UOP to expand adsorbents and catalysts production at its Mobile plant

Abstract

Listen

Translate article

The primary health effect of ingested nitrate in drinking water at higher than 45 ppm, the current drinking water standard, is methemoglobinemia in infants after nitrate conversion to nitrite in vivo. This results in reduced oxygen transport by hemoglobin to tissues in the body, producing symptoms of oxygen deficiency. Bacterial contamination of water, gastrointestinal infection (leading to nitrate and nitrite synthesis), and inflammation, which could produce nitric oxide are contributing factors. Ascorbic acid has been shown to have a protective effect. Active secretion of nitrate in saliva and nitrate to nitrite conversion occur in humans and some laboratory species but not in rats. When the water standard is not exceeded, food is the major source of nitrate exposure. Epidemiological studies are suggestive but not conclusive of an association between elevated nitrate levels in drinking water and reproductive effects, birth defects, thyroid effects, and childhood diabetes mellitus. Animal studies with nitrate showed it to be goitrogenic and negative for carcinogenicity. However, most reproductive/development animal studies have been conducted on nitrite, not nitrate, since it is capable of inducing methemoglobinemia in animal studies. For nitrate alone, there is no evidence of carcinogenicity from food or drinking water. Combined animal and human data suggest an increased carcinogenic risk associated with ingested nitrate under conditions that result in endogenous nitrosation.