can be applied individually or in combination, depending on patient preference, symptoms, OSA severity, comorbidities and other health risk factors (Box 2). Development of a personalised treatment plan requires the active involvement of the patient, partner and family in goal-setting.14 For the health professional, it requires that they be sufficiently familiar with the field and the practical application of each of the available OSA investigations and treatment options. The complexity of this process has meant that OSA has been traditionally managed by a relatively small specialised workforce using the gold standard, in-laboratory PSG. However, patient access to specialist sleep services has been limited and alone will not be able to cope with the evidently large burden of disease.12

Given these service barriers, various simplified, lower-cost clinical models have been developed for OSA. These have incorporated screening questionnaires to identify patients at high risk of OSA,15–19 simplified testing with home-based PSG or limited channel sleep studies (typically without sleep electroencephalography) and selected use of automatically titrating CPAP devices that lessen the need for supervised in-laboratory CPAP titrations. If patients are identified as having a high pretest probability of OSA and if major comorbidities and overlapping sleep disorders are excluded (Box 3), the use of home-based PSG or limited channel sleep testing and automatically titrating CPAP has been shown to produce similar or non-inferior patient outcomes to more traditional specialist referral and in-laboratory PSG approaches.20–23 Further, it has been shown that with suitable training and support from a specialist sleep centre, these management approaches can be applied effectively to uncomplicated OSA patients by nurses and primary care physicians.24

A major challenge is how to translate and upscale these research findings from controlled settings to the “real world” to meet the demonstrably high community burden of disease while ensuring high-quality, holistic patient care. The current availability of open-access PSG has enabled primary care practitioners to become more involved in the care of OSA patients. However, few of these services currently select for high pretest probability of disease, nor do they train or adequately support the referring health care professional to ensure that they are sufficiently knowledgeable in assessment and personalised treatment of OSA. Some patients accessing this service model who are found to have uncomplicated moderate to severe symptomatic OSA may adhere to CPAP treatment and be successfully managed in primary care. However, there are no data available on the overall adequacy of CPAP treatment for patients with milder or complex OSA, or overlapping sleep disorders and adverse lifestyle issues. There is also a lack of such data for patients who refuse CPAP treatment or for whom the treatment is unsuccessful.

If sleep service delivery at the primary care level is to be upscaled and the recently validated simplified models of care for OSA translated into routine care, there will need to be greater awareness around clinical assessment, goals of OSA treatment and the various available treatment options. Objectives of the clinical assessment are to determine the motivating factor(s) for presentation and the patient’s symptom profile and pretest probability of disease, and to identify modifiable adverse lifestyle factors and co-occurring sleep problems. Collectively, these factors will have an important influence on the investigation and management pathway.

In Australia, Medicare reimbursement is provided for full PSG, conducted in either supervised (in-laboratory) or unsupervised (home) settings. For home-based PSG, patients are connected to the electrodes and sensors at the facility on the afternoon of the test and return home, or self-connect in their own home before bed, according to written, verbal or audiovisual instructions. Patients may perceive an increased level of convenience and comfort with testing in their own home, sensing a more sleep-conducive environment. When directly compared, one study showed 50% of patients preferred home-based testing, 25% preferred laboratory-based testing and 25% had no preference.28 Comparison of home-based versus in-laboratory PSG showed reduced total cost for home testing28 and high overall satisfaction rates for both forms of testing.28 However, home-based PSG is associated with higher test-failure rates, partial signal loss producing equivocal results,28,29 and a tendency to underestimate sleep apnoea severity.29 More severe sleep apnoea (high pretest probability) may overcome the shortfalls of partial signal loss and any tendency to underestimate severity, and this will improve diagnostic accuracy.

