efsa-opinion-chromium-food-drinking-water

Chromium in food and drinking water
149.8 ng/kg b.w. per day (maximum UB, infants). The 95 th percentile exposure ranged from
0.0 (minimum LB) to 148.7 ng/kg b.w. per day (maximum UB, ‘Toddlers’).
An additional contribution to the exposure to Cr(VI) was considered from the water used to prepare
certain foods (coffee, tea infusions, and infant dry and follow-on food mainly, but also some others
such as instant soup, evaporated and dried milk, and dehydrated fruit juice). A worst-case scenario,
with no reduction of the Cr(VI) present in water into Cr(III) when the foods are ingested immediately
after their preparation, was assumed. This scenario led to an increase up to two-fold in the exposure
levels to Cr(VI), in comparison to those estimated via the consumption of drinking water only.
The CONTAM Panel concluded that the exposure via the diet likely represents the most important
contribution to the overall exposure to Cr in the general population. Inhalation of Cr compounds
present in particular in cigarette smoke may contribute to the overall exposure levels but the currently
available information does not allow quantification of its relative contribution.
Cr(III) compounds present low oral toxicity because they are poorly absorbed. Cr(III) compounds
have the potential to react with DNA in acellular systems, however restricted cellular access limits or
prevents genotoxicity. The CONTAM Panel decided to use the data from the chronic toxicity studies
of the National Toxicology Programme (NTP) on chromium picolinate monohydrate to derive a
health-based guidance value (HBGV) for the risk characterization of Cr(III). In the two year NTP
chronic oral toxicity study in rats and mice, no carcinogenic or other adverse effects have been
observed. The lowest no-observed-adverse-effect level (NOAEL) value derived from these studies
amounted to 286 mg/kg b.w. per day in rats, which was the highest dose tested. Effects of Cr(III) on
reproduction and developmental toxicity have been reported in some studies with the lowest lowestobserved-adverse-effect
levels (LOAELs) in the order of 30 mg/kg b.w. per day, but the Panel noted
that these studies had methodological limitations. In addition, no effects have been reported on
reproductive organ weights, sperm parameters and oestrous cyclicity in subchronic dietary studies in
rats or mice at the highest doses tested (506 mg/kg b.w. per day and 1090 mg/kg b.w. per day,
respectively) (NTP studies). Taking these observations together, the Panel derived a Tolerable Daily
Intake (TDI) of 300 µg Cr(III)/kg b.w. per day from the relevant NOAEL in the long-term rat NTP
study of 286 mg/kg b.w. per day, applying a default uncertainty factor of 100 to account for species
differences and human variability and an additional uncertainty factor of 10 to account for the absence
of adequate data on reproductive and developmental toxicity.
Under the assumption that all chromium in food is Cr(III), the CONTAM Panel noted that the mean
dietary exposure levels across all age groups (minimum LB of 0.6 μg/kg b.w. per day and maximum
UB of 5.9 μg/kg b.w. per day) as well as the 95 th percentile exposure (minimum LB of
1.1 μg/kg b.w. per day and maximum UB of 9.0 μg/kg b.w. per day) are well below the TDI of
300 µg Cr(III)/ kg b.w. per day.
Regarding the vegetarian population, although based on limited consumption data, the dietary
exposure to Cr(III) seems to be similar to that estimated for the general population. Thus, also the
dietary exposure of vegeterians is well below the TDI of 300 µg Cr(III)/ kg b.w. per day.
A significant exposure to Cr(III) may occur via dietary supplement intake. Considering the exposure
via dietary supplement intake (13 g/kg b.w. per day and 22 g/kg b.w. per day, for typical and upper
intake from fortified foods, PARNUTS and food supplements, respectively, for an adult of 70 kg b.w.)
and the maximum estimated contribution coming from the diet for adults (95 th percentile of
2.6 µg/kg b.w. per day), the total exposure remains below the TDI of 300 µg Cr(III)/ kg b.w. per day.
After oral exposure, Cr(VI) has been shown to be carcinogenic in rats and mice of both sexes and
genotoxic in some in vivo studies. The data available so far support that the reduction of Cr(VI) to
Cr(III) along the gastrointestinal tract is efficient but it cannot be excluded that even at low dose levels
a small percentage of Cr(VI) escapes gastrointestinal reduction to Cr(III). Once taken up in the cells,
Cr(VI) is reduced to Cr(III) with formation of Cr-DNA adducts and production of oxidative stress (due
to formation of reactive intermediates). Both modes of action can contribute to the genotoxicity and
carcinogenicity of Cr(VI).
EFSA Journal 2014;12(3):3595 4