Higher exposure to particulate matter among infants increases all-cause and infection-related ED visits

10th March 2023

Greater particulate matter exposure during the first year of life is linked to higher all-cause and infection-related visits to the ED

Work by researchers from San Diego, La Jolla in the US, has shown that an increased exposure to particulate matter 2.5 μm or less in diameter (PM2.5), increases the risk for all-cause and infection-related visits to an emergency department among infants during their first year of life.

It has been recognised for several years that particulate matter comprising particles with a diameter of less than 2.5 micrometres, can penetrate deeply into the lungs, causing irritation and corrosion of the alveolar wall and therefore impairing lung function. PM2.5 comes from a wide range of sources including natural (i.e., dust, sea salt), anthropogenic emissions, e.g., vehicles, as well as household wood burning and from industry. The composition of PM2.5 is a complex mix of inorganic components such as heavy metals, organics (polycyclic aromatic hydrocarbons) and biologicals e.g., bacteria, viruses and fungi. Prior studies have shown that exposure to PM2.5 during pregnancy can increase adverse outcomes and stillbirth and early childhood exposure to air pollutants may play a role in the development of asthma. However, research to data on the impact of early PM2.5 exposure and the risk of hospitalisation during infancy is conflicting, indicating either an increased risk of bronchiolitis or no noticeable effect compared to older children.

In the current study, researchers examined all live births in California between 2014 and 2018 and estimated weekly exposure to particular matter based on the postal (zip) codes using a machine learning model. They set the outcomes of interest as both the first all-cause emergency department (ED) visit and the first infection-related visit based on birth status (pre or full-term).

Particulate matter and ED visits

A total of 983,700 infants, (49.4% female) were included in the analysis.

During the first year of life, the odds of an ED visit for any cause was higher for both pre-term (odds ratio, OR = 1.05, 95% CI 1.04 – 1.06) and full-term infants (OR = 1.05, 95% CI 1.04 – 1.05) for each 5-μg/m3 increase in exposure to PM2.5.

Similarly, there were elevated odds for a respiratory infection-related ED visit, pre-term (OR = 1.03) and full-term (OR = 1.05). In fact, the highest risks for an ED in both types of infant occurred between 18 to 23 weeks.

The authors concluded these elevated risks associated with exposure to particulate matter, may have implications for minimising exposure to air pollution.

Citation
Teyton A et al. Exposure to Air Pollution and Emergency Department Visits During the First Year of Life Among Preterm and Full-term Infants. JAMA Netw Open 2023

Particulate matter in air pollution may cause lung cancer in never smokers

23rd September 2022

Exposure to particulate matter from air pollution appears associated with an increased risk of lung cancer in those who have never smoked

The exposure to particulate matter derived from air pollution represents a mechanism through which lung cancer can develop among individuals who have never smoked according to the findings of research presented at the European Society for Medical Oncology (ESMO) Congress 2022 by scientists of the Francis Crick Institute and University College London.

Globally in 2020 there were an estimated 2.21 million cases of lung cancer and 1.80 million deaths. There are two primary forms of lung cancer, small cell lung cancer and non-small cell lung cancer (NSCLC) with this latter form accounting for approximately 84% of all cases. It has been recognised for several years that particulate matter in outdoor air pollution with a size of at least 2.5 micrometers, leads to an 18% higher risk of lung cancer among those who had never smoked. However, the mechanisms driving this increased risk among those who do not smoke has remained unclear.

In the study presented at the ESMO congress, researchers focused on lung cancers due to a mutation in the epidermal growth factor receptor (EGFR), which is a transmembrane receptor tyrosine kinase protein, expressed in some normal epithelial, mesenchymal, and neurogenic tissue. Moreover, research suggests that EGFR protein expression is a risk factor in patients with NSCLC. Using normal lung tissue samples from humans and mice, the team investigated the consequences of increasing 2.5um particulate matter (PM2.5) concentrations with cancer risk.

Particulate matter exposure and cancer risk

Samples were analysed from 463,679 individuals and the team found that increasing PM2.5 levels were associated with a greater risk for EGFR mutated NSCLC samples from England, South Korea and Taiwan. This was also associated with an increased risk of mesothelioma (hazard ratio, HR = 1.19), lung (HR = 1.16), anal (HR = 1.23), small intestine (HR=1.30), glioblastoma (HR=1.19), lip, oral cavity and pharynx (HR = 1.15) and laryngeal carcinomas (HR = 1.26) in UK Biobank samples, for each 1 ug/m³ PM2.5 increment. 

A further interesting finding was the presence of EGFR driver mutations in 18% of normal lung samples and a further mutation (KRAS) in 33% of samples. The team also showed that PM promoted a macrophage response and a progenitor-like state in lung epithelium harbouring mutant EGFR. Consistent with particulate matter promoting NSCLC in at-risk epithelium harbouring driver mutations, PM increased tumour burden in three EGFR or KRAS driven lung cancer models in a dose-dependent manner.

In a press release discussing their findings, Charles Swanton who presented the findings at ESMO, said ‘We found that driver mutations in EGFR and KRAS genes, commonly found in lung cancers, are actually present in normal lung tissue and are a likely consequence of ageing. In our research, these mutations alone only weakly potentiated cancer in laboratory models. However, when lung cells with these mutations were exposed to air pollutants, we saw more cancers and these occurred more quickly than when lung cells with these mutations were not exposed to pollutants, suggesting that air pollution promotes the initiation of lung cancer in cells harbouring driver gene mutations. The next step is to discover why some lung cells with mutations become cancerous when exposed to pollutants while others don’t.‘

Citation
Mechanism of action and an actionable inflammatory axis for air pollution induced non-small cell lung cancer: Towards molecular cancer prevention