How Pollution Can Cause Skin Peeling And Damage

Skin peeling can be caused by a variety of factors, including:

- Dry skin: This is often the result of insufficient sebum and sweat production, leading to dry and flaky skin.

- Sunburn: Prolonged exposure to the sun without protection can cause UV damage, resulting in skin redness and peeling.

- Contact dermatitis: Allergens like perfume, cosmetics, or cleaning products can trigger an allergic reaction, causing skin peeling, redness, and itching.

- Psoriasis: An inflammatory disease characterised by pink or red rashes with white, peeling skin.

- Atopic dermatitis: An inflammatory disease causing dry skin due to impaired water retention and reduced fat production by the sebaceous glands.

- Seborrheic dermatitis: A condition causing oily skin peeling, often associated with itching and redness, commonly found in areas with a higher concentration of sebaceous glands, such as the scalp.

- Fungal infections: Transmissible infections caused by various types of fungi, leading to skin peeling, cracking, and itching, especially in humid areas.

- Cutaneous lupus erythematosus: A condition characterised by red skin lesions with a darker border and skin peeling, typically found in sun-exposed areas like the face, ears, and scalp.

- Skin cancer: Prolonged sun exposure without protection can increase the risk of skin cancer, which may present as skin lesions, rashes, or peeling.

Oxidative stress and potential interactions of airborne pollutants with UV light

Yes, your skin can peel due to pollution.

Ultraviolet (UV) light, which emits UV in the range of 320–400 nm, has been used worldwide in light trapping of insect pests. In this article, we test the hypothesis that one of the effects of UV light irradiation is to increase oxidative stress on insects. The effects of UV light irradiation on total antioxidant capacity, malondialdehyde (MDA) and protein carbonyl contents and the activities of superoxide dismutase (SOD), catalase (CAT), peroxidases (POX) and glutathione-S-transferase (GST) were investigated in Helicoverpa armigera adults. The adults were exposed to UV light for various time periods (0, 30, 60 and 90 min). We found that exposure to UV light for 30 min resulted in increased total antioxidant capacity, protein carbonyl content and activities of SOD, CAT, POX and GST. When the exposure time lasted for 60 and 90 min, the protein carbonyl content and activities of CAT and GST remained significantly higher than the control. However, the antioxidant capacity and SOD activity returned to control levels, and POX activity decreased at 60 and 90 min. Our results confirm the hypothesis that UV light irradiation increases the level of oxidative stress in H. armigera adults.

Oxidative stress responses to reactive oxygen species (ROS) and subsequent inflammation resulting from air pollution exposure may be one of these important mechanisms. However, epidemiologic evidence in humans that ambient PM or gaseous pollutant exposures increases biomarkers of oxidative stress is limited. The following review assesses the importance of addressing this gap to the field of air pollution research and we offer some possible methods of doing so by focusing on a few selected biomarkers that can be measured in the blood for large population studies. We will not discuss the use of other body fluids to measure oxidative stress that are reviewed elsewhere, for example exhaled breath condensates and urine. We also focus on inhalation and pulmonary deposition as the route of exposure for cardiovascular effects of interest in the paper (we do not discuss dermal, gastrointestinal, or transplacental routes). Finally, the air pollutants of primary focus in the review are those associated with particles.

Direct and indirect pollution uptake – Biochemical and clinical effects of pollutants and potential interactions with UV light. Direct dermal uptake with the accumulation of airborne pollutants (PAHs, PM, O3; black dots) on the stratum corneum and subsequent penetration. Indirect dermal uptake in the dermis and basal epidermal layer with the systemic blood distribution of inhaled or ingested pollutants that may have been metabolized (black dots). Left panel: Airborne pollutants (black dots) penetrate the skin directly or indirectly (black arrows) and induce biochemical effects such as an increase in the production of ROS via the aryl hydrocarbon receptor, an elevation of lipid peroxidation, protein oxidation and cell death (apoptosis), and a reduction in cell proliferation and antioxidant and ATP levels. Clinically, the effects of pollutants correspond to the exacerbation of skin ageing processes, the symptoms of inflammatory diseases (e.g. atopic dermatitis) and the deregulation of skin moisture. Right panel: UV radiation penetrates the skin where it might induce the production of ROS. In addition, some pollutants located at the surface or within the skin might induce the production of ROS (red and black filled circles). The combination of UV radiation and pollutants might exacerbate the biochemical and clinical effects of airborne pollutants. ATP, adenosine triphosphate; O3, ground-level ozone; PAHs, polycyclic aromatic hydrocarbons; PM, particulate matter; ROS, reactive oxygen species; UV, ultraviolet.

