Summary: Two new studies from USC reveal the implications of air pollution on brain development and neurological health in children and older women.
A pair of recently published USC studies add to our growing understanding of how fine particle pollution — the tiny, inhalable pollutants from cars and power plants — impacts our brains.
The first study, published in Environment International, found that these fine particles — known as PM2.5 — may alter the size of a child’s developing brain, which may ultimately increase the risk for cognitive and emotional problems later in adolescence.
“At this young age, the neurons in children’s brains are expanding and pruning at an incredible rate. As your brain develops, it wants to create efficient pathways,” said lead author Megan Herting, an assistant professor at the Keck School of Medicine of USC. “If these pathways are altered by PM2.5 exposure, and different parts of the brain are maturing and making connections at different rates, that might set you up for individual differences later on.”
USC, located in what the American Lung Association frequently cites as the most polluted city in the nation, is home to a robust air pollution research program. Findings from its studies have led to changes in state and federal guidelines to improve air quality standards. One of its cornerstones is the USC Children’s Health Study, one of the largest and most detailed studies of the long-term effects of air pollution.
Herting’s team used MRI scans from nearly 11,000 children aged 9 and 10 from 21 cities across the United States and matched each scan with yearly pollution data for each child’s residence. This is the first study of its kind to show that, even at relatively low levels, current PM2.5 exposure may be an important environmental factor that influences patterns of brain development in American children.
When they compared highly exposed kids with those who had less exposure to PM2.5, they saw differences. For example, areas associated with emotion were larger in highly exposed kids, while other areas associated with cognitive functioning were smaller.
Herting plans to follow the progress of the children, who are part of the ABCD Study, the largest long-term study of brain health and child development in the United States.
Eating fish could help protect women’s brains against fine particle pollution The second study, published in Neurology, found that omega-3 fatty acids from consuming fish may protect against PM 2.5-associated brain shrinkage in older women.
Previous USC research showed that women in their 70s and 80s who were exposed to higher levels of air pollution experienced greater declines in memory and more Alzheimer’s-like brain atrophy than their counterparts who breathed cleaner air.
For this study, researchers looked at the brain MRIs of 1,315 women aged 65 to 80 and blood test results to determine levels of healthy omega-3 fatty acids in their blood.
“We found that women with higher blood levels of omega-3s had larger volumes of white matter in their brains. Women living in locations with higher PM2.5 tended to have smaller white matter in their brains, but such damage that may be caused by PM2.5 was greatly reduced in women with high blood levels of omega-3 fatty acids,” said corresponding author Jiu-Chiuan Chen, an associate professor at the Keck School of Medicine of USC.
The brain’s white matter, in contrast to gray matter, makes up most of the volume of the brain. It is the vast, intertwining system of neural connections that unites different regions of the brain that perform various mental operations. White matter loss may be an early marker of Alzheimer’s disease.
About the Environment International study: In addition to Herting, other authors of the study include Dora Cserbik, Jiu-Chiuan Chen, Rob McConnell, Elizabeth R. Sowell, Daniel A. Hackman, all of USC; Kiros Berhane of Mailman School of Public Health of Columbia University; Eric Kan of Children’s Hospital Los Angeles; Joel Schwartz of Harvard T.H. Chan School of Public Health; and Chun C. Fan of UC San Diego.
Funding: The study was supported with grants from the National Institute of Environmental Health Sciences (P30ES007048-23S1, 3P30ES000002-55S1, P01ES022845), the Environmental Protection Agency (RD 83587201, RD 83544101) and the Rose Hills Foundation. The larger ABCD study is also supported by the National Institutes of Health (U01DA041048, U01DA050989, U01DA051016, U01DA041022, U01DA051018, U01DA051037, U01DA050987, U01DA041174, U01DA041106, U01DA041117, U01DA041028, U01DA041134, U01DA050988, U01DA051039, U01DA041156, U01DA041025, U01DA041120, U01DA051038, U01DA041148, U01DA041093, U01DA041089, U24DA041123 and U24DA041147).
