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The skin aging exposome

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The skin aging exposome

TL;DR

Foundational consensus review from a European board of environmental-medicine and skin-biology specialists. Proposes a formal definition of the skin aging exposome and catalogues the evidence base for each component factor: solar radiation (UVR + visible light + IRA), air pollution (PM, NO₂, ozone), tobacco smoke, nutrition, and a miscellaneous cluster (stress, sleep deprivation, temperature, cosmetics). Key thesis: these factors do not act additively — molecular crosstalk between exposure components produces net effects on skin aging that exceed the sum of individual contributions. Concludes that daily broad-spectrum UVA+UVB sunscreen is the best-evidenced single protective intervention, citing the only adequately powered adult RCT at that date (Hughes et al. 2013). 669 citations (FWCI 24.8; 100th percentile) as of 2026 archive record; functionally foundational to the exposome-in-dermatology literature.

What is the skin aging exposome?

The exposome concept was coined in 2005 by cancer epidemiologist Christopher Wild to describe the totality of non-genetic exposures a human individual is subject to from conception to death 1. The skin aging exposome, as defined in this paper, encompasses:

“External and internal factors and their interactions, affecting a human individual from conception to death as well as the response of the human body to these factors that lead to biological and clinical signs of skin aging.”

The review argues skin is a paradigmatic organ for exposome research because: (i) it is the primary interface with the external environment, (ii) the biological responses of skin to environmental threats are well characterised at cellular and molecular levels, and (iii) prior research had almost exclusively studied exposure components in isolation rather than as an interacting system.

Components of the skin aging exposome

ComponentSub-categoriesEvidence levelPrimary mechanism
Solar radiation — UVUVB (280–315 nm); UVA₂ (315–340 nm); UVA₁ (340–400 nm)Strong (decades of mechanistic + epidemiological data)MMP induction via AP-1/NF-κB; DNA oxidation; ROS generation; fibroblast senescence
Solar radiation — visible light400–740 nm; blue-violet (415 nm) most bioactiveEmergingROS via carotenoid depletion; pigmentation via distinct pathway (not ROS-mediated for VL-specific effect)
Solar radiation — infrared-A (IRA)740–1400 nm; IRA = 30% of total IRR; 65% of IRA reaches the dermisEmergingMMP-1 induction via heat/ROS; elastotic material accumulation
Air pollutionPM₂.₅, PM₁₀; NO₂; ozone; polycyclic aromatic hydrocarbonsModerate (epidemiological + in vitro)AhR activation → MMP-1; oxidative stress; pigmentation
Tobacco smoke3,800+ compounds; nicotine, N-nitrosonornicotine, acroleinModerate (epidemiological + in vitro)MMP-1 via AhR; MITF-mediated melanogenesis; reduced microcirculation; oxidative fibroblast damage
NutritionDietary antioxidants, glycaemic load, fat/CHO balanceLimited–moderate (epidemiological)AGE formation; ROS balance; skin pigmentation
StressPsychological/chronic; HPA axis activationLimited (indirect evidence only)ROS; DNA damage; epidermal barrier disruption via cortisol/catecholamines/neuropeptides
Sleep deprivation<5 h/night; sleep-disturbed subjectsLimited (experimental studies, small n)Epidermal permeability barrier impairment; perceived skin aging (observer-rated)
TemperatureHeat (IRA-driven + occupational ovens/glass blowers); cold not shown to age skinLimitedTropoelastin/fibrillin-1/MMP-12 accumulation in dermis; angiogenesis
CosmeticsTopical products; endocrine-disrupting compounds in poorly-regulated productsVariableBarrier function alteration; chemical penetration

Solar radiation: key mechanistic claims

UV radiation (UVB/UVA)

Photoaging affects all three skin compartments — epidermis, dermis, and hypodermis. Dermal changes are primary; epidermal changes are often secondary, propagated by paracrine signals from aged fibroblasts. Key mechanistic points extracted from the review:

