Hubbry Logo
HydroquinoneHydroquinoneMain
Open search
Hydroquinone
Community hub
Hydroquinone
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Hydroquinone
Hydroquinone
Hydroquinone
View on Wikipedia
from Wikipedia

Hydroquinone
Hydroquinone
Hydroquinone
Names
Preferred IUPAC name
Benzene-1,4-diol[1]
Other names
Hydroquinone[1]
Idrochinone
Quinol
4-Hydroxyphenol
1,4-Dihydroxybenzene
p-Dihydroxybenzene
p-Benzenediol
Identifiers
3D model (JSmol)
605970
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard 100.004.199 Edit this at Wikidata
EC Number
  • 204-617-8
2742
KEGG
RTECS number
  • MX3500000
UNII
UN number 3077, 2662
  • InChI=1S/C6H6O2/c7-5-1-2-6(8)4-3-5/h1-4,7-8H checkY
    Key: QIGBRXMKCJKVMJ-UHFFFAOYSA-N checkY
  • InChI=1/C6H6O2/c7-5-1-2-6(8)4-3-5/h1-4,7-8H
    Key: QIGBRXMKCJKVMJ-UHFFFAOYAX
  • c1cc(ccc1O)O
Properties
C6H6O2
Molar mass 110.112 g·mol−1
Appearance White solid
Density 1.3 g cm−3, solid
Melting point 172 °C (342 °F; 445 K)
Boiling point 287 °C (549 °F; 560 K)
5.9 g/100 mL (15 °C)
Vapor pressure 10−5 mmHg (20 °C)[2]
Acidity (pKa) 9.9[3]
−64.63×10−6 cm3/mol
Structure
1.4±0.1 D[4]
Pharmacology
D11AX11 (WHO)
Hazards
GHS labelling:
GHS05: CorrosiveGHS07: Exclamation markGHS08: Health hazardGHS09: Environmental hazard
Danger
H302, H317, H318, H341, H351, H400
P201, P202, P261, P264, P270, P272, P273, P280, P281, P301+P312, P302+P352, P305+P351+P338, P308+P313, P310, P321, P330, P333+P313, P363, P391, P405, P501
NFPA 704 (fire diamond)
[6]
NFPA 704 four-colored diamondHealth 2: Intense or continued but not chronic exposure could cause temporary incapacitation or possible residual injury. E.g. chloroformFlammability 1: Must be pre-heated before ignition can occur. Flash point over 93 °C (200 °F). E.g. canola oilInstability (yellow): no hazard codeSpecial hazards (white): no code
2
1
Flash point 165 °C (329 °F; 438 K)
Lethal dose or concentration (LD, LC):
490 mg/kg (mammal, oral)
245 mg/kg (mouse, oral)
200 mg/kg (rabbit, oral)
320 mg/kg (rat, oral)
550 mg/kg (guinea pig, oral)
200 mg/kg (dog, oral)
70 mg/kg (cat, oral)[5]
NIOSH (US health exposure limits):
PEL (Permissible)
 TWA 2 mg/m3[2]
REL (Recommended)
 C 2 mg/m3 [15-minute][2]
IDLH (Immediate danger)
 50 mg/m3[2]
Related compounds
Related benzenediols
 Pyrocatechol
Resorcinol
Related compounds
 1,4-benzoquinone
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
checkY verify (what is checkY☒N ?)

Hydroquinone, also known as benzene-1,4-diol or quinol, is an aromatic organic compound that is a type of phenol, a derivative of benzene, having the chemical formula C6H4(OH)2. It has two hydroxyl groups bonded to a benzene ring in a para position. It is a white granular solid. Substituted derivatives of this parent compound are also referred to as hydroquinones. The name "hydroquinone" was coined by Friedrich Wöhler in 1843.[7]

In 2023, it was the 274th most commonly prescribed medication in the United States, with more than 800,000 prescriptions.[8][9]

Production

[edit]

Hydroquinone is produced industrially in two main ways.[10]

  • The most widely used route is similar to the cumene process in reaction mechanism and involves the dialkylation of benzene with propene to give 1,4-diisopropylbenzene. This compound reacts with air to afford the bis(hydroperoxide), which is structurally similar to cumene hydroperoxide and rearranges in acid to give acetone and hydroquinone.[11]
  • A second route involves hydroxylation of phenol over a catalyst. The conversion uses hydrogen peroxide and affords a mixture of hydroquinone and its ortho isomer catechol (benzene-1,2-diol):
C6H5OH + H2O2 → C6H4(OH)2 + H2O

Other, less common methods include:

The latter three methods are generally less atom-economical than oxidation with hydrogen peroxide, and their commercial practice in China produced serious pollution in 2022.[20]

Reactions

[edit]

The reactivity of hydroquinone's hydroxyl groups resembles that of other phenols, being weakly acidic. The resulting conjugate base easily undergoes O-alkylation to give mono- and diethers. Similarly, hydroquinone is highly susceptible to ring substitution via Friedel–Crafts alkylation. This reaction is often used for the production of several popular antioxidants, namely 2-tert-butyl-4-methoxyphenol (BHA). The useful dye quinizarin is produced by diacylation of hydroquinone with phthalic anhydride.[10]

Redox

[edit]

Hydroquinone can be reversibly oxidised under mild conditions to give benzoquinone. Naturally occurring hydroquinone derivatives, such as coenzyme Q, exhibit similar reactivity, wherein one hydroxyl group is exchanged for an amino group. Given the conditional reversibility and relative ubiquity of reagents, oxidation reactions of hydroquinones and hydroquinone derivatives are of significant commercial use, often used at an industrial scale.

When colorless hydroquinone and benzoquinone - bright yellow in solid form - are cocrystallized at a 1:1 ratio, a dark-green crystalline charge-transfer complex (melting point 171 °C), known as quinhydrone (C6H6O2·C6H4O2), is formed. [citation needed]This complex dissolves in hot water, dissociating both quinone molecules in solution.[21]

Amination

[edit]

An important reaction involves the conversion of hydroquinone to its mono- and di-amine derivatives. One such derivative, methylaminophenol, used in photography, is produced according to the stochiometry:[10]

C6H4(OH)2 + CH3NH2 → HOC6H4NHCH3 + H2O

Diamines - used in the rubber industry as antiozone agents - aminated from aniline, are formed via a similar pathway:

C6H4(OH)2 + 2 C6H5NH2 → C6H4(N(H)C6H5)2 + 2 H2O

Uses

[edit]

Hydroquinone has a variety of uses principally associated with its action as a reducing agent that is soluble in water. It is a major component in most black and white photographic developers for film and paper where, with the compound metol, it reduces silver halides to elemental silver.

There are various other uses associated with its reducing power. As a polymerisation inhibitor, exploiting its antioxidant properties, hydroquinone prevents polymerization of acrylic acid, methyl methacrylate, cyanoacrylate, and other monomers that are susceptible to radical-initiated polymerization. By acting as a free radical scavenger, hydroquinone serves to prolong the shelf life of light-sensitive resins such as preceramic polymers.[22]

Hydroquinone can lose a hydrogen cation from both hydroxyl groups to form a diphenolate ion. The disodium diphenolate salt of hydroquinone is used as an alternating comonomer unit in the production of the polymer PEEK.

