Superfund Research Program
Investigating the Human Health Effects of Vanadium -- Recent Studies Show Significant Acute Respiratory Effects in Occupationally-Exposed Workers, Even at Permissible Exposure Limits
Found on about one-quarter of the country's Superfund sites, vanadium is a transition metal that has been an important hardening agent in steels and other alloys since the early 1900s. Its use in pigments and dyes, and as a chemical catalyst dates back to the 1860s. The industrial importance of vanadium has contributed to contamination at several types of Superfund sites including mines where vanadium ores were extracted, mills and metallurgical operations where these ores were processed and refined, and manufacturing plants where vanadium compounds were produced.
Vanadium is also a major contaminant of the oil burned to produce electric power. One result of building high-efficiency boilers in the last 20 years is that fuel oil is continuously re-burned until the remaining ash is primarily comprised of metals and sulfates. The vanadium content of this ash, which collects on the walls and at the bottom of the boiler, can be as high as 45%, most of which is oxidized. Vanadium oxides are water soluble and therefore readily inhaled into the lungs, where they are absorbed into the bloodstream and eventually excreted by the kidneys. This is noteworthy because respiratory exposure to high-vanadium-content dusts often occurs in boilermakers, the workers who clean and repair fuel oil boilers.
In the respiratory system, vanadium has been shown to have a variety of adverse health effects. Early studies of boilermakers found elevated rates of cough, wheeze, rhinitis, and nasal irritation in workers. Similar effects have been observed in workers exposed to the metal in vanadium manufacturing and processing plants. The early studies of boilermakers also noted that several workers had developed green tongues, a classic sign of vanadium exposure.
Later studies of boilermakers in the early 1980s confirmed these findings and also found that lung function was acutely impaired in workers during the repair and cleaning of boilers (usually referred to as an overhaul). These changes were sometimes accompanied by severe acute conditions, such as a condition resembling acute bronchial asthma. Improvements in working conditions and protective gear have significantly reduced exposure to fuel oil ash in boiler repair jobs. However, one important finding of the later studies was that many of the adverse respiratory effects experienced by the boilermakers occurred at relatively low levels of vanadium exposure, sometimes at levels below the permissible exposure limit.
The respiratory and systemic effects of low vanadium exposures are still poorly characterized. Moreover, little is known about the possible long-term effects of repeated exposures to this transition metal.
Since the early 1990s, a team of researchers at the Harvard School of Public Health has been studying the health effects of low-level vanadium exposure in boilermakers. The scientists have been testing the hypotheses that exposure to relatively low levels of airborne vanadium compounds causes bronchial hyperreactivity and asthmatic bronchitis via an inflammatory mechanism, and that upper airway (nasal) responses due to vanadium are well-correlated with the lower airway (bronchial) responses. This work includes ongoing studies of boilermakers that combine analyses of inflammation in the upper airway with an assessment of lung or lower airway function. The researchers have also begun to explore the possible effects of vanadium and particulate matter on cardiac function.
In support of these goals, the scientists have been developing and applying sensitive biomarkers of vanadium exposure and early response. One biomarker technique that has been successfully developed and used is the measurement of biological markers of acute inflammation in the upper airway. The markers are collected via nasal lavage, a technique in which a small amount of sterile saline is put into the nasal cavity and allowed to remain for 10 seconds. The resulting fluid includes samples of the cell population in the upper airway, which can then be analyzed for specific cell types and inflammatory molecules.
In an early study using this technique, the scientists found a significant increase in polymorphonuclear leukocytes (PMNs) in non-smoking boilermakers after only three days of boiler work. PMNs are among the first cells to appear at a site of cellular or tissue injury in the body. Their presence signifies the early stages of inflammation.