  • All three UV wavelengths (UVB, UVA₂, UVA₁) contribute to photoaging 2; UVA₁ penetrates deepest (reaching dermis), contributing most to chronic low-dose collagen degradation.
  • Susceptibility to photoaging is influenced by endogenous protection: skin pigmentation, DNA-repair capacity, and antioxidant defence, all of which vary between ethnic groups and individuals.
  • Sub-erythemogenic UV dose is sufficient — photoaging results principally from daily exposure to non-extreme, low doses that cause no visible redness. Krutmann et al. state this as a key conclusion (item vi, p.154) citing a block of review papers (refs [13–19]) rather than a single primary source. The independent mechanistic demonstration that MMP mRNA, protein, and activity are induced in human skin in vivo within hours of a sub-erythemogenic dose is from Fisher 1996 3, which is cited in the broader photoaging literature but does not appear in Krutmann 2017’s reference list. needs-canonical-id — Krutmann 2017 does not directly cite Fisher 1996; sub-erythemogenic MMP induction evidence attributed to refs [13–19] (review block) in Krutmann.
  • Acute stress responses (MMP induction, proinflammatory cytokines) and chronic responses (accumulation of macromolecular damage — mitochondrial DNA, oxidised proteins) both drive the skin aging process.
  • Evidence is high that daily sunscreen use can delay photoaging [see Sunscreen section below].

Visible light and IRA

Visible light (400–740 nm) and IRA (740–1400 nm) are more recently recognised contributors. The review characterises them as less well-established than UV but with growing mechanistic evidence:

  • VL and IRA from natural sunlight induce MMP-1 production in exposed skin — confirmed when UV was filtered out by black clothing, leaving only VL and IRA to act 4. The IRA response may be partially heat-mediated.
  • IRA induces radical species in the skin measurable in vivo 5; exposure modulates stratum corneum ceramide subclasses and squalene.
  • Blue-violet light (415 nm) induces marked, prolonged dose-related pigmentation at physiological doses — via a distinct pathway from UVB-induced pigmentation, not associated with ROS production 6. This has implications particularly for darker-skinned individuals.
  • At cellular level: red light (632 nm, 648 nm) and IRA (850 nm, 940 nm) have no impact on proliferation; blue light (412 nm, 419 nm, 426 nm) decreases proliferation and promotes keratinocyte differentiation 7.

needs-replication: the relative contribution of IRA-driven skin aging to overall lifetime photoaging burden has not been quantified in a dedicated human intervention study as of the review date.

Air pollution

A relationship between air pollution and skin aging was first shown in the SALIA study (epidemiological study of elderly Caucasian women), demonstrating that traffic-related PM contributes to skin aging signs 8. Further cross-sectional studies in China (rural vs urban) provided additional epidemiological evidence.

  • NO₂ and pigment spot formation: An increase of 10 µg/m³ NO₂ was associated with 25% more pigment spots on cheeks in German women and 24% in Chinese women 9. needs-replication in other cohorts.
  • Ozone and wrinkling: Ground-level ozone exposure may be associated with wrinkle formation in the face (epidemiological) 10; ozone depletes antioxidants from the stratum corneum and increases lipid peroxidation in mouse skin 11.
  • Mechanism — AhR activation: In vitro, ozone and PM (soot + polycyclic aromatic hydrocarbons) activate the aryl hydrocarbon receptor (AhR) in cultured keratinocytes 12. AhR activation induces MMP-1, consistent with PM-driven matrix degradation. Gene-environment interaction studies demonstrate women with high genetic risk scores for AhR pathway variants developed 52% (95% CI: 14–104%) more lentigines after an increase of 4.45 µg/m³ PM₂.₅ 13.

Practical implication from the review: daily rinse-off cleansing to reduce particle load on the skin surface; topical antioxidants to reduce harm from ozone and IRA.

Tobacco smoke

The relationship between cigarette smoking and skin aging is supported by epidemiological and in vitro mechanistic evidence. Points extracted from the review:

  • Epidemiology: One twin study estimated that 10 years of smoking corresponds to approximately 2.5 years’ older appearance 14. Female Japanese smokers have darker skin colour than non-smokers (epidemiological) 15.
  • Facial wrinkling: Smoking is associated with increased wrinkles, tissue laxity, and pigmentary changes — especially around the mouth and upper lip — documented in twin studies 16.
  • Microcirculation: One inhalation from a cigarette produces reduced blood flow in skin microcirculation for up to 2 minutes after consumption, regardless of nicotine concentration 17.
  • MMP-1 mechanism: MMP-1 mRNA is elevated in smoker vs non-smoker skin; AhR pathway activation is implicated 18. Cigarette smoke extract also significantly increases MITF expression in melanocytes in a dose-dependent manner via AhR-mediated mechanisms, promoting melanin production 19.
  • Fibroblast damage: Cigarette smoke extract impairs fibroblast growth and proliferation and leads to features similar to those seen in senescent fibroblasts. Oxidative stress injury and inhibition of antioxidant defence activity are proposed mechanisms 20.

