AP Syllabus focus:
‘When stratospheric ozone decreases, more UV radiation reaches Earth’s surface, increasing risks such as skin cancer and cataracts in humans.’
Stratospheric ozone normally filters harmful ultraviolet light.
NASA’s “ozone density vs. altitude” profile is overlaid with UV-A, UV-B, and UV-C penetration, showing that UV-C is essentially eliminated and UV-B is strongly reduced as sunlight passes through the ozone-rich stratosphere. The figure reinforces why a thinner ozone layer disproportionately increases biologically damaging UV-B at the surface, even when UV-A changes much less. Source
When ozone thins, especially for UV-B, human exposure rises. This page explains how increased UV damages tissues, elevates disease risk, and affects public health.
The UV increase that matters for human health
Ozone depletion increases the fraction of biologically damaging UV that reaches Earth’s surface, raising the dose received during everyday outdoor activities.
Ultraviolet (UV) radiation: Electromagnetic radiation from the Sun with wavelengths shorter than visible light; UV-B (280–315 nm) is strongly linked to DNA damage and many health risks.
How UV harms the body
Higher UV exposure increases the rate of cellular injury because UV energy can alter biomolecules.
Direct DNA damage: UV can create lesions in DNA that, if unrepaired, increase mutation rates.
This structural diagram illustrates a thymine photodimer (a cyclobutane pyrimidine dimer), a common UV-induced lesion where two adjacent thymine bases become covalently linked. Such lesions can distort DNA and increase replication errors if not repaired, providing a concrete molecular pathway from higher UV exposure to higher mutation rates and, ultimately, increased skin cancer risk. Source
Oxidative stress: UV promotes formation of reactive molecules that damage cell membranes and proteins.
Inflammation: Acute exposure triggers sunburn, a visible sign of tissue damage.
Skin cancer risk
Increased UV exposure raises the probability that mutations accumulate in skin cells, increasing cancer risk over time.
Key links between UV and skin cancer
More exposure = higher lifetime dose: Ozone loss can raise the cumulative UV dose, especially in high-UV settings (high elevation, low latitude, reflective surfaces).
DNA mutations in skin cells: Mutations in genes that control cell division can lead to uncontrolled growth.
Reduced effectiveness of immune surveillance: UV can suppress local immune responses in the skin, making it harder to eliminate abnormal cells early.
Major health outcomes in the skin
Non-melanoma skin cancers (commonly basal and squamous cell cancers) are strongly associated with long-term UV exposure and are among the most UV-linked cancers.
Melanoma risk is also increased by UV exposure, particularly patterns involving intense, intermittent exposure that can cause severe sunburns.
Cataracts and other eye damage
The eye is vulnerable because UV can damage transparent tissues, especially the lens. With less ozone, more UV reaches the surface and increases the risk of cataracts in humans (clouding of the lens that impairs vision).
Why cataract risk rises with UV
Protein damage in the lens: UV alters lens proteins, which can clump and reduce transparency.
Cumulative exposure: Cataract formation often reflects long-term exposure; small increases in daily UV can matter over decades.
Limited natural repair: The lens has limited ability to remove damaged proteins once they accumulate.
Additional UV-related eye effects
Photokeratitis: A painful, sunburn-like injury to the cornea after intense exposure (for example, strong sun with high reflectivity).
Pterygium: Abnormal tissue growth on the eye surface, associated with chronic UV exposure.
Immune system and broader health effects
Higher UV exposure can affect health beyond the skin and eyes by altering immune function.
Immune suppression: UV can reduce certain immune responses, potentially increasing susceptibility to some infections and reducing the effectiveness of immune surveillance against abnormal cells.
Skin aging: UV accelerates breakdown of structural proteins, contributing to wrinkling and loss of skin elasticity.
Indirect public health impacts: Increased disease burden can strain healthcare systems through more screening, treatment, and vision care needs.
Who is most at risk (and why)
Health impacts are not evenly distributed; risk depends on both exposure and vulnerability.
Outdoor workers and athletes: Higher daily UV dose from time spent outside.
Children and adolescents: More time outdoors and a longer future window for damage to manifest.
People at high altitude or near highly reflective surfaces (snow, water, sand): Greater UV intensity due to thinner atmosphere and reflection.
People with lower natural skin pigmentation: Less melanin protection against UV-induced DNA damage.
Communities with limited access to eye care and skin screening: Later detection can worsen outcomes.
FAQ
UV-B more efficiently causes direct DNA lesions (such as cyclobutane pyrimidine dimers), which can become mutations if not repaired.
UV-A penetrates deeper and contributes more via oxidative stress; it is harmful, but its carcinogenic pathways are often less direct.
Cells use DNA repair pathways (including nucleotide excision repair) to remove UV-caused lesions.
Repair can fail when exposure is frequent/intense, repair genes are less effective, or damage occurs faster than repair, allowing mutations to persist.
Reflective surfaces increase the amount of UV reaching the eyes from below and multiple angles.
Cold temperatures can reduce perceived risk, increasing exposure time without protection.
Cataracts involve the lens and usually develop gradually from cumulative damage.
Photokeratitis affects the cornea and can occur within hours after intense UV exposure, often resolving over days but causing significant pain.
They combine:
Satellite/ground UV measurements and UV index trends
Health surveillance (skin cancer incidence, cataract surgery rates)
Long-term cohort studies that account for behaviour, latitude, and occupational exposure
Practice Questions
Explain how decreased stratospheric ozone can increase the risk of cataracts in humans. (2 marks)
States that less ozone allows more UV (especially UV-B) to reach Earth’s surface (1).
Links increased UV exposure to damage of the eye lens (e.g., protein damage/clouding), increasing cataract risk (1).
Describe two human health effects of increased UV radiation reaching Earth’s surface due to ozone depletion, and explain the biological mechanism for each effect. (6 marks)
Identifies a valid health effect: skin cancer and/or cataracts (1 + 1).
Mechanism for skin cancer: UV causes DNA damage/mutations in skin cells leading to uncontrolled cell division (1).
Mechanism detail for skin cancer: reduced immune surveillance and/or cumulative exposure increasing mutation accumulation (1).
Mechanism for cataracts: UV damages lens proteins causing clouding and impaired vision (1).
Mechanism detail for cataracts: cumulative/long-term exposure increases damage with limited repair in lens (1).
