32 SKIN CARE A
Skin permeability is reduced, limiting negative effects of pollution on skin
With pollution
500% 400% 300% 200% 100% 0%
-45% *
Non-exposed untreated
B
Stratum corneum Epidermis
Dermis Placebo
Without Pollution Untreated
Blend 0.1% * p-value < 0.05 With Pollution Placebo Blend 0.1%
red colour in the epidermis= skin permeability
Degradation of skin barrier function
minor red colour in the epidermis= low skin permeability
Protection of skin barrier function
3000% 2500% 2000% 1500% 1000% 500% 0%
Collagen remains protected against pollution, maintaining its integrity as before exposure
With pollution -102% **
Non-exposed untreated
Placebo Blend 0.1% ** p-value < 0.01
400% 300% 200% 100% 0%
Skin is protected from oxidation due to pollution, maintaining its integrity close to before exposure
With pollution
-91% **
Non-exposed untreated
Placebo
Blend 0.1% ** p-value < 0.01
Epidermis Dermis
red spots = CHP
Collagen degradation induced by pollution
minor red spots = low CHP Collagen is protected from
pollutants, similar to its state before pollution
Epidermis Dermis
green spots colour = ROS Increase of skin oxidation
minor green spots = low ROS The skin is protected from
oxidation, close to its state before pollution
Figure 7: A: Bar graphs depict skin permeability, collagen damage and ROS level in response to pollution determined by respective stainings. B: Micrographs of ingredient and urban dust treated skin explants stained with respective dyes for image analysis of skin permeability, collagen damage and ROS protection
COX-2 and PGE2, and reduce filaggrin expression, culminating in barrier dysfunction.9 Reviews of skin inflammaging similarly describe a close relationship between environmental stress, declining barrier performance, and chronic low-level inflammation.4,10,11
by urban dust after 45 minutes, for three days. Semi-quantitative evaluation of skin permeability was performed by Rhodamine B (fluorescent dye) infiltration method. Collagen damage was visualized using a
The ‘exposome’ thus contributes
to sensitive-skin persistence through repeated oxidative and inflammatory triggers, while ageing skin exhibits barrier and microenvironment shifts that heighten susceptibility to daily insults and slow recovery, reinforcing a vulnerability loop. Within this context, our ex vivo data demonstrate that the blend, even at low use levels, can reduce oxidative stress, enhance resistance to pollution- driven permeability changes, and protect collagen integrity under daylight UV and urban-dust challenge conditions (Figure 7). Notably, following UV daylight and pollution
exposure, 0.1% of the blend reduced collagen damage as assessed by collagen hybridizing peptide (CHP) detection (Figures 7 and 8) and Rhodamine B (fluorescent dye) infiltration (Figure 7). Figure 7 shows skin explants treated daily with 0.1% of the ingredient or placebo followed
PERSONAL CARE MAGAZINE May 2026
fluorescently labelled Collagen Hybridizing Peptide (CHP) and ROS level were determined using HDCF. Images were analysed using Fiji software (fluorescence intensity and distribution). The placebo was 90% water and 10% DMSO. It was demonstrated that 0.1% safeguards skin
barrier and collagen structure against pollution stress possibly via ROS protection — helping preserve skin architecture and support long-term resilience and skin’s natural external shield. Figure 8 shows an ex vivo study in which skin was repetitively irradiated with UV daylight over three days. After each treatment, the blend was topically applied to the respective samples. After further three days, samples were harvested and processed for damaged collagen staining using CHP. Images were analyzed using Fiji software (fluorescence intensity and distribution). Placebo: 90% water and 10% DMSO. These results not only highlight the blend’s
anti-irritation potential but also supports its role in ‘skin longevity’ by reducing stress-linked matrix damage. Collectively, these findings emphasize that an ingredient capable of soothing irritated skin can also help mitigate the impact of environmental insults that perpetuate sensitivity, bridging acute comfort with long-term prevention.
From pathway modulation to visible skin benefit For all the value of mechanistic data, a soothing ingredient ultimately has to perform on skin. Our in vivo studies provide that translational layer. In an SDS-induced irritation model, a formulation containing 0.05% of the blend reduced visible redness by 49% within two days and returned skin to baseline within five days, outperforming the individual components alone (Figure 9). This is particularly meaningful because it indicates synergy rather than simple addition of benefits. Figure 9 Study A shows a test performed on 20 panelists subjected to redness induced by SDS treatment. Application on forearms: four to six hours after SDS treatment, then for seven days, twice daily. Evaluation before SDS treatment, four to six
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Rhodamine B infiltration (Relative % to non-exposed untreated)
CHP content (Relative % to non-exposed untreated)
ROS production (Relative % to non-exposed untreated)
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