About . Birth before 37 weeks can lead to a cascade of health risks, both immediate and long-term, making prevention a vital tool for improving public health over generations.��

In recent years, researchers have identified a potential link between wildfire smoke — one of the fastest-growing sources of air pollution in the United States — and preterm birth, but no study has been big or broad enough to draw definitive conclusions. A new study led by the 91̽�� makes an important contribution, analyzing data from more than 20,000 births to find that pregnant people who are exposed to wildfire smoke are more likely to give birth prematurely.

“Preventing preterm birth really pays off with lasting benefits for future health,” said lead author , a 91̽��postdoctoral researcher in environmental and occupational health sciences. “It’s also something of a mystery. We don’t always understand why babies are born preterm, but we know that air pollution contributes to preterm births, and it makes sense that wildfire smoke would as well. This study underscores that wildfire smoke is inseparable from maternal and infant health.”

In the study, ,��researchers used data from the , a federal research project focused on how a wide range of environmental factors affect children’s health. The sample included 20,034 births from 2006-2020 across the contiguous United States.

Researchers estimated participants’ average daily exposure to fine particulate matter, or PM2.5, generated by wildfire smoke, and the total number of days they were exposed to any amount of smoke. They estimated the intensity of smoke exposure by how frequently participants were exposed to wildfire PM2.5 levels above certain thresholds.

They found that pregnant people exposed to more intense wildfire smoke were more likely to give birth prematurely. In mid-pregnancy, exposure to any smoke was associated with an elevated risk of preterm birth, with that risk peaking around the 21st week of gestation. In late pregnancy, elevated risk was most closely associated with exposure to high concentrations of wildfire PM2.5, above 10 micrograms per cubic meter.

“The second trimester is a period of pregnancy with the richest and most intense growth of the placenta, which itself is such an important part of fetal health, growth and development,” said co-author , a 91̽��professor of environmental and occupational health sciences and of pediatrics in the 91̽��School of Medicine. “So it may be that the wildfire smoke particles are really interfering with placental health. Some of them are so tiny that after inhalation they can actually get into the bloodstream and get delivered directly into the placenta or fetus.”��

The link was strongest and most precise in the Western U.S., where people were exposed to the highest concentrations of wildfire PM2.5 and the greatest number of high-intensity smoke days. Here, the odds of preterm birth increased with each additional microgram per cubic meter of average wildfire PM2.5.

It’s possible those results were more precise simply because the West experiences more wildfire smoke on average, making the exposure model perform better, Sherris said. But there may be other factors behind the regional differences.��

The composition of wildfire smoke is different across the country. In the West, smoke tends to come from fires nearby, while in places like the Midwest, smoke has typically drifted in from faraway fires. and reacts with sunlight and airborne chemicals, which could have affected the results. Researchers also noted that external factors like co-occurring heat or housing quality may have effects that aren’t fully understood.��

Researchers hope that future studies will examine the exact mechanisms by which wildfire smoke might trigger preterm birth. But in the meantime, Sherris said, evidence for a link is now strong enough to take action.��

“There are a couple avenues for change,” Sherris said. “First, people already get a lot of public health messaging and information throughout pregnancy, so there’s an opportunity to work with clinicians to provide tools for pregnant people to protect themselves during smoke events. Public health agencies’ messaging about wildfire smoke could also be tailored to pregnant people and highlight them as a vulnerable group.”

Co-authors include , doctoral student of environmental and occupational health sciences at the UW; , clinical associate professor of environmental and occupational health sciences at the UW; , professor of biostatistics at the UW; , associate professor of environmental and occupational health sciences and of epidemiology at the UW; , postdoctoral fellow of epidemiology at the UW; and , assistant professor of environmental and occupational health sciences at the UW. A full list of co-authors is included with the paper.

This research was funded by the Environmental influences on Child Health Outcomes (ECHO) program at the National Institutes of Health under multiple awards. A full list of ECHO funding awards is included with the paper.��

For more information or to contact the researchers, email Alden Woods at acwoods@uw.edu.