Cumulative dose uncertainty: How much is due to direct skin exposure vs systemic exposure following inhalation has not been established.

Nutrition

  • Dietary antioxidants (vitamins C, E; carotenoids; flavonoids; polyphenols) appear to delay aging effects; higher vitamin C intake is associated with lower likelihood of wrinkled appearance in an epidemiological study (n not specified in review) 21.
  • Higher fat and carbohydrate intake were associated with higher likelihood of wrinkled appearance in the same study.
  • AGEs and skin: Consuming too much sugar promotes glycation (Maillard reaction in vivo); AGE deposits have been observed in fibronectin, laminin, elastin, and collagen in the dermis from age 35. Exogenous glycation via food-derived AGEs (grilling, frying) also contributes.
  • Beta-carotene supplementation (30 mg/day) and retinyl palmitate (25,000 IU/day, taken long-term) were associated in one large study with increased incidence of lung cancer (28%), death (17%), and cardiovascular disease mortality in the intervention group vs placebo 22. The review warns against high-dose isolated antioxidant supplementation; fruit and vegetable consumption is recommended as a balanced, safe approach.
  • Nutrition contribution to skin aging is estimated to account for up to 30% of wrinkle formation in Japanese women 23. needs-replication

Miscellaneous factors

Stress

There is clinical evidence that psychological stress affects skin integrity, but the review reports no direct evidence that stress exacerbates skin aging as of 2017. The underlying mechanisms — chronic HPA activation, catecholamines, neuropeptides, elevated ROS, DNA damage, epidermal barrier disruption — are individually plausible but not causally linked to skin aging in humans with adequately powered studies 24.

Sleep deprivation

  • Sleep-deprived subjects appear markedly less healthy and attractive; rating studies document changes in skin colour parameters (observer and instrument) 25.
  • A cross-sectional study of 60 women found that those who slept <5 h/night had more intrinsic aging signs by SCINEXA score 26.
  • Reduced epidermal permeability barrier function is observed during periods of psychological stress due to lack of sleep 27.

Temperature

  • IRA drives heat deposition in the skin; skin temperature can exceed 40°C under direct IRR.
  • In vivo buttock skin study at 43°C × 90 min: increased tropoelastin expression in epidermis and dermis; increased MMP-12 expression; modulation of fibrillin-1 28.
  • “Thermal aging” has been proposed as a concept by Seo and Chung 29.

Cosmetics

The review discusses cosmetics as part of the exposome with a focus on their safety framework. “Traditional” cosmetics or those made without strict safety rules can be harmful and contribute negatively to the skin exposome 30. unsourced — the specific harmful-ingredient claim lacks primary evidence citations in the review itself.

Factor interactions and non-additivity

Section 4 of the paper is its most conceptually novel contribution. Key claims:

  • UVA × UVB crosstalk: Sequential UVA+UVB irradiation of human epidermal keratinocytes produces a third, distinct ERK1/2 and p38/JNK phosphorylation pattern — neither additive nor intermediate — relative to each wavelength alone 31. This represents an evolutionarily conserved molecular defence strategy that has developed to handle the combined, simultaneous solar radiation signal.
  • Wavelength × wavelength: IRA can modulate UV-induced photoaging via different signalling transduction pathways. Red light irradiation decreased SA-β-galactosidase expression, upregulated SIRT1, and decreased MMP-1 in human fibroblasts exposed to UVA in vitro [^niu2015] — suggesting red light may partially counteract UVA-photoaging effects.
  • PM × UV: PM may not only interact at the skin-cell level but also upstream — airborne PM exposure to UV radiation is thought to cause “particle aging” through photochemical processes. UVA radiation of polycyclic aromatic hydrocarbons in air pollution may be a separate metabolic activation pathway 32.
  • Gene × environment interactions: Women with high-risk AhR pathway genotypes show amplified pigmentation responses to PM₂.₅, demonstrating that genetic background modulates the biological impact of the same environmental exposure dose 13.

The review concludes that future research must map exposure-interaction networks, not just individual-factor dose-responses, to optimise anti-skin-aging strategies.

