efsa-opinion-chromium-food-drinking-water

Chromium in food and drinking water
chromium in humans which, in some studies, could be related specifically to Cr(III) or Cr(VI)
exposure.
Increased chromium (unspecified) concentrations in biological fluids may occur as a consequence of
malfunctioning metal-on-metal prostheses of the hip and the knee. Early reports have been reviewed
by Sunderman et al. (1989), but the problem became a public health issue only over the last ten
years, after the publication of several case reports of severe poisoning in patients with hip implants
based on Cobalt-Chromium ( sometimes Chromium-Molybdenum) alloys (Delaunay et al., 2010;
Sampson and Hart, 2012). After lumbar disc arthroplasty median serum Cr levels before operation or
3, 6, 12, 24, and 36-months post-operation were found as 0.06, 0.49, 0.65, 0.43, 0.52, and 0.50 ng/mL,
respectively (Gornet et al., 2013).
7.3.1. Observations in humans related to Cr(III)
Only very limited information from few case studies was not suitable to assess human toxicity after
oral exposure to Cr(III) compounds.
Few occupational exposure studies and case reports indicate that respiratory effects can occur from
exposure to Cr(III). Workers exposed to high concentrations of chromium trioxide in a chrome plating
plant experienced nausea and vomiting and symptoms of dyspnea, dizziness, headache, and weakness
(Lieberman, 1941). Anemia and liver damage was reported following swallowing of plating fluid
containing Cr trioxide (Fristedt et al., 1965). Musculoskeletal and renal effects were observed in two
cases of ingestion of Cr(III) picolinate equivalent to 2.2 μg of Cr(III)/kg b.w. over a 48-hour period
(Martin and Fuller, 1998) and 1.1 μg Cr(III)/kg b.w. per day for 6 weeks (Wasser et al., 1997).
The interpretation of studies on Cr(III) in humans is complicated by the proposed beneficial effects of
dietary supplements containing high levels of Cr(III), e.g. up to 0.1 - 0.2 mg Cr(III) picolinate/ kg b.w.
per day (EFSA ANS Panel, 2010a).
Cr(III) can induce allergic sensitisation in humans after dermal exposure as observed in a few small
studies (Fregert and Rorsman, 1964, Estlander et al., 2000, Iyer et al., 2002, Chou et al., 2008). The
ATSDR, however, noted that it is unclear if individuals were sensitized to both Cr(VI) and Cr(III) or if
cross-sensitivity occurs between Cr(VI) and Cr(III) since positive responses were also observed after
challenge with Cr(VI) compounds (ATSDR, 2012). Furthermore, co-exposure to other more
significant sources of daily contact, including nickel and cobalt,time of exposure and other factors
such as humidity and pH may play a role when assessing the risk of induction and elicitation of an
allergic response (Basketter et al., 1993).
Khan et al. (2012) conducted a cross-sectional study on 100 Cr(III) -exposed persons living near
tanning industry at Jajmau, Kanpur (India) and 100 unexposed persons living away from tanning
industry (reported an increased prevalence of dermal effects, pulmonary tuberculosis, diabetes, asthma
and bronchitis and gastrointestinal effects) in the exposed group. Although the authors adjusted for
confounding, some confounding cannot be excluded since there were statistically significant
differences (p