Pollution's Link To Lung Cancer: A Deadly Connection

Air pollution has been linked to lung cancer for decades, with studies suggesting that air pollution, particularly from the incomplete combustion of fossil fuels, may be responsible for increased rates of lung cancer. While smoking remains the biggest risk factor for lung cancer, outdoor air pollution causes roughly 1 in 10 cases of lung cancer in the UK. Globally, around 300,000 lung cancer deaths in 2019 were attributed to exposure to PM2.5, fine particulate matter with an aerodynamic diameter of less than 2.5 micrometers. These particles are emitted from vehicle exhaust, coal-fired power plants, and other industrial sources, and they can get trapped deep in the lungs, causing damage and increasing the risk of early death.

Particulate matter (PM2.5) in the air promotes the growth of cells in the lungs which carry cancer-causing mutations

Air pollution is the second-largest risk factor for lung cancer, after smoking. Particulate matter (PM2.5) is a pollutant that is found in high concentrations in large cities due to high air pollution. PM2.5 is composed of tiny solid and liquid particles, and is small enough to enter deep into the lungs and even enter the bloodstream.

PM2.5 has been found to promote the growth of cells in the lungs which carry cancer-causing mutations. This occurs through the activation of the aryl hydrocarbon receptor (AhR), which regulates the expression of xenobiotic-metabolising enzymes (XMEs) and increases polycyclic aromatic hydrocarbon (PAH) metabolism, leading to the formation of reactive metabolites, oxidative stress, DNA damage, and mutagenesis.

PM2.5 exposure has been linked to an increased risk of developing lung cancer, with higher rates of EGFR mutant lung cancer found in people living in areas with higher levels of PM2.5 pollution. PM2.5 exposure can also increase the proliferation, migration, and chemoresistance of lung cancer cells, suggesting that exposure to PM2.5 may stimulate the malignancy of tumour cells.

Particle pollution increases the risk of early death, heart disease, asthma attacks, and interferes with lung growth and function

Particle pollution, also known as particulate matter or soot, is a mix of tiny solid and liquid particles in the air we breathe. These particles are emitted directly from sources like wood stoves, forest fires, and vehicles, and they can also form from other types of pollution, such as power plants. The particles are so small that they get trapped deep in the lungs and can even enter the bloodstream, causing serious damage to our health.

The health effects of particle pollution are extensive and range from respiratory symptoms such as cough, phlegm, and wheezing to more severe issues like inflammation of the airways and lungs, bronchial hyperreactivity, and acute phase reactions. One of the most concerning impacts of particle pollution is its contribution to early death, heart disease, and asthma attacks.

Particle pollution increases the risk of early death by causing or exacerbating serious health conditions. Fine and ultrafine particles can lead to cardiovascular events such as heart attacks, heart failure, and strokes, resulting in hospitalizations and, in some cases, premature death. The evidence suggests that both short-term acute exposure and long-term chronic exposure to particle pollution can have deadly consequences.

Heart disease is another serious concern associated with particle pollution. The particles can cause or contribute to cardiovascular disease by inducing inflammation and damaging the cardiovascular system. Studies have found a clear link between particle pollution and an increased risk of heart attacks and strokes, with vulnerable populations bearing the brunt of these adverse effects.

Additionally, particle pollution interferes with lung growth and function, particularly in children and teenagers. It can slow lung function growth and development, leading to long-term respiratory issues. Particle pollution has also been linked to an increased risk of asthma attacks and hospitalizations among children, as well as a higher likelihood of developing asthma in the first place.

The impact of particle pollution on lung health is significant and far-reaching. It not only affects those with pre-existing respiratory conditions but also increases the risk of developing respiratory diseases like asthma and chronic obstructive pulmonary disease (COPD). The interference with lung growth and function can have lasting consequences for overall health and quality of life, especially in vulnerable populations such as children and the elderly.

Inflammation triggered by particle pollution wakes up normally inactive cells in the lungs which carry cancer-causing mutations

How Pollution Can Cause Lung Cancer

Overview

Particle pollution in the air we breathe is a serious health risk, causing an estimated 9 million preventable deaths globally each year. Outdoor air pollution is the leading cause of lung cancer, with vehicle exhaust, coal-fired power plants, and other industrial sources being significant contributors. These particles are a mixture of tiny solid and liquid particles, including acids, organic chemicals, metals, soil, and dust. They are so small that they can get trapped deep in our lungs and even enter our bloodstream, causing damage to our health.

Inflammation and Cancer-Causing Mutations

Now, a recent study by scientists at the Francis Crick Institute and UCL has revealed a new mechanism by which air pollution can cause lung cancer, even in people who have never smoked. Led by Professor Charles Swanton, the research found that exposure to particulate matter (PM2.5) in the air promotes the growth of cells in the lungs which carry cancer-causing mutations. These mutations naturally accumulate as we age but remain dormant. However, when exposed to air pollution, these cells are "woken up," and inflammation is triggered, leading to uncontrolled cell growth and the potential formation of tumours.

