Table 1.

A summary table of the main biological mechanisms and clinical effects of acute exposure to exposome factors

Acute stress	Skin function affected	Main biological mechanisms	Clinical manifestations
Solar radiation	Barrier	TEWL	Dryness
	Pigmentation	Melanogenesis	PIHP, tanning, melasma exacerbation, dark spots
	Defences	Oxidative stress, 31 DNA damage, inflammation, 19 decrease in epidermal Langerhans cells, 35 Treg expansion, 36 , 37 microbiome alteration, 21 photoimmunosuppression 19	Sunburn, photosensitivity, photoallergy, actinic keratoses, viral reactivation, herpes labialis. Improvement of some dermatoses (psoriasis, atopic dermatitis), Koebner phenomenon, photodermatoses (e.g. polymorphous light eruption)
	Neuroendocrinology	Neurogenic inflammation, 44 , 45 upregulation of CRH, 46 , 47 vitamin D synthesis, opioid release, 42 decreased blood pressure 39	Pruritus, hypersensitivity, atopic dermatitis, rosacea
	Thermoregulation function and systemic effect	Vasodilatation 49 , 50	Fever, erythema, rosacea flushes
	Skin structure	Hyaluronic acid degradation from epidermis and dermis extracellular matrix degradation via oxidative stress	Dryness, wrinkles, skin laxity
Pollution	Barrier	Change in sebum, squalene peroxidation 58	Dryness, skin sensitivity Flares of acne, atopic dermatitis
	Pigmentation	Pigmentation 57	Dark spots
	Defences	Oxidative stress, 60 , 61 microbiome alteration, 65 pro‐inflammatory immune response	Flares of acne, atopic dermatitis
	Neuroendocrinology	Neurotrophic factor artemin 69	Pruritus, flares of atopic dermatitis
Pollution and ultraviolet radiation	Defences	Oxidative stress 74 , pigmentation, oxinflammation 64	Photoaging, dark spots and wrinkles
Meteorological changes	Barrier	TEWL, 75 , 78 sebum production	Dryness, oily skin and scalp, pruritus, flares/improvement of atopic dermatitis, psoriasis
	Structure	Hypersudation	Sweat
	Defences	Inflammation 67	Skin sensitivity, flares of atopic dermatitis, rosacea
Psychosocial stress	Barrier	TEWL, tight junction dysfunction	Dryness, transgression of microbes, toxins, allergens
	Structure		Piloerection, sweating, hair loss by anagen termination and telogen effluvium, alopecia
	Defences	Oxidative stress, inflammation 102 , immune suppression	Flares of acne, rosacea, psoriasis, alopecia areata, vitiligo, seborrhoeic dermatitis, atopic dermatitis, skin superinfection, viral reactivation
	Neuroendocrinology	Neurogenic inflammation, hyper‐innervation, 87 , 88 , 90 upregulation of CRH 94 , 95 , 96	Erythema, oedema, pruritus, pain
	Thermoregulation	Vasodilation, vasoconstriction	Pale skin, hypothermia, redness
Sleep deprivation	Barrier	TEWL 7	Dryness, dullness
	Defences	Oxidative stress, 111 inflammation 107	Pruritus, flares of psoriasis, atopic dermatitis, seborrhoeic dermatitis, acne, skin superinfection, viral reactivation
Nutrition	Barrier	Lipid/ sebum production 121 , 124	Dry skin, oily skin
	Defences	Antioxidant, inflammation, 123 allergic reactions, 130 microbiome 122	Acne, atopic dermatitis, systemic contact dermatitis
	Neuroendocrinology		Flushing, rosacea exacerbations
Hormonal variations	Skin barrier		Oily skin, dry skin
	Structure	Hypersudation	Telogen effluvium, androgenic alopecia
	Defences	Oxidative stress, melatonin (antioxidant), oxytocin 140 , inflammation 136 , 138	Acne, atopic dermatitis, aphtous ulcers
	Neuroendocrinology	Stimulation of the HPA, 142 , 143 GC, 144 modulation of skin neuropeptides 145	Progesterone dermatitis
Medications and procedures	Skin barrier		Irritation, dryness and erythema
	Defences	Inflammation, antimicrobial response, 152 , 153 changes in microbiome	Acne, superinfection, viral reactivation
Mask use, disinfectants, frequent washing	Barrier and defence	Skin temperature, sebum, TEWL 158	Dryness, pruritus, skin sensitivity, erythema, acne and rosacea flares

CA, cholinergic axis; CRH, corticotrophin‐releasing hormone; HPA, hypothalamus–pituitary–adrenal axis; PIHP, postinflammatory hyperpigmentation; TEWL, trans‐epidermal water loss;