Asthma affects more than 6% of U.S. children, making it the most common chronic disease in kids nationwide. It’s difficult to isolate any single cause, but one of the most common contributors is air pollution: Studies have shown that breathing air with high levels of fine particulate matter, nitrogen dioxide and other environmental pollutants can increase children’s risk of developing asthma. But it’s been unclear whether long-term, early childhood exposure to ozone, the pollutant that most frequently exceeds U.S. air quality standards, contributes to the disease.����

, a doctoral student at the 91̽��, set out to find a possible link. In a study , Dearborn and collaborators identified a puzzling trend: Children exposed to higher levels of ozone in their first two years of life were significantly more likely to be diagnosed with asthma or wheezing at ages 4-6 — but researchers didn’t observe the increased risk of asthma at ages 8-9.����

While the researchers couldn’t pin down the exact reason, possible explanations include the changing nature of asthma as kids age, which could lead to a drop-off in formal diagnoses, and the influence of other risk factors and pollutants on asthma as children’s lungs grow.��

“It’s a puzzling finding,” said Dearborn, who led the research in the 91̽��Department of Environmental & Occupational Health Sciences. “It’s something we spent a long time trying to consider, and I don’t know if we ever came up with a satisfying answer. But these findings are important. Even if we only see the effects early in life,��there are still all kinds of associated health care costs and stresses for families. There are all sorts of larger contextual factors about having this chronic disease at any point in life.”��

This study relied on data from the (ECHO) program, a federal research project focused on how a wide range of environmental factors affect children’s health. Researchers drew 1,118 participants from six cities, including Seattle and Yakima, who had low-risk pregnancies and completed validated surveys that asked if their children had been diagnosed with asthma or had experienced wheezing.����

Researchers estimated exposure in the first two years of a child’s life using a model developed by co-author , a 91̽��professor of environmental and occupational health sciences, of epidemiology and of medicine. They found that a relatively small increase in ozone exposure — 2 parts per billion — in a child’s first two years of life was associated with a 31% increase in asthma and 30% increase in wheeze at age 4-6 years. Asthma and wheeze risk at ages 8-9 was not found to be associated with their early life ozone concentration.��

Researchers also analyzed how exposure to mixtures of three common air pollutants — ozone, nitrogen dioxide and fine particulate matter (PM2.5) — affected asthma outcomes. In this analysis, ozone stood out.��

“We interpret trends, and what we can conclude from this analysis is that when ozone within the air pollution mixture was higher than about 25 parts per billion, we saw a higher probability of asthma regardless of the concentration of nitrogen dioxide,” Dearborn said. “We found a relationship between ozone and asthma only when fine particulate matter was at or above median concentrations, giving novel evidence that the relationship between ozone and childhood asthma may depend on the concentration of other pollutants, like fine particulate matter.”��

The study’s findings highlight the need for more research into the effects of long-term ozone exposure in early life, Dearborn said. Further study could determine why the increased asthma risk related to ozone is not evident at ages 8-9, and whether it increases again later in childhood.����

In the meantime, Dearborn said, researchers and public health officials should pay more attention to the effects of long-term exposure to ozone.��

“In the United States, ozone regulations only consider a very short time period,” Dearborn said. “We don’t regulate ozone over the long term, and that’s where this analysis fits in. Maybe we should be considering both a short- and a long-term threshold for the regulation of ozone.”����

Other authors are , a 91̽��professor of environmental and occupational health sciences and of pediatrics in the 91̽��School of Medicine; postdoctoral researchers and , research scientist , and clinical associate professor , all of the 91̽��Department of Environmental & Occupational Health Sciences; , a 91̽��professor of biostatistics; , a graduate student in the 91̽��Department of Epidemiology; of Seattle Children’s Research Institute and an assistant professor of pediatrics in the 91̽��School of Medicine; Margaret Adgent and Paul Moore of Vanderbilt University Medical Center; Yu Ni of San Diego State University; Marnie Hazlehurst and Drew Day of Seattle Children’s Research Institute; Ruby Nguyen of the University of Minnesota; Kaja LeWinn of the University of California, San Francisco; and Kecia Carroll of the Icahn School of Medicine at Mount Sinai in New York City.����

