The link between air pollutants and lung cancer
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The effects on human health due to poor air quality mainly involve the respiratory system and the cardiovascular system. Individual reactions to air pollutants depend on the type of pollutant a person is exposed to, the degree of exposure, the individual's state of health and genetics.
Indoor air pollution and poor urban air quality are listed as two of the world's worst toxic pollution problems in the 2008 report. Outdoor air pollution causes 2.1 to 4.21 million dead every year. Collectively, air pollution causes the deaths of approximately 7 million people worldwide each year and is the largest single environmental health risk in the world.
There are many studies done to understand the link between the percentage of COHb in the blood and the macroscopic health effects. The damage caused by COHb to human health is essentially linked to the effects on the cardiovascular system and the nervous system.
The Lung adenocarcinoma promotion by air pollutants study, published in the Nature, explained: "A complete understanding of how exposure to environmental substances promotes cancer formation is lacking. More than 70 years ago, tumorigenesis was proposed to occur in a two-step process: an initiating step that induces mutations in healthy cells, followed by a promoter step that triggers cancer development1.
Here we propose that environmental particulate matter measuring ≤2.5 μm (PM2.5), known to be associated with lung cancer risk, promotes lung cancer by acting on cells that harbor pre-existing oncogenic mutations in healthy lung tissue.
on EGFR-driven lung cancer, which is more common in never-smokers or light smokers, we 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 tumorigenesis.
Ultradeep mutational profiling of histologically normal lung tissue from 295 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively.
These findings collectively support a tumour-promoting role for PM2.5 air pollutants and provide impetus for public health policy initiatives to address air pollution to reduce disease burden."