Arsenic in food.
There has been less concern, internationally or nationally, over the potential public health risks associated with residues of growth promoters in meat products, although the discovery of chloramphenicol in Asian shrimp in 2002 resulted in a requirement that all shrimp be tested before sale in the EU (Delegation of the European Commission to Thailand 2002). Arsenicals--arsanilic acid and roxarsone--are permitted for nontherapeutic uses as growth promoters in animal feeds in the United States [National Research Council (NRC) 1999]. Lasky et al. (2004) serve notice that we must re-evaluate this use of arsenicals not solely for environmental impacts (Jackson et al. 2003) but also for their role in human dietary exposures to arsenic. It is noteworthy that most studies of dietary sources of arsenic exposure do not examine flesh poultry or pork products (e.g., NRC 2000; Ryan et al. 2001).
However, in two respects, the conclusions drawn by Lasky et al. (2004) probably underestimate the true risks. First, as the authors carefully noted, they had to estimate the concentrations of arsenic in muscle using the only U.S. Department of Agriculture (USDA) data available, analyses of liver concentrations. It would be interesting to know why the USDA does not analyze arsenic in muscle, the tissue most commonly consumed by humans. [In 1981, Westing et al. (1981) reported higher levels of arsenic in edible muscle tissue from cattle given feeds containing poultry litter.] In the absence of real data, Lasky et al. used information from the drug manufacturer, Alpharma (Fort Lee, NJ), which supported an inference of a liver:muscle ratio of 2.9-11, depending on withdrawal time before slaughter. However, these assertions must be supported by data, particularly because broiler chickens are fed arsenicals throughout their lifespan. I was unable to find any article on the toxico-kinetics of arsenic in birds under controlled conditions; however, following the guidance of the World Health Organization/Food and Agrigulture Organization (WHO/FAO) Joint Expert Committee on Food Additives (JECFA) 2000], I examined recent studies on arsenic metabolism in mammals. Hughes et al. (2003) reported that the body burden of arsenic in mice under repeated-dose exposure was significantly higher than that under acute exposures; moreover, elimination of arsenic after repeated doses was significantly slower than after an acute dose. Under repeated doses, the ratio of liver to muscle arsenic changed dramatically over time, and at day 17, arsenic in muscle was higher than in liver. Thus, it is likely that the actual concentrations of arsenic in edible portions of broiler poultry are higher than the estimates of Lasky et al. (2004).
In addition, Lasky et al. (2004) referred to a 20-year-old assessment of the human health risks of ingesting arsenic (JECFA 1983). Much more recently, in a risk assessment of arsenic in drinking water, the NRC (2000, 2001) concluded that the excess cancer risks associated with dietary exposures are considerably greater than those previously assumed by the WHO and other authorities. In its analysis of cancer risks (NRC 2001), the committee concluded that exposure to 50 ppb arsenic in drinking water could be associated with excess cancer risks on the order of 1 in 100 (all cancers). Exposure to 1.38-5.24 [micro]g/kg/day As from chicken consumption, as estimated by Lasky et al. (2004), would be a significant addition to drinking-water exposure based on the NRC's recommended maximum contamination level (MCL) of 10 [micro]g/L (~ 3 L/day, or 30 [micro]g/day; for an adult weighing 70 kg, a daily exposure of 0.43 [micro]g/kg/day).
Surely it is time for the U.S. government and international organizations to reconsider the acceptability of arsenic use in food-animal production. Arsenic contributes to the rise in drug resistance among pathogens (Liu et al. 2001), and its use contaminates the land when animal wastes are used as fertilizers (Arai et al. 2003; Garbarino et al. 2003; Rutherford et al. 2003; Wing and Wolf 2000). Also, direct consumer exposures via food may well be a significant and preventable portion of overall exposures to this human carcinogen.
The author declares she has no competing financial interests.
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Ellen K. Silbergeld
Johns Hopkins University
Bloomberg School of Public Health
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|Author:||Silbergeld, Ellen K.|
|Publication:||Environmental Health Perspectives|
|Article Type:||Letter to the Editor|
|Date:||May 1, 2004|
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