No abstract

Caramel color has been used in foods and beverages for over 150 years and is globally regulated as a color additive. The four distinct classes of caramel color (Plain Caramel, Sulfite Caramel, Ammonia Caramel, and Sulfite Ammonia Caramel) are well characterized and each have specifications that take into account processing variables including reactants that can give rise to low molecular weight constituents (e.g., 4-MeI and THI) that may have toxicological significance for evaluating safety. Extensive safety testing has been conducted with the different classes of caramel color and its constituents, including toxicokinetics, genotoxicity, subchronic toxicity, carcinogenicity, and reproductive/developmental toxicity studies. In addition, data is available on uses and use levels that have been used to estimate intakes of caramel colors and their constituents. No Observable Adverse Effect Levels (NOAEL) have been identified for all classes and Acceptable Daily Intakes have been established to ensure safety of use. Available studies support a conclusion that caramel colors are not genotoxic or carcinogenic, and exposure estimates indicate that intake of caramel colors and constituents do not pose undue safety risks. This update summarizes available relevant safety studies and authoritative reviews on caramel colors and its toxicologically important constituents, 4-MeI and THI.

Ozone is a potent oxidant gas and a common constituent of photochemical smog. This investigation evaluated the numbers and functional capabilities of alveolar macrophages (AM) recovered from rabbits undergoing acute and subchronic ozone exposure. Bronchoalveolar lavage was performed immediately, 24 h, and 7 d after acute (2-h) exposure to 0.1 or 1.2 ppm ozone, and on d 3, 7, and 14 during subchronic (2 h/d X 13 d) exposure to 0.1 ppm ozone. After acute exposure to 1.2 ppm, a marked increase in lavaged neutrophils was observed at 24 h. A single exposure to 0.1 ppm resulted in increased AM at 7 d, while repeated exposures resulted in an increase in AM and neutrophils on d 7 and 14. AM phagocytosis was depressed immediately and 24 h after acute exposure to 0.1 ppm, and at all time points after exposure to 1.2 ppm. Repeated exposures to 0.1 ppm produced reductions in the numbers of phagocytically active AM on d 3 and 7, with a return to control levels by d 14. Substrate attachment by AM was impaired immediately after exposure to 1.2 ppm; AM mobility was not altered by any of the ozone exposures. The results of these studies demonstrated significant alterations in the numbers and functional properties of AM as a result of single or repeated exposure to 0.1 ppm ozone, a level below the current National Ambient Air Quality Standard. These findings indicate that levels of ozone frequently encountered in areas of high photochemical air pollution can elicit a pulmonary inflammatory response and can impair pulmonary defense capabilities.