What a pregnant mom eats, drinks, and breathes can obviously affect her baby. We know this from studies of alcohol consumption and cigarette smoking, among other things. But how does air pollution affect her baby? Can the pollution a pregnant mom inhales, such as fine particles, or soot, unknowingly cause health problems years down the line, when that baby is a teenager?
Dr. Frederica Perera, a professor at Columbia University’s Mailman School of Public Health and director of the Columbia Center for Children’s Environmental Health, focuses her research on just this question. She has been examining the effects of environmental exposures on pregnant women and their children for 15 years. Using personal air monitoring “backpacks” combined with ambient air monitors, Dr. Perera has been investigating the effects of air pollution on more than 700 mothers and their children in Northern Manhattan, with other ongoing studies in Poland and China.
Dr. Perera’s research explores the relationship between air pollution – specifically, exposure to polycyclic aromatic hydrocarbons (PAHs) – and birth weight, cancer markers, asthma, learning and behavior, obesity, and other health effects. PAHs are a group of chemicals released into the air when organic matter is burned, such as coal, gasoline, diesel fuel, firewood, and tobacco.
I spoke with her recently about her research.
Why do you study air pollution?
I study air pollution because it is a common and widespread exposure, in this country and of course globally. We have learned during the last several decades that exposure to air pollution has multiple adverse outcomes. Our work is focused on the prenatal window of susceptibility and the early period of child development because we know from many lines of evidence that this is a particularly important period for the potential disruption of normal development by environmental exposures. That’s been shown experimentally [in laboratory animals] and also in some studies, such as ours, in humans.
What are the major sources of air pollution for the population that you study?
We can talk about indoor and outdoor air pollution and sometimes people think that they’re completely separate, but they’re not. There is a great deal of exchange of air between the outdoor and indoor environment. Buildings are quite permeable, surprisingly so. The major sources of air pollution are combustion of organic material. Of course fossil fuel combustion is a major source in urban areas. We’re talking about diesel, oil for heating, gasoline for vehicles, and coal burning. In addition, tobacco smoking causes air pollution. That’s a major indoor source, and it’s an indoor source of some of the very pollutants found in outdoor air from these other combustion sources.
Correlations between the levels of indoor and outdoor pollutants indicate that there is a considerable transfer from the outdoor to the indoor environment.
What are the health effects that you’re looking for?
Birth outcomes is the first thing we look at – birth weight, length, head circumference – and then we look at child development using standardized, validated measurements and instruments. We do the assessments periodically from the time the child is born all the way through adolescence. Our oldest children in the study are now 14. Of course the instruments change over time. They are age-appropriate tests and we’re able to gather more and more information, more refined information, on child development in different domains that are not accessible or would not have emerged at the early ages. Neurobehavioral development and cognitive development are important outcomes of interest for us in our research.
[What are Dr. Perera's findings on fetal growth and developmental effects? From her Center's website:]
- Prenatal exposure to PAH reduced birth weight and head circumference in African-American babies born to women who were more highly exposed to the air pollutants. Several studies have reported that reduction in head circumference at birth or during the first year of life correlates with poorer cognitive functioning and school performance in childhood.
- Children with high prenatal exposure to PAH had significantly lower test scores at age 3 on the Bayley test for cognitive development and were more likely to be developmentally delayed.
- Prenatal exposure to PAH at levels encountered in NYC air can adversely affect child IQ scores at 5 years of age. After adjustment for potential confounders, highly exposed children had Full-scale and Verbal IQ scores that were 4.31 and 4.67 points lower compared to less exposed children. These reductions are similar in magnitude to the effects of low-level lead exposure.
Also we’re looking at asthma as an outcome. We have been publishing results on our findings with respect to both prenatal and postnatal exposure to Polycyclic Aromatic Hydrocarbons [PAHs] and asthma in childhood. We’re continuing to follow the kids to be able to look at whether these conditions are persisting, are resolving, or even worsening. So respiratory health is a major outcome.
[What are Dr. Perera's findings on asthma and air pollution? From her Center's website:]
- Combined prenatal exposure to airborne PAHs and postnatal secondhand smoke results in the increased likelihood of respiratory and asthma-like symptoms at one and two years of age and at five to six years of age.
- CCCEH has linked epigenetic alterations associated with prenatal exposure to PAH in cord blood with parental report of asthma by age 5. Epigenetic changes may disrupt the normal functioning of genes by affecting how they are expressed, but do not cause structural changes or mutations in the genes.
- Exposure shortly after birth to ambient metals such as nickel, vanadium, and carbon is associated with wheeze and cough in children aged two and younger.
We’re also interested in potential risk of cancer. In our cohort we’re not able to look at cancer as an outcome because we don’t have the very large sample sizes needed for such studies. But we are able to look at what we call “procarcinogenic biomarkers.” We’re evaluating those particular chromosomal abnormalities, or chromosomal changes, attributable to or associated with the exposures. We look at this prenatally, we look at cord blood, and then we take repeat blood samples as the children are getting older, and are looking further at the chromosomal abnormalities in those older samples.
Research from our center has shown that in newborns, PAHs were associated with chromosomal aberrations. It’s not cancer per se but it is a biomarker that has been shown in adults to be related to risk of cancer, so it’s a biomarker of concern.