Sunscreen as the best-evidenced protective intervention

The review identifies daily broad-spectrum UVA+UVB sunscreen as the single best-evidenced skin-aging protective intervention. Evidence chain:

  1. Mechanistic basis: UV radiation induces MMP-mediated collagen degradation at sub-erythemogenic doses; repeated daily exposures accumulate damage 3.
  2. Sub-erythemal dose repeated exposure RCT (human skin simulant): Broad-spectrum SPF 15 sunscreen with 2% avobenzone UVA protection prevents cumulative damage from repeated sub-erythemal UV in a reconstructed human skin model 33.
  3. Adult population RCT (Hughes et al. 2013): The first and, as of the review, only adequately powered adult RCT. Randomised SPF 15 broad-spectrum sunscreen (daily vs discretionary use) in adults aged 25–55 at latitude 26° south (Queensland, Australia). After 4.5 years, the daily sunscreen group showed no detectable increase in skin aging as assessed by microtopography of a silicone skin cast; skin aging from baseline to end of trial was 24% less in the daily-use group than in the discretionary-use group 34. · n=903 (903 enrolled, 903 analysed) · rct · p<0.05 (silicone skin cast microtopography score).

The review recommends daily use of a well-balanced, broad-spectrum sunscreen containing both UVA1/UVA and UVB photoprotection with a critical wavelength >370 nm. Genetic background and latitude should be considered when adapting SPF recommendations.

Caveats from the review: Interactions between UVA and UVB suggest choosing a photoprotection profile that filters both in a ratio resembling natural exposure; the optimal ratio had not been defined as of 2017. needs-replication: evidence for sunscreen protection against pollution-driven or IRA-driven skin aging was absent at review date.

Knowledge gaps surfaced by Krutmann et al.

The review explicitly identifies the following research needs (paraphrased):

  1. VL and IRA net contribution: The relative contribution of visible light and IRA to total lifetime skin photoaging burden is not quantified; dedicated human intervention trials needed.
  2. Interaction mapping: No study had mapped the full interaction network of all major exposome components simultaneously acting on skin.
  3. Cold temperatures: No evidence for cold temperature accelerating skin aging was found; proposed as a research gap.
  4. Pollution counter-strategies: Whether topical antioxidants prevent pollution-specific skin aging is unknown and remains unproven; sustained clean air policies are the most important long-term approach.
  5. Stress and skin aging: No direct causal evidence as of 2017; the mechanistic link from HPA activation to measurable skin aging phenotype is not established.
  6. Non-physiological antioxidant dosing: High-dose supplemental antioxidants appear harmful; the optimal dietary strategy for ROS balance in skin aging is undetermined.
  7. Cosmetics safety gaps: “Traditional” cosmetics lacking safety assessment may negatively contribute to the skin exposome.

Limitations

  • Review methodology: PubMed search without systematic review-grade protocol (no PRISMA reporting, pre-registration, or risk-of-bias assessment). Evidence grading is descriptive, not quantitative (no formal GRADE).
  • Funding conflict: Vichy Laboratoires (France) provided funding for the board meetings and writing support; three authors (Anne Bouloc, Gabrielle Sore, Bruno A. Bernard) are L’Oréal employees; corresponding author Krutmann (JK) and co-author Passeron (TP) received consultancy fees from L’Oréal (per COI statement p.159). The clinical recommendations (Table 1) include cosmetic product use, which is within the funder’s commercial interest. Biological claims about solar radiation and pollution mechanisms are broadly consistent with independent literature and do not appear to be influenced by this conflict; cosmetics-specific claims warrant heightened scrutiny.
  • Currency: Literature cutoff is 2016; the exposome/skin field has expanded substantially since then, including more VL/IRA mechanistic work, blue-light-specific pigmentation studies in darker skin types, and additional cohort data for pollution-skin aging associations. long-term-unknown: no review update by the same group had been published as of the wiki’s current literature check window.
  • Quantitative claims are often secondary citations: The review cites primary papers for most quantitative claims (percentage changes, dose values). Where quantitative claims appear in this study page, we have traced attribution back to the original primary source where possible (Fisher 1996 for sub-erythemogenic UV; Hughes 2013 for the RCT result). Downstream users should verify such claims against the cited primary studies, not against this review.

