This review article seeks to provide an overview of allergic contact dermatitis (ACD) as a significant environmental and occupational skin disease, the phases of ACD, its causes from the occupational and environmental perspectives, its detection, the effects of ACD with respect to the social, psychological, occupational, and financial perspectives, and its cure and/or prevention. Human skin is very sensitive and as the largest organ in the body, it is highly prone to direct and indirect contact with the substances from its environment. The skin reacts to these substances (xenobiotics) differently depending on the individual’s tolerance level or threshold. Allergic contact dermatitis is a significant environmental and occupational skin disease that should not be ignored in our society because it can affect the quality of life of an affected individual. There are multiple causes of ACD, and these causes of ACD have been discussed from two perspectives: environmental and occupational. The effects of ACD can be psychological, social, financial, and occupational. There is need for more public enlightenment on the effects of ACD as well as a precise understanding that it is not a contagious disease so as to significantly reduce the psychological and social effects of ACD on these patients.
There are several xenobiotics (allergens) in the environment which may induce allergic contact dermatitis (ACD), an occupational and environmental health disease. This health disease is of global concern because it has no cure and can only be managed in affected individuals by preventing them from further exposure to these allergens. The following quinones (Q) are known to be air pollutants: 1,2‐naphthoquinone (1,2‐NQ), 1,4‐naphthoquinone (1,4‐NQ), 9,10‐phenanthraquinone (PQ), and 9,10‐anthraquinone (AQ). There have been studies on the cytotoxicity of these air pollutants, but no kinetic studies have been carried out on them to determine their chemical reactivity and, more especially, their interaction with model proteins so as to ascertain if they can react with skin proteins thereby causing allergic reactions. This article provides details on the kinetics studies carried out on the protein‐haptenation reactions of these quinones with 4‐nitrobenzenethiol (NBT), a model nucleophile, as well as the mechanisms of their reactions. The NBT−Q reactions were investigated under pseudo‐first‐order conditions at various concentration ratios at a temperature of 25 °C at three different pH values by either ultraviolet‐visible (UV‐Vis) or stopped‐flow spectrophotometry, as appropriate. The reaction rate constants obtained for the NBT−Q reactions were in the following order: at pH 7.42: 1,2‐NQ>1,4‐NQ>PQ>AQ while at pH 5.65, the order was observed to be 1,2‐NQ>1,4‐NQ>PQ>AQ and at pH 8.41, it was 1,4‐NQ>PQ>AQ>1,2‐NQ. These trends for the reaction rate constants of the Q at the three pH values can be attributed to inductive effects and the position of oxo‐groups on the phenyl rings. The NBT−Q reactions were further investigated by determining the effect of ionic strength on the reaction rate constants with potassium sulphate as the background electrolyte. Our findings showed that there are no charged species at the transition state of the NBT−Q reactions. The products of the NBT−Q reactions were isolated and characterized by means of UV‐Vis and FTIR spectrophotometry and NMR and TOF‐MS spectrometry. The deduced mechanisms for the NBT−Q reactions were validated by computer simulation with “Simkine3” software.
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