Skin depigmentation

[edit]

Hydroquinone is used as a topical application in skin whitening to reduce the color of skin. It does not have the same predisposition to cause dermatitis as metol does. This is a prescription-only ingredient in some countries, including the member states of the European Union under Directives 76/768/EEC:1976.[23][24]

In 2006, United States Food and Drug Administration revoked its previous approval of hydroquinone and proposed a ban on all over-the-counter preparations.[25] The FDA officially banned hydroquinone in 2020 as part of a larger reform of the over-the-counter drug review process.[26] The FDA stated that hydroquinone cannot be ruled out as a potential carcinogen.[27] This conclusion was reached based on the extent of absorption in humans and the incidence of neoplasms in rats in several studies where adult rats were found to have increased rates of tumours, including thyroid follicular cell hyperplasias, anisokaryosis (variation in nuclei sizes), mononuclear cell leukemia, hepatocellular adenomas and renal tubule cell adenomas. The Campaign for Safe Cosmetics has also highlighted concerns.[28]

Numerous studies have revealed that hydroquinone, if taken orally, can cause exogenous ochronosis, a disfiguring disease in which blue-black pigments are deposited onto the skin; however, skin preparations containing the ingredient are administered topically. The FDA had classified hydroquinone in 1982 as a safe product - generally recognized as safe and effective (GRASE), however additional studies under the National Toxicology Program (NTP) were suggested in order to determine whether there is a risk to humans from the use of hydroquinone.[25][27][29] NTP evaluation showed some evidence of long-term carcinogenic and genotoxic effects.[30]

While hydroquinone remains widely prescribed for treatment of hyperpigmentation, questions raised about its safety profile by regulatory agencies in the EU, Japan, and USA encourage the search for other agents with comparable efficacy.[31] Several such agents are already available or under research,[32] including azelaic acid,[33] kojic acid, retinoids, cysteamine,[34] topical steroids, glycolic acid, and other substances. One of these, 4-butylresorcinol, has been proved to be more effective at treating melanin-related skin disorders by a wide margin, as well as safe enough to be made available over the counter.[35]

In the anthraquinone process substituted hydroquinones, typically anthrahydroquinone are used to produce hydrogen peroxide which forms spontaneously on reaction with oxygen. The type of substituted hydroquinone is selected depending on reactivity and recyclability.

Natural occurrences

[edit]

Hydroquinones are one of the two primary reagents in the defensive glands of bombardier beetles, along with hydrogen peroxide (and perhaps other compounds, depending on the species), which collect in a reservoir. The reservoir opens through a muscle-controlled valve onto a thick-walled reaction chamber. This chamber is lined with cells that secrete catalases and peroxidases. When the contents of the reservoir are forced into the reaction chamber, the catalases and peroxidases rapidly break down the hydrogen peroxide and catalyze the oxidation of the hydroquinones into p-quinones. These reactions release free oxygen and generate enough heat to bring the mixture to the boiling point and vaporize about a fifth of it, producing a hot spray from the beetle's abdomen.[36]

Hydroquinone is thought to be the active toxin in Agaricus hondensis mushrooms.[37]

Hydroquinone has been shown to be one of the chemical constituents of the natural product propolis.[38]

It is also one of the chemical compounds found in castoreum. This compound is gathered from the beaver's castor sacs.[39]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Hydroquinone

View on Grokipedia
from Grokipedia
Hydroquinone, chemically known as benzene-1,4-diol (C₆H₆O₂), is a white crystalline solid and a benzenediol featuring two hydroxyl groups in the para position on a ring. With a of 172 °C and of 1.3 g/cm³, it exhibits strong reducing properties due to its phenolic structure, enabling it to act as an and in various chemical reactions. First isolated in 1820 via of , hydroquinone has been industrially produced since the , primarily through routes involving oxidation or similar processes akin to the method. In , hydroquinone serves as a primary developing agent in black-and-white film and , where it reduces exposed silver halides to metallic silver, often combined with for enhanced activity and finer grain. Beyond imaging, it functions as a inhibitor and rubber in industrial applications. In , hydroquinone is employed as a topical depigmenting agent to treat conditions such as , solar lentigines, and post-inflammatory by inhibiting , the rate-limiting enzyme in synthesis. Despite its efficacy, hydroquinone's use is marred by toxicity concerns, including potential carcinogenicity, skin irritation, and exogenous ochronosis with prolonged application, prompting regulatory restrictions. The U.S. FDA has deemed over-the-counter hydroquinone products illegal due to safety risks, while it is banned outright in the European Union, Australia, and Japan for cosmetic use. Occupational exposure limits are set at 2 mg/m³ to mitigate inhalation hazards, reflecting its classification as a hazardous substance capable of causing burns, sensitization, and systemic effects. Global production exceeds tens of thousands of tonnes annually, underscoring its continued industrial relevance amid ongoing debates over risk-benefit profiles in medical contexts.

Chemical Properties

Molecular Structure and Physical Characteristics

Hydroquinone has the molecular formula C6H6O2 and the IUPAC name benzene-1,4-diol, consisting of a ring with hydroxyl groups attached at the 1 and 4 positions. This para substitution differentiates it from the ortho isomer (benzene-1,2-diol), with which it shares the dihydroxybenzene structure but exhibits distinct chemical behaviors due to positional effects. As a white granular solid or crystalline powder, hydroquinone displays low volatility, with a of 0.12 Pa at 20°C. Its is 172°C, and the is 287°C under standard . The measures 1.32 g/cm³ at 15°C, providing a baseline for its handling in solid form.

Stability, Solubility, and Reactivity

Hydroquinone displays moderate solubility in , approximately 72 g/L at 25 °C, increasing with and in alkaline media due to of its phenolic hydroxyl groups. It exhibits high solubility in polar organic solvents, including (around 300 g/L at 25 °C), , acetone, and , but limited solubility in nonpolar solvents like or . As a weak diprotic acid with pKa values of 9.85 and 11.40, its solubility profile is -dependent, with enhanced dissolution above pH 10 via formation of hydroquinonate ions that facilitate bonding with . The compound remains chemically stable under standard ambient conditions (, neutral , exclusion of light and air), but pure dry hydroquinone darkens slowly upon prolonged exposure to oxygen or light due to auto-oxidation forming p-benzoquinone. This oxidative instability accelerates in alkaline solutions or with trace metals, necessitating storage with antioxidants (e.g., ) or in sealed, inert environments to prevent degradation. Thermally, hydroquinone melts at 172 °C and begins to sublime, with decomposition occurring above 200 °C, potentially yielding , , and phenolic fragments under oxidative heating. Reactivity stems primarily from its two phenolic hydroxyl groups, which enable intermolecular hydrogen bonding—contributing to its solid-state lattice and solution behavior—and impart weak acidity for salt formation with bases. These groups also activate the ring for , directing incoming electrophiles to ortho/para positions relative to the OH substituents, as seen in facile bromination or without catalysts. Unlike aliphatic alcohols, the phenolic C-O bond resists nucleophilic attack, emphasizing its aromatic character over aliphatic-like reactivity.