Significance

This review effectively launched the skin aging exposome as a named concept. Its value is threefold: (i) it provides a practical vocabulary and classification schema for the field, (ii) it situates UV photoaging within a multi-factor framework that includes pollution, tobacco, and lifestyle, and (iii) it makes the epistemic shift from individual-factor thinking to interaction-aware systems thinking explicit. It is cited extensively in subsequent epidemiological studies linking air pollution to lentigines and in cosmetics-science literature justifying broad-spectrum photoprotection strategies.

Cross-referenced from: skin-aging, skin, dermis, epidermis, chronic-inflammation, genomic-instability

Forward reference: uv-protection (R42 forward-ref; page seeded and verified 2026-05-19)

Footnotes

Footnotes

  1. doi:10.1158/1055-9965.EPI-05-0456 · Wild CP · Cancer Epidemiol Biomarkers Prev 2005 · introduced the “exposome” concept · review ↩

  2. krutmann-2017-skin-aging-exposome · n=N/A · review · model: human skin (review of epidemiological + in vitro + ex vivo + clinical studies) ↩

  3. doi:10.1038/379335a0 · Fisher GJ, Datta SC, Talwar HS et al. · Nature 1996 · MMP mRNA, protein, and activity induced in human skin in vivo within hours of sub-erythemogenic UVB; mechanism via AP-1/NF-κB; primary source for sub-erythemogenic UV dose claim · in-vivo · model: human skin in vivo (Fisher cohort; dose not specified in this footnote — see primary source for exact MED fraction) ↩ ↩2

  4. doi:10.1111/j.1365-2133.2008.08598.x · Cho M, Lee MS, Kim S et al. · J Dermatol Sci 2008 · MMP-1 upregulation observed after natural sunlight exposure even when UV filtered out by black clothing, confirming VL/IRA contribution · in-vivo · model: human skin in vivo ↩

  5. Lohan SB, Müller R, Albrecht S, Mink K, Tscherch K, Ismaeel F, Lademann J, Rohn S, Meinke MC · “Free radicals induced by sunlight in different spectral regions — in vivo versus ex vivo study” · Exp. Dermatol. 25(5) (2016) 380–385 · cited as Krutmann 2017 ref [28] · in-vivo/ex-vivo · model: human skin · needs-canonical-id — DOI not confirmed; original wiki DOI (10.3109/09546634.2014.951119) and journal (J Dermatol Treat) appear to belong to a different paper; correct journal is Exp. Dermatol. Note: year is 2016, not 2015; journal is Exp. Dermatol., not J Dermatol Treat. ↩

  6. doi:10.1111/pcmr.12297 · Duteil L, Cardot-Leccia N, Queille-Roussel C et al. · Pigment Cell Melanoma Res 2014 · blue-violet light (415 nm) induces marked prolonged pigmentation at physiological doses via distinct pathway from UVB-induced pigmentation · in-vivo · model: human skin (dorsal skin, types III–IV) ↩

  7. doi:10.1016/j.jdermsci.2009.10.002 · Liebmann J, Born M, Kolb-Bachofen V · J Invest Dermatol 2010 · blue-light irradiation regulates proliferation and differentiation in human skin cells · in-vitro · model: human keratinocytes and fibroblasts ↩

  8. doi:10.1038/jid.2010.204 · Vierkötter A, Schikowski T, Ranft U et al. · J Invest Dermatol 2010 · SALIA study; traffic-related PM correlates with extrinsic skin aging signs (pigment spots) in elderly Caucasian women · observational · model: human epidemiological ↩

  9. doi:10.1038/jid.2016.35 · Hüls A, Vierkötter A, Gao W et al. · J Invest Dermatol 2016 · 10 µg/m³ NO₂ increase associated with 25% more pigment spots (German women), 24% (Chinese women) · observational · model: human epidemiological (German + Chinese cohorts) ↩

  10. Hüls A, Schikowski T, Krämer U, Sugiri D, Stolz A, Vierkoetter A, Krutmann J · “Ozone exposure and extrinsic skin aging: results from the SALIA cohort” · J Invest Dermatol 135 (2015) 286 (S49, Abstract) · cited as Krutmann 2017 ref [32] · conference abstract · observational · model: human epidemiological (SALIA cohort) · needs-replication — single cohort; abstract only, no full-text DOI. Note: this is a 2015 conference abstract, not the same paper as 9 (doi:10.1038/jid.2016.35). ↩