A comprehensive overview of all treatment options is beyond the scope of this manuscript, and international guidelines are available.31 Options are summarised in Box 2. Identification of sleep apnoea is a teachable moment for the health care professional to guide the patient and suggest interventions to modify lifestyle and reduce weight. Thereafter, treatment considerations ought to extend beyond CPAP. Studies have shown large variation (17%–71%) in adherence to optimal CPAP (defined as average of ≥ 4 hours per night).32 More recent randomised controlled trial evidence suggests that mandibular advancement splints may be as effective as CPAP across a range of OSA severity,33 although there is limited information on longer-term compliance. Newer surgical techniques are emerging for OSA and the combination of uvulopalatopharyngoplasty, tonsillectomy where appropriate, and a low-morbidity technique to reduce tissue volume at the tongue base shows promise in highly selected patients for whom conventional therapies such as CPAP or a mandibular advancement splint have been unsuccessful.34 Adults with gross tonsillar hypertrophy and sleep apnoea are uncommon but often do very well following tonsillectomy. Some preliminary success is reported with nasal positive expiratory pressure devices,35 although long-term adherence to treatment is unknown and patient selection needs more evaluation.

Overall, treatment for OSA includes a range of options, all of which have their unique challenges. Cost is a consideration and commitment is required to achieve long-term adherence. There is a risk that patients may not persevere with the treatment plan if the clinical assessment was not patient-focused and did not address key presenting symptoms or motivators. A negative experience has consequences in terms of lost opportunity if the patient withdraws from the therapeutic process. All patients should be clinically reassessed after a treatment option is tried, to ensure the treatment has been effective in controlling both OSA and its symptoms.

The specialty of sleep medicine now has a robust curriculum, encompassing both respiratory and non-respiratory sleep disorders, and requires a full year of dedicated training. This will see larger numbers of specialists with sufficient skills to assist with managing the public health burden of OSA. Telehealth will also enable sleep specialists to assist health care practitioners and patients in rural and regional communities.

However, the large burden of disease is likely to be best served in the long term by an expanded trained pool of primary care and other health care providers working alongside sleep and respiratory specialists. In this model of care, sleep specialists working in a multidisciplinary environment would have as their major clinical focus complex or atypical OSA cases (eg, those with comorbidities or overlapping sleep disorders) or treatment failures. All modalities of sleep testing will be used in accordance with existing validated algorithms. These models of care will take time to evolve and will require changes to clinical guidelines and accreditation standards, the upskilling of the health care workforce, and government and private sector policy changes with respect to reimbursement.

1 Algorithm for management of obtructive sleep apnoea (OSA) in the community

PSG = polysomnography.

Patients with obstructive sleep apnoea (OSA) have a high prevalence of insulin resistance (IR), type 2 diabetes mellitus and cardiovascular disease (CVD), indicating a strong association among the conditions. Intermittent hypoxia with fragmentation of normal sleep contributes to significant autonomic dysfunction plus proinflammatory and procoagulopathy states,1 leading to IR and CVD (Box 1). Although obesity is a common risk factor for OSA, IR and particularly CVD, current evidence suggests that OSA itself is an independent risk factor for both IR and CVD. Clinical data suggest that this effect is most likely mediated via intermittent oxygen desaturation. However, teasing out the precise role that OSA plays in IR and CVD, independent of obesity, is difficult given the confounding effects of inactivity, sleep deprivation, diet and OSA variability in terms of age of onset, duration and severity. With this in mind, this paper attempts to review the epidemiological and interventional evidence connecting OSA with IR and CVD (Box 2).

Obesity is the major risk factor for OSA, particularly central adiposity with visceral fat. Large epidemiological studies have reported a dose–response association between OSA prevalence and increased body mass index (BMI) plus neck and waist circumferences. One large prospective epidemiological study reported that a 10% weight gain led to a sixfold increase in the odds of developing moderate to severe OSA, independent of confounding factors.22

Conversely, weight loss improved OSA, but to a lesser extent than weight gain worsened it (10% weight loss predicted a 26% decrease in the apnoea–hypopnoea index [AHI]). The latter observation underscores the potential for weight loss as a treatment for OSA. Observational data suggest an improvement in OSA with weight loss, although results from randomised controlled trials (RCTs) have been available only more recently. Trial data indicate that patients with mild OSA substantially improve their OSA with weight loss, although only 22% achieved a “cure” (AHI < 5/h).23 However, among obese patients with severe OSA, results from weight loss studies are more unpredictable. Data from lifestyle interventions show an improvement in OSA, with weight loss of at least 10 kg, but only a minority of patients achieved an AHI < 5/h.24,25