The nasal lavage technique was used again in a recent collaborative study with colleagues at the National Institute of Occupational Safety and Health and Allegheny Health Sciences University. Lavages were performed in a group of boilermakers before, during and after the overhaul of a large oil-fired boiler. Two molecular markers of inflammation were measured: the cytokine interleukin-8 (IL-8) and the enzyme myeloperoxidase (MPO). IL-8 is a protein messenger that is known to play a key role in acute inflammatory processes. Released by cells of the immune system, it is responsible for the recruitment of PMNs to sites of inflammation. MPO, which is part of the defense system of PMNs, catalyzes the production of hypochlorous acid, a powerful oxidant that breaks down injured tissues in response to inflammatory conditions.
During boiler work, there was a significant increase in IL-8 and MPO, which are reliable indicators of an active inflammatory process. At two weeks post-exposure, the levels of these markers had declined almost to baseline. These findings suggest that exposure to fuel oil ash results in acute upper airway inflammation and that this inflammatory process may be mediated by IL-8 and the recruitment and activation of PMNs.
Another study measured the lung function of a group of boilermakers exposed to fuel oil ash during two separate overhauls. During the first overhaul, the researchers observed a significant decline in lung function, especially forced expiratory volume and maximum mid-expiratory flow. This is noteworthy in that these acute decrements occurred even though workers were exposed to levels of vanadium and PM10 (particulate matter less than 10 microns) substantially lower than what was observed in studies carried out between 1950 and the early 1980s.
During the second overhaul, exposure levels were lower and of a shorter duration than what were observed in the previous overhaul. Although the lung function of the workers was not affected in this latter study, the scientists noted significantly increased upper and lower airway symptoms including rhinitis, wheezing, cough, throat irritation and sputum production. This is consistent with the IL-8 and MPO findings and suggests that boilermakers can experience acute airway inflammation and symptoms without necessarily exhibiting any significant changes in lung function.
The researchers are currently following this group of boilermakers to assess the possible long-term effects of repeated exposure to vanadium, including the risk of developing chronic respiratory conditions and the possible effects on cardiac function. Preliminary results from a cardiac evaluation of boilermakers suggest that exposure to ash particulates may affect heart rate and rhythm.
The findings of these studies demonstrate that vanadium is a respiratory irritant capable of causing significant airway symptoms that are accompanied by an influx of inflammatory molecules. Even at levels encountered in the workplace today, vanadium, and the fuel-oil ash with which it is associated, is correlated with acute declines in lung function. The possibility that cardiac function may also be affected by this metal must be considered. Given the ubiquity of oil-fired burners in the United States and the presence of vanadium on many hazardous waste sites, the potential for above-average exposure exists in both occupational groups and the general public. The results provided in these studies will aid in a more accurate evaluation of the risks that vanadium poses to humans, which is crucial to establishing appropriate environmental and occupational standards for this metal.
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To learn more about this research, please refer to the following sources:
- Woodin MA, Hauser R, Liu Y, Smith TJ, Siegel PD, Lewis DM, Tollerud DJ, Christiani DC. 1998. Molecular markers of acute upper airway inflammation in workers exposed to fuel-oil ash. Am J Respir Crit Care Med 158:182-187. PMID:9655727
- Meng ZH, Costa DL, Hauser R, Christiani DC. 1997. Lung injury, leachable metals, and oxidation potential of fly ash. Am J Respir Crit Care Med 155:A244.
- Woodin MA, Hauser R, Liu Y, Smith TJ, Christiani DC. 1997. Respiratory symptom incidence in workers overhauling an oil-fired boiler. Am J Respir Crit Care Med 155:A811.
- Hauser R, Daskalakis C, Christiani DC. 1996. A regression approach to the analysis of serial peak-flow among fuel-oil ash-exposed workers. Am J Respir Crit Care Med 154:968-974. PMID:8887594
- Hauser R, Godleski J, Hatch V, Christiani DC. 1996. Ultrafine particles in human lung macrophages and their relationship with lung function. Am J Respir Crit Care Med 153:A544.
- Woodin MA, Hauser R, Siegel RD, Tollerud DJ, Lewis DM, Liu Y, Smith TJ, Christiani DC. 1996. Nasal lavage inflammatory mediators as biomarkers of upper airway exposure to fuel oil ash. Am J Respir Crit Care Med 153:A475.
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