  11. Thiele JJ, Traber MG, Polefka TG, Cross CE, Packer L · “Ozone-exposure depletes vitamin E and induces lipid peroxidation in murine stratum corneum” · J. Invest. Dermatol. 108(5) (1997) 753–757 · cited as Krutmann 2017 ref [33] · in-vivo · model: mouse skin · needs-canonical-id — DOI not confirmed; original wiki DOI (10.1172/JCI119386) is a JCI-format DOI inconsistent with a J Invest Dermatol paper. Note: journal is J Invest Dermatol (not J Clin Invest); full author list from Krutmann ref [33]. ↩

  12. doi:10.1016/j.jdermsci.2009.04.023 · Afaq F, Zaid MA, Pelle N et al. · J Dermatol Sci 2010 · aryl hydrocarbon receptor is an ozone sensor in human skin keratinocytes · in-vitro · model: human keratinocytes ↩

  13. Hüls A, Vierkoetter A, Kraemer U, Stolz S, Haarmann-Stemmann T, Felsner I, Brenden H, Grether-Beck S, Krutmann J, Schikowski T · “Epidemiological and mechanistic evidence that AHR signaling is involved in airborne particle-induced damage” · J Invest Dermatol 136 (2016) 188 (S33, Abstract) · cited as Krutmann 2017 ref [37] · conference abstract · observational (gene–environment interaction); AhR pathway GRS × PM₂.₅ → 52% (95% CI 14–104%) more lentigines per 4.45 µg/m³ PM₂.₅ increase · model: human epidemiological · needs-canonical-id — abstract only; no full-text DOI. Note: this is a separate 2016 conference abstract, not the same paper as 9 (doi:10.1038/jid.2016.35). ↩ ↩2

  14. Rowe DJ, Guyuron B · “Environmental and genetic factors in facial aging in twins,” in: Farage MA, Miller KW, Maibach HI (Eds.), Textbook of Aging Skin, Springer Berlin Heidelberg, 2010, pp. 441–446 · cited as Krutmann 2017 ref [44] for twin-study 2.5-year appearance estimate · book chapter · needs-canonical-id — book chapter; no DOI. Note: year is 2010, not 2000; footnote label retained for citation continuity. ↩

  15. Tamai Y, Tsuji M, Wada K, Nakamura K, Hayashi M, Takeda N, Yasuda K, Nagata C · “Association of cigarette smoking with skin colour in Japanese women” · Tob. Control 23(3) (2014) 253–256 · cited as Krutmann 2017 ref [42] · observational · model: human (Japanese women) · needs-canonical-id — DOI not confirmed. Note: author is Tamai Y (not Yamai T) and year is 2014 (not 2001); footnote label retained for citation continuity. ↩

  16. Doshi DN, Hanneman KK, Cooper KD · “Smoking and skin aging in identical twins” · Arch. Dermatol. 143(12) (2007) 1543–1546 · cited as Krutmann 2017 ref [38] · observational (twin study) · model: human epidemiological · needs-canonical-id — correct DOI for Arch Dermatol 2007 paper not confirmed; original wiki DOI (10.1001/archderm.1997.03890370053007) belongs to a different 1997 paper and is wrong. Note: year is 2007, not 1997; footnote label retained for citation continuity. ↩

  17. Richardson D · “Effects of tobacco smoke inhalation on capillary blood flow in human skin” · Arch. Environ. Health 42(1) (1987) 19–25 · cited as Krutmann 2017 ref [47] · in-vivo · model: human skin · needs-canonical-id — no DOI confirmed for this Arch Environ Health 1987 article. Note: author is Richardson D (not Rickards D); Krutmann ref number is [47] (not [46]). ↩

  18. doi:10.1111/j.1524-475X.2009.00488.x · Morita A, Torii K, Maeda A, Yamaguchi · J Investig Dermatol Symp Proc 2009 · molecular basis of tobacco smoke-induced premature skin aging; MMP-1 via AhR pathway · review/in-vitro · model: human skin (in vitro + ex vivo) ↩

  19. doi:10.1016/j.expdermatol.2011.10.009 · Nakamura M, Ueda Y, Hayashi M et al. · Exp Dermatol 2012 · tobacco smoke-induced skin pigmentation mediated by AhR; MITF upregulation · in-vitro · model: human melanocytes ↩

  20. doi:10.7150/ijbs.6424 · Yang CL, Zhang XC, Liu G et al. · Int J Biol Sci 2013 · cigarette smoke extract impairs fibroblast growth and proliferation; senescent features · in-vitro · model: human skin fibroblasts ↩

