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U.S. Department of Health and Human Services

Database of Select Committee on GRAS Substances (SCOGS) Reviews

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Sulfur dioxide

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Report No.:  15
Type of Conclusion:  2
ID Code:  7446-09-5
Year:  1976
CFR Section:  182.3862
SCOGS Opinion:  Based upon chronic toxicity tests in animals, primarily in rats, the no observed adverse effect level of SO2 is estimated to be in the range of 30 to 100 mg of SO2 per kg of body weight per day. These values are considerably higher than the estimated average per capita consumption of about 0.2 mg of SO2 equivalent per kg body weight per day, and well above the estimates of up to 2 mg per kg body weight per day that some individuals may consume if they select foods and beverages relatively high in SO2 content. The margin of only about fifteenfold between the SO2 that may be ingested by high-intake consumers and the lowest estimated no observed adverse effect level is relatively narrow. However, consideration of the significance of this difference should recognize the difficulties in estimating with confidence the components which are the basis of the calculated margin. While the biological effects of sulfiting agents are still incompletely understood, certain conclusions are warranted. There is no reason to believe the direct, local, irritating effects of sulfite, seen in high-dose acute toxicity tests, constitute a hazard from ingestion of sulfiting agents as they are presently used in foods. Orally administered sulfite is very rapidly oxidized to sulfate in all species studied. The metabolic removal of sulfite appears to be the critical defense mechanism, and this points to the important role of the enzyme, sulfite oxidase. Congenital deficiency of hepatic sulfite oxidase has been described as a rare metabolic disorder in man. There is also paucity of data on the normal development of this enzyme with age in various species, and on the possible effects of dietary factors and disease on sulfite oxidase activity. Moreover, sulfite is capable of deaminating cytosine in vitro and inhibiting several enzymes requiring NAD or pyridoxal as cofactors which suggests that sulfite might be toxic in vivo if sulfite oxidase activity were sufficiently impaired or this metabolic mechanism were sufficiently overloaded, to prevent rapid oxidation of ingested sulfite to sulfate. Information in these respects would be helpful in assessing any special risk factors that may apply for select subpopulations. Destruction of thiamine can occur as a result of the sulfiting of foods but suffiecient thiamine is present in usual mixed diets, particularly because use of sulfiting agents is prohibited by regulation in foods known to be major sources of the vitamin. While there is no evidence that the sulfiting agents are teratogenic, there is evidence that directly added sulfite produces mutations in bacteria by alteration of nucleic acids. None of the available mammalian in vivo studies confirms these observations. Because the same organisms are not affected in the host-mediated assay, it seems reasonable to infer that rapid destruction of sulfite by the host's sulfite oxidase provides protection. In view of the foregoing, the Select Committee concludes that: There is no evidence in the available information on potassium bisulfite, potassium metabisulfite, sodium bisulfite, sodium metabisulfite, sodium sulfite, and sulfur dioxide that demonstrates, or suggests reasonable grounds to suspect, a hazard to the public when they are used at levels that are now current and in the manner now practiced. However, it is not possible to determine, without additional data, whether a significant increase in consumption would constitute a dietary hazard.