History

Discovery and Initial Applications

Hydroquinone, chemically known as 1,4-dihydroxybenzene, was first isolated in 1820 by French chemists Pierre-Joseph Pelletier and Joseph Bienaimé Caventou through the of , a compound derived from plant sources such as bark. This empirical process yielded the white crystalline substance, marking its initial chemical characterization prior to large-scale synthetic methods. The compound occurs naturally in certain plants, notably as the aglycone of in species like (), where enzymatic or hydrolytic breakdown releases hydroquinone; early 19th-century observations of such plant-derived reducing agents laid groundwork for its recognition, though pure isolation relied on the 1820 technique. By the mid-19th century, German chemist contributed to its nomenclature and further synthesis, emphasizing its phenolic structure and . Hydroquinone's practical utility emerged prominently in photography when British scientist Sir William de Wiveleslie Abney identified its developing properties in 1880 through systematic reduction experiments on silver halide emulsions. Abney demonstrated that hydroquinone efficiently reduced exposed silver ions to metallic silver while minimizing fogging in unexposed areas, attributing this to its selective electron-donating capacity under alkaline conditions. This application rapidly supplanted earlier developers like pyrogallol, establishing hydroquinone as a cornerstone of black-and-white film processing due to its controllable reaction kinetics and stability. In the late , hydroquinone's inherent reducing nature prompted exploratory uses beyond , including as an intermediate in dye production—such as the synthesis of quinizarin via oxidation—and as an to prevent oxidation in organic preparations, leveraging direct observations of its ability to quench . These early deployments stemmed from empirical testing of its electrochemical behavior rather than theoretical prediction, predating formalized industrial scaling.

Evolution in Industrial and Medical Contexts

During the early , hydroquinone's industrial applications expanded beyond initial uses, with its role as a —recognized since 1880—scaling amid rising demand for film processing in documentation and . accelerated this through heightened production of photographic materials for military purposes, while hydroquinone also proved essential in stabilizing rubber for tires in jeeps and , supporting wartime . By mid-century, its integration as a precursor in rubber antioxidants further entrenched industrial reliance, with consumption patterns reflecting broad adoption in polymers and stabilizers prior to later regulatory scrutiny. In medical contexts, hydroquinone's depigmenting properties emerged serendipitously in the early 1950s when it was incorporated into sunscreens in the , where users observed unintended skin lightening effects attributed to inhibition of , the enzyme central to synthesis. This led to targeted exploration for disorders like . In 1961, dermatologist Malcolm Spencer conducted the first clinical evaluation, treating 98 subjects with 1.5% to 2% hydroquinone formulations and reporting lightening in 45% of cases across White and African American males, marking its formal introduction for . Subsequent studies in the confirmed efficacy against abnormal pigmentation via topical application, shifting its status from incidental observation to evidence-based dermatological tool. By the 1970s, hydroquinone transitioned to prescription formulations in , driven by accumulating data demonstrating reversible inhibition of melanogenesis without initial evidence of permanent harm at low concentrations, enabling regulated use for conditions involving localized . This evolution reflected causal prioritization of biochemical mechanisms over anecdotal reports, with formulations standardized for medical oversight rather than over-the-counter availability.

Production

Industrial Synthesis Methods

Hydroquinone is produced industrially via three principal routes: oxidation of , direct of phenol, and oxidative cleavage of diisopropylbenzene dihydroperoxide. These methods rely on feedstocks, primarily derivatives, with aniline historically sourced from but now predominantly from nitrobenzene reduction using petroleum-derived . The oxidation process, the earliest industrial method dating to the early 20th century, involves oxidizing to p-benzoquinone using (typically 15-20% excess) in aqueous at elevated temperatures, followed by reduction of the quinone to hydroquinone via catalytic hydrogenation over or gaseous . This route achieves yields exceeding 90% in optimized steps but requires stoichiometric oxidants, generating manganese sludge and sulfate waste, which reduces overall . Phenol hydroxylation employs as oxidant over heterogeneous catalysts such as titanium-modified zeolites (e.g., TS-1), yielding a mixture of and hydroquinone (typically in a 2:1 ratio favoring ) under mild conditions around 60-80°C and 1-10 bar pressure. Selectivity to dihydroxybenzenes can reach 90-95%, with hydroquinone subsequently isolated by or extraction; this method emphasizes peroxide efficiency, minimizing over-oxidation, though separation costs impact scalability. The diisopropylbenzene route, analogous to the for phenol, begins with selective monoalkylation of with to p-diisopropylbenzene, followed by air oxidation to the dihydroperoxide and acid-catalyzed (e.g., ) rearrangement-cleavage to hydroquinone and acetone (1:2 molar ratio). This process delivers hydroquinone yields of 85-95% based on the , benefiting from the marketable acetone coproduct and air as the terminal oxidant, thus improving over stoichiometric alternatives.

Economic and Scalability Factors

Global production of hydroquinone was approximately 80,000 metric tons in 2024, reflecting demand from stabilizers, rubber antioxidants, and pharmaceutical intermediates. is concentrated in , which accounts for a majority of output through numerous suppliers, supplemented by U.S.-based firms like that emphasize integrated production capabilities. This regional dominance facilitates but exposes supply chains to geopolitical and trade disruptions. Scalability challenges arise from differing purity requirements across applications: pharmaceutical-grade hydroquinone demands impurities below parts-per-million levels, necessitating multi-stage purification such as recrystallization or , which elevates energy use and capital investment compared to industrial grades used in or polymers. Oxidation-based synthesis routes, typically from phenol or , involve high-temperature and catalyst-intensive steps that limit rapid capacity expansion without significant process optimization. Key cost drivers include feedstock phenol prices, which averaged about 1 USD per kg in major markets during 2024, propagating through to hydroquinone at roughly 3.5-4 USD per kg amid steady supply-demand balance. Fluctuations in benzene-derived phenol, combined with energy costs for oxidation, can compress margins during low-demand periods, while for high-purity variants adds fixed expenses that hinder small-scale operations.

Chemical Reactions

Redox Behavior

Hydroquinone undergoes reversible two-electron oxidation to p-benzoquinone, serving as a classic example of a quinone-hydroquinone couple with a of approximately +0.70 V versus the (SHE) under acidic conditions. This potential reflects the thermodynamic favorability of the oxidized form in oxidizing environments, enabling hydroquinone's role as a through . The oxidation mechanism proceeds via a semiquinone radical intermediate, formed by one-electron transfer, which has been characterized spectroscopically; (EPR) detects this with characteristic hyperfine splitting patterns during oxidative processes. The semiquinone exhibits absorption maxima around 400-430 nm in its anionic form and is stabilized transiently before or further oxidation to the . This intermediate underscores the stepwise nature of the two-electron process, influenced by dynamics. Autoxidation of hydroquinone in aqueous solutions is oxygen-dependent, with kinetics showing sensitivity: rates increase markedly above 7 due to enhanced reactivity of the mono- or di-deprotonated species (pK_a values ≈9.9 and 11.4), facilitating or intermediates. Empirical studies report stoichiometric formation of p-benzoquinone and during at pH 7.4 and 37°C for concentrations below 1 mM, with observed pseudo-first-order rate constants on the order of 10^{-3} to 10^{-2} min^{-1} in buffered media, highlighting causal oxygen mediation via radical chain propagation.

