Abstract
Context: This mini-review describes the toxic effects of vanadium pentoxide inhalation principally in the workplace and associated complications with breathing and respiration. Although there are some material safety data sheets available detailing the handling, hazards and toxicity of vanadium pentoxide, there are only two reviews listed in PubMed detailing its toxicity. Aim: To collate information on the consequences of occupational inhalation exposure of vanadium pentoxide on physiological function and wellbeing. Materials and Methods: The criteria used in the current mini-review for selecting articles were adopted from proposed criteria in The International Classification of Functioning, Disability and Health. Articles were classifi ed from an acute and chronic exposure and toxicity thrust. Results: The lungs are the principal route through which vanadium pentoxide enters the body. It can injure the lungs and bronchial airways possibly involving acute chemical pneumonotis, pulmonary edema and/or acute tracheobronchitis. It may adversely influence cardiac autonomic function. It stimulates the secretion of cytokines and chemokines by hepatocytes and disrupts mitochondria function. It disrupts the permeability of the epithelium and promotes access of inflammatory mediators to the underlying neuronal tissue causing injury and neuronal death. When renal brush border membrane vesicles are exposed to vanadium pentoxide, there is a time-dependent inhibition of citrate uptake and Na+K+ATPase in the membrane possibly contributing to nephrotoxicity. Exposure results in necrosis of spermatogonium, spermatocytes and Sertoli cells contributing to male infertility. Conclusion: Vanadium pentoxide certainly has adverse effects on the health and the well-being and measures need to be taken to prevent hazardous exposure of the like.
Extracts
This mini-review describes the toxic effects of vanadium pentoxide inhalation principally in the workplace and associated complications with breathing and respiration.[1] Vanadium is a by-product of oil-burning furnaces when vanadium pentoxide (MR 181.88) is deposited in the flues. It is an odorless gas.[2] Inhalation is the principal route of entry into the body and may result acutely in severe pneumonitis with associated mucus membrane irritation and gastrointestinal disturbances. Ambient vanadium pentoxide dust produces irritation of the eyes, nose and throat.[3] Over long periods, inhalation may potentiate chronic bronchitis, eczematous skin lesions, fine tremors of the extremities and greenish discoloration of the tongue.[1] As it has a rapid renal clearance, it may be monitored in urine specimens to determine exposure to vanadium pentoxide (American Conference of Governmental Industrial Hygienists, ACGIH and British Education Index, BEI) 50 ìg.g-1 creatinine for an end-ofshift, end-of-workweek sample.[1] Most absorbed vanadium is excreted in the urine within one day after a long-term moderate exposure to vanadium dust.[4] ... The workplace exposure limit for vanadium pentoxide is according to the Health and Safety Executive (HSE), 0.05 mg.m-3/8h.[1] MSDS[2] details airborne exposure limits of 0.5 mg.m-3 (ceiling) for vanadium respirable dust and 0.1 mg.m-3 (ceiling) for vanadium fumes. ...
Although there are some material safety data sheets available detailing the handling, hazards and toxicity of vanadium pentoxide,[2,24] there are only two reviews listed in PubMed detailing its toxicity.[25,26] The aim of this article therefore was to collate information on the consequences of occupational inhalation exposure of vanadium pentoxide on physiological function and wellbeing. An attempt to classify the like according to functionality of certain selected organ systems was decided. ...
Lungs: Vanadium pentoxide is regarded as a less soluble form of vanadium and is therefore eliminated from the lungs at a slow rate.[28] Inhalation of vanadium pentoxide can injure the lungs and bronchial airways,[2] possibly involving acute chemical pneumonotis, pulmonary edema and/or acute tracheobronchitis.[25] Symptoms include irritation and inflammation of the mucus membranes, nasal passages and pharynx.[2] Clinical complications include a persistent cough, shortness of breath, bronchiolar constriction, tightness of the chest and a pseudo-asthmatic inflammation.[2] In a study of 40 plant workers previously free of lung disease and exposed to vanadium pentoxide, 12 had bronchial hyper-reactivity and symptoms of asthma.[29] Vanadate acts directly on human bronchial smooth muscle promoting the release of Ca2+ from intracellular store via the production of inositol phosphate second messengers and inhibition of Ca2+-ATPase and causing spasms.[30] Occasionally pulmonary edema and/or pneumonia may result with fatal consequences.[2] First aid measures following inhalation include removing the patient into fresh air and applying artificial respiration if breathing has expired. Oxygen is needed if breathing is labored and it is essential to seek medical attention.[2] Vanadium pentoxide dust may be a potential mutagen via induced chromosomal aberrations in man[31] and hamsters.[32] ... There may be a pathological pattern within the lung which may be associated with the pattern and/or extent of vanadium deposition.[40] Its cumulative effect in lung tissue possibly contributes to the development lung cancer. ...
