Rosalind J. Wright , Hsiao-Hsien Leon Hsu , Yueh-Hsiu Mathilda Chiu , Brent A. Coull , Matthew C Simon , Neelakshi Hudda , Joel Schwartz , Itai Kloog , and John L Durant. Prenatal Ambient Ultrafine Particle Exposure and Childhood Asthma in the Northeastern United States. Am J Respir Crit Care Med. 2021 May 21. https://doi.org/10.1164/rccm.202010-3743OC.

The study focused on mothers and their full-term singleton-born children in a lower-income ethnically mixed urban sample in the northeastern U.S. The measurement of ambient UFP exposure occurred during pregnancy and the first year after birth. The researchers then followed children's asthma outcomes through interviews at approximately 4-month intervals from birth to age 30 months, then annually thereafter.

Sex differences were found in the broader effect of UFPs on childhood asthma outcomes. Of the children studied, 18.4% developed asthma. Despite there being no identifiable differences in pollutant exposures based on sex, males were impacted more than females (22.3% vs 14.6%, respectively).

Timing of the exposure was also a factor. When the researchers modeled using trimester-specific exposure averages, they found that regardless of sex, the most critical window for exposure leading to asthma is the third trimester.

For females, the exposure timing associated with the highest risk of childhood asthma was during the third trimester of pregnancy. For males, all windows of exposure were estimated to be “equally important with risk elevated across the entire pregnancy.”

Asthma affects an estimated 10% of school-aged children in the U.S. It impacts children’s ability to attend school, to participate in sports or play outdoors, and their overall quality of life. Due to environmental racism, substandard housing, lack of quality health care, and other factors, Black children are twice as likely to be hospitalized for asthma and are four times as likely to die from asthma as white children. Air pollution contributes significantly to the exacerbation of asthma symptoms in children and is associated with increased hospitalizations and death from the disease.

This study is one of the very few that considers UFP exposure, as most research linking prenatal air pollution exposures and childhood asthma only considers larger particulate matter and other criteria air pollutants such as carbon monoxide, ground-level ozone, lead, nitrogen dioxide, and sulfur dioxide. UFPs may exert far more toxic effects on our children than criteria pollutants, due to their ability to penetrate more deeply into the lungs and cause more inflammation.

The U.S. Environmental Protection Agency (EPA) does not regulate UFPs. The agency continues to wait for additional research findings to meet its minimum threshold for causality.

Greater investment into further research surrounding the impacts of ultrafine particles on children’s health is critical to building the evidence base necessary for EPA to regulate. Child health advocates should continue to keep this issue before the agency and to push for reviews and consideration of the latest research findings to shorten the lag between established causality and protective policy.

Because traffic-related pollution is the primary source of UFPs in urban areas of the U.S., and because families of color and those in under-resourced communities are more likely to reside closer to major highways, continued prioritization of air quality interventions in these communities is needed. These interventions need to include considerable investments in clean energy, accessible and affordable public transit, and electric vehicle infrastructure.