Mothers Matter: Looking for a Healthy Start
EPA researchers and their partners are exploring the links between early exposures to pollution and potential health effects later in life.
There's a lot that expectant mothers can do to give their babies a better chance for a healthy start: get plenty of rest, take prenatal vitamins, get regular checkups, and avoid alcohol and smoking.
What they can't do: stop eating, drinking water, or breathing.
EPA scientists and their partners, including researchers supported by grants from the Agency's Science to Achieve Results (STAR) Program and sister Federal agencies such as the National Institute of Environmental Health Sciences (NIEHS) are exploring potential links between a mother's everyday exposures to environmental pollutants during pregnancy and the health consequences those exposures might have for her baby in the future.
The results of the research will help mothers know what they can add to their "to do" (or "to not do") lists when preparing for a healthy new arrival. The research will also provide important information to public policy officials and healthcare providers.
Reducing Children’s Health Risks from Exposure to Pesticides
Every year, approximately one billion pounds of pesticides are used in the United States. Unfortunately, the early life stages can be particularly vulnerable to unintended consequences from pesticide exposure.
Children’s health research has already identified—and helped diminish—increased risks that children face from pesticide exposure through everyday activities. By exploring possible links between prenatal exposures to pesticides and potential health effects after birth, researchers and their partners are further advancing the science of protecting children’s health.
There is strong evidence that prenatal exposure to even low levels of organophosphate (OP) pesticides can harm children’s health. Studies by university-based scientists funded by EPA and NIEHS have revealed links between prenatal exposure to two OP pesticides—chlorpyrifos and diazinon—and reduced birth weight and length.
While EPA has banned the use of both pesticides in residential settings, they (and other OP pesticides) are still widely used in agriculture and can be applied in public spaces such as parks and golf courses. As a result, children living in agricultural communities can still be exposed, and residues of the pesticides can be present on some conventionally-grown produce.
Recent advances in OP pesticide exposure research gained national attention in 2011, when several landmark scientific papers were published by three of the EPA/NIEHS Children’s Environmental Health and Disease Prevention Research Centers (see also Protecting Children’s Health for a Lifetime in this issue). The results of those studies revealed links between prenatal exposure to OP pesticides and disrupted brain and nervous system development.
Beginning in 1998 and 1999, the three studies measured OP pesticide levels in mothers’ blood, urine, and in-home environments during pregnancy and after children were born. The multi-year studies allowed researchers to gather health information from birth to childhood, allowing them to investigate early life stage exposures, behavior, and other health outcomes later in childhood.
One of these studies, by scientists at the Center for Environmental Research and Children’s Health (CERCH) at the University of California, Berkeley, found that higher prenatal levels of OP pesticides in mothers’ urine were associated with lower scores for working memory (memory the brain uses while actively engaged in a task), verbal comprehension, Intelligence Quotient (IQ), and other measures in children from the “CHAMACOS” cohort at age seven. CHAMACOS stands for Center for the Health Assessment of Mothers and Children of Salinas, a study looking at the health impacts of pesticides and other environmental chemicals that may affect children’s health, growth, and brain development.
Similar results were obtained by scientists at the EPA/NIEHS Center for Children’s Environmental Health at Columbia University. In that study, high cord-blood measures of the OP pesticide chlorpyrifos were linked to lowered IQ and deficits in working memory in children at age seven.
And in the third study, scientists at the EPA/NIEHS Children’s Center at the Mount Sinai School of Medicine found that prenatal exposure to OP pesticides was associated with deficits in mental and perceptual reasoning among six- to nine-year-old children.
Although the studies are not directly comparable, all three studies in three different groups of children show similar results linking prenatal exposure to OP pesticides with adverse effects on cognitive function in childhood. The results add to the weight of evidence that prenatal exposure to OP pesticides can have detrimental effects on children’s cognitive development.
