**3.4 Irritation and chromium burn**

*Trace Metals in the Environment - New Approaches and Recent Advances*

cancer in human.

mammals including humans.

reduction of chromium(VI) by endogenous antioxidant to produce ROS and chromium(III), and alteration of DNA directly by chromium(VI) or indirectly by ROS [86]. The alteration of DNA then produces different types of products including Cr-DNA adducts, DNA–protein and DNA interstrand cross-links, DNA breaks, and DNA base damage [87]. Carcinogenicity of chromium(VI) has induced lung cancer in workers from various chromium-based industries [88–90] and has been associated to incidence of other cancers [91]. However, the meta-analysis study showed that the correlation between exposure of chromium(VI) and the high mortality in skin cancer is not significant [91]. This study indicated that there is no supporting data confirming the chromium species as carcinogen in inducing skin

Several studies, however, showed that chromium species could induce skin cancer in rats and mice either as single carcinogen or cocarcinogen. Oral administrations of drinking water containing sodium dichromate dehydrate to male F344/N rats for 2 years showed that the sample developed various types of skin cancer [92]. Two other studies using hairless SK1-hrBR mice also exhibited that chromium(VI) could act as cocarcinogen in promoting UV-induced skin tumor [93, 94]. Davidson and co-workers [93] showed that oral administration of chromium(VI)-containing drinking water and UV irradiation to hairless mice have synergistic effect in promoting skin tumor. Exposure of chromium(VI) or UV radiation alone did not induce skin tumors [93]. Uddin and co-worker also conducted the same experiment and found that systemic administration of exogenous antioxidant (vitamin E and selenomethionine) did not improve skin condition [94]. It indicated that chromium(VI) cocarcinogenicity may be occurred in different mechanisms without involving ROS [94]. These three studies indicate that acute or chronic oral administration of chromium(VI) species has a great potency in promoting skin cancer in

*Simplified mechanism of chromium carcinogenesis adapted from several references [86, 95].*

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**Figure 3.**

Irritation and chemical burn are caused by dermal exposure of chromium(VI) particle, solution, or mist in large quantities. Solid deposition of chromium(VI) would develop to "chromium ulcers" or "chrome holes" [67], while high concentration of chromium(VI) solution would lead to chromium burn. A mechanism for this ulcer formation is still unclear, but it may be related to the disruption of actin cytoskeleton by chromium(VI) leading to mitochondria-dependent apoptosis in skin fibroblasts cells [96]. Several reports exhibited these irritation and burning effects from different chromium species such as solid CrO3 [97], chromic acid solution [98–100], hot chromium(III) sulphate solution [101, 102], and chromium acid mist [103].

Management of irritation is conducted by considering preventive and treatment approaches. Prevention of irritation is conducted by using barrier creams, moisturizers, etc., while treatment could be done by using moisturizers and corticosteroids [50]. For chromium burn, treatment is conducted by combining mechanical excision, hemofiltration, and systemic administration of chelating agent and antioxidant [100].