Mechanisms of injury from air pollution

Air pollution is a leading environmental health risk and is responsible for numerous adverse health outcomes. It is defined as the contamination of the atmosphere by one or more harmful substances, such as dust, fumes, gas, mist, odour, smoke or vapour. The main pathway of exposure from air pollution is through the respiratory tract, but some pollutants are small enough to penetrate the bloodstream via the lungs and circulate throughout the entire body, leading to systemic inflammation and carcinogenicity.

Cardiovascular injury

Inhalation of air pollutants affects heart rate, heart rate variability, blood pressure, vascular tone, blood coagulability, and the progression of atherosclerosis. Major mechanisms of inhalation-mediated cardiovascular toxicity include activation of pro-inflammatory pathways and generation of reactive oxygen species.

Neurological impairment

Short-term exposure to air pollution has been linked to neurological impairments, including decreased motor activity, memory/cognitive impairment, and neurobehavioural performance impairment, which are related to injury-related factors such as distractibility/attention deficits, impaired judgment, and executive dysfunction.

Skin damage

The skin, along with the lungs, is the main target organ affected by the harmful insults of air pollution. Air pollutants can affect the physiology of the skin and are responsible for cutaneous damage. Some polycyclic aromatic hydrocarbons are photoreactive and could be activated by ultraviolet radiation (UVR). Therefore, such UVR exposure would enhance their deleterious effects on the skin.

Air pollution also affects vitamin D synthesis by reducing UVB radiation, which is essential for the production of vitamin D3, tachysterol, and lumisterol derivatives. Ambient air pollutants, photopollution, blue-light pollution, and cigarette smoke compromise cutaneous structural integrity, can interact with human skin microbiota, and trigger or exacerbate a range of skin diseases through various mechanisms.

Generally, air pollution elicits an oxidative stress response on the skin that can activate the inflammatory responses. The aryl hydrocarbon receptor (AhR) can act as a sensor for small molecules such as air pollutants and plays a crucial role in responses to (photo)pollution.

Injury from external causes

Short-term exposure to ambient air pollution has been found to increase the risk of injuries, particularly unintentional and assault injuries. The risk of injuries caused by falls, blunt objects, penetration, traffic accidents, machinery, and slips was found to be associated with specific air pollutants.

Skin disorders associated with pollution

• Atopic dermatitis/eczema: Atopic dermatitis is a chronic inflammatory skin disorder that can be caused by air pollution. It is characterised by intense itching, which reduces quality of life. A study found that atopic dermatitis symptoms were associated with levels of outdoor air pollutants, including PM, toluene, and VOCs.
• Acne: Acne is a common inflammatory skin disease that can be exacerbated by air pollution. A study found that exposure to increased levels of PM, NO2, and SO2 was associated with a higher number of acne lesions and increased sebum production.
• Skin ageing: Air pollution can cause premature skin ageing, including wrinkles and age spots. A study found that exposure to soot and traffic particles was associated with a 20% increase in pigment spots on the forehead and cheeks.
• Melasma: Melasma is a skin disorder characterised by light-to-dark-brown hyperpigmentation. Recent studies suggest that pollution is a possible risk factor for the development of melasma.
• Pigment spots: Air pollution can cause pigment spots on the skin, particularly on the forehead and cheeks.

Prevention strategies

• Use a gentle, fragrance-free cleanser.
• Avoid products that dry out your skin.
• Dry your face gently with a soft towel.
• Take shorter showers with lukewarm water.
• Drink plenty of water.
• Wear sunscreen every day.

Air quality guidelines

Yes, air pollution can cause skin peeling. Air pollution can cause oxidative stress, which can lead to skin damage and peeling.

Frequently asked questions