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.��