Attempts to assess psychological stress rely heavily upon subjective techniques which measure changes in perceived mental loading and situational awareness (Hart and Staveland 1988, Reid and Nygren 1988, Lemyre and Tessier 2003, 1998). Although quantitative methodologies do exist, for example monitoring changes in the cardiopulmonary system (Gelfand et al. 2004, Harada et al. 2006), such parameters are subject to influence by factors other than stress. Psychological stress is known to influence the effectiveness of the innate immune system, leading to an increased risk of infection and immune-related disease (Dhabhar et al. 1996, Boscarino et al. 1999, Altemus et al. 2006). Leukocytes, primarily neutrophils have been identified as an essential component of this mechanism - periods of increased psychological stress have been shown to stimulate neutrophils to release reactive oxygen species into surrounding healthy tissues (Mian et al. 2003). The exact biochemical pathways by which this occurs have not yet been fully elucidated. However, this mechanism has become the basis for a novel in vitro technique (McLaren et al. 2003) which has the potential and sensitivity to rapidly quantify and discriminate between changes in psychological stress, resulting from exposure to short-term low-level everyday life-stressors. Aims The overall aim of this research was to further explore the relationship between short-term psychological stress and altered immune responsiveness. Leukocyte coping capacity (LCC) is a luminol-dependent chemiluminescent technique for the assay of reactive oxygen species production in whole blood samples. The feasibility of applying this test as an objective, quantitative, diagnostic measure of altered mental workload (mental stress), in the assessment of ergonomics within automotive research and development was examined. Methods Leukocyte activity was determined from whole blood, using a luminol-dependent, in vitro, chemiluminescent technique referred to as Leukocyte Coping Capacity (LCC). 2 The technique measures reactive oxygen species production following phorbol 12-myristate 13-acetate (PMA) stimulation. Subjective psychological measures, including likert scales and the NASA task load index were employed to assess perceived stress and altered mental workload. Other traditional physiological parameters including heart rate, systolic and diastolic blood pressure and core body temperature were also measured. The ability of each parameter to detect and discriminate between related short-term stressors was investigated, and results were correlated with post-test changes in leukocyte activity. To investigate the mechanism of stress induced leukocyte activation, standard ELISA was used to assess post-stressor plasma concentration changes in nine mediators including Adrenaline, Noradrenaline, Cortisol, E-Selectin, L-Selectin, Interleukin-1β, Interleukin-6, Endothelin-1, and Tumour Necrosis Factor-α. All 5 studies involved the use of mental stressors that were associated with either driving or the ergonomics of driving. Participants were moderately fit and healthy, aged between 20 and 65 years. Study one assessed the ability of the LCC technique to objectively discriminate between two closely related stressors (performing a simple manoeuvre in two different vehicles). Study two investigated leukocyte sensitivity, by testing whether a quantifiable response was elicited following exposure to a low-level stressor lasting seconds. The third study was used to explore the mechanism of leukocyte activation following short-term low-level stress. In addition to testing the viability of leukocyte responsiveness as an objective quantitative ergonomic assay for use within the motor industry, study four investigated how the magnitude of leukocyte responsiveness changed following repeated exposure to the same stressor. The final study used leukocyte reactivity to investigate how mental loading was affected during the interaction with three different motor vehicle control interfaces, whilst simultaneously maintaining lane discipline within a simulated driving environment.

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