This research was funded by the National Institutes of Health’s ECHO-PATHWAYS program; the National Center for Advancing Translational Health Sciences; the National Heart, Lung, and Blood Institute; the National Institute of Environmental Health Sciences; the 91̽��Pediatric and Reproductive Environmental Health Scholars K-12 program; the U.S. Environmental Protection Agency; the 91̽��EDGE Center; the National Institute on Aging; and the Urban Child Institute.��

A new study found that pregnant women exposed to higher levels of air pollutants had children with lower IQs, compared to the children of women exposed to lower levels.

The study, led by researchers at the 91̽�� and UCSF as part of the ECHO PATHWAYS consortium, will be published in the September issue of Environmental Research and is currently available��.

Researchers looked at 1,005 pregnant women participating in the Conditions Affecting Neurodevelopment and Learning study, set in Shelby County, Tenn., and assessed the IQs of their offspring between the ages of 4 and 6. They found that exposure to PM10 — pollutant particles with a diameter of one-seventh the width of a human hair that are produced by industry, power plants, cars, air traffic and railways�� — was negatively associated with IQ. Children whose mothers were in the highest 10 percent of exposure had IQ scores that were 2.5 points lower than those in the lower 10 percent.

When the researchers looked at plasma levels of maternal folate, which is found naturally in leafy vegetables, beans and citrus fruit, and is recommended for all pregnant women in its synthetic form as folic acid, they found that the difference between offspring IQs in the highest and lowest PM10-exposed groups had widened to 6.8 points among those whose mothers had the lowest levels (bottom 25 percent)�� of folate.

PM10 exposure had no impact on IQ if maternal levels of folate were higher, the researchers found.

While the study underlines the importance of folic acid in pregnancy, there may be such a thing as too much folic acid supplementation, said first author Christine Loftus, an epidemiologist from the UW’s Department of Environmental & Occupational Health Sciences.

“Although supplementation has been shown to be protective against neural tube defects, which are devastating birth defects of the central nervous system, recent research suggests that too much prenatal folic acid may impair healthy fetal neurodevelopment,” Loftus said. “The dose of folic acid is something that pregnant women should discuss with their doctors.”

Long-term exposure to PM10 has been linked to reduced lung function and the development of cardiovascular and respiratory diseases. In this study, other pollutants, including nitrogen dioxide, which is a marker for high-concentration motor traffic, were not found to impact IQ.

The authors said that they could not explain the mechanism by which PM10 exposure contributed to lower IQ, but said that animal studies indicated that air pollution exposure increased maternal inflammation and oxidative stress. “This could result in placental inflammation and may interfere with placental or fetal epigenetic programming,” said senior author��, ScD, associate professor of psychiatry at the UCSF School of Medicine.

“While it’s beyond the scope of our paper to understand how folate might alter this association, it is possible that higher folate levels increase the antioxidant capability of the diet, buffering oxidative stress associated with PM10 exposure,” said LeWinn.

“It may also be that folate itself is protective, since it plays an important role in healthy neurodevelopment, regardless of air pollution exposure.”

Co-authors includes Marnie F. Hazlehurst, Adam Szpiro, Yu Ni and Catherine J. Karr also of the UW; Sheela Sathyanarayana of the 91̽��and the Seattle Children’s Research Institute; Frances Tylavsky of the University of Tennesee; Nicole Bush of UC San Francisco; Kecia Carroll of Vanderbilt University Medical Center.

The study was supported by grants from the NIH and the Urban Child Institute.

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For more information, contact Loftus at��cloftus@uw.edu.