The Impact of Particle Pollution

The study's findings have important implications for understanding the early stages of lung cancer and other types of cancer. By examining data from over 400,000 people, the researchers found higher rates of EGFR mutant lung cancer and other types of cancer in areas with higher levels of PM2.5 pollution. This research provides valuable insights into the complex relationship between air pollution and cancer risk, highlighting the urgent need to reduce people's exposure to harmful particle pollution.

Protecting Ourselves from Particle Pollution

While individual actions can help reduce our contribution to local pollution sources, such as not burning wood or idling vehicles, collective efforts are also necessary. Joining organisations working to reduce air pollution and advocating for policies that protect our health from air pollution are crucial steps in creating a cleaner and healthier environment for everyone.

In conclusion, inflammation triggered by particle pollution awakens normally inactive cells in the lungs that carry cancer-causing mutations. This mechanism sheds light on how air pollution contributes to lung cancer, even in non-smokers, and underscores the importance of taking steps to mitigate particle pollution to improve public health.

Air pollution is linked to a variety of health problems, including asthma, chronic obstructive pulmonary disease (COPD), heart disease and dementia

Air pollution is a major public health issue, affecting all parts of the world. It is linked to a variety of health problems, including asthma, chronic obstructive pulmonary disease (COPD), heart disease, and dementia.

Asthma

Air pollution can cause asthma and worsen its symptoms, leading to more hospital visits and even early death. Small airborne particles, found in haze, smoke, soot, and dust, can irritate the airways and lungs, causing serious air quality problems. People with asthma are at greater risk from breathing in these particles and irritating gases.

COPD

Air pollution is closely linked to COPD, with exposure to polluted air causing exacerbation of existing symptoms, impaired lung function, and increased hospitalisation and mortality rates. Long-term exposure to air with high levels of pollutants may also increase the incidence of COPD.

Heart Disease

Air pollution is a risk factor for cardiovascular disease, which includes conditions affecting the health of the heart or blood vessels. Research has shown that air pollution can exacerbate existing heart disease and contribute to the development of the disease. Fine particulate matter (PM2.5) in particular can increase the risk of cardiovascular events, including heart attacks and death.

Dementia

A recent study found a link between higher levels of fine particulate matter (PM2.5) in the air and an increased number of dementia cases developing over time. The strongest link was seen with PM2.5 from agriculture and wildfires. While the reason for this connection is not yet fully understood, it is thought that fine particulates may affect the lungs, circulate in the blood, and move into the brain, causing potential damage.

Overall, air pollution has been linked to a range of serious health issues, and it is important to take steps to reduce exposure and limit contributions to local pollution sources.

Pollution might spark defects in DNA repair function, alterations in the body's immune response, or inflammation that triggers angiogenesis, allowing tumours to spread

Pollution might spark defects in DNA repair function

Pollution can cause DNA damage, which, if left unrepaired, can lead to mutations and cancer. Pollution can cause DNA damage through the production of reactive oxygen species (ROS) and other intracellular damaging agents. ROS can directly produce oxidatively damaged bases, abasic sites, and single-strand breaks (SSBs).

Oxidative base lesions include 8-oxoguanine (8-oxoG), thymine glycol, 8-hydroxyadenine, 2-hydroxyadenine, 2,6-diamino-4-hydroxy-5-formamidopyrimidine, and 4,6-diamino-5-formamidopyrimidine (the so-called FaPys). 8-oxoG, one of the most frequent oxidative base lesions, causes little change to the DNA helical structure, yet frequently mispairs with adenine, causing G→T transversions.

Abasic sites, which lack the instructional information of the base, are non-coding templates that can cause mutagenic end-points or serve as blocks to replicative DNA or RNA polymerases.

SSBs represent interruptions in the phosphodiester backbone and thus can collapse a progressing DNA or RNA polymerase complex or drive recombination events when encountered during replication.

Alterations in the body's immune response

The immune system is comprised of multiple types of immune cell that act together to generate (or fail to generate) immune responses. In health, the immune system must respond effectively to infections and neoplastic cells, with a response tailored to the insult, but must tolerate the healthy body and benign commensal bacteria.

Air pollution can trigger pro-inflammatory immune responses across multiple classes of immune cells. It can enhance T helper lymphocyte type 2 (Th2) and T helper lymphocyte type 17 (Th17) adaptive immune responses, as seen in allergy and asthma, and dysregulate anti-viral immune responses.

Inflammation that triggers angiogenesis, allowing tumours to spread

During carcinogenesis, advanced tumours are surrounded by both stromal and immune cells, which support tumour development. In addition, inflammation and angiogenesis are processes that play important roles in the development of cancer, from the initiation of carcinogenesis, tumour in situ and advanced stages of cancer.

Tumours have a high metabolic rate and require a constant supply of nutrients, along with the exclusion of waste material. These processes are successfully achieved through the induction of angiogenesis. To preserve physiological homeostasis, angiogenesis is rigorously linked with the inflammatory processes. However, in deregulated inflammatory processes that lead to chronic inflammation, pathological angiogenesis can be initiated.

An intimate connection between immune cells and the endothelium occurs during inflammation. In addition, several studies have indicated that immune/endothelium cell interactions are maintained and encourage tumour development.

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