Amination and Other Transformations

Hydroquinone undergoes selective monoetherification with primary alcohols such as under acidic conditions catalyzed by (NaNO₂), producing 4-alkoxyphenols like (4-methoxyphenol) with yields up to 70% and high selectivity, minimizing diether formation. The mechanism involves initial nitrosation of one hydroxyl group, facilitating nucleophilic attack by the alcohol while the para-hydroxy group activates the ring . This transformation is valuable for synthesizing intermediates and pharmaceutical precursors, where selective protection of one phenolic hydroxyl is required. For bulkier alkyl groups, such as tert-butyl, hydroquinone reacts with tert-butanol or methyl tert-butyl ether over acidic catalysts like H-beta at 100–150°C, yielding tert-butylhydroquinone in industrially relevant quantities as an precursor, though exact lab-scale yields vary with catalyst loading (typically 50–80% conversion reported in optimization studies). Esterification of hydroquinone proceeds via reaction with derivatives, such as acid chlorides or anhydrides, under basic conditions (e.g., or triethylamine in ), forming mono- or diesters that serve as protected forms for further synthetic manipulations or as bioactive derivatives. For instance, hydroquinone benzoate esters have been synthesized in laboratory settings with yields ranging from 40% to 75%, depending on substituent effects and purification steps like . These esters exhibit utility in , where they act as monomers for polyesters, and in for inhibitors, with the ester linkage providing hydrolytic stability under neutral conditions. Mechanistically, the para relationship of the hydroxyls enhances reactivity due to intramolecular bonding in the diester, influencing and crystallinity. Beyond ether and ester formation, hydroquinone's phenolic framework enables limited cycloaddition reactivity, particularly when its oxidized benzoquinone form (generated in situ) serves as a dienophile in Diels-Alder reactions with dienes like cyclopentadiene, yielding bridged adducts under electrochemical conditions at potentials around 0.5–1.0 V vs. SCE. Direct Diels-Alder participation of hydroquinone as a diene is rare due to aromatic stabilization, but it can act as an activator in oxidative dehydrogenative variants, lowering activation barriers by stabilizing transition states through hydrogen bonding, as evidenced by DFT calculations showing reduced energy barriers by 5–10 kcal/mol. These transformations highlight hydroquinone's role in constructing polycyclic scaffolds for natural product synthesis, though industrial application remains constrained by competing redox pathways and the need for precise control to avoid over-oxidation. Electrophilic aromatic substitution patterns, directed ortho/para by the hydroxyl groups, further enable nitration or halogenation at C-2/C-6 positions under mild conditions (e.g., Br₂ in acetic acid yielding 2-bromo-1,4-hydroquinone in >80% yield), providing handles for diversified derivatives without disrupting the core symmetry.

Applications

Photographic Development

Hydroquinone functions as a key in black-and-white photographic developers, selectively converting exposed crystals in emulsions—primarily and —to metallic silver, thereby forming the visible image. This reaction occurs in alkaline conditions, where the hydroquinone (in its quinol form) donates electrons to the sites, oxidizing to p-benzoquinone, with unexposed halides remaining largely unaffected to minimize . Its high makes it particularly effective for generating dense, contrasty negatives, as evidenced by steeper characteristic curves in densitometric analyses of developed films compared to single-agent developers. In common metol-hydroquinone (MQ) formulations, hydroquinone is paired with (N-methyl-p-aminophenol sulfate) at ratios typically around 1:4 to 1:10 (metol to hydroquinone by weight), exhibiting superfadditivity—a synergistic acceleration of development rate beyond the additive effects of each agent alone, as demonstrated in early 20th-century patents optimizing density and speed. Working solutions often contain hydroquinone at concentrations of 0.5–2 g/L in alkaline baths buffered with or , though higher levels up to 5–8 g/L appear in stock concentrates for dilution. This combination yields fine grain and balanced shadow detail from metol's initial reduction, complemented by hydroquinone's capacity for highlights and contrast, per empirical tests showing reduced development times (e.g., 5–10 minutes at 20°C for ISO 100 films). Use of hydroquinone in peaked mid-20th century but declined sharply after the 2000s amid the transition to , which eliminated chemical development needs for most applications. Nonetheless, it persists in niche analog and archival workflows, including motion picture preservation and specialized lithographic , where its proven photochemical reliability ensures reproducible results unavailable in digital alternatives.

Industrial Antioxidants and Polymers

Hydroquinone functions as an in rubber processing, where it and its derivatives, such as dialkyl hydroquinones, protect against oxidative and ozonolytic degradation by scavenging free radicals and suppressing radical chain reactions. This stabilization extends the of vulcanized rubber products, with hydroquinone derivatives demonstrating superior and efficacy compared to unsubstituted hydroquinone in sulfur-vulcanized formulations. Approximately 25% of global hydroquinone production is directed toward synthesizing such rubber antioxidants and antiozonants. In polymer manufacturing, hydroquinone primarily serves as a polymerization inhibitor for monomers like and , preventing premature radical-initiated polymerization during storage, transport, and . The inhibition mechanism relies on hydroquinone's phenolic structure, which donates a or to nascent free radicals, forming a resonance-stabilized semiquinone radical that terminates chain propagation without propagating further reaction. This application exploits hydroquinone's properties to maintain monomer purity, with typical addition levels ranging from parts per million to low percentages based on monomer reactivity and storage conditions. Rubber-derived antioxidants from hydroquinone account for about 65% of total hydroquinone consumption, underscoring its dominant role in industrial stabilization. Hydroquinone also acts as a precursor in and synthesis, contributing to approximately 10% of market demand through intermediates that impart color stability in formulations. Global hydroquinone production, supporting these uses, reached around 80 thousand tonnes in 2024.

Other Specialized Uses

Hydroquinone serves as a reference standard in for titrations, leveraging its well-characterized reversible oxidation to p-benzoquinone via semiquinone intermediates, with the National Institute of Standards and Technology providing thermochemical and spectral data for precise potential measurements. Its two-electron couple, exhibiting a standard potential of approximately 0.699 V vs. SHE under standard conditions, facilitates accurate in cerimetric or iodometric procedures. In , hydroquinone functions as a component in chemical doping processes for , particularly through equilibria with to generate charge carriers and control conductivity in aqueous media. Developments since the have demonstrated its role in achieving tunable electrical conductivities up to several S/cm in flexible devices, enhancing p-type doping efficiency without issues common in traditional methods. Medically, hydroquinone acts as an inhibitor in biochemical assays studying toxicity, where it suppresses signaling pathways at micromolar concentrations, mimicking metabolite-induced cellular responses. In veterinary applications, it and its ethers exhibit rare depigmenting effects in animal models, such as inducing dose-dependent in black guinea pigs at 1-5% concentrations, informing treatments for refractory melanistic conditions.

