Environmental factors influence the frequency and type of DNA damage through several ways. Environmental exposures can directly damage DNA or affect cellular processes involved in DNA repair. The ability of cells to effectively detect and repair DNA damage (DNA capacity) is influenced by these factors. Exposure to genotoxic agents such as UV radiation, ionizing radiation, chemical carcinogens, and oxidative stressors can induce various types of DNA lesions. UV radiation (particularly in the form of UVB and UVC) can induce the formation of thymine dimers. Thymine dimers distort the DNA helix structure, leading to structural abnormalities and interfering with DNA replication and transcription if not repaired. Single-strand breaks (SSBs) can occur through different mechanisms: they can result directly from the breakdown of the deoxyribose backbone, as unintended byproducts of topoisomerase 1 or indirectly as part of the normal process of base-excision repair. Exposure to ionizing radiation is associated with an increased risk of DNA double-strand breaks (DSBs). Some examples include X-rays, gamma rays, and cosmic radiation. DSBs are highly cytotoxic and can lead to chromosomal rearrangements, loss of genetic material, and cell death if not repaired accurately. Additionally, chronic exposure to environmental toxins, pollutants, and lifestyle factors such as smoking, alcohol consumption, and diet can also influence DNA repair capacity. As an example, smoking over an extended period of years raises one’s risk of developing lung cancer and COPD.