Triclocarban

Triclocarban is an antibacterial chemical once common in, but now phased out of, personal care products like soaps and lotions. It was originally developed for the medical field. Research suggests that it is similar in its mechanism to triclosan and can be effective in fighting infections by targeting the growth of bacteria such as Staphylococcus aureus. Additional research seeks to understand its potential for causing antibacterial resistance and its effects on organismal and environmental health. Triclocarban is an antibacterial chemical once common in, but now phased out of, personal care products like soaps and lotions. It was originally developed for the medical field. Research suggests that it is similar in its mechanism to triclosan and can be effective in fighting infections by targeting the growth of bacteria such as Staphylococcus aureus. Additional research seeks to understand its potential for causing antibacterial resistance and its effects on organismal and environmental health. Triclocarban was used as an antimicrobial and antifungal compound since the 1960s. It was commonly found in personal care products as an antimicrobial in soaps, lotions, deodorants, toothpaste, and plastic. As of 2005 about 80% of all antimicrobial bar soap sold in the United States contained triclocarban. In 2011 United States consumers were spending nearly 1 billion dollars annually on products containing triclocarban and triclosan. In December 2013, the Food and Drug Administration (FDA) required all companies to prove within the next year, that triclocarban is not harmful to consumers. Companies like Johnson & Johnson, Procter & Gamble, Colgate-Palmolive, and Avon began phasing out antibacterial ingredients due to health concerns. By 2016 usage of triclocarban in soaps had declined to 40%, and that September the FDA banned triclocarban, triclosan and 17 other common antibacterial chemicals by September 2017, for their failure to be proven safe, or more effective than plain soap and water. Triclocarban, 3-(4-chlorophenyl)-1-(3,4-dichlorophenyl)urea, is a white powder that is insoluble in water. While triclocarban has two chlorinated phenyl rings, it is structurally similar to carbanilide compounds often found in pesticides (such as diuron) and some drugs. Chlorination of ring structures is often associated with hydrophobicity, persistence in the environment, and bioaccumulation in fatty tissues of living organisms. For this reason, chlorine is also a common component of persistent organic pollutants. Triclocarban is incompatible with strong oxidizing reagents and strong bases, reaction with which could result in safety concerns such as explosion, toxicity, gas, and heat. There are two commercial routes used for the production of triclocarban, using the reaction of isocyanates with nucleophiles such as amines to form ureas: The purity specification in the draft USP monograph for triclocarban is: not less than 97.0% w/w. The purity of commercial production is greater, 98% w/w. Triclocarban is predominantly active against gram positive bacteria (bacteria with a thick peptidoglycan wall). The precise mechanism of action of triclocarban is unknown, but it is shown to be bacteriostatic, which prevents bacterial proliferation. Unlike other antibacterial compounds, triclocarban does not interfere with the membrane. As a result, it is hypothesized that triclocarban’s molecular mechanism resembles that of triclosan, which inhibits bacterial fatty acid synthesis. By mimicking the natural substrate of the enoyl-acyl-carrier protein reductase (ENR) enzyme, triclosan acts as a site-directed inhibitor and disrupts lipid, phospholipid, lipopolysaccharide and lipoprotein synthesis. ENR is a highly conserved enzyme of lipid biosynthetic pathways in both Gram-negative and Gram-positive bacteria and mycobacterial species and is absent in humans. The specific mechanism of action for triclocarban's health effects on humans, like in bacteria, is unclear. Generally, triclocarban enhances the gene expression of other steroid hormones, including androgens, estrogens, and cortisol. It is hypothesized that the compound acts similar to cofactors or coactivators that modulate the activity of estrogen receptors and androgen receptors. Experiments show that triclocarban activates constitutive androstane receptor and estrogen receptor alpha both in vivo and in vitro and might have the potential to alter normal physiological homeostasis. Activation of these receptors amplifies gene expression and, in doing so, may be the mechanistic base of triclocarban's health impact on humans. However, further investigation is needed to determine whether triclocarban increases the activity of sex steroid hormones by binding to the receptors or by binding to and sensitizing the receptor coactivators.