Ultrafine pollutants may prime unborn children to develop asthma

May 21, 2021
Asthma has been linked to prenatal exposure to air pollution. (Shutterstock)

Asthma has been linked to prenatal exposure to air pollution. (Shutterstock)

A new study of hundreds of mothers and their children is one of the first to link exposure to ultrafine particulate matter before birth to the development of asthma in early childhood.

The paper, published Friday in the American Journal of Respiratory and Critical Care Medicine, found that women in the Boston area who were exposed to high amounts of ultrafine particulate matter were more likely to have children who eventually developed asthma.  

The researchers drew from data from 376 pregnant mothers and their children enrolled in two different health studies, as well as estimations of ultrafine particulate matter around the subjects' homes in the Boston area. There, the researchers detected particle number concentrations, a measure of very small particles, between 10,000 and 40,000, with effects seen at 15,000 to 30,000. This difference could signify a home on a quiet side street or one on a major highway, where heavy traffic can spew these particles at higher rates.

Controlling for obesity; exposure to nitrogen dioxide, another common pollutant; and other factors, the researchers found that 18.4% of children eventually developed asthma after accentuated exposure to ultrafine particulates in an urban area, whereas across the U.S., only 7% of children have asthma.  

Prior research has focused mainly on fine particles, the largest of which are 2.5 micrometers. Unlike large particles, ultrafine particles are 0.1 micrometers and smaller, and they are not monitored by the U.S. Environmental Protection Agency. Often, these ultrafine particles enter the environment through car exhaust, though research has revealed other sources, such as indoor cooking and smoking.

According to the study, ultrafine particles are particularly dangerous because, when inhaled, they can better penetrate the lungs and cause oxidative stress, an imbalance between the body's antioxidant defense mechanism and invading free radicals that can damage tissues. When this exposure occurs in utero, either by causing oxidative stress directly to the placenta or by moving past the placenta and into the fetus's bloodstream, it may prime a child to develop asthma, though the exact mechanism is still unknown and may be a combination of exposures in utero and ex utero. 

"It might be a two-hit thing: You get hit in pregnancy, and it sort of tweaks your systems to go this way, and now you're born, now you're breathing the air yourself. That's a different mechanism altogether," said lead author Rosalind Wright, a professor of environmental medicine and public health at the Icahn School of Medicine at Mount Sinai. "And if you've already been kicked that way, it might actually be more of an interaction of pre- and post-exposure."

The study collected information from mothers involved in one of two cohort studies: the Asthma Coalition on Community, Environment and Social Stress project and the Programming of Intergenerational Stress Mechanisms study. Recent research has shown how deadly air pollution disproportionately hurts Black, Hispanic and Asian people. In this study, 37.8% of the mothers were Black, and 43.9% were Hispanic, and researchers followed up with them in interviews once every four months to assess asthma in their children, and annually after the children reached 30 months old.

Because ultrafine particles are not routinely monitored, Wright collaborated with the Tufts Air Pollution Monitoring Laboratory, which provided ultrafine particle data, to estimate ultrafine particulate exposure based on each mother's address. These mothers lived around the Boston area, and some of them lived around major roadways, where vehicle exhaust accounted for most of the ultrafine particulate matter. 

Along with over 18% of the 376 children developing asthma, Wright and her colleagues also discovered that sensitivity to ultrafine particles varied between girls and boys in the womb. In the third trimester, girls seemed to be most vulnerable to ultrafine particles, while boys were vulnerable throughout pregnancy. 

The mechanism behind this difference remains unclear. Prior research, however, suggests that boys may be more susceptible to oxidative stress during pregnancy, which could be causing asthma later on, according to Wright. For girls, endocrine disruption — which can alter the natural function of hormones by mimicking them, blocking them or changing their production — may invoke this vulnerability, rather than oxidative stress. 

"This is a big area where science is moving towards trying to elucidate differences in boys and girls as they develop," Wright said in an interview with The Academic Times. "Men and women over the lifetime were very different in lots of different ways. And that starts right at conception. We develop in a different hormonal soup."

While Wright would like this paper and others to inspire better regulation of vehicular emissions and air quality, she understands these changes can take a long time. For instance, getting the auto industry to reduce engine emissions, or governments to improve air-quality management, will probably take longer than nine months of pregnancy. Instead, Wright intends for her research to inspire short-term changes on an individual level that can reduce the threat of ultrafine particles. 

"You don't want to just scare people; you just want balance," Wright said. "Staying healthy is all about balancing. We know we're going to encounter exposures and challenges that we're going to need to handle and deal with, but a lot of times you can mitigate the risk if you do other helpful behaviors."

Some of these behaviors include eating a more anti-inflammatory diet bolstered with fruits and vegetables, keeping windows closed and using air conditioning, if it's available. According to Wright, pregnant women ultimately should be made aware that they are in a vulnerable period of not just their life but also their child's.

In future research, Wright wants to better understand why girls tend to be more vulnerable to ultrafine particles during the third trimester of pregnancy, and she may examine biological specimens to test her and her colleagues' hypothesis that endocrine disruption somehow governs this vulnerability.

Wright also notes that her study and one completed in Toronto are two of the first to link prenatal ultrafine particulate exposure to asthma development early in life, and that additional research to replicate their findings, as well as investigate health outcomes aside from asthma, should be completed.

"Our exposures up until now kind of have programmed us in a way that makes us more or less vulnerable to a given exposure that we might encounter currently," Wright said. "We're all a product of where we've been."

The study, "Prenatal ambient ultrafine particle exposure and childhood asthma in the northeastern United States," published May 21 in the American Journal of Respiratory and Critical Care Medicine, was authored by Rosalind Wright, Hsiao-Hsien Leon Hsu, Yueh-Hsiu Mathilda Chiu and Itai Kloog, Icahn School of Medicine at Mount Sinai; Brent A. Coull and Joel Schwartz, Harvard University; Matthew C. Simon, U.S. Department of Transportation; and Neelakshi Hudda and John L. Durant, Tufts University.

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