The Journal of Biological Physics and Chemistry

2014

 

Volume 14, Number 3, pp. 34–53

 

 

 

Autoantibody markers of neural degeneration are associated with post-mortem histopathological alterations of a neurologically injured pilot

M.B. Abou-Donia,1 F.R.W. van de Goot2 and M.F.A. Mulder3

1 Duke University Medical Center, Durham, North Carolina 27710, USA
2 Symbiant BV, Wilhelminalaan 12, 1815 JD Alkmaar, The Netherlands
3 Aviation Medical Consult, Karbouwstraat 14, 1402 VC Bussum, The Netherlands

There are numerous concerns regarding the neurotoxicity of contaminated air inside pressurized aircraft. Neurological symptoms have been seen in many aircrew members who have reportedly been exposed to the breathable, yet potentially toxic, air in airliners. Symptoms allegedly contracted by aircrew and passengers are thought to be caused by a single large exposure or repetitive cumulative low-level exposures to toxic chemicals in the airliner internal air. Genetic variation plays a rôle. We report here the case of a 43-year old airline pilot who presented with neurological deficits and other symptoms. The pilot died without regaining good health. In vivo blood had been collected ante mortem. Analysis of the serum confirmed grossly elevated levels of serum autoantibody biomarkers for neuronal cell degeneration compared with a control group. At autopsy, various tissues underwent histopathological assessment. Brain and spinal tissues exhibited axonal degeneration and demyelination. Peripheral nerves showed T-lymphocyte infiltration and demyelination. T-lymphocytes had infiltrated the heart muscle tissue. The post-mortem tests and pathological examination of the nervous system confirmed the autoantibody biomarker results. Differential diagnosis showed that the work environment, clinical condition, histopathology and serum biomarkers for nervous system injury are consistent with organophosphate-induced neurotoxicity. The results also indicated that the inferred exposure to organophosphates sensitized the nervous system and heart tissue towards further injury.

Keywords: neural degeneration, lymphocytic myocarditis, pain

 

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