Young children from low-income homes whose mothers reported frequent use of toxic chemicals such as household cleaners were more likely to show delays in language development by age 2, a new study found.
In addition, the children scored lower on a test of cognitive development.
These developmental delays were evident even when the researchers took into account factors such as the education and income of mothers, which are also linked to their children’s language and cognitive skills.
The findings provide additional evidence of the need for pediatricians and other health care providers to counsel parents of young children to restrict their use of toxic household chemicals, said Hui Jiang, lead author of the study and senior research associate at The Ohio State University.
“We found that a significant percentage of mothers with young children may commonly expose their children to toxic household chemicals, possibly because they are unaware that such materials may be harmful,” said Jiang, who is with Ohio State’s Crane Center for Early Childhood Research and Policy.
The study was published online recently in the journal Clinical Pediatrics.
The researchers used data on 190 families from the Kids in Columbus Study, a Crane Center research project that followed children born into low-income families in Columbus for five years after birth.
When they first started the study, mothers were asked about their use of household chemicals such as floor and toilet cleaners and solvents during pregnancy.
They were asked again when their child was 14 to 23 months old. Mothers also reported whether they had mold in the home, their use of pesticides, and neighborhood pollution sources.
Children’s language development was measured when they were between 14 and 23 months old and again when they were 20 to 25 months old.
The researchers used a standardized test that examines children’s understanding and expression of language – for example, recognition of objects and people, following directions, and naming objects and pictures.
Findings showed that neighborhood pollution, mold in the house and pesticide use were not significantly linked to child outcomes.
But the more household chemicals mothers reported using regularly after childbirth, the lower the child language and cognitive outcomes at 2 years of age.
There was no link between chemical use during pregnancy and child outcomes, possibly because mothers reported using significantly fewer chemicals during pregnancy.
Exposure to toxic chemicals was reported by about 20 percent of mothers during pregnancy, but that increased to 30 percent when their children were between 1 and 2 years old.
Mothers also reported using more household chemicals after childbirth.
“A lot of mothers seem to know to limit exposure to toxic chemicals during pregnancy, but once their child is born, they may think it is no longer a problem,” Jiang said.
But research has shown these early years of a child’s life are key in many ways, said Laura Justice, co-author of the study and professor of educational psychology at Ohio State.
“When kids reach about 2 years old, that is a peak time for brain development,” said Justice, who is executive director of The Crane Center.
“If the use of toxic chemicals is interfering with that development, that could lead to problems with language and cognitive growth.”
While many mothers may use household cleaners and other toxic chemicals when their children are young, low-income mothers may face particular challenges, Jiang said.
For example, they often live in smaller apartments where it may be more difficult to keep children away from chemicals, particularly while they are cleaning.
Jiang noted that this study simply analyzed the relationship between mothers’ use of toxic chemicals and later child development and as such can’t prove that chemical use caused the developmental delays.
“Future studies are need to more carefully examine the mechanisms through which household toxicants may disrupt early language development,” she said.
The findings do show that pediatricians need to emphasize that pregnancy is not the only time for mothers to be concerned about chemical use, Justice said.
“Parents need to understand the delicacy of brain development in the first several years of life and their children’s susceptibility to chemical exposure,” she said.
Other co-authors were Kelly Purtell and Randi Bates, both of Ohio State.
Children are exposed prenatally and in early childhood to multiple environmental stressors that can adversely affect their cognitive abilities, academic performance and consequent educational trajectories, adult health, wealth, and social status.1,2
Project TENDR (Targeting Environmental Neurodevelopmental Risks), a unique collaboration of leading scientists, health professionals, and children’s and environmental health advocates, points to growing scientific evidence linking exposure to toxic chemicals during early brain development with brain disorders and calls on individuals, industries, and policymakers to reduce these exposures.3
Developmental disabilities, such as learning disabilities, developmental delays, autism, and attention-deficit/hyperactivity disorder (ADHD), affect one in six children in the United States, and the rate of these disorders is rising.4
The estimated annual cost (medical care, lost economic productivity) of environmentally mediated neurodevelopmental disorders in US children is $74.3 billion.5
Evidence linking combustion-related air pollution with adverse neurodevelopment is mounting. Sources of these pollutants include fossil fuel burning for power generation and transportation, wildfires, and burning of agricultural waste.
