Abstract. Cancer is a disease caused by changes (mutations) to nuclear DNA. Cancer in humans is a large group of diseases with the common characteristic of normal cells becoming cancerous and multiply uncontrollably with the ability to grow and spread to normal human body tissues. Cancer is the second most common cause of death in developed countries after cardiovascular diseases. In 2014, globally, 17.7 million people died annually from cardiovascular diseases, whereas cancer accounts for 8.8 million deaths per year. Early detection and innovative treatments are curing cancer and helping people with cancer live longer. Survival rates from cancer are improving for many types of malignant neoplasms, thanks to improvements in cancer screening, medical and anticancer drugs treatments and prevention. Living biological organisms are continuously exposed to a myriad of DNA damaging agents. Mutations in cellular DNA accumulate throughout human life, and some of these mutations contribute to cancers. Mechanisms of DNA repair decline with age and accumulated mutations in crucial genes are inextricably linked with cancer. In the last decade, researchers have established experimentally that inflammation plays a critical role in tumourigenesis and some of the underlying molecular mechanisms have been elucidated. An international team of researchers in UK, Canada and USA has made a breakthrough in identifying how a new mechanism of air pollution causes lung cancer in people who have never smoked. Researchers found that fine particles and extremely small particulate matter, (PM10, PM2.5, etc) in polluted air cause inflammation in the lungs, which activates pre-existing cancer genes that had been dormant. It was established that through toxicological results, the PM particles caused inflammation, which activated pre-existing mutations in genes that drive the development of many lung cancers. The inflammatory mechanism identified could ultimately help researchers to find better ways to prevent and treat lung cancer in never smokers. The next step of research discovered why some lung cells with mutations become cancerous when exposed to PM pollutants while others do not. The findings may be applicable to other cancers associated with air pollution, including mesothelioma (typical cancer of asbestos miners) and for tumours of the throat and mouth. These results are very important because a high proportion  of the world’s population lives in big cities with high concentrations of airborne particulate matter (PM10, PM2.5), which exceed annual World Health Organization (WHO) limits for pollution. These results underlining the public health challenges posed by PM air pollution across the globe. Researchers focused on epidermal growth factor receptor (EGFR) lung cancer, which is more common in never-smokers or light smokers. They found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in four within-country cohorts. Functional mouse models revealed that air pollutants cause an influx of macrophages into the lung and release of interleukin-1β. This process results in a progenitor-like cell state within EGFR mutant lung alveolar type II epithelial cells that fuels tumourigenesis.