About the Neurology study: In addition to Chen, other authors of the study include Xinhui Wang and Helena Chui of Keck; Cheng Chen and Ka He of Columbia University; Pengcheng Xun of Indiana University; Joel Kaufman of the University of Washington; Kathleen Hayden and Mark Espeland of Wake Forest School of Medicine; Eric Whitsel, Marc Serre and William Vizuete of University of North Carolina Chapel Hill; Tonya Orchard of Ohio State University; and William Harris of the University of South Dakota.
Funding: The study was supported with grants from the National Institutes of Health (R01AG033078, RF1AG054068 and RF1AG056111) and the National Institute of Environmental Health Sciences (R01ES025888).
About this neuroscience research article
Source: USC Contacts: Leigh Hopper – USC Image Source: The image is credited to USC.
Objective: To examine whether LCn3PUFA levels modify the potential neurotoxic effects of PM2.5 exposure on normal-appearing brain volumes among dementia-free elderly women.
Methods: A total of 1,315 women (aged 65 to 80 years) free of dementia were enrolled in an observational study between 1996-9 and underwent structural brain MRI in 2005-6. Based on prospectively collected and geocoded participant addresses, we used a spatiotemporal model to estimate the 3-year average PM2.5 exposure before the MRI. We examined the joint associations of baseline LCn3PUFAs in red blood cells (RBCs) and PM2.5 exposure with brain volumes in generalized linear models.
Results: After adjustment for potential confounders, participants with higher levels of RBC LCn3PUFA had significantly greater volumes of white matter and hippocampus. For each inter-quartile increment (2.02%) in omega-3 index, the average volume was 5.03 cm3 (P<0.01) greater in the white matter, and 0.08 cm3 (P=0.03) greater in the hippocampus. The associations with RBC DHA and EPA levels were similar. Higher LCn3PUFA attenuated the inverse associations between PM2.5 exposure and white matter volumes in the total brain and multi-modal association areas (frontal, parietal, and temporal; all P for interaction <0.05), while the associations with other brain regions were not modified. Consistent results were found for dietary intakes LCn3PUFAs and non-fried fish.
Conclusions: Findings from this prospective cohort study among elderly women suggest that the benefits of LCn3PUFAs on brain aging may include the protection against potential adverse effects of air pollution on white matter volumes.
Fine particulate matter exposure during childhood relates to hemispheric-specific differences in brain structure
Background Emerging findings have increased concern that exposure to fine particulate matter air pollution (aerodynamic diameter ≤ 2.5 μm; PM2.5) may be neurotoxic, even at lower levels of exposure. Yet, additional studies are needed to determine if exposure to current PM2.5 levels may be linked to hemispheric and regional patterns of brain development in children across the United States.
Objectives We examined the cross-sectional associations between geocoded measures of concurrent annual average outdoor PM2.5 exposure, regional- and hemisphere-specific differences in brain morphometry and cognition in 10,343 9- and 10- year-old children.
Methods High-resolution structural T1-weighted brain magnetic resonance imaging (MRI) and NIH Toolbox measures of cognition were collected from children at ages 9–10 years. FreeSurfer was used to quantify cortical surface area, cortical thickness, as well as subcortical and cerebellum volumes in each hemisphere. PM2.5 concentrations were estimated using an ensemble-based model approach and assigned to each child’s primary residential address collected at the study visit. We used mixed-effects models to examine regional- and hemispheric- effects of PM2.5 exposure on brain estimates and cognition after considering nesting of participants by familial relationships and study site, adjustment for socio-demographic factors and multiple comparisons.
Results Annual residential PM2.5 exposure (7.63 ± 1.57 µg/m3) was associated with hemispheric specific differences in gray matter across cortical regions of the frontal, parietal, temporal and occipital lobes as well as subcortical and cerebellum brain regions. There were hemispheric-specific associations between PM2.5 exposures and cortical surface area in 9/31 regions; cortical thickness in 22/27 regions; and volumes of the thalamus, pallidum, and nucleus accumbens. We found neither significant associations between PM2.5 and task performance on individual measures of neurocognition nor evidence that sex moderated the observed associations.
Discussion Even at relatively low-levels, current PM2.5 exposure across the U.S. may be an important environmental factor influencing patterns of structural brain development in childhood. Prospective follow-up of this cohort will help determine how current levels of PM2.5 exposure may affect brain development and subsequent risk for cognitive and emotional problems across adolescence.