Dermatological Efficacy

Mechanism of Action in Pigmentation Disorders

Hydroquinone primarily inhibits melanin production by targeting , the -dependent enzyme that catalyzes the initial steps of melanogenesis, converting to dopaquinone and subsequently to pigments. This inhibition occurs through competitive binding at the enzyme's , where hydroquinone chelates the binuclear copper ions required for tyrosinase's catalytic activity, thereby disrupting the oxidation process. Enzymatic studies report IC50 values for hydroquinone against tyrosinase in the range of approximately 50-100 μM, depending on assay conditions and tyrosinase source, with melanocyte tyrosinase showing sensitivity in the micromolar range under physiological substrates. At higher concentrations (typically >1 mM ), hydroquinone exhibits cytotoxic effects on melanocytes, inducing or , which reduces the population of melanin-synthesizing cells and further diminishes overall pigmentation. This melanocytotoxicity involves redox cycling, where hydroquinone is oxidized to semiquinone radicals that generate , overwhelming cellular antioxidants and leading to degradation. Skin permeation studies demonstrate that topically applied hydroquinone readily diffuses across the into the viable , achieving intradermal concentrations sufficient for inhibition (e.g., 0.1-1% formulations yield epidermal levels of 10-50 μM), with absorption rates of 30-45% of the applied dose in human skin models. In combination therapies, hydroquinone's efficacy is enhanced by retinoids such as tretinoin, which accelerate epidermal cell turnover, improve hydroquinone penetration, and upregulate expression to amplify inhibition targets, as shown in pharmacokinetic models from the 1980s and 1990s. Sunscreens complement this by blocking UV-induced activation and that promote melanogenesis, yielding additive reductions in synthesis through complementary pathways. These synergies stem from hydroquinone's rapid oxidation and short dermal residence time ( ~1-2 hours), necessitating adjuncts to sustain inhibition.

Clinical Studies and Evidence of Effectiveness

Clinical trials have established that topical hydroquinone (HQ) at 2-4% concentrations effectively reduces melasma severity, with randomized controlled trials (RCTs) reporting mean reductions in Melasma Area and Severity Index (MASI) scores of approximately 40-60% after 3 months of use. In one open-label study of moderate-to-severe melasma, a 4% HQ regimen combined with tretinoin yielded a 62.8% ± 19.4% mMASI reduction over 3 months, with sustained improvements observed in follow-up assessments. Meta-analyses of RCTs confirm these findings, though variability exists across comparators; for instance, HQ showed statistically significant MASI improvements versus baseline but was outperformed by azelaic acid in direct comparisons (mean difference -1.23, 95% CI -2.05 to -0.40). Comparative RCTs highlight HQ's superiority over certain alternatives, such as 0.75% , where 4% HQ achieved faster and greater MASI reductions (e.g., mean change of 7.553 ± 5.289 by week 12 versus delayed onset with ). Relapse rates post-treatment average around 50%, with approximately 47% of patients experiencing recurrence within 6 months despite initial response, underscoring the need for maintenance therapy. Subgroup analyses from RCTs indicate enhanced efficacy in Fitzpatrick skin types III-V, populations prone to melasma, with 4% HQ plus regimens showing marked pigmentation improvement and tolerability in these groups over 12-24 weeks. Long-term studies up to 1 year demonstrate sustained benefits with intermittent or low-dose HQ application under dermatological monitoring, reducing relapse while preserving efficacy gains.

Safety and Toxicology

Acute Toxicity and Irritation Potential


Hydroquinone exhibits moderate acute oral toxicity, with an LD50 value in rats ranging from 298 to 367 mg/kg body weight, classifying it as harmful if swallowed under GHS criteria. Dermal acute toxicity is lower, evidenced by LD50 values exceeding 2000 mg/kg in rabbits and rats, indicating minimal risk from single skin exposures. Inhalation exposure to high concentrations can cause respiratory tract irritation, though specific LC50 data are limited. Acute exposure symptoms include gastrointestinal distress such as nausea and vomiting, neurological effects like tinnitus and dizziness, and hematological changes including , which may lead to and dyspnea. These effects arise from hydroquinone's activity forming reactive intermediates that oxidize . Occupational exposure limits, such as the OSHA PEL of 2 mg/m³ as a time-weighted , aim to prevent such acute irritative and systemic responses. Hydroquinone demonstrates irritant potential to and eyes, classified under GHS as causing irritation (Category 2) and serious eye irritation (Category 2). contact at concentrations above 1-2% may induce mild erythema and per 404 guidelines, while ocular exposure results in redness, tearing, and potential corneal damage per 405. Dermal absorption occurs rapidly, with in vivo human studies showing up to 45% penetration over 24 hours from 2% formulations, though systemic levels remain low in controlled patch tests due to .

Long-Term Effects and Ochronosis

Exogenous , a rare complication of prolonged topical hydroquinone application, manifests as persistent bluish-black primarily in sun-exposed areas such as the malar cheeks and periorbital regions, resulting from deposition of ochre-colored polymers in the . Histopathologically, it is characterized by banana-shaped, ochronotic fibers within the papillary , often accompanied by solar elastosis and collagen degeneration, distinguishing it from endogenous forms linked to metabolic disorders like . This condition arises from the accumulation of metabolites or hydroquinone-derived polymers, which bind to dermal fibers, but it is not a universal outcome of hydroquinone use and typically requires cumulative high exposure. In human cohorts using supervised 4% hydroquinone formulations, the incidence of exogenous remains below 1%, with most reports confined to unregulated over-the-counter products containing higher concentrations (>5%) applied for years without medical oversight. Dermatological studies emphasize that early irritant effects, such as or mild pigmentation changes, are generally reversible upon discontinuation, whereas established proves more recalcitrant, underscoring the importance of periodic treatment cycling to mitigate risks—reducing potential incidence from approximately 0.9% to 0.05% in compliant patients. Predisposing factors include darker Fitzpatrick skin types (V-VI), which account for over 50% of documented cases, likely due to enhanced activity facilitating metabolite formation. Ultraviolet exposure exacerbates risk by promoting hydroquinone oxidation and elastotic changes, with histopathological evidence showing preferential involvement in chronically photoexposed sites; unprotected sun exposure thus acts as a causal potentiator rather than an isolated trigger. Animal models, which demonstrate ochronotic changes at lower doses and shorter durations than observed clinically, overestimate human dermal risks owing to species-specific differences in absorption, , and expression, rendering them less predictive for supervised topical regimens in humans. Empirical data from long-term follow-ups prioritize these modulated human outcomes over extrapolated preclinical alarms, highlighting that emerges primarily from misuse patterns rather than inherent compound toxicity at therapeutic levels.

Carcinogenicity: Animal Data vs. Human Evidence

In male F344 rats administered hydroquinone by gavage at doses up to 100 mg/kg body weight daily for two years, the National Toxicology Program observed increased incidences of renal tubular cell adenomas, particularly at higher doses, alongside exacerbation of chronic progressive nephropathy (CPN), a common age-related in this strain. These tumors were not evident in female F344 rats or in B6C3F1 mice of either sex under similar exposure conditions, where no consistent carcinogenic effects were reported across multiple studies. The International Agency for Research on Cancer (IARC) classified hydroquinone as Group 3 (not classifiable as to its carcinogenicity to humans), citing limited evidence in experimental animals primarily confined to this strain- and sex-specific renal effect. Human epidemiological data, including cohorts of photographers with occupational exposure via photographic developers and dermatology patients using topical formulations, show no consistent elevation in cancer incidence, with studies failing to demonstrate increased risks for renal, skin, or other malignancies. Genotoxicity assessments, such as the , are negative for mutagenicity, while equivocal results with metabolites like reflect potential for formation under extreme conditions but lack direct relevance to typical human exposures. Physiologically based pharmacokinetic modeling reveals species differences, with male F344 rats exhibiting disproportionately higher renal concentrations of toxic metabolites due to enhanced oxidation and lower rates compared to humans, supporting a nonlinear, threshold-based mechanism tied to CPN rather than genotoxic applicable across species. This disconnect underscores the limited human hazard from hydroquinone's rodent findings, as human metabolic profiles predict minimal bioactivation at dermal or low oral doses.

