efsa-opinion-chromium-food-drinking-water

Human observations
Chromium in food and drinking water
No well-designed prospective human studies were identified for oral exposure to total
chromium, Cr(III) or Cr(VI).
The very limited information from few case studies was not suitable to assess human toxicity
after oral exposure to Cr(III) compounds.
At very high doses Cr(VI) after accidental or intentional intoxication exerted acute health
effects in the respiratory, haematological, hepatic and renal system and in the gastrointestinal
tract where acute effects include abdominal pain, vomiting, ulceration, haemorrhage,
necrosis, and bloody diarrhea.
Cr(VI) was classified by IARC as carcinogenic for humans with respect to the cancer of the
lung and also cancer of the nose and nasal sinuses based on evidence from occupational
studies. The data on oral exposure are limited and provide no convincing evidence of an
association with adverse health effects including cancer.
Available data were insufficient to assess developmental and reproductive toxicity and the
allergenic potential of Cr(VI) after oral exposure from food or water.
Biomonitoring
Biological monitoring of exposure to Cr(VI) compounds is a common practice in occupational
settings. In principle, an accurate assessment of systemic exposure to Cr(VI) escaping
reduction, can be obtained measuring chromium in red blood cells (RBC), since only Cr(VI)
is able to cross RBC membranes and is very slowly released from these cells.
No biomonitoring data are available on chromium concentrations in RBCs from the general
population.
Dose response assessment
The available human data did not provide information on dose-response relationships for
Cr(III) or Cr(VI) upon oral exposure.
For Cr(III) no dose-response modelling was possible for data in experimental animals since no
effects were observed even at the highest dose in the relevant studies.
For Cr(VI) dose-responses could be assessed for neoplastic effects and for non-neoplastic
lesions in male and female rats and mice, and for haematotoxic effects in male rats.
Dose-response data on squamous neoplastic lesions on the epithelium of the oral cavity in rats
and on epithelial cell neoplastic lesions in the small intestine in mice were suitable for
applying the BMD approach and calculating the BMDL 10 for neoplastic effects of Cr(VI).
Since there were no statistically significant differences between males and females, the
CONTAM Panel derived for the incidence of adenoma or carcinoma combined a BMDL 10 of
1.0 mg/kg b.w. per day and for the incidence of carcinoma only at all sites a BMDL 10 of
3.8 mg/kg b.w. per day.
From the dose-response data for effects in the liver, pancreas and small intestine in mice, the
CONTAM Panel identified incidences of chronic inflammation of the liver in female rats,
diffuse epithelial hyperplasia in the duodenum in male and female mice, and histiocytic
cellular infiltration in mesenteric lymph nodes in male and female mice as relevant nonneoplastic
endpoints suitable for applying the BMD approach.
When applying the BMD approach most dose response data did not allow identification of a
BMDL 10 value, since the BMD/BMDL ratios and the range of the acceptable BMDL values
were larger than one order of magnitude.
EFSA Journal 2014;12(3):3595 125