nated water.” Nitrate exposures were known for 214 cases, and all of them exceeded 50 mg/L; of the 214 cases, 81% occurred above 220 mg/L, 17% at 90-220 mg/L, and only 2% at 50-90 mg/L. The presence of nitrite, of bacteriologic contamination, and of gastrointestinal disease and methemoglobin concentrations were not reported.
In a similar survey in Germany, 745 cases of methemoglobinemia among infants were identified (Simon et al. 1964); data on exposure were available for 249 of the cases. Nitrate concentration in water exceeded 100 mg/L in 84%, was 50-100 mg/L in 12%, and was less than 50 mg/L in only 4%. The only three cases that occurred at concentrations below 20 mg/L were associated with nitrite and substantial dietary nitrate exposure as well. Of the 306 cases for which additional information was available, 98% occurred in infants aged 3 months old or younger, and 53% of the infants had diarrhea, an indicator of bacterial contamination and a factor associated with endogenous nitrate formation.
Dose-response relationships for nitrate exposure and methemoglobin concentrations have been reported in several studies of infants. For example, normal methemoglobin concentrations (less than 3%) were observed in infants fed water that contained nitrate at up to 50 mg/L, with mean methemoglobin concentrations increasing with nitrate intake up to 6.6% in those consuming over 100 mg/L (Würkert 1978; Toussaint and Würkert 1982). Similar dose-response relationships have not been observed in children or adults, in whom increasing nitrate exposure has little or no effect on methemoglobin concentration (Craun et al. 1981). In adults, methemoglobinemia has been reported only in cases of accidental ingestion of large amounts of nitrite. However, the concentration of methemoglobin that constitutes an adverse health effect has not been established definitively. Other factors, such as infantile diarrhea, can influence methemoglobin concentrations in the absence of increased concentrations of nitrate in food or water.