Hydroquinone and its analogues in dermatology – a potential health risk

  title={Hydroquinone and its analogues in dermatology – a potential health risk},
  author={Wiete Westerhof and T J Kooyers},
  journal={Journal of Cosmetic Dermatology},
Hydroquinone has been used for decades as a skin lightening agent. Since January 1, 2001, its use in cosmetics has been banned. This ban is as a result of mid‐term effects such as leukoderma‐en‐confetti/occupational vitiligo and exogenous ochronosis. However, a recent literature search on hydroquinone as a skin lightening agent suggests that possible long‐term effects such as carcinogenesis may be expected as well. 

Hydroquinone and its analogues in dermatology – a risk‐benefit viewpoint

Hydroquinone (HQ) has been used since the 1950s in commercially available over‐the‐counter skin lightener products and since the 1960s as a commercially available medical product. It is also used in

The safety of hydroquinone

Despite 40-50 years use of hydroquinone for medical conditions, there has not been a single documented case of either a cutaneous or internal malignancy associated with this drug.

Hydroquinone-induced depigmentation: case report and review of the literature.

  • T. JowB. Hantash
  • Medicine, Biology
    Dermatitis : contact, atopic, occupational, drug
  • 2014
The development of depigmentation and paradoxical hyperpigmentation in 2 patients with Fitzpatrick skin type III/IV after brief treatment of their melasma with the HQ-containing Nu-Derm and Reverse systems is described for the first time.

Hyperpigmentation: Its Historical Treatment and the Development of Hydroquinone

The history of treatments for hyperpigmentation and the development of hydroquinone, currently the medication of choice for hyperPigmentation are reviewed.

Exogenous ochronosis: a review for clinicians

The clinical findings, pitfalls in diagnosis, etiopathogenesis and possible treatment options of this difficult-to-treat condition are discussed.

Hydrolysis of arbutin to hydroquinone by human skin bacteria and its effect on antioxidant activity

Normal skin microflora may increase the skin lightening effect of arbutin due to the antioxidant action of hydroquinone, which is more potent 1,1‐diphenyl‐2‐picrylhydrazyl radical scavenging activity and tyrosinase inhibition than arbuting.

Naturally occurring and synthetic peptides: Efficient tyrosinase inhibitors

Among a wide range of compounds possessing anti‐tyrosinase activity, peptides both natural and synthetic derivatives have attracted attention due to high potency and safety.

Hydroquinone, a benzene metabolite, and leukemia: A case report and review of the literature

A case of a 43-year-old male diagnosed with antecedent myelodysplastic syndrome and acute myeloid leukemia following 16 years of occupational exposure to hydroquinone in radiographic developer solution is reported.

Isobutylamido thiazolyl resorcinol for prevention of UVB‐induced hyperpigmentation

Isobutylamido thiazolyl resorcinol (ITR, Thiamidol®) has been proposed as a potent tyrosinase inhibitor and has recently shown promising efficacy for the treatment of some hyperpigmentary conditions.



Topical use of hydroquinone as a depigmenting agent.

Therapy with topically applied hydroquinone did not lead to complete disappearance of pathological hypermelanosis, but results were satisfactory enough to help most patients become less self-conscious about their pigmentary abnormalities.

A new formula for depigmenting human skin.

The formula was therapeutically effective in treatment of melasma, ephelides, and postinflammatory hyperpigmentation and Senile lentigines were resistant to this therapy.

Hypothesis: Phenol and hydroquinone derived mainly from diet and gastrointestinal flora activity are causal factors in leukemia

The hypothesis predicts that susceptibility to the disease would be related to diet, medicinal intake, genetics and gut-flora composition, and thus dietary modification and reduced use of medicines that elevate phenol levels may be the best intervention strategies for lowering leukemia risk.

Carcinogenicity of a nephrotoxic metabolite of the "nongenotoxic" carcinogen hydroquinone.

Although HQ is generally considered a nongenotoxic carcinogen, the data suggest that HQ nephrocarcinogenesis is probably mediated by the formation of the quantitatively minor yet potent nephrotoxic metabolite TGHQ, which induces sustained regenerative hyperplasia, loss of tumor suppressor gene function, and the subsequent formation of renal adenomas and carcinomas.

Mechanism of depigmentation by hydroquinone.

Findings indicate that HQ affects not only the formation, melanization, and degradation of melanosomes, but that it affects also the membraneous structures of melanocytes and eventually causes necrosis of whole melanocytes.

Human in vivo and in vitro hydroquinone topical bioavailability, metabolism, and disposition.

Risk assessment should not only involve the bioavailability of intact topical hydroquinone, but also consider phase I and phase II metabolism in both humans and any animal for which toxicity potential was assessed.

Hydroquinone, a Bioreactive Metabolite of Benzene, Inhibits Apoptosis in Myeloblasts

The ability of hydroquinone to induce a program of differentiation in the myeloblast that proceeds only to the myELocyte stage coupled with its ability to inhibit the CPP32 protease and, thereby, apoptosis of the proliferating myelocytes, may have important implications for benzene‐induced acute myeloid leukemia.

Development of a physiologically based pharmacokinetic model for hydroquinone.

An initial physiologically based pharmacokinetic model was developed to characterize the role of kinetics in the strain differences observed in HQ-induced renal toxicity and tumorigenicity and represents the first stage in the development of a biologically based dose-response model for improving the scientific basis for human health risk assessments of HQ.

Hydroquinones cause specific mutations and lead to cellular transformation and in vivo tumorigenesis.

Benzo(a)pyrene and benzene are human carcinogens. The metabolic activation of these compounds into ultimate mutagenic and carcinogenic metabolites is prerequisite for their carcinogenic effects. In