Project TENDR identified these air pollutants—polycyclic aromatic hydrocarbons, nitrogen dioxide, fine particulate matter (PM2.5, including ultrafine particulate matter [UFP]; ≤ 100 nm), and other pollutants for which nitrogen dioxide and PM2.5 are markers—as exemplary targets for action. The purpose of this commentary is to present Project TENDR’s recommendations to reduce combustion-related air pollutant emissions to protect healthy brain development.Go to:
NEURODEVELOPMENTAL EFFECTS OF AIR POLLUTION
Air pollution exposure has been linked with preterm birth and low birth weight,6,7 known risk factors for many neurodevelopmental disorders in children.8,9 A growing body of human studies associate exposure to combustion-related air pollutants (PM2.5, polycyclic aromatic hydrocarbons, nitrogen dioxide, black carbon) with adverse effects on brain development, including deficits in intelligence, memory, and behavior.10–12
Polycyclic aromatic hydrocarbons, a component of PM2.5, have been associated with developmental delay; reduced IQ; symptoms of anxiety, depression, and inattention13; ADHD; and reduced size of brain regions important for processing information and impulse control.14 Other studies have linked roadway proximity,15 traffic-related PM,16 elemental carbon, or nitrogen dioxide17 to decreased cognitive function, including deficits in memory and attention.
The effect of polycyclic aromatic hydrocarbon exposures during fetal development on cognitive and behavioral outcomes is magnified by material hardship or maternal demoralization.18 Low-income communities are thus disproportionately exposed and uniquely vulnerable because of family and community economic hardship. Increasing evidence links prenatal exposure to traffic-related air pollutants19 and PM2.520 to autism spectrum disorder.
Laboratory studies provide support for the neurotoxic effects of exposure to air pollutants. In mice, prenatal exposures to fine and ultrafine particles caused enlarged lateral ventricles, an early and excessive myelination pattern, an increase in the size of the corpus callosum (the bridge connecting the two brain hemispheres), and a decrease in the hippocampal area (involved in emotional regulation, spatial navigation, and memory).21
Prenatal diesel exhaust exposure produced inflammation in fetal brain, decreased activity, increased anxiety, and brain microglial activation (indicating a pathological process) in males as adults.22 Prenatal diesel exhaust exposure in mice reduced locomotor activity and altered levels of neurotransmitters (dopamine, norepinephrine) in a region-specific manner.23
Chronic exposure of young adult mice to UFP produced depressive-like behaviors and impaired spatial learning and memory.24 In a series of studies, postnatal UFP exposures of mice produced a pattern of developmental neurotoxicity notably similar to the hypothesized mechanistic underpinnings of autism spectrum disorder.
Both sexes exposed during early postnatal life, a period considered equivalent to the human third trimester, to concentrated ambient UFP showed disrupted development of the corpus callosum and persistent elevation of brain glutamate levels—an excitatory neurotransmitter—with effects more pronounced in males and persistent through adulthood.
UFP is likely the most toxic fraction of particulate air pollution and once inhaled can migrate to the central nervous system via the nasal cavity, circulating blood, or sensory nerves found in the gastrointestinal tract.25 Exposures in these studies were at levels consistent with high-traffic areas of major US cities and thus highly relevant.
Although specific autism spectrum disorder–defining behaviors were not examined in this series of studies, impaired learning and short-term memory and increased impulsivity were observed.26
Potential cellular mechanisms responsible for air pollution–induced neurological damage include persistent glial activation with concomitant neuroinflammation and oxidative stress.22,27–29 The findings in controlled laboratory studies are consistent with and provide mechanistic evidence for air pollutant effects on neurocognitive and neurobehavioral outcomes observed in humans.
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Ohio State University