Subsequent studies have continued to build on the work. Researchers at the Columbia Children’s Center followed up their analysis by looking at MRI brain scans of some of the children in the original study. Results, published in 2012 in the Proceedings of the National Academy of Sciences, revealed links between children whose mothers had higher levels of chlorpyrifos exposure and structural changes in their brains that are consistent with lower IQ scores in the exposed children. In addition, gender differences between the male and female brain appeared to be disrupted.
Studies from the UC Berkeley/CERCH Children’s Center, in collaboration with other Children’s Center researchers, have shown that there can be significant genetic differences between individuals in the ability to detoxify OP pesticides in the body through differing efficiency and quantity of an enzyme called paraoxonase (PON). They also found that until the age of nine, children in general have lower capacity than adults to detoxify OP pesticides.
Another part of EPA’s research on prenatal exposures is looking at the potential future health effects that may result from air pollution exposure. Two recent publications from that work provide important clues into two potential effects: weight gain and neurobehavioral problems.
EPA researchers collaborated with partners from Duke University Medical Center on a laboratory study that explored how prenatal exposure to diesel exhaust might be linked to obesity later in life.
To conduct the study, researchers exposed a group of pregnant laboratory mice to air containing diesel exhaust at levels similar to those found in some U.S. cities. Another group of pregnant mice was exposed to clean (filtered) air.
The researchers then evaluated the offspring, recording weight as the mice grew. Half the mice in each group were raised on a regular diet and half on a high fat diet.
While all the offspring weighed roughly the same at birth, male offspring whose mothers had been exposed to diesel exhaust became much heavier once they reached adulthood, whether or not they were fed a high fat diet. Male offspring from the diesel exposed group also developed insulin resistance, a risk factor for diabetes and heart disease. In contrast, female offspring from the diesel group only gained more weight, as compared to the female control group, when fed high-fat diets.
“Preventing such diesel exposures to pregnant women may be one strategy, along with better diet and more exercise, to combat the obesity epidemic,” said Sally Perreault Darney, PhD, coordinator of children’s health research for EPA. (Also see Closing the Asthma Gap in this issue.)
To further advance the research, EPA scientists are now exploring clues that will help explain the observed obesity-inducing effect of diesel exhaust. EPA’s Ian Gilmour, Ph.D, the co-author of the study, said it’s possible that prenatal exposures to diesel exhaust produces inflammatory reactions in the developing brain that prime mice for weight gain as they get older.
In the second study, scientists at the EPA/NIEHS-funded Columbia Center for Children’s Environmental Health showed that prenatal exposure to air pollution can make children more likely to develop behavioral problems. The study focused on substances called polycyclic aromatic hydrocarbons (PAHs), a group of structurally-similar chemical compounds commonly found in vehicle and other exhaust.
During the study, non-smoking expectant women living in New York City were fitted with air monitors to passively measure PAH levels from the surrounding air as they went about their daily routines throughout the third trimester of pregnancy. The scientists also measured PAH levels in the mothers’ cord-blood after their babies were born. Both the ambient air and cord-blood measures were combined to estimate how much PAH the growing babies were exposed to.
The researchers continued to follow the children after birth and about 250 children from the cohort, then six to seven years of age, were evaluated for neurobehavioral and other problems by having their mothers fill out a detailed questionnaire.
Published in the June 2012 issue of Environmental Health Perspectives, the findings showed a link between higher levels of PAH exposure and increased symptoms of anxiety, depression, and attention problems. The new results extend findings from an earlier study with the same children that linked high PAH exposure to lower IQ and developmental delays.
“Neurobehavioral problems can affect a child’s ability to succeed in school so they can have lifelong impacts,” said the study’s lead author, Frederica Perera, DrPH, a professor of environmental health at Columbia University, who said the effects of PAHs are comparable to those of low-level lead exposure. “Therefore, research aimed at understanding the role of prenatal exposure to air pollution is a key to preventing behavioral and cognitive problems that can have long-term effects on children and impose a major burden on society.”