Circulatory system: Chronically, exposure to airborne metals including vanadium may result in alterations in cardiac autonomic function.[43] Vanadium induces thrombocytosis and may be associated with various thromboembolic diseases.[44] Acute studies of vanadium pentoxide inhalation on the heart in experimental animals revealed that there was myocardial vascular congestion was observed, with focal perivascular haemorrhages.[6] Studies in humans has revealed palpitation of the heart, high incidence of extrasystoles, changes in the blood picture (anemia, leukopenia, punctatebasophilia of the erythrocytes) and reduced levels of cholesterol in the blood.[45] Limited studies have suggested a positive correlation between vanadium inhalation in urban air and mortality from cardiac failure, despite an absence of lifestyle determination.[46]
Liver: Acutely, vanadium is a potent inhibitor of many enzymes, while it stimulates adenylate cyclase. It has been shown to inhibit cholesterol biosynthesis and lower plasma cholesterol levels. Vanadium can also directly influence glucose metabolism in vitro and may play a role in its regulation. Lipid peroxidation of rat liver microsomes and mitochondria was induced by sulphite and accelerated by the presence of vanadium compounds.[6] Severe acute exposure (tens of mg/m3) is responsible for systemic effects. Most frequent findings in animal experiments were in the liver, kidneys, gonads and the nervous, hematological and cardiovascular systems.[45] Chronically, histopathological changes observed in the liver following the higher level of inhalation exposure (27 ìg/m3 for 70 days) included central vein congestion with scattered small hemorrhages and granular degeneration of hepatocytes.[6] ...
CNS: Severe acute exposure to vanadium pentoxide has major patho-physioloogical manifestations on the nervous system.[6] Inhalation thereof produces a time-dependent loss of dendritic spines, necrotic-like cell death and considerable alterations of the hippocampus CA1 neurophile, all associated with spatial memory impairment.[51] Additionally, there is a decrease in the number of tyrosine hydroxylase immunreactive neurones in the substatia nigra pars compacta.[52] Within the ependymal epithelium, cilia loss, cell sloughing and cell layer detachment occur after vanadium pentoxide inhalation.[53] The damage results in disrupted permeability of the epithelium and promotes access of inflammatory mediators to the underlying neuronal tissue causing injury and neuronal death.[53] In humans, severe chronic exposure results in general symptomatology including nervous disturbances, neurasthenic or vegetative symptoms.[6]
Kidneys: Severe acute exposure (tens of mg/m3) is responsible for aberrations in renal function.[6] Vanadium concentrations of 25 μg/g dwt. in the kidneys are associated with mortality in ducks acutely exposed to sodium metavanadate.[47] Chronic exposure to increasing dietary concentrations of sodium metavanadate (38.5-2651 ppm) over 67 days resulted in vanadium accumulation in the kidneys of 13.6 μg/g dw.[47] It is unlikely though that such concentrations would have been achieved via inhalation. ...
Testicles: Chronic ingestion of vanadium may have significant consequences for infertility by damaging spermatogenesis. Studies in mice have demonstrated that inhalation of vanadium pentoxide results in necrosis of spermatogonium, spermatocytes and Sertoli cells.[58] Vanadium accumulates in the testes and attenuates the percentage of gammatubulin in all analysed testicular cells, suggesting changes in microtubules used in cell division.[59] Vanadium also induces DNA damage.[60] Leydig cells may not be affected by vanadium pentoxide as testosterone levels remain unchanged.[61]
Discussion
This mini-review has contributed to a brief synthesis of the literature which is currently rather scattered in nature into a compact format. Its main thrust was from both an acute and chronic exposure and toxicity angle. Vanadium pentoxide has adverse effects on health and well-being and measures need to be taken to prevent hazardous exposure of the like. Medical monitoring of workers exposed to the dust or fumes; workplace monitoring and measurement of ambient concentrations; dealing with contaminated attire and establishing personal hygienic procedures; dealing with emergency spills of dust; enforcing protocols for emergencies and hazardous waste management; and the use of inspected respiratory and personal protective equipment, are all essential in reducing toxic exposure.
Vanadium pentoxide exposure (acutely and chronically) in both experimental animal and human studies indicates a systemic patho-physiological and pathological influence on cell metabolism and tissue function. Therefore procedures need to be implemented in environments which potentially expose workers to vanadium pentoxide including influences on respiratory function and appropriate quality guidelines enforced. The lungs are likely to accumulate more vanadium particles than elsewhere particularly from polluted air. The lowest observed-adverse-effect level for acute exposure can be considered to be 60 μg vanadium per m3. Indeed, chronic exposure emanates as slight changes in the upper respiratory tract, with irritation, coughing and injection of pharynx, to more serious effects such as chronic bronchitis and pneumonitis. Persons suffering from lung problems including asthma and cystic fibrosis would need to ensure that they take adequate measures to prevent vanadium irritation of the mucosae. Obviously, however, a systemic assessment via renal and liver function tests needs to be completed in order to make an accurate clinical assessment of the influence of vanadium on body function and ultimately the efficient maintenance of homeostasis. More research is required to establish and add to the limited existing knowledge on the toxicokinetic and toxicological database on vanadium pentoxide. Indeed, there is limited understanding of the potential for dermal absorption and the potential long term effects as a result of sequestration in body tissues such as bone.
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