In this population-based study, we found that occupational vanadium exposure appears to be associated with increased HDL-C and apoA-I levels and decreased atherogenic indexes (TC/HDL-C, LDL-C/HDL-C and apoB/apoA-I). Furthermore, among male workers, exposure to vanadium was found to be significantly negatively associated with low HDL-C level and abnormal atherogenic index and this association cannot be attributed to confounding factors such as age, or unhealthy lifestyle (alcohol and tobacco consumption). This suggests vanadium may have beneficial effects on blood levels of HDL-C and apoA-I, which in a long term may reduce the risk of atherosclerosis.
Previous studies have demonstrated that a low plasma HDL-C concentration is a well-established risk factor for atherosclerosis and subsequent coronary heart disease, and several studies have reported higher concentrations of HDL-C in women compared to men [19–23]. According to our study, higher levels of HDL-C could be observed in the vanadium exposed group compared with the control group. What’s more interesting is when we stratified the study groups by gender, we found that compared with the control group, the exposed group had a much higher level of HDL-C in male workers, while in females, the levels showed no difference. A negative association still existed between vanadium exposure and low HDL-C level, independent of age, smoking and drinking. It seems that vanadium has a pronounced effect on male workers. Despite the well-documented gender difference and other identified metabolic factors responsible for the difference in HDL-C and apoA-I concentrations [20, 21], it remains to be elucidated whether it is because of susceptibility of the men. ApoA-I is the primary protein component of HDL and is a direct protect factor against atherosclerosis independent of HDL-C . ApoA-I facilitates selective uptake of HDL cholesterol by the liver by activating lecithin-cholesterol acyltransferase  and acting as a specific ligand for SR-BI . In our study, we found higher apoA-I level and smaller HDL-C/apoA-I in the vanadium exposure group. This suggests vanadium may mainly increase apoA-I by increasing the synthesis or by inhibiting its catabolism and accordingly increase the apoA-I-rich HDL-C level. But the mechanisms about how vanadium influences the HDL-C, apoA-I and HDL-C/apoA-I need more researches.
Furthermore, since lipid is a well-established risk factor for cardiovascular diseases and diabetes, the relationship between lipid, lipoprotein profiles and vanadium may provide another explanation for the effect of vanadium treatment on cardiovascular function in the hyperinsulinemic, insulin-resistant conditions. High values of atherogenic indexes (TC/HDL-C, LDL-C/HDL-C and apoB/apoA-I) have been reported to be risk factors for cardiovascular disease that led to insulin resistant [27–31]. According to our study, atherogenic indexes values were lower in vanadium exposure group than in control group, which may be one possible mechanism of its insulino-mimetic and anti-diabetic effects. Among male workers, a significantly negative association existed between occupational vanadium exposure and abnormal atherogenic index after adjusting for age, smoking and drinking. Whether it is because of longer services or the susceptibility of men remains to be elucidated.
The question as to how exactly vanadium causes lipid and lipoprotein alterations remains elusive. Vanadate is reported to decrease plasma cholesterol and inhibit cholesterol biosynthesis and this effect is ascribed to a possible inhibition of oxidase , which may be important in mediating lipid effects induced by vanadium. Biomedical importance of vanadium confirmed by numerous studies is mostly based on its interaction with proteins, including enzymatic systems and cellar constituents [32–34], which may influence the lipid and lipoprotein synthesis or interfere with catabolism. Also, the stimulation of lipoprotein lipase activity by vanadate and stimulation of 2,3-diphosphoglycerate hydrolysis by vanadium may play a role as well [35, 36].
This study finds that occupational exposure to vanadium in a low-dose, long-term exposure condition is associated with lipid and lipoprotein profiles alterations. One limitation of this study is that we did not have personal exposure measurements, which disabled us from further exploration of the relationship between lipids, lipoprotein levels and vanadium. In addition to occupational exposure measurements, biomarkers such as vanadium concentration in whole blood, serum, plasma or urine samples would be more accurate and convincing in terms of dose-response effects. Although it could be adjusted using statistical methods, higher prevalence of smoking and drinking in the exposed group could also be confounding variables. Lack of information on other factors known to influence lipid and lipoprotein levels such as levels of exercise and body mass index (BMI) may have an impact on the strength of the association. Also, because of the cross-sectional and observational nature of our study, results of this study should not be taken as evidence of a causal relationship. Future studies, preferably prospective cohort designs, are needed to clarify whether or not vanadium exposure leads to lipid and lipoprotein profiles changes, whether this effect is pronounced in certain subgroups such as the male workers and whether the association is dose-dependent. However, this study provides the initial epidemiological exploration demonstrating the association between vanadium exposure and altered lipid and lipoprotein profiles. The data may be of value for environmental exposure assessment of vanadium function.