A recent Australian RCT assessing the effect of laparoscopic gastric banding surgery in morbidly obese patients with moderate to severe OSA showed that although surgical patients lost more weight, there was no significantly greater reduction in AHI in the surgical group compared with the control group who undertook lifestyle measures.26 In both groups, there were significant improvements in symptoms of sleepiness and mood, despite only about a 50% reduction in the group AHI, suggesting that weight loss per se, rather than OSA reversal, contributed to improved quality of life. Metabolic parameters also improved with weight loss and were greatest in the surgical group, who lost more weight. This trial underlines two important points. First, obese patients with mild OSA may be “cured” by weight loss, but those with moderate to severe OSA are rarely “cured” by either surgical or medical weight loss strategies. Second, many significant health benefits (relating to quality of life, depression and diabetes control) can be achieved by weight loss in obese OSA patients, even if OSA persists.

OSA and systemic hypertension commonly coexist — the prevalence of OSA in populations with systemic hypertension has been reported to vary from 30% to 83%.27 Several large epidemiological cross-sectional studies of community dwellers indicate that the presence of untreated OSA is associated with a greater prevalence of hypertension when controlled for known confounding factors,2 although the association is weaker in prospective incidence studies.3 Although some prospective incidence studies of middle-aged adults have found untreated OSA to be associated with a two- to threefold risk of developing hypertension over a 4–8-year period,4 not all studies have found a positive association between OSA and hypertension.3 In addition, the relationship between OSA and hypertension has not been confirmed in patients aged > 65 years,5 probably because of additional accumulating risk factors.

Treatment of OSA with continuous positive airway pressure (CPAP) has been shown to lead to reductions in mean systemic blood pressure measured over 24 hours, although these falls are small (about 2–3 mmHg), with the greatest benefit seen in patients with more severe OSA.6 There is also evidence that treatment with mandibular advancement splints leads to an improvement in hypertension,7 suggesting that the benefit of OSA treatment with respect to blood pressure is independent of the treatment modality.

Despite this, pharmacological antihypertensive therapy (valsartan) is more effective than CPAP (9 mmHg v 2 mmHg fall in mean 24-hour blood pressure) over 8 weeks, according to one RCT of 23 patients with hypertension and OSA.28

Four important messages need consideration regarding OSA and hypertension. First, clinicians should assess for OSA symptoms and consider a sleep study in patients with resistant hypertension.29 Second, OSA treatment in hypertensive OSA patients may improve blood pressure control but without large reductions, while snoring and quality of life should improve. Third, CPAP is not a substitute for pharmacological treatments. Fourth, obesity is a unifying factor and, accordingly, assistance with weight loss should be the primary objective for clinicians.

Metabolic disorders of glucose control and OSA share the same major risk factor of central obesity with excess visceral fat and, unsurprisingly, the disorders commonly coexist. Mechanistically, OSA may aggravate IR and type 2 diabetes via intermittent hypoxia, fragmented sleep and elevated sympathetic activity. Diabetes may contribute to OSA via neuropathy and weight gain related to insulin use. The prevalence of OSA in patients with type 2 diabetes has been reported to vary between 23%8 and 86%,9 with differences in study populations and OSA definitions explaining the marked variation in results.10 Most cross-sectional studies have demonstrated that OSA is independently associated with IR and type 2 diabetes in adult sleep clinic populations and in unselected communities, independent of age and BMI, but prospective incidence studies have been less convincing.

The effect of OSA treatment with CPAP on insulin sensitivity and glucose control (ie, HbA1c levels) is unclear. A recent meta-analysis11 of five RCTs (four with crossover design) suggested that reversal of OSA with CPAP for 1–12 weeks has a beneficial effect on IR, as measured by homoeostatic model assessment in OSA patients without diabetes, although the effect size was small (− 0.44) in contrast to pharmacological effects (− 0.9). The only RCT of CPAP treatment of OSA among adults with type 2 diabetes indicated that CPAP did not improve homoeostatic model assessment scores, HbA1c levels or BMI in 42 patients with moderate to severe OSA and type 2 diabetes, although patients were symptomatically and objectively less sleepy.30 A larger and longer international trial is nearing completion (NCT00509223). Some authors suggest the variable effects of CPAP on glucose control may relate to duration of CPAP treatment (potentially > 3 months) and that the effects may be greatest in patients who are less obese.31

The observations above indicate that factors for developing IR other than obesity, sedentary lifestyle and age, such as OSA and loss of normal sleep, should be considered, especially among patients with difficult-to-control diabetes. Moreover, it is important to realise that the OSA and IR pathophysiological association may be bidirectional.