Regulatory Framework and Controversies

United States Regulations

The U.S. (FDA) classifies over-the-counter (OTC) skin lightening products containing hydroquinone as unapproved new drugs, rendering their sale illegal without prior FDA approval via a . This status stems from a 2006 proposed rule citing insufficient evidence of safety, including animal data suggesting carcinogenic potential from topical application, and was reinforced in 2020 under the Coronavirus Aid, Relief, and Economic Security (CARES) Act, which deemed such products not and effective (GRAS/E). Prescription formulations with 2–4% hydroquinone, including FDA-approved 4% monotherapy creams and combination therapies like Tri-Luma (hydroquinone 4% with tretinoin and ), are permitted for short-term dermatological use in treating conditions such as , with oversight to mitigate risks like or irritation based on clinical benefit-risk evaluations. In non-cosmetic contexts, hydroquinone is authorized as an indirect food additive under 21 CFR 175–178 for uses in food contact materials like adhesives and polymers, with limitations such as concentrations below 0.02% in specific applications to prevent migration into food. It lacks GRAS affirmation for direct food use or cosmetic skin lightening. FDA enforcement targets illegal OTC marketing through warning letters to distributors and import alerts; for instance, in August 2025, a letter addressed unapproved hydroquinone-based skin bleaching products like Vivant True Tone. Recalls in 2025 addressed adulterated imported skin lighteners containing undeclared mercury alongside hydroquinone, due to mercury's neurotoxic and dermatotoxic effects, while preserving prescription access for verified medical needs.

International Bans and Restrictions

In the , hydroquinone has been banned from use in cosmetic products since March 1, 2001, under Annex II of Regulation (EC) No 1223/2009, due to its classification as a Category 2 , which indicates suspected human carcinogenicity based on animal data. This prohibition extends to all leave-on and rinse-off , reflecting harmonized risk assessments prioritizing precautionary measures against potential long-term dermal absorption risks. Australia and Japan have implemented full prohibitions on hydroquinone in cosmetics, with Australia's Therapeutic Goods Administration restricting it post-2000 amid concerns over ochronosis and carcinogenicity, while Japan's Ministry of Health, Labour and Welfare enacted a similar ban in the early 2000s, classifying it as unsuitable for over-the-counter skin lightening. These outright bans contrast with more nuanced allowances elsewhere, underscoring inconsistencies in global risk harmonization, where empirical evidence of human harm remains debated yet prompts stringent controls in developed markets. In developing markets across and , unregulated imports of high-concentration hydroquinone products persist despite partial bans, with surveys indicating widespread misuse for skin lightening; for instance, a WHO-reported 77% prevalence among Nigerian women highlights enforcement gaps and associated adverse events like irritation and pigmentation rebound. The has cautioned against such unregulated applications, emphasizing risks from unmonitored formulations exceeding safe thresholds, though comprehensive data remains limited in these regions. Certain Asian countries permit hydroquinone under prescription-only conditions with mandated monitoring, such as in where the Health Sciences Authority prohibits it in cosmetics but allows therapeutic use for disorders under medical supervision to mitigate misuse risks. Similar frameworks in places like involve regulatory crackdowns on illegal over-the-counter sales, relying on to track post-marketing adverse effects, though compliance varies and contributes to uneven international standards.

Debates on Risk Assessment and Policy Overreach

Critics of hydroquinone regulations argue that bans on its cosmetic use, implemented in 2001, exemplify precautionary overreach by prioritizing genotoxicity data over extensive epidemiological evidence showing no causal link to carcinogenicity or widespread at therapeutic doses. Animal studies indicating mutagenicity in high-dose models have driven restrictions despite metabolic differences between species—such as ' rapid conjugation and excretion of hydroquinone versus slower processing—and the absence of corresponding tumors in long-term users. Dermatologists, including those responding to proposed U.S. restrictions, contend that such extrapolations ignore real-world safety, with exogenous occurring primarily from chronic high-dose misuse in unregulated contexts rather than supervised low-concentration application. The American Society for Dermatologic Surgery (ASDS) maintains that hydroquinone remains a cornerstone for treating disorders like when used judiciously, critiquing blanket bans for disregarding its proven efficacy and safety profile in clinical practice. Policy decisions influenced by cultural stigma against skin lightening—often conflating cosmetic vanity with medical necessity—undermine therapeutic access, as hydroquinone's tyrosinase inhibition provides unmatched for conditions unresponsive to alternatives. Post-ban proliferation of illegal markets in restricted regions has exacerbated risks, with unregulated products frequently containing hydroquinone concentrations exceeding 5-10% or adulterants like mercury, leading to higher incidences of adverse effects than regulated use would entail. Advocates for evidence-based reform call for dose-specific approvals, citing over 40 years of U.S. prescription and over-the-counter data (up to 2% concentrations) demonstrating minimal systemic absorption and rare side effects under dermatologic oversight, which outweigh hypothetical risks from animal models. Such barriers impose economic costs, including reduced access for patients with —prevalent in diverse populations—and drive reliance on inferior or hazardous substitutes, underscoring the need to balance rare misuse concerns against broad clinical utility. Recent reviews affirm hydroquinone's safety in intermittent, supervised regimens, challenging precautionary policies that prioritize theoretical harms over human outcomes.

Natural and Environmental Aspects

Natural Biosynthesis and Sources

Hydroquinone is biosynthesized in plants primarily as the glucoside arbutin (β-D-glucopyranoside of hydroquinone), which serves as a storage form and is hydrolyzed to free hydroquinone by β-glucosidases upon need, such as in response to environmental stress or microbial attack. In bearberry (Arctostaphylos uva-ursi) leaves, arbutin concentrations reach up to 10% of dry weight, making it a prominent natural source; similar but lower levels occur in pear bark, wheat germ, and other species like Pyrus and Triticum. This glycosylated form predominates in plant tissues to mitigate the compound's reactivity and potential toxicity. In certain animals, hydroquinone functions as a biochemical precursor in defensive mechanisms. Bombardier beetles (Brachinus and related genera) store hydroquinone in abdominal reservoirs alongside ; upon threat, enzymes catalyze its oxidation to p-benzoquinone, generating (up to 88°C) and for explosive ejection as a deterrent spray. Microbial pathways contribute to hydroquinone production via enzymatic of phenol or related aromatics, as seen in methylotrophic and fungi capable of position-specific ring modifications under aerobic conditions. These processes occur in natural environments, such as or decaying plant matter, though yields remain low without optimization. Trace dietary exposure to free hydroquinone occurs through common foods, with concentrations of 0.2 ppm in , 0.2–0.4 ppm in cereals, 0.5 ppm in , and 0.1 ppm in ; additional intake derives from hydrolysis in the gut from bearberry-derived teas or similar. Overall, such endogenous and dietary levels are orders of magnitude below anthropogenic inputs from industrial emissions and consumer products.

