Ann. occup. Hyg., Vol. 46, No. 2, pp. 269-270, 2002
© 2002 British Occupational Hygiene Society
Published by Oxford University Press
Letters to the Editor |
Effect of Cr(VI) Exposure on Sperm Quality
The Edinburgh Centre for Toxicology 43 Mansionhouse Road Edinburgh EH9 2JD, UK
Received 30 October 2001;
I have a number of difficulties with Li et al. (2001), starting with its title ‘Effect of Cr(VI) exposure...’. The chemical species Cr(VI) does not exist as a free entity under normal conditions. Normally it is found in the form of the anion chromate associated with a cation. Hence, ‘Effect of chromate exposure...’ might have been a more accurate statement with regard to both the workers in the electroplating factory and the rats (but see below). Even then, the cation(s) present should have been stipulated as they may well determine how the body reacts to chromate, particularly at high exposures.
However, I can see no evidence that the workers studied were actually exposed to any form of chromate. It may be so, but no data are presented for exposure or exposure conditions. The presence of the element chromium in the blood does not establish exposure to chromate since the analytical methods used on the blood and semen samples do not permit determination of this chemical species, or indeed of any chemical speciation (Ebdon et al., 2001). Since no measurements of exposure are reported, there is no possibility of considering the effects of other substances to which these workers may have been exposed. Not even their smoking habits are reported. Nor is there any consideration of nutritional exposures or, indeed, of the nutritional status of the workers in the study. Both sperm quality and uptake of chromate (or other forms of chromium) must be dependent on the nutrition of those at risk. This is particularly important in animal experiments where rats are exposed by oral feeding.
The relevance of oral feeding of CrO3, chromic anhydride, must also be questioned. I hope that the workers were not exposed to chromic anhydride orally in the workplace. No description of possible exposure routes is given and so I suppose it may be a theoretical possibility. It should certainly not occur where there is good occupational hygiene practice. The most likely exposure of workers in an electroplating factory is by inhalation or skin exposure to a cation-bound chromate and so the relevance of the animal experiments is highly doubtful. The feedstuffs given to the rats and the feeding regime are not described. If the chromic anhydride were given without feedstuff dilution, it would immediately react with water to form chromic acid, which is corrosive. Either the rats would not touch it, or the mouth and oesophagus would be severely damaged. If it were given by gavage, it would damage the stomach directly. If it were given diluted in feedstuffs which contained significant amounts of anti-oxidants such as vitamins C and E, or -SH compounds such as glutathione, the Cr(VI) present in the chromic acid would quite readily be reduced to the Cr(III) form. No attempt seems to have been made to ascertain how far this may have happened. In the presence of high phosphate or sulfate, chromate will not be absorbed to any extent because of competition for carrier sites (Jennette, 1981; Martell, 1981). If the Cr(III) became bound to a fat-soluble organic compound, it might be absorbed quite readily. Thus, the resultant internal exposure would be to Cr(III) in some appropriate chemical species and not Cr(VI). Further, even if Cr(VI) species were absorbed, there is good evidence of the potential for reduction of Cr(VI) in compounds to Cr(III) by enzymes in human cells (Myers and Myers, 1998). This makes it imperative for the chemical speciation of chromium in both exposure media and in body fluids to be determined before jumping to the conclusion that exposure to a compound containing Cr(VI) necessarily results in significant levels of Cr(VI) anywhere in the body. At the very least, control experiments with chromic oxide (Cr2O3) should have been carried out.
Editorial note: The authors of the paper discussed were invited to reply, but decided not to do so.
REFERENCES
Ebdon L, Pitts L, Cornelis R, Crews H, Donard OFX, Quevauviller P. (2001) Trace Element Speciation for Environment, Food and Health. Cambridge: Royal Society of Chemistry. ISBN 0 85404 459 0.
Jennette KW. (1981) The role of metals in carcinogenesis: biochemistry and metabolism. Environ Health Perspect; 40: 233–52.[Web of Science][Medline]
Li H, Chen Q, Li S, Yao W, Li L, Shi X, Wang L, Castranova V, Vallyathen V, Ernst E, Chen C. (2001) Effect of Cr(VI) exposure on sperm quality: human and animal studies. Ann Occup Hyg; 45: 505–11
Martell AE. (1981) Chemistry of carcinogenic metals. Environ Health Perspect; 40: 207–26.[Medline]
Myers C, Myers JM. (1998) Iron stimulates the rate of reduction of hexavalent chromium by human microsomes. Carcinogenesis; 19: 1029–39.
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