Patients with untreated OSA have an elevated risk of developing stroke, and the data are more consistently positive than for cardiac disease,18 including in the elderly.32 Mechanisms include large swings in systemic blood pressure, local vibrational damage to the carotid artery bifurcation, increased coagulopathy, surreptitious development of atrial fibrillation during sleep with thrombus formation and paradoxical emboli through asymptomatic patent foramen ovale opening during transient sleep-related hypoxaemia with pulmonary hypertension.33

Prospective observational studies show increasing risk for ischaemic stroke with increasing OSA severity.19 A large epidemiological study in the United States found that the risk for stroke in men increased almost three times once the AHI was > 19/h, but that the risk in women was much smaller and did not become significant until AHI was > 25/h.19

CPAP treatment may reduce stroke risk; however, large RCTs are lacking. Observational studies have shown that treatment of OSA reduces stroke risk. The only RCT assessing the effect of CPAP on risk of mortality and subsequent stroke did not show a benefit, but had only small numbers and was not adequately powered to address the issue.34

The prevalence of OSA is high (estimated to be 30%–58%) in patients with ischaemic heart disease (IHD).12 In the general community, cross-sectional epidemiological evidence supports a link between OSA and IHD. OSA is associated with a greater risk for acute myocardial infarction than are smoking or hypertension.13 Further, the presence of OSA in patients with established IHD is associated with greater 7-year mortality compared with patients without OSA.12 Whether underlying OSA contributes to the well described circadian distribution of myocardial infarction (peak incidence around 8 am) remains to be determined. RCTs of OSA treatment on the development or outcomes of IHD are presently lacking.

Benign cardiac arrhythmias are commonly present in OSA. Examples include cyclic tachycardia–bradycardia, atrial and ventricular ectopics, bigeminy, heart block and atrial fibrillation.35 In a large study, subjects with severe OSA (AHI > 30/h) were found to be more likely to have atrial fibrillation (fourfold risk), non-sustained ventricular tachycardia (4.4-fold risk) and quadrigeminy (twofold risk) compared with subjects without OSA.14 The clinical significance of this is unknown. Similar data were provided for Australians with moderate OSA (AHI > 15/h), with an odds ratio of 3 for having atrial fibrillation.35

Some data suggest that all arrhythmias improve with CPAP treatment,36 whereas other data are not as supportive.37 One study suggested the 12-month recurrence of atrial fibrillation after cardioversion was significantly lower if coexistent OSA was treated with CPAP compared with untreated OSA.38

Although the risk of fatal arrhythmias from OSA is unknown, an increased risk is suggested from data showing that subjects with OSA who die of sudden cardiac death are more likely to do so at night compared with those without OSA.39

Although RCTs of the effect of OSA treatment on cardiac arrhythmia frequency and severity are lacking, it does appear prudent to question for OSA symptoms in patients with difficult-to-control arrhythmias, such as cyclic tachycardia–bradycardia or atrial fibrillation, especially when they occur during sleep.

Both diastolic and systolic heart failure (HF) are common in OSA populations. In addition to the proposed effect of OSA on CVD, large swings in negative intrathoracic and positive intravascular pressures that result from OSA are thought to contribute to the development of cardiomyopathy as well as hypertension, hypoxia, hypoxic pulmonary hypertension and oxidative stress.1 Epidemiological data indicate a threefold greater prevalence of diastolic and systolic HF in community dwellers with severe OSA (AHI > 30/h) compared with those without OSA.15 Further, the risk of developing incident HF due to untreated OSA is estimated to be 1.6 times greater, based on 4422 community dwellers (controlled for age, sex, race, diabetes and hypertension) followed for a mean of 8.7 years.16

OSA and central sleep apnoea (defined by about 30 seconds of hyperventilation followed by about 30 seconds of apnoea with no respiratory effort and usually absence of snoring) are also commonly seen within HF populations. A study demonstrated that 55%–85% of HF patients have sleep apnoea (either obstructive or central) when patients were tested several times over a 12-month period.40 In general, central sleep apnoea is seen in the more advanced severe spectrum of HF and can be explained by additional pathophysiology to that seen in pure OSA. The high prevalence of each type of apnoea does not appear to have been affected by the introduction of β-blockers or spironolactone.41

