ABSTRACT
Type 3 diabetes (T3D) accurately reflects that dementia, e.g., Alzheimer's disease, represents insulin resistance and neurodegeneration in the brain. Similar retinal microvascular changes were observed in Alzheimer's and chronic stressed individuals. Hence, we aimed to show that chronic stress relates to T3D dementia signs and retinopathy, ultimately comprising a Stress syndrome prototype reflecting risk for T3D and stroke. A chronic stress and stroke risk phenotype (Stressed) score, independent of age, race or gender, was applied to stratify participants (N = 264; aged 44 ± 9 years) into high stress risk (Stressed, N = 159) and low stress risk (non-Stressed, N = 105) groups. We determined insulin resistance using the homeostatic model assessment (HOMA-IR), which is interchangeable with T3D, and dementia risk markers (cognitive executive functioning (cognitiveexe-func); telomere length; waist circumference (WC), neuronal glia injury; neuron-specific enolase/NSE, S100B). Retinopathy was determined in the mydriatic eye. The Stressed group had greater incidence of HOMA-IR in the upper quartile (≥5), larger WC, poorer cognitiveexe-func control, shorter telomeres, consistently raised neuronal glia injury, fewer retinal arteries, narrower arteries, wider veins and a larger optic cup/disc ratio (C/D) compared to the non-Stressed group. Furthermore, of the stroke risk markers, arterial narrowing was related to glaucoma risk with a greater C/D, whilst retinal vein widening was related to HOMA-IR, poor cognitiveexe-func control and neuronal glia injury (Adjusted R2 0.30; p ≤ 0.05). These associations were not evident in the non-Stressed group. Logistic regression associations between the Stressed phenotype and four dementia risk markers (cognitiveexe-func, telomere length, NSE and WC) comprised a Stress syndrome prototype (area under the curve 0.80; sensitivity/specificity 85%/58%; p ≤ 0.001). The Stress syndrome prototype reflected risk for HOMA-IR (odds ratio (OR) 7.72) and retinal glia ischemia (OR 1.27) and vein widening (OR 1.03). The Stressed phenotype was associated with neuronal glia injury and retinal ischemia, potentiating glaucoma risk. The detrimental effect of chronic stress exemplified a Stress syndrome prototype reflecting risk for type 3 diabetes, neurodegeneration and ischemic stroke.
ABSTRACT
OBJECTIVES: The objectives of this study were to assess dermal exposure of cell workers to nickel at a South African base metal refinery and to characterize their skin condition by measuring the skin hydration and trans epidermal water loss (TEWL) indices. METHODS: The skin hydration index of the index finger, palm, neck, and forehead was measured before, during and at the end of the shift. The TEWL index was measured before and at the end of the shift. Dermal exposure samples were collected with Ghostwipes from the index finger and palm of the dominant hand, before, during, and at the end of the shift. Neck and forehead samples were collected before and at the end of the shift. Wipe samples of various surfaces in the workplace were also collected. Wipes were analyzed for nickel according to NIOSH method 9102, using inductively coupled plasma-atomic emission spectrometry. RESULTS: Hydration indices measured on the hands decreased significantly during the shift, but recovered to normal levels by the end of the shift. TEWL indices for the index finger and palm of the hands are indicative of a low barrier function even before commencement of the shift, which further deteriorated significantly during the shift. During the shift, substantial nickel skin loading occurred on the index finger and palm of the hand. Levels on the neck and forehead were much lower. Various workplace surfaces, which workers come into contact with, were also contaminated with nickel. CONCLUSIONS: The skin condition and high levels of nickel on the skin were most probably caused by inadequate chemical protection provided by protective gloves. Although, the permeability of nickel through intact skin is considered to be low, a decreased barrier function of dehydrated or slightly damaged skin will increase its permeability for nickel. The ethnicity of these exposed workers may contribute significantly toward the low incidence of allergic contact dermatitis observed. Several measures to lower dermal exposure to nickel are also recommended.