  21. doi:10.1093/ajcn/86.4.1225 · Cosgrove MC, Franco OH, Granger SP et al. · Am J Clin Nutr 2007 · dietary nutrient intakes and skin-aging appearance in middle-aged American women; higher vitamin C intake associated with lower likelihood of wrinkled appearance · observational · model: human epidemiological ↩

  22. doi:10.1056/NEJM199601043340101 · Omenn GS, Goodman GE, Thornquist MD et al. (CARET study) · N Engl J Med 1996 · beta-carotene + retinyl palmitate supplementation associated with increased lung cancer incidence (28%), death (17%), and cardiovascular mortality vs placebo · rct · n=18,314 · model: human (high-risk smokers and asbestos workers) ↩

  23. doi:10.1046/j.1365-4362.2001.01263.x · Purba MB, Kouris-Blazos A, Wattanapenpaiboon N et al. · Int J Dermatol 2001 · skin wrinkling in populations with different dietary intakes; olive oil, fish, vegetables associated with less wrinkling · observational · model: human (Greek, Swedish, Anglo-Celtic, and Greek-Australian populations) ↩

  24. doi:10.1046/j.1365-2133.2001.04605.x · Garg A, Chren MM, Sands LP et al. · J Invest Dermatol 2001 · psychological stress perturbs epidermal permeability barrier homeostasis · in-vivo · model: human skin ↩

  25. doi:10.1136/bmj.c6614 · Axelsson J, Sundelin T, Ingre M et al. · BMJ 2010 · sleep deprivation affects perceived health and attractiveness; skin colour parameters changed · experimental · n=23 (small) · model: human ↩

  26. doi:10.1111/cos.12175 · Oyetakin-White P, Suggs A, Koo B et al. · Clin Exp Dermatol 2015 · poor sleep quality affects skin aging; cross-sectional study; <5 h/night associated with higher SCINEXA score · observational · model: human ↩

  27. doi:10.1111/j.1365-2133.2003.05360.x · Denda M, Tsuchiya T, Elias PM, Feingold KR · Br J Dermatol 2003 · psychological stress perturbs epidermal permeability barrier via sleep-restriction mechanism · in-vivo · model: human skin ↩

  28. doi:10.1111/j.1365-4632.2005.02467.x · Chen JY, Seo JY, Kim SS et al. · J Dermatol Sci 2005 · heat modulation of tropoelastin, fibrillin-1, and MMP-12 in human skin in vivo; buttock skin at 43°C · in-vivo · model: human skin ↩

  29. doi:10.1016/j.jdermsci.2005.10.005 · Seo JY, Chung JH · J Dermatol Sci 2006 · thermal aging as a new concept of skin aging · review · model: human/mouse skin ↩

  30. doi:10.3109/10408440903572638 · Witorsch RJ, Thomas JA · Crit Rev Toxicol 2010 · personal care products and endocrine disruption; critical review of literature · review ↩

  31. doi:10.1038/sj.jid.5700264 · Schieke SM, Ruwiedel K, Gers-Barlag H et al. · J Invest Dermatol 2005 · molecular crosstalk between UVA and UVB signalling at MAPK level in human epidermal keratinocytes; sequential exposure produces non-additive third response pattern · in-vitro · model: human keratinocytes ↩

  32. doi:10.1093/toxsci/kfv181 · Xia HM, Chiang JJ, Yin S et al. · Toxicol Sci 2015 · UVA photoirradiation of benzo[a]pyrene metabolites: cytotoxicity, ROS, lipid peroxidation · in-vitro · model: human cell lines ↩

  33. doi:10.1111/j.1468-3083.2009.03332.x · Seité S, Christiaens F, Bredoux C et al. · J Eur Acad Dermatol Venereol 2010 · broad-spectrum SPF 15 sunscreen prevents cumulative damage from repeated sub-erythemal solar UV · in-vivo (reconstructed human skin model) · model: in vitro/reconstructed skin ↩

  34. doi:10.7326/0003-4819-158-11-201306040-00002 · Hughes MCB, Williams GM, Baker P, Green AC · Ann Intern Med 2013 · n=903 · rct · daily SPF 15 broad-spectrum sunscreen vs discretionary use for 4.5 years at latitude 26° south; skin aging 24% less in daily-use group by microtopography silicone cast · model: adults aged 25–55, Queensland Australia ↩

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