Evidence suggests that coexistent OSA worsens HF and is improved by CPAP therapy. An RCT found that treatment of patients with OSA (AHI > 20/h) and systolic HF with fixed pressure CPAP over 3 months was associated with improvements in systolic function, quality of life, exercise capacity and autonomic control.17 Nevertheless, the data are not universally positive. The study was not large enough to assess mortality; however, an observational study suggests an improvement in survival with long-term CPAP treatment, compared with untreated OSA.42

Several large, longitudinal epidemiological studies have consistently indicated that in middle-aged populations, severe untreated OSA (AHI > 30/h) is associated with greater mortality compared with treated OSA, mild to moderate OSA or no OSA.20 These data suggest that severe OSA confers a mortality risk, which is prevented by CPAP treatment. Nevertheless, these studies were not RCTs and, given that unrecognised bias may confound the results, whether OSA is a reversible risk factor for mortality remains inconclusive.

The mortality effects of untreated OSA are less certain in the elderly. In a large cohort of 14 589 Israeli patients, severe OSA led to increased mortality only for those aged < 50 years.21 Similarly, a large US study also failed to show increased mortality in patients aged > 70 years.20 However, a recent Spanish observational trial reported that elderly patients (> 65 years of age) with severe untreated OSA (AHI > 30/h) had 2.25 times increased mortality — due largely to stroke and HF, but not to IHD.21 No excess mortality was seen in severe OSA treated with CPAP, or in less severe OSA.

Observational studies suggest that CPAP improves survival in severe OSA, although formal long-term RCTs are needed. The SAVE trial (ANZCTR 12608000409370; NCT00738179), instigated by the Adelaide Institute for Sleep Health, is currently underway. The trial aims to randomly allocate 2500 high CVD-risk patients with OSA to either CPAP or no CPAP, with a primary end point of time to cardiovascular event or death (results are expected in 2016). Several other large outcome-based trials are also underway, including a Spanish trial (NCT01335087) of CPAP treatment of OSA in patients with acute coronary artery syndromes. These and other studies will provide valuable clarification about whether OSA is a reversible cardiovascular risk factor. In addition, newer variants of positive airway pressure, such as adaptive servoventilation, are being tested in patients with sleep-disordered breathing and HF (NCT01164592 and NCT01128816), and we also await the results of these large multinational trials.

1 Schematic summary of precipitating factors towards obstructive sleep apnoea, with physiological consequences and downstream cardiovascular consequences

Nearly 1.5 million Australians are employed in shift work, representing 16% of the working population. Shift work is associated with adverse health, safety and performance outcomes. Circadian rhythm misalignment, inadequate and poor-quality sleep, and sleep disorders are thought to contribute to these associations.

The most immediate consequence of shift work is impaired alertness, which has widespread effects on core brain functions — reaction time, decision making, information processing and the ability to maintain attention. This impairment leads to preventable errors, accidents and injuries, especially in high-risk environments. Long-term health consequences of shift work have been reported, including increased vascular events.1

This review evaluates the health burden associated with shift work and discusses strategies for the clinical management of sleep–wake disturbances in shift workers. Evidence-based management strategies require consideration of the key physiological sleep–wake determinants of alertness (Box 1).

The mismatch between the endogenous circadian pacemaker and the sleep–wake cycle results in immediate sleep–wake disturbances, chronic sleep restriction and possibly internal desynchronisation of the circadian system (Box 1). This results in deleterious effects on alertness, cognitive function, mood, social and work activities, and health. Sleepiness is common, increased by more than 50% in truck drivers working night shift and associated with brief sleep episodes.12 Falling asleep during night shift occurred at least weekly in 36% of rotating shift workers, 32% of permanent night workers and 21% of day and evening nurses working an occasional night shift.13