Environmental Persistence and Biodegradation

Hydroquinone demonstrates limited environmental persistence primarily due to abiotic degradation pathways, including photo-oxidation and auto-oxidation in aqueous media. In sunlit surface waters, photo-oxidation proceeds rapidly, with a conservatively estimated of 20 hours driven by reaction with hydroxyl radicals. Auto-oxidation to p-benzoquinone occurs upon exposure to air and light, further reducing its stability in oxic environments. These processes confine hydroquinone's aqueous to hours rather than days or weeks under typical environmental conditions. Biodegradation further limits persistence, as hydroquinone is classified as readily biodegradable under standardized conditions. In Test Guideline 301C assays using inoculum, it achieved 70% degradation within 28 days, meeting the criteria for ready biodegradability (≥60% theoretical oxygen demand in ≤10 days). Laboratory studies report primary degradation within 1 day, while microbial cometabolism by species such as facilitates rapid breakdown in and natural systems. Products of biodegradation, including polymerization to humic-like acids, integrate into without accumulating. The compound's (log Kow) of 0.59–0.61 indicates low hydrophobicity and negligible potential in aquatic or terrestrial organisms, as values below 3 typically preclude significant partitioning into lipids. Releases to the environment occur mainly through wastewater effluents from , rubber production, and , though dilution and treatment in sewage systems promote effective removal via processes. Acute ecotoxicity is evident, with LC50 values for (e.g., Pimephales promelas), , and ranging from 0.050–0.335 mg/L, reflecting sensitivity in short-term exposures. However, the compound's rapid degradation kinetics and microbial cometabolism reduce chronic exposure risks in receiving waters.

