**2. Epidemiology of risk factors for cardiovascular disease in aircrew**

#### **2.1 Traditional risk factors for cardiovascular disease in aircrew**

Several studies mentioned the established risk factors for CVD continuum including hypertension, type-2 diabetes, dyslipidemia, smoking, overweight and mainly abdominal adiposity, physical inactivity and Mets [9]. Recent data suggest disturbing increases in the prevalence of these risk factors for CVD (**Figure 1**) [10].

#### *2.1.1 Hypertension*

Worldwide, hypertension is the leading etiology of morbidity and mortality [11, 12]. Hypertension is the first issue for pilots to secure their medical certificate [1, 13]. Through complications such as myocardial infarction, stroke, renal failure and death, hypertension constitutes a risk of in-flight incapacitation. In-flight CV events are believed to be scarce although allegation of in-flight CV incapacitation misdiagnosis has once been put forth [14]. Exposure to flight stress could be listed as a plausible explanation as weighted by total flight time at baseline. Indeed, considering the responsibility to fly the plane, flight crew is exposed to chronic stress that might trigger both hypothalamo-pituitary- adrenocortical and sympatho-adreno-medullary pathways to raise arterial blood pressure. In addition, it has been reported that chronic stress could lead to hypertension, which is triggered by angiotensin II through either lymphocyte T activation or vascular inflammation.

#### *2.1.2 Types-2 diabetes*

Type-2 diabetes either through chronic complications (heart disease, hypertension, and stroke) or acute complications (hypoglycemia or hyperglycemia episodes) *Risk Factors for Cardiovascular Diseases in Aircrew DOI: http://dx.doi.org/10.5772/intechopen.99905*

#### **Figure 1.**

*Relationship between risk factors and CVD among aircrew. ASCVD: atherosclerotic cardiovascular disease; CVD: cardiovascular disease; TFH: total flight hours.*

can grievously compromise flight safety and harm not only the aircrew himself but also the passengers, the aircraft, and the environment [15]. The relationship between blood glucose control and the establishment of CVD in diabetes remains a matter of controversy. Whilst several glucose-lowering trials in diabetes showed significant reduction in microvascular complications, they systematically failed to achieve significantly in macrovascular complications. Still, it should be mentioned that some systematic reviews and meta-analysis have recommended that efforts to improve blood glucose lower the incidence of CVD [16].

#### *2.1.3 Smoking*

Smoking has long been considered as the major risk factor for the establishment of CVD. Tobacco use, the single largest preventable cause of CV morbidity, is responsible for 10% of all of CVDs and doubles the 10-y mortality rate [17]. Worldwide, nearly a billion people are smokers and newly smokers are men from low- and middle-income countries (LMICs). Smoking delirious effect is dose related with no safe limit observed. It has been shown that passive smoking produces noticeable interferences in the normal autonomic nervous system functioning characterized by increased sympathetic drive and reduced HR variability (HRV) and parasympathetic modulation.

#### *2.1.4 Overweight/obesity*

Obesity, a significant determinant of CVDs, is extensively related to hypertension even if the exact mechanisms remain not totally unraveled [18]. This relation should now focus on weight variation across time along with visceral or intraabdominal fat that is likely linked to the insulin resistance syndrome, an indicator of generalized metabolic disorder [18]. Obesity interacts with aviation duties. In fact, not only does obesity increase the risk of sudden CV incapacitation, but the risk of sudden and subtle incapacitation consequential to sleep apnea and the risk of pulmonary embolus do [19]. On the other hand, obesity can jeopardize the egress of

aircraft in emergency [19]. The current results demonstrated that short term commercial flying significantly altered cardiovascular function including the reduction of parasympathetic modulations. Further, greater physical fitness and lower body fat composition were associated with greater cardiac autonomic control for passengers during flights. Enhanced physical fitness and leaner body composition may enable passengers to cope better with the cardiovascular stress and high allostatic load associated with air travel for enhanced passenger well-being [20]. In an observational cross-sectional study among Brazilian pilots, Palmeira found that more than half of and nearly a quart pilots were overweighed and obese, respectively. These authors concluded that overweight and obesity among the commercial airline pilots was high and represents a serious health problem in this population [21].

#### *2.1.5 Physical inactivity*

The lack of physical activity has contributed increasingly to overweight and obesity in young persons and adults. Physical activity is significant for primary and secondary prevention as well notwithstanding of BMI. Aircrew have little physical activity and eat higher caloric foods away from home at unscheduled time intervals [21]. Physical inactivity and unhealthy diet are responsible of raised BP, increased blood glucose, increased blood lipids, and overweight and obesity.

#### *2.1.6 Total flight hours*

The relationship between higher TFH and ASCVD risk in pilots have been established [22] as well as how TFH expresses the likelihood of crash involvement significantly compared with aging, which encompasses a conflict between decreasing cognitive functions that jeopardizes flight safety and increasing flying expertise that enhances fight safety [23]. Similarly, having 5,000 tfh or more protects against crash involvement but this protection levels off at a threshold of 10,000 tfh [23]. Likewise, inverse nonlinear relationship has been found between crash involvement and total flight time [23].

#### *2.1.7 High altitude exposure*

Pilots have to cope with stress due to 6,000 to 8,000 feet pressurized environment, and working hours [21]. It is known that the increase of BP with high altitude exposure 3000 m above sea level (asl) [24]. The explanation among several is the sympathetic activation (increased BP, HR, cardiac output, myocardial twist) through peripheral chemoreceptor [24]. Individuals with grade 2 hypertension and increased ASCVD risk should check their BP values before and during HA (>2500 m) exposure. Individuals with grade 1 hypertension may reach very HA (>4000 m) with adequate medical therapy; uncontrolled severe hypertensive individuals (grade 3) should avoid exposure to very HA [24]. At HA, left ventricular experiences changes such as an increase of systolic function with elevated sphericity index, but a decrease of diastolic function [25, 26]. Moreover, HA exposure may increase risk of cerebral ischemia for individuals with antecedent of ischemic stroke [26–28]. Background contributors are increased hematocrit and greater blood viscosity. HA exposure increases risk of hemorrhagic stroke in those with cerebral aneurysms and arterial/venous malformation [29]. HA may be at benefit for arrhythmia [24]. High altitude less than 4000 m does not affect pacing and implantable cardioverter devices [30].

At sea level, barometric pressure is 760 mmHg, and air has a partial pressure of oxygen (PO2) of 160 mmHg. Airline flight usually cruises at altitudes of 9,150–13,000 m (30–40,000 feet) asl where the atmospheric PO2 is usually ≤38 mmHg, which would normally result in a lethal level of airway (alveolar) hypoxia. Aircraft cabins are therefore environmentally modified (pressurized) to atmospheric pressures of 1,530–2,440 m (5,000–8,000 feet) asl [24].
