Two of the major causes of death worldwide are cardiovascular disease and Type II diabetes. Although death due to these diseases is assessed separately, the physiological process that is attributed to the development of cardiovascular disease can be linked to the development of Type II diabetes and the impact that this disease has on the cardiovascular system. Physiological, genetic, and personal factors contribute to the development of both these disorders. It has also been hypothesized that work-related stress may contribute to the development of Type II diabetes and cardiovascular disease. This review summarizes some of the studies examining the role of work-related stress on the development of these chronic disorders. Because women may be more susceptible to the physiological effects of work-related stress, the papers cited in this review focus on studies that examined the difference in responses of men or women to work-related stress or on studies that focused on the effects of stress on women alone. Based on the papers summarized, it is concluded that (1) work-related stress may directly contribute to the development of cardiovascular disease by inducing increases in blood pressure and changes in heart rate that have negative consequences on functioning of the cardiovascular system; (2) workers reporting increased levels of stress may display an increased risk of Type II diabetes because they adopt poor health habits (ie, increased level of smoking, inactivity etc), which in turn contribute to the development of cardiovascular problems; and (3) women in high demand and low-control occupations report an increased level of stress at work, and thus may be at a greater risk of negative health consequences.

Research regarding the risk of developing hand-arm vibration syndrome after exposure to impact vibration has produced conflicting results. This study used an established animal model of vibration-induced dysfunction to determine how exposure to impact vibration affects peripheral blood vessels and nerves. The tails of male rats were exposed to a single bout of impact vibration (15 min exposure, at a dominant frequency of 30 Hz and an unweighted acceleration of approximately 345 m/s(2)) generated by a riveting hammer. Responsiveness of the ventral tail artery to adrenoreceptor-mediated vasoconstriction and acetylcholine-mediated re-dilation was measured ex vivo. Ventral tail nerves and nerve endings in the skin were assessed using morphological and immunohistochemical techniques. Impact vibration did not alter vascular responsiveness to any factors or affect trunk nerves. However, 4 days following exposure there was an increase in protein-gene product (PGP) 9.5 staining around hair follicles. A single exposure to impact vibration, with the exposure characteristics described above, affects peripheral nerves but not blood vessels.

Welding generates complex metal aerosols, inhalation of which is linked to adverse health effects among welders. An important health concern of welding fume (WF) exposure is neurological dysfunction akin to Parkinson's disease (PD), thought to be mediated by manganese (Mn) in the fumes. Also, there is a proposition that welding might accelerate the onset of PD. Our recent findings link the presence of Mn in the WF with dopaminergic neurotoxicity seen in rats exposed to manual metal arc-hard surfacing (MMA-HS) or gas metal arc-mild steel (GMA-MS) fumes. To elucidate the molecular mechanisms further, we investigated the association of PD-linked (Park) genes and mitochondrial function in causing dopaminergic abnormality. Repeated instillations of the two fumes at doses that mimic approximately 1 to 5 yr of worker exposure resulted in selective brain accumulation of Mn. This accumulation caused impairment of mitochondrial function and loss of tyrosine hydroxylase (TH) protein, indicative of dopaminergic injury. A fascinating finding was the altered expression of Parkin (Park2), Uchl1 (Park5), and Dj1 (Park7) proteins in dopaminergic brain areas. A similar regimen of manganese chloride (MnCl2) also caused extensive loss of striatal TH, mitochondrial electron transport components, and Park proteins. As mutations in PARK genes have been linked to early-onset PD in humans, and because welding is implicated as a risk factor for parkinsonism, PARK genes might play a critical role in WF-mediated dopaminergic dysfunction. Whether these molecular alterations culminate in neurobehavioral and neuropathological deficits reminiscent of PD remains to be ascertained.