Northbrook, IL, October 11, 2004 — Children prenatally exposed to pollutants, such as motor vehicle exhaust, and postnatally exposed to environmental tobacco smoke (ETS) may be more likely to suffer from asthma and related symptoms early in life. A new study in the October issue of CHEST, the peer-reviewed journal of the American College of Chest Physicians, shows that young children who are exposed to these pollutants may be significantly more likely to develop respiratory conditions at ages 12 and 24 months.
“A great deal of new evidence suggests that the respiratory system may be vulnerable to damage caused by inhaled environmental agents during the prenatal period,” said Rachel L. Miller, MD, the study’s lead author at the Columbia Center for Children’s Environmental Health, part of the Columbia University Mailman School of Public Health, New York, NY.
“This study indicates that the combination of exposure to combustion by-products in the womb and to second-hand smoke during infancy can cause significantly more respiratory problems than either exposure on its own,” added Dr. Frederica Perera, the study’s Principal Investigator and Director of the Center.
Researchers from the Columbia Center for Children’s Environmental Health studied 303 pregnant Dominican and African-American women, all nonsmokers, who were enrolled as part of a large prospective cohort study following mothers and their children for several years after delivery to examine effects of environmental pollutants. The researchers measured each woman’s prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAHs) through personal air monitors and questionnaires, and distributed additional periodic questionnaires to monitor the children’s respiratory health. Study results show that children exposed prenatally to PAHs and postnatally to ETS were more likely to cough and wheeze at 12 months of age and experienced more difficulty breathing, as well as higher incidences of asthma symptoms, at 24 months of age. Although the researchers found increased respiratory symptoms at 12 and 24 months, they did not find a relationship between PAHs, ETS, and respiratory symptoms when the children were 6 months old. These findings may suggest that the harmful effects on the lung develop after prolonged or later exposure to ETS.
“At this point we can only speculate how PAH exposure, in conjunction with ETS, causes respiratory damage,” said Dr. Miller. “One possibility is that PAHs, which easily reach the fetus and damage DNA, affect the child’s developmental programming, which then leaves the child’s airways at risk for future harm.”
People living in high-traffic areas and poor housing are at especially high risk for PAH and ETS exposure. PAHs can come from motor vehicle emissions, residential heating, power generation, tobacco smoking, and other combustion sources. While PAHs and ETS can harm boys and girls, the study found preliminary evidence that the combination more often leads to cough and wheeze in boys, possibly because boys tend to have smaller airways, which may increase the risk for airway hyperreactivity or inflammation-induced respiratory symptoms.
“The congestion and pollution found in most large cities can compromise the respiratory health of children in these areas,” said Richard S. Irwin, MD, FCCP, President of the American College of Chest Physicians. “This study reinforces the importance of society doing a better job protecting the health of children living in inner-cities, even before they are born.”
CHEST is a peer-reviewed journal published by the ACCP. It is available online each month at www.chestjournal.org. ACCP represents 16,000 members who provide clinical respiratory, critical care, sleep, and cardiothoracic patient care in the United States and throughout the world. The ACCP’s mission is to promote the prevention and treatment of diseases of the chest through leadership, education, research, and communication. For more information about the ACCP, please visit the ACCP Web site at www.chestnet.org.