Workplace Stress: A Potential Killer

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Introduction
Having a job or source of income plays a critical role in improving people’s health as
well as shaping their attitude towards life. However, workers in various social constructions are
today faced with a new challenge that threatens their well-being, and that is stress. Workplace
stress has become a critical issue for many people to the extent that outweighs the possible
benefits and exposes individuals to various health challenges. The National Institute for
Occupational Safety and Health defines workplace stress as “harmful physical and emotional
responses that occur when the requirements of the job do not match their capabilities, resources
as well as the needs of the employee or worker.” As a consequence of stress, workers can suffer
injuries and poor health. A collective majority of the workers occasionally report experiencing
workplace stress, and that compromises their health and performance. While stress levels may
vary from workplace to another, it is imperative to underscore that some employees are
confronted with greater risks than the others. To this extent, therefore, it can be stated that work
stress is a potential killer.
Literature Review
Emotional and chronic psychosocial distress impacts the immune functions to a greater
extent. As a consequence, the alteration of the immune function increases the risk of contracting
diseases. Breen et al. (2016) argue that the recent estimates indicate that by 2030 the stress-
related pathologies will be the most widespread and debilitating health disorders. Chronic stress
has both adverse and protective effects on individuals. For instance, chronic stress can enhance
the expression and the acquisition of immunoprotection by activating the bodily defences before
infection or wounding (Breen et al., 2016). Alternatively, acute stress can induce

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immunopathology through the exacerbation of autoimmune inflammation, with cardiovascular
and respiratory consequences. One of the primary mechanisms through which acute
psychological stress induces an immune response is through the rapid changes in the distribution
of leukocyte in the peripheral circulation (Bosch et al., 2005). Some of the studies on acute short-
term stressors in humans have reported increases on natural killer cell numbers as well as other
leukocyte subtype cell numbers (Breen et al., 2016). Additionally, acute stress in humans causes
a reduction in the proliferation of lymphocyte and increased pro-inflammatory cytokine
production. Therefore, it can be determined that work-related stress can have negative
implications for the health of an individual, especially when the immune functions are altered.
It has also been established that work-related stress causes hypertension. In a study
conducted by Babu et al. (2014), cohort and case-control studies indicated that there was a
positive correlation between job strain and hypertension. In 2010 there were increased cases of
circulatory and cardiovascular disorders. Prevalence of hypertension has increased globally, and
it is projected that by 2025 about 500 million people will have hypertension (Babu et al., 2014).
Evidence suggests that hypertension reduction reduces the chances of contracting communicable
diseases. According to Babu et al. (2014), environmental, psychological, social and potential
biological contributors are likely to impact the pathogenesis of hypertension. Previous studies
have demonstrated that there is a correlation between job strain and coronary diseases
(Netterstrom, 2014). Job strain has significant consequences on the well-being of a person to the
extent that they create conditions that cause heart diseases, leading to hypertension. The study
conducted by Babu et al. (2014) indicate that both home and work-related stress have the
potential of causing hypertension.

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Work-related stress has also been associated with coronary heart disease. Chandola et al.
(2008) conducted a study in London among civil servants with the aim of understanding the
correlation between work stress and coronary heart disease. The study established that work-
related stress may be a significant determinant of coronary heart disease (CHD) among working-
age populations. Today, strain in the workplace is more related to an increased risk of heart
complications (Chandola et al., 2008). According to Chandola et al. (2008), work stress may
cause CHD through the direct activation of neuroendocrine responses to the stressors or
indirectly through unhealthy tendencies that may increase the risk of CHD. Some of the
unhealthy behaviours include smoking, excessive alcohol consumption and smoking.
Additionally, it has been established that work stress can cause dysregulation of the
hypothalamic pituitary adrenal axis that is associated with circadian rhythm disturbances and the
development of metabolic syndrome (Chandola et al., 2008). Further, accumulation of work
stress has been associated with higher risk of incident obesity and metabolic syndrome.
Therefore, cumulative work stress is considered a risk factor for coronary heart disease (CHD) as
well as neuroendocrine stress responses.
On the other hand, stress in the workplace also causes cardiovascular diseases. According
to Fishta and Backe (2015), psychosocial stress has been determined as one of the causes of
cardiovascular diseases (CVD). Similar to the findings by Chandola et al. (2008), Fishta and
Backe (2015) note that repeated and long-term stress predicts CV mortality and morbidity. Acute
or short-term stress might cause CV events, especially among individuals with advanced
atherosclerosis. Additionally, Fishta and Backe (2015) argue that long-term stress in the
workplace increases the risk of recurrent CHD and predicted CV mortality and morbidity. Many
studies continue to link work-related stress (short and long-term) with heart complications. A