References

  1. https://pubchem.ncbi.nlm.nih.gov/compound/Hydroquinone
  2. https://byjus.com/chemistry/hydroquinone/
  3. https://www.chemicalbook.com/ChemicalProductProperty_EN_CB6717931.htm
  4. https://ijdvl.com/history-of-hydroquinone/
  5. https://inchem.org/documents/ehc/ehc/ehc157.htm
  6. https://www.eastman.com/en/products/product-detail/71001349/hydroquinone-photographic-grade
  7. https://pmc.ncbi.nlm.nih.gov/articles/PMC10723018/
  8. https://www.ncbi.nlm.nih.gov/books/NBK539693/
  9. https://www.fda.gov/consumers/skin-facts-what-you-need-know-about-skin-lightening-products/skin-product-safety
  10. https://nj.gov/health/eoh/rtkweb/documents/fs/1019.pdf
  11. https://www.osha.gov/chemicaldata/175
  12. https://www.ncbi.nlm.nih.gov/books/NBK499038/
  13. https://chemicalsafety.ilo.org/dyn/icsc/showcard.display?p_card_id=0166
  14. https://www.chemicalbook.com/ChemicalProductProperty_US_CB6717931.aspx
  15. https://cameochemicals.noaa.gov/chemical/3626
  16. https://www.sigmaaldrich.com/US/en/sds/sial/h9003
  17. https://www.statlab.com/pdfs/sds/Hydroquinone_Safety_Data_Sheet.pdf
  18. https://stacks.cdc.gov/view/cdc/19410/cdc_19410_DS1.pdf
  19. https://ijdvl.com/content/126/2022/0/1/pdf/IJDVL-657-2021.pdf
  20. https://www.britannica.com/biography/Sir-William-de-Wiveleslie-Abney
  21. https://www.encyclopedia.com/science/dictionaries-thesauruses-pictures-and-press-releases/abney-william-de-wiveleslie
  22. https://www.sciencedirect.com/topics/chemistry/hydroquinone
  23. https://www.eastman.com/en/who-we-are/history/timeline
  24. https://blog.drbrandtskincare.com/ingredient-spotlight-hydroquinone/
  25. https://onlinelibrary.wiley.com/doi/full/10.1002/der2.134
  26. https://pubmed.ncbi.nlm.nih.gov/17177740/
  27. https://www.dermatologytimes.com/view/hydroquinone-has-long-history
  28. https://www.chemicalbook.com/synthesis/hydroquinone.htm
  29. https://patents.google.com/patent/CN102351656B/en
  30. https://www.sciencedirect.com/science/article/pii/S0926961496800268
  31. https://www.sciencedirect.com/science/article/abs/pii/S0920586115001340
  32. https://www.researchgate.net/figure/Synthesis-of-hydroquinone-HQ-from-benzene-by-the-conventional-route-A-the-newly_fig1_329398775
  33. https://patents.google.com/patent/US3798277
  34. https://www.sciencedirect.com/science/article/abs/pii/S0926860X00007146
  35. https://www.chemanalyst.com/industry-report/hydroquinone-market-3129
  36. https://www.pharmacompass.com/manufacturers-suppliers-exporters/hydroquinone
  37. https://www.linkedin.com/pulse/north-america-high-purity-hydroquinone-market-hjpbc/
  38. https://patents.google.com/patent/CN115043710A/en
  39. https://www.imarcgroup.com/phenol-pricing-report
  40. https://www.imarcgroup.com/hydroquinone-pricing-report
  41. https://www.chemanalyst.com/Pricing-data/hydroquinone-1392
  42. https://dash.harvard.edu/bitstreams/7312037d-dc27-6bd4-e053-0100007fdf3b/download
  43. https://pubs.aip.org/aip/jcp/article/131/15/154504/317172/Redox-potentials-and-pKa-for-benzoquinone-from
  44. https://chemistry-europe.onlinelibrary.wiley.com/doi/10.1002/cctc.202401048
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC4643184/
  46. https://www.researchgate.net/publication/232744044_Role_of_PCET_in_the_Redox_Interconversion_between_Benzoquinone_and_Hydroquinone
  47. https://www.sciencedirect.com/science/article/pii/000927979190022Y
  48. https://pmc.ncbi.nlm.nih.gov/articles/PMC2936108/
  49. https://www.researchgate.net/publication/284274797_Selective_Monoetherification_of_14-Hydroquinone_Promoted_by_NaNO2
  50. https://www.sciencedirect.com/science/article/abs/pii/S0920586100003436
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC10870825/
  52. https://www.sciencedirect.com/science/article/abs/pii/S0022072808003070
  53. https://www.sciencedirect.com/science/article/abs/pii/S1093326321000085
  54. https://pubs.acs.org/doi/10.1021/acs.joc.4c02662
  55. http://www.michaelandpaula.com/mp/developerintro.html
  56. https://www.photomemorabilia.co.uk/Developer_Chemistry.html
  57. https://patents.google.com/patent/US2805947
  58. https://timlaytonfineart.com/black-and-white-developer-formulas/
  59. https://www.reportsanddata.com/report-detail/hydroquinone-market
  60. https://www.archivemarketresearch.com/reports/photographic-grade-hydroquinone-61751
  61. https://hpvchemicals.oecd.org/UI/handler.axd?id=7ca97271-99ed-4918-90e0-5c89d1ce200c
  62. https://patents.google.com/patent/US2875174A/en
  63. https://www.chempoint.com/insights/eastman-hydroquinone-inhibitors-for-polymerization
  64. https://www.researchgate.net/figure/llustration-of-the-mechanism-of-hydroquinone-as-a-polymerization-inhibitor_fig3_366343399
  65. https://www.archivemarketresearch.com/reports/solid-hydroquinone-420386
  66. https://www.globalgrowthinsights.com/market-reports/hydroquinone-market-109833
  67. https://webbook.nist.gov/cgi/cbook.cgi?ID=123-31-9
  68. https://pubs.rsc.org/en/content/articlelanding/2022/ay/d2ay01631a
  69. https://www.nims.go.jp/eng/press/2023/10/202310180.html
  70. https://www.eurekalert.org/news-releases/1030957
  71. https://pmc.ncbi.nlm.nih.gov/articles/PMC2625402/
  72. https://www.sciencedirect.com/science/article/abs/pii/S0278691598001276
  73. https://www.sciencedirect.com/science/article/pii/S0022202X15479783
  74. https://pubmed.ncbi.nlm.nih.gov/1899343/
  75. https://www.tandfonline.com/doi/full/10.3109/14756366.2015.1004058
  76. https://www.nature.com/articles/srep34993
  77. https://www.sciencedirect.com/topics/medicine-and-dentistry/hydroquinone
  78. https://pmc.ncbi.nlm.nih.gov/articles/PMC9532501/
  79. https://karger.com/spp/article/29/6/300/295889/In-vitro-Dermal-Absorption-of-Hydroquinone
  80. https://pmc.ncbi.nlm.nih.gov/articles/PMC2807702/
  81. https://www.researchgate.net/publication/8992810_Safety_and_efficacy_of_4_hydroquinone_combined_with_10_glycolic_acid_antioxidants_and_sunscreen_in_the_treatment_of_melasma
  82. https://link.springer.com/article/10.1007/s40257-024-00863-2
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC3848650/
  84. https://www.cureus.com/articles/167988-azelaic-acid-versus-hydroquinone-for-managing-patients-with-melasma-systematic-review-and-meta-analysis-of-randomized-controlled-trials
  85. https://pmc.ncbi.nlm.nih.gov/articles/PMC3657227/
  86. https://pubmed.ncbi.nlm.nih.gov/21623930/
  87. https://jddonline.com/articles/clinical-evaluation-of-a-4-hydroquinone-1-retinol-treatment-regimen-for-improving-melasma-and-photod-S1545961616P1435X
  88. https://www.jaad.org/article/S0190-9622%2811%2901988-8/fulltext
  89. https://pubmed.ncbi.nlm.nih.gov/17030380/
  90. https://www.cdc.gov/niosh/idlh/123319.html
  91. https://westliberty.edu/health-and-safety/files/2012/08/Hydroquinone.pdf
  92. https://ec.europa.eu/health/scientific_committees/consumer_safety/docs/sccs_o_183.pdf
  93. https://www.phfscience.nz/media/1rgelgbc/esr-health-risk-assessment-hydroquinone-skin-lightening-products.pdf
  94. https://cir-safety.org/sites/default/files/hyrdoquinone.pdf
  95. https://pubmed.ncbi.nlm.nih.gov/9638901/
  96. https://pubmed.ncbi.nlm.nih.gov/34486734/
  97. https://pubmed.ncbi.nlm.nih.gov/10379810/
  98. https://pmc.ncbi.nlm.nih.gov/articles/PMC10755631/
  99. https://www.tandfonline.com/doi/abs/10.1080/10408449991349221
  100. https://ntp.niehs.nih.gov/sites/default/files/ntp/htdocs/lt_rpts/tr366.pdf
  101. https://www.sciencedirect.com/science/article/pii/027869159290075V
  102. https://publications.iarc.who.int/_publications/media/download/2310/335e6c753bb32e16b6226bc84df2e9c5cacbd319.pdf
  103. https://pubmed.ncbi.nlm.nih.gov/18027166/
  104. https://www.cir-safety.org/sites/default/files/Hydroq_032014_Rep.pdf
  105. https://pubmed.ncbi.nlm.nih.gov/10828212/
  106. https://academic.oup.com/toxsci/article/82/1/9/1651540
  107. https://www.federalregister.gov/documents/2006/08/29/E6-14263/skin-bleaching-drug-products-for-over-the-counter-human-use-proposed-rule
  108. https://www.fda.gov/drugs/drug-safety-and-availability/fda-works-protect-consumers-potentially-harmful-otc-skin-lightening-products
  109. https://www.asds.net/Portals/0/PDF/asdsa/asdsa-position-statement-hydroquinone.pdf
  110. https://www.hfpappexternal.fda.gov/scripts/fdcc/index.cfm?set=IndirectAdditives&id=HYDROQUINONE
  111. https://www.fda.gov/inspections-compliance-enforcement-and-criminal-investigations/warning-letters/confer-707691-08012025
  112. https://www.foodresearchlab.com/insights/recall/2025-fda-skin-lightening-product-recall-mercury-hydroquinone/
  113. https://www.mdpi.com/2076-3417/12/6/3177
  114. https://www.safecosmetics.org/chemicals/hydroquinone/
  115. https://www.medicinenet.com/fda_proposes_hydroquinone_ban/views.htm
  116. https://mederbeauty.com/blogs/blog/ingredient-ban
  117. https://www.dermatologytimes.com/view/distant-decisions
  118. https://www.nature.com/articles/s41598-023-47160-2
  119. https://www.hsa.gov.sg/announcements/safety-alert/hsa-updates-on-products-found-overseas-that-contain-potent-ingredients-%28april-2022%29
  120. https://asianews.network/indonesian-drug-regulator-cracks-down-on-illegal-prescription-skincare-products/
  121. https://www.jaad.org/article/S0190-9622%2807%2900431-8/abstract
  122. https://pmc.ncbi.nlm.nih.gov/articles/PMC12335261/
  123. https://www.hmpgloballearningnetwork.com/site/thederm/article/6562
  124. https://pubmed.ncbi.nlm.nih.gov/38850450/
  125. https://pmc.ncbi.nlm.nih.gov/articles/PMC6766929/
  126. https://www.frontiersin.org/journals/bioengineering-and-biotechnology/articles/10.3389/fbioe.2022.914280/full
  127. https://biotechnologyforbiofuels.biomedcentral.com/articles/10.1186/s13068-024-02540-2
  128. https://pmc.ncbi.nlm.nih.gov/articles/PMC3565695/
  129. https://www.chemistrysteps.com/the-chemistry-behind-bombardier-beetles-spray/
  130. https://www.sciencedirect.com/science/article/pii/016816569090008Y
  131. https://pmc.ncbi.nlm.nih.gov/articles/PMC3727088/
  132. https://pubmed.ncbi.nlm.nih.gov/8568910/
  133. https://www.tandfonline.com/doi/pdf/10.1080/009841096161915
  134. https://cdnservices.industrialchemicals.gov.au/statements/EVA00106%2520-%2520Evaluation%2520Statement%2520-%252022%2520December%25202022.pdf
  135. https://echa.europa.eu/de/registration-dossier/-/registered-dossier/14417/5/1
Add your contribution
Related Hubs
User Avatar
No comments yet.