Hydrocarbon Keratosis

Clinical and Pathological Features

Causes and Risk Factors

• Sources of Chronic PAH Exposure:
  • Industrial occupations: asphalt and tar workers, coke-oven workers, chimney sweeps, oil refinery workers, mechanics and machinists with long-term exposure to lubricating and mineral oils (crankcase oil/cutting oils), and woodworkers using creosote (a wood preservative).
  • Medical treatment: years of using coal tar preparations to treat psoriasis or atopic dermatitis.
• How PAHs Damage Cells and Cause Epidermal Dysplasia (Carcinogenesis):
  • Formation of DNA adducts: once PAHs (benzo[a]pyrene is the classic example) enter the skin, cytochrome P450 enzymes (CYP1A1, CYP1B1) convert them into a reactive epoxide (BPDE). This binds covalently to guanine in DNA, forming PAH–DNA adducts.
  • Mutation of the tumor suppressor gene TP53: these DNA adducts cause copying errors that lead to point mutations in TP53 (mainly G>T transversions), so damaged keratinocytes can no longer self-destruct (apoptosis).
  • Synergy with ultraviolet (UV) light: PAHs act as photosensitizers. When PAH-contaminated skin is exposed to sunlight, a phototoxic reaction multiplies the production of reactive oxygen species (ROS) and speeds up malignant change.

Clinical Features

Lesions usually appear after 10–20 years of chronic exposure, on skin that is in direct contact with, or rubbed by clothing soaked in, oil or tar:

• Typical sites: the backs of the hands, forearms, face and neck (exposed skin) and, notably, the scrotum and groin folds in men (from touching the area with oily hands when using the toilet, or from oil-soaked work clothes rubbing against it).
• Appearance:
  • Gray-brown, dark brown or grayish-black scaly papules or plaques, 2–8 mm across.
  • A dry, rough surface that feels like sandpaper and is firmly stuck to the skin beneath.
  • Often found on skin showing other PAH-related changes: patchy or spotty hyperpigmentation (tar melanosis), fine dilated vessels, or oil/tar acne with many blackheads and blocked sebaceous follicles. (Chloracne is a different condition, caused by halogenated hydrocarbons such as dioxins and PCBs.)
• Malignant transformation:
  • A hydrocarbon keratosis that thickens, develops a broad base, ulcerates, cracks or becomes firm and indurated is a sign of progression to Bowen's disease (cSCC in situ) or invasive squamous cell carcinoma (invasive cSCC).
  • Hydrocarbon keratoses turn malignant more often than ordinary actinic keratoses because PAHs are directly genotoxic.

Microscopic Features (Histopathology)

• Hyperkeratosis and papillomatous acanthosis: a markedly thickened stratum corneum with alternating columns of parakeratosis (retained nuclei) and orthokeratosis (no nuclei).
• Basal keratinocyte dysplasia:
  • Keratinocytes in the basal and parabasal layers are enlarged, with dark, irregular nuclei and loss of polarity.
  • The rete ridges are elongated and extend into the upper dermis.
• Pigment deposits and dermal inflammation:
  • Pigment incontinence, with many macrophages in the upper dermis that have engulfed melanin and carbon particles.
  • A chronic inflammatory infiltrate of lymphocytes and plasma cells around dilated blood vessels.

Differential Diagnosis and Immunohistochemistry (IHC)

Our Approach to Treating Hydrocarbon Keratosis

At Haute-Derma, we manage hydrocarbon keratosis on two principles: removing occupational exposure and using tissue-sparing destructive treatment:

• Cutting off PAH exposure: we guide patients to wear proper protective workwear and chemical-resistant gloves, stop using coal tar products, and keep strict personal hygiene (changing out of oily clothes right after work and washing the scrotum and groin thoroughly).
• Regular dermoscopic screening of all exposed skin and the scrotum: every at-risk site is checked periodically so precancerous lesions are caught before they become invasive.
• Field-directed therapy combined with targeted destruction: visible keratotic papules are destroyed while hidden microscopic damage across the affected skin is cleared at the same time.

How We Diagnose Hydrocarbon Keratosis at Haute-Derma

• Detailed Occupational and Medical History: we record how long and how heavily you have been exposed to asphalt, coal, machine oils or creosote, and any past use of coal tar for psoriasis.
• High-Resolution Dermoscopy:
  • Hydrocarbon keratosis papules: gray-brown to black scale, a rhomboidal or "strawberry" pattern, and follicular openings plugged with dark keratin.
  • Surrounding skin: an irregular gray-brown pigment network (tar melanosis) and blackheads of oil/tar acne.
• Skin Biopsy for Histopathology (Punch Biopsy): required for raised, thickened, cracked or bleeding papules, or any with a firm base, to rule out invasive squamous cell carcinoma.
• Immunohistochemistry (p53, Ki-67): stratifies the risk of malignancy using the Ki-67 proliferation index and the TP53 mutation pattern.

Specialized Treatments at Haute-Derma

• UltraPulse CO2 Laser Ablation: our preferred option at Haute-Derma for precisely removing the dysplastic epidermis. The CO2 laser vaporizes keratotic lesions quickly and seals blood vessels, so the procedure is bloodless, recovery is fast and there are no contracting scars (making it especially safe for thin skin such as the scrotum and backs of the hands).
• Topical Field Therapy:
  • 5-fluorouracil cream (5-FU 5%): applied once or twice daily for 2–4 weeks. It selectively destroys abnormally proliferating keratinocytes.
  • Imiquimod 5% cream: applied 3 times a week for 4–8 weeks. It stimulates the local immune system to clear PAH-damaged cells.
• Photodynamic Therapy (PDT): the photosensitizer 5-ALA is applied and left on for 3 hours, then activated with red laser light (630 nm). This treats widespread microscopic damage across chronically PAH-exposed forearms or face.
• Mohs Surgery / Wide Excision: required once a hydrocarbon keratosis has progressed to invasive squamous cell carcinoma (invasive cSCC) or to extensive Bowen's disease on the scrotum.