[What are Dr. Perera's findings on cancer and air pollution? From her Center's website:]
- Approximately 40% of babies in the study were born with DNA damage associated with PAH. In other studies such damage has been tied to an increased risk of cancer. Of particular concern, newborns had higher (approximately 10-fold) levels of adducts than mothers per unit of estimated exposure, indicating greater fetal susceptibility and potential risk from these pollutants.
- Prenatal exposure to PAH was linked to structural changes in babies’ chromosomes. Such genetic alterations have been related in other studies to increased risk of cancer in children and adults.
- Prenatal maternal exposure to polycyclic aromatic hydrocarbons (PAH) from polluted air is associated with chromosomal abnormalities in cord blood. Chromosomal aberrations have been associated with increased risk of cancer in adults. These results suggest that the carcinogenic process may begin in the womb.
The other endpoints that we’re looking at are obesity and metabolic disorder. We are following up on some work in laboratories that had suggested that air pollution we’re interested in, the PAH, might be associated with increased weight and obesity. We have published from the Center the first finding that in fact there was a significant link between prenatal PAH exposure as we measured it and later body mass index of the children.
If these chromosomal abnormalities show up – does this mean that people are more likely to develop cancer 10 years down the line, 15 years down the line?
No. This is a general finding at the population level. We can’t make any risk predictions for any one child. And in fact some of the chromosomal aberrations may disappear. So we don’t really know what the life course is going to be. It’s simply that the finding is an early warning of potential risk in terms of cancer. But we really have to emphasize that it is not cancer. We cannot make risk predictions based on it.
If you had unlimited resources, how long would you want to follow your cohort?
If we could, we’d want to follow this group just as long as they would be willing to have us follow them. There are no studies like this with such in-depth assessment of early-life exposures and also other risk factors that then follow the children through their early years and on through adolescence. We know that adolescence is another vulnerable period where there are many hormonally related changes and reorganization of the brain. All kinds of things are happening that are important to track.
How do race and poverty fit into the picture of environmental exposures?
Race and poverty are important in that there are racial and economic disparities in exposure. Although air pollution affects everyone and it’s not confined to any one area, the levels tend to be higher in the lower income and inner city neighborhoods. Our population is drawn from one such community here in NYC. There are disparities both in exposure and in rates of the different outcomes that we’re concerned about.
Do you feel like there are parts of your research that are relevant to area outside of NYC?
Oh, I think so. The exposures we’re measuring are prevalent, they’re widespread, and they’re common in urban environments. We see consistent effects in our cohorts in Poland and in China. Those studies have not been going for so long and are not as in-depth as the one in New York, but we do have parallels in terms of the methods and the outcomes. The effects seem to be consistent, certainly for birth outcomes and neurodevelopment.
What are the questions you would like to answer in the future?
We’re very interested in prevention. Our focus more than anything is on research that can lead to prevention. That’s our reason for being. To prevent disease you need to have understanding of the associations between certain preventable risk factors and your outcomes of concern. Certainly all the outcomes I’ve mentioned [low birthweight, developmental delays, asthma, cancer] are of enormous concern. These are all health problems in children that have been increasing in recent years, and they have enormous individual and social costs, so obviously we want our research to help find ways to reduce those burdens.
The environment is one source that by its nature is amenable to intervention. What we would like to do in the future is keep the research going to document the long-term consequences of early life exposure, and to carefully document and then translate that work so it’s accessible and usable by policymakers. We also want to begin to understand better how the social environment, how the psychosocial factors, may interact with the physical environment in terms of either exacerbating the health effects or preventing and improving those outcomes.
Are there prevention measures or policy measures that you want to see in place now, that you wish would happen, that you think we have enough evidence to implement?
We know what can work. We’ve been able to see in our own cohort that efforts to clean up the air in New York City have led to decreasing levels of the PAH air pollutant. We know that over a period of time when we were monitoring the personal air that women were breathing in during pregnancy – the years between 1998 and 2006 – there were measures taken to reduce diesel fuel and other pollutant sources. And we’ve seen a decrease in our monitored levels.
We’ve seen that also in China, where a coal-burning power plant was shut down. We saw direct benefits in the subsequent group of children that were born in that city. We also have seen that regulations of pesticides work. The pesticide that we have been concerned about, chlorpyrifos, was banned for residential use for spraying and use for pest control in homes and in apartments [in 2000]. We were able to see that in cord blood after the phase-out ban, the levels [of chlorpyrifos] were dramatically lower.
So the good news is that these interventions can work. There are ways of reducing these exposures and directly measuring those benefits. Of course, we do need to do much better, and there are readily available means to reduce air pollution levels.
What can moms and dads do to try to protect their children from harmful exposures?
Certainly moms and dads have control in their own house of the smoking issue: not smoking themselves, and asking others not to smoke in the home. They also control other exposures to potentially toxic chemicals: cleaning and pest control. There are alternatives for those. And so we can make our home environment as safe as possible.
This doesn’t take care of the problem of outdoor air. There are strategies that are effective in reducing air pollution emissions to the air, and those have included the cleanup of the diesel bus fleet in New York. The bus fleet now has standards for diesel fuel and restrictions on idling. These standards, plus idling restrictions for school buses and trucks – these are things we know can work.