Examining the molecular mechanisms, health implications, and therapeutic approaches
Every breath we take may contain invisible air pollutants that potentially harm our health. From fine particles to ozone gas, air pollution not only damages the environment but also triggers a series of molecular reactions in the human body. One key mechanism that occurs is oxidative stress, an imbalance condition that can cause cell damage and trigger various diseases. This article will thoroughly examine how air pollution affects oxidative stress based on a systematic review of current scientific literature, and explain its implications for human health.
Over 90% of the world's population lives in areas where air quality levels exceed WHO limits, leading to increased oxidative stress in billions of people.
Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body's ability to neutralize them through antioxidant systems. ROS are actually produced naturally in the body as a result of normal metabolic processes, and at low levels even play a role in important cell signaling . However, when exposure to air pollutants excessively increases ROS production, the antioxidant defense system becomes overwhelmed, leading to oxidative damage to cellular components including lipids, proteins, and DNA .
The systematic review conducted by Kusmiyati et al. (2022) is a comprehensively designed study to evaluate the effect of air pollutants on oxidative stress 1 . Researchers conducted literature searches through the Science Direct database for articles published between 2017-2021. Keywords used were combinations of "air pollutant", "oxidative stress", and "air pollution" 1 .
From the initial search results, articles were selected based on predetermined inclusion criteria. Article eligibility was assessed using The JBI Critical Appraisal Tool, and only 15 articles met the criteria for further review 1 . This strict selection process ensures that only research with high methodological quality is included in the review.
Science Direct database with specific keyword combinations
Articles published between 2017-2021
Using JBI Critical Appraisal Tool
15 articles meeting all criteria
| Air Pollutant Type | Oxidative Stress Biomarker | Observed Changes |
|---|---|---|
| PM₂.₅ | 8-OHdG | Significant increase |
| PM₁₀ | Malondialdehyde (MDA) | Significant increase |
| NO₂ | Glutathione (GSH) | Decreased levels |
| Ozone (O₃) | Reactive Oxygen Species | Increased production |
| CO | Antioxidant enzymes | Activity changes |
Tropospheric ozone (ground-level ozone) is a main component of photochemical smog and is formed from reactions between nitrogen oxides and volatile organic compounds in the presence of sunlight 2 . Chronic exposure to low-level ozone can cause loss of redox system regulation and induce a state of chronic oxidative stress 2 . In mouse models, low-dose ozone exposure (0.25 parts per million) caused progressive changes resembling neurodegeneration in Alzheimer's and Parkinson's diseases 2 .
Although known as a harmful pollutant, ozone also has therapeutic applications when used in controlled conditions. Medical ozone at appropriate doses can activate anti-oxidative stress mechanisms and achieve therapeutic effects 3 . Administration methods include ozonated autohemotherapy (O-AHT), ozonated water, ozonated oil, and ozone injections 3 .
Ozone therapy mechanism involves the induction of hydrogen peroxide (H₂O₂) and aldehydes that act as redox signaling molecules 3 . At appropriate concentrations, H₂O₂ can activate various transcription factors including Nrf2 which induces the expression of antioxidant enzymes 3 9 . Ozone therapy has shown potential in treating various conditions including liver disease, diabetes, and neurological disorders 3 9 .
Controlled ozone exposure at 0.5-1 ppm can activate Nrf2 pathway, increasing antioxidant production by up to 40% in experimental models 9 .
| Reagent/Tool | Function | Example Application |
|---|---|---|
| 8-OHdG Assay | Detects oxidative damage to DNA | Measuring impact of air pollution on oxidative stress 1 |
| ELISA for cytokine | Measures inflammatory markers | Assessing inflammatory response to pollutants 6 |
| Glutathione kit | Measures glutathione levels | Evaluating antioxidant capacity 1 |
| ROS Probe | Detects reactive oxygen species | Monitoring intracellular ROS production |
| Medical ozone generator | Produces ozone at precise concentrations | Ozone therapy research 3 |
| Pollutant exposure chamber | Simulates controlled pollutant exposure | Air pollution toxicology studies 2 |
| UHPLC-MS system | Targeted metabolomic analysis | Identifying metabolic changes due to exposure 5 |
Exposure to air pollutants and the resulting oxidative stress affects various organ systems. In the respiratory system, oxidative stress causes chronic inflammation, emphysema, and fibrosis 6 . In the cardiovascular system, oxidative stress triggers atherosclerosis through LDL oxidation and inflammatory response . In the nervous system, oxidative stress causes neurodegeneration through mitochondrial damage, neuronal death, and neuroinflammation 7 .
Certain populations such as the elderly, children, and individuals with underlying diseases are more vulnerable to the effects of air pollution due to less competent antioxidant systems or existing disease burden 6 . Additionally, inequalities in air pollution exposure also contribute to health disparities, where low-income communities often live in areas with worse air quality.
The good news is that global efforts to reduce air pollution are showing positive results. Recent research confirms that the Antarctic ozone layer is in the process of recovery as a direct result of global efforts to reduce ozone-depleting substances like CFCs 8 . This proves that with proper commitment and policies, humans can solve complex environmental problems.
Projections indicate that with continued adherence to the Montreal Protocol, the Antarctic ozone hole is expected to gradually close, with complete recovery anticipated by the 2060s.
Based on existing systematic reviews, there is strong evidence that exposure to air pollutants causes changes in biological markers of oxidative stress which are early indications of health disorders 1 . Pollutants such as PM₂.₅, NO₂, and ozone can increase ROS production, decrease antioxidant capacity, and cause oxidative damage to DNA, proteins, and lipids.
The story about air pollution and oxidative stress is not just about dangers but also about human resilience and adaptation. Recent research shows that low-level exposure to certain oxidative stressors may induce a hormesis response—where low-dose exposure can actually trigger beneficial adaptive mechanisms 5 .
Research on mice shows that exposure to negative air ions (NAIs) generated through cold atmospheric plasma (CAP) can induce metabolic adaptations that increase mitochondrial efficiency and reduce oxidative stress 5 .
Looking ahead, innovative approaches such as exposome modification (the totality of environmental exposures throughout life) and therapies targeting redox pathways may help reduce the adverse health effects of air pollution. With a combination of effective pollution control policies, innovative therapeutic approaches, and individual awareness of the importance of air quality, we can breathe easier toward a healthier future.