Para-dichlorobenzene toxicity - a review of potential neurotoxic manifestations

Abstract

Background: Para-dichlorobenzene (PDCB) is an active ingredient of mothballs, deodorizers and fumigants. Due to the easy availability of this chemical, there is a considerable risk for accidental or intentional toxic exposure. Recently, multiple cases of PDCB toxicity due to mothball ingestion were reported. PDCB toxicity can affect multiple organ systems including liver, kidneys, skin, lung and the central nervous system (CNS). CNS toxicity often results in leukoencephalopathy and heterogeneous neurological manifestations.

Objectives: The objective of this study was to illustrate the clinical presentation, imaging findings, diagnosis and management of PDCB toxicity.

Methods: We carried out a literature review of the pharmacological and toxicological properties of PDCB.

Conclusions: PDCB and other aromatic hydrocarbons are capable of CNS tissue damage and in promoting functional neurological decline. While very little is currently known about prevalence of PDCB addiction, it cannot be ruled out that its illicit use among young people is under-recognized. The number of cases of PDCB toxicity might also rise due to the increasing industrial and domestic use of this chemical.

Keywords: Paradichlorobenzene; aromatic hydrocarbons; demyelination; leukoencephalopathy; mothballs; neurotoxicity.

Figure 1.

Para-dichlorobenzene (PDCB) structure and metabolism. PDCB is metabolized in the liver by the cytochrome P450 system (CYP2E1, 2B1, 3A1 and 3A4) to 2,5-dichlorophenol, 2,5-dichlorohydroquinone, 2,5-dichlorophenylmethyl sulfide and 2,5-dichlorophenylmethyl sulfone.

Figure 2.

Pharmacodynamics properties of para-dichlorobenzene (PDCB) and potential therapeutic interventions in individuals who have clinical manifestations from prolonged exposure. Potential therapeutic options are listed grey text boxes. (A) In cases of acute PDCB toxicity, the amount of absorbed toxin can be reduced by using either charcoal or emetics (e.g. Ipecac) [Gervais et al. 2010]. (B) The rate of metabolism of PDCB by CYP 2E1 enzymes can potentially be increased by various enzyme inducers including acetaminophen, isoniazid and ethanol [Flockhart et al. 2007, Kim et al. 2007]. (C) Serum level of the PDCB may be reduced by hemodialysis [Daum et al. 1978]. (D) The phenomenon of coasting due to mobilization of fat stores of PDCB following cessation of oral ingestion can be regulated by prevention of starvation (adequate diet or tube feeds) and use of hormones preventing lipolysis in adipose tissue through administration of insulin [Herron et al. 2002; Schweigert et al. 2002]. (E) Extent of neuronal damage could be limited by preventing hyperthermia, hyper/hypoglycemia. (F) Renal excretion of PDCB following acute ingestion can be increased by preventing its deposition in adipose tissue by using intra venous fat emulsion agents, including propofol [Avila et al. 2006; Hernandez et al. 2010].