Air pollution is linked to adverse birth outcomes in India

Prenatal exposure to ambient fine particulate matter and climatic factors, such as temperature and rainfall, are associated with adverse birth outcomes in India, according to a study published in PLOS Global Public Health 

Ambient air pollution poses a global threat to human health, with a disproportionate burden of its detrimental effects falling on those residing in low and middle-income countries. Referred to as the silent killer, ambient air pollution is among the top five risk factors for mortality in both males and females.

With a diameter of less than 2.5 microns, ambient fine particulate matter 2.5 (PM2.5), which primarily originates from the burning of fossil fuels and biomass, is considered the most harmful air pollutant. In the 2023 World Air Quality Report, India was ranked as the third-most polluted country out of 134 nations based on its average yearly PM2.5 levels.

Ambient air pollution has been associated with a range of pediatric morbidities, including adverse birth outcomes, asthma, cancer, and an increased risk of chronic diseases.

To address the knowledge gap, the researchers investigated the impact of ambient air pollution on adverse birth outcomes at the national level, focusing on  low birth weight and preterm birth, and used different geospatial models to highlight vulnerable areas. The analysis provided evidence of the association between in-utero exposure to PM2.5 and adverse birth outcomes by leveraging satellite data and large-scale survey data.

The individual-level analysis revealed that an increase in ambient PM2.5 is associated with a greater likelihood of low birth weight and preterm birth. Climatic factors such as rainfall and temperature were also linked to adverse birth outcomes. Children residing in the Northern districts of India appeared to be more susceptible to the adverse effects of ambient air pollution.

PLOS Global Public Health (2025). DOI: 10.1371/journal.pgph.0003798

Unlocking the mystery behind Barrett's esophagus

A research team has shed light on the process that drives Barrett's esophagus formation. This condition affects the lining of the esophagus—the tube that carries food from the mouth to the stomach—and increases the risk of developing esophageal adenocarcinoma, a serious and often deadly cancer.

The study, published in the Journal of Clinical Investigation, reveals that two important genes involved in guiding and maintaining the identity of the esophagus and intestine, SOX2 and CDX2, are altered in Barrett's esophagus. The findings not only deepen our understanding of how the disease develops but also open the door to new ways of identifying people at risk and potentially preventing the condition from progressing to cancer.

It is known that Barrett's esophagus usually develops after long-term exposure to acid and bile reflux, which transforms the cells of the lining of the esophagus into cells that look more like those in the stomach and the intestine.

The esophagus, which is not normally exposed to acid, adapts to acid reflux by becoming more like the stomach or the intestine, organs that are used to an acidic or bile-rich environment.

Eliminating acid reflux with medication does not heal Barrett's esophagus; the cells do not revert to their typical esophagus characteristics.

Under the microscope, Barrett's lesions show increased cell proliferation and a disorganized tissue with stomach-like and intestine-like cells where only esophageal cells should be.

To gain insight into what drives the transformation of esophageal cells into stomach and intestinal cells, the team investigated transcription factors SOX2 and CDX2, which are proteins that regulate the identity of esophageal and intestinal cells, respectively.

The findings support the idea that Barrett's esophagus may arise from the acid- and bile-triggered reprogramming of normal esophageal cells by altering the balance of SOX2 and CDX2. This new understanding could help scientists find strategies to intervene earlier in the disease process as well as develop new ways to provide an early diagnosis.

Ramon U. Jin et al, SOX2 regulates foregut squamous epithelial homeostasis and is lost during Barrett's esophagus development, Journal of Clinical Investigation (2025). DOI: 10.1172/JCI190374

Food contact articles as source of micro- and nanoplastics