Given this impairment in alertness and cognitive function, it is not surprising that, compared with day workers, the risk of accidents and near-miss events is significantly elevated in shift workers, including those involved in safety-critical industries such as health care, law enforcement and commercial driving.14 Major catastrophes such as the industrial accidents at Three Mile Island, Chernobyl and Bhopal have been linked to human error related to shift work.2 Shift workers have impaired driving performance and a two to four times increased risk of crashing during their commute to and from work.6,13 Sleep-related accidents are most common during the night shift in transportation fields, peaking towards the end of the night shift, and the risk of occupational accidents is also increased when working outside regular daytime hours (relative risk, 1.6).15 These findings are consistent with those from the general population showing increased risk of motor vehicle crash during the night and after sleep restriction.16 In addition to personal and public safety risks, productivity is impaired, with frequent workplace errors and increased absenteeism.17 Conversely, an intervention based on circadian principles significantly improved productivity in rotating shift workers.18 There is a marked increase in preventable medical errors, including those resulting in fatalities, when medical residents work frequent extended-duration night shifts.6 In police officers, poor sleep associated with shift work is also related to impaired function at work, including administrative and safety errors, falling asleep in meetings, uncontrolled anger and absenteeism.10 Hence, shift work can impact on the safety of the worker and others, as well as reducing productivity.

Shift work is associated with a higher risk of several medical conditions, particularly metabolic syndrome, cardiovascular diseases and mood disorders.6 Increased cancer risk has also been described, potentially through disruption of the circadian system from light exposure at night.19 Circadian misalignment is related to cardiometabolic changes, and together with altered food choice and physical activity, leads to increases in obesity, dyslipidaemia and impaired glucose metabolism. Rotating shift workers are 20%–30% more likely to have impaired glucose metabolism (elevated HbA1c levels) with a 70% increase in metabolic syndrome among transport workers.20 In large epidemiological studies, mortality from diabetes, cardiovascular disease and stroke is higher in long-term shift work, although all-cause mortality is not clearly increased.21 Mood disturbance is common during rotating and night shifts, although the longer-term effects of shift work on mood are less clear. Doctors experience symptoms of anxiety, depressed mood and reduced motivation, in conjunction with impaired cognition, during prolonged night shifts.22 A recent US study of police found that anxiety and depression were more than twice as common in those who had symptoms of disordered sleep.10 Depressive symptoms in shift workers are also linked to increased absenteeism and occupational errors.23 Although impaired mood is common during shift cycles, it remains unclear as to whether shift work results in longer-term mood disturbance.

The health and economic costs of shift work-related sleep–wake disturbances are high, taking into account the combined effects of impaired sleep, workplace and road accidents, mood disorders, lost productivity and cardiovascular health. Precise economic costs have not been quantified, although the economic impact of individual elements provides some idea. The average cost per year to a person suffering from regular insomnia, as occurs with shift work, is estimated at over $5000. Excessive sleepiness occurs in more than 30% of shift workers. The combined cost of road and workplace accidents caused by excessive sleepiness is estimated for 2009 at $71–$93 billion per annum in the US, with shift work a major contributor to this cost.24

The key aims of managing sleep–wake problems in shift workers are to ensure sustained alertness during wake episodes when working and during social activities, and to facilitate restorative sleep when sleep is required. In part, this is achieved by prevention or minimisation of factors that worsen sleep–wake function and therefore impair alertness, such as long work hours or rotating shift schedules, an approach that has been shown to reduce adverse events related to shift work in the health sector. Forward rotation of shifts (from day to afternoon to night) is preferable. Second, given the interindividual variability in sleep–wake responses to shift work, it is also important to develop algorithms that predict whether a shift worker is fit for duty or potentially vulnerable to alertness failure. There have been major efforts to develop biomathematical models using information such as work and sleep–wake schedules to evaluate safety risk associated with particular shift rosters. The use of such approaches outside of the research setting is considered premature. In high-risk industries, such as transportation, companies should have systems in place to minimise the risk related to shift work.

With shift work, sleep–wake disorders are highly probable at some stage in all workers, and an approach to mitigate the consequences of shift work should be adopted in the workplace as occupational health policy; for example, through screening programs for sleep disorders and general health.

1 Multiple pathways potentially explaining the link between shift work and adverse health outcomes*

* Modified with permission from Knutsson A. Health disorders of shift workers. Occup Med (Lond) 2003; 53: 103-108.