Meeting Report
11/14/2006

Smoking during pregnancy linked to congenital heart defects

Abstract 3274

CHICAGO, Nov. 14 — Women who smoke or are exposed to tobacco smoke early in their pregnancies are more likely to have children with certain types of congenital heart defects, researchers reported at the American Heart Association’s Scientific Sessions 2006.

“The heart’s basic structures develop very early in pregnancy, before many women realize they are pregnant,” said Sadia Malik, M.B.B.S., M.P.H., the study’s lead author and an assistant professor of pediatrics at the University of Arkansas for Medical Sciences in Little Rock, AR.  “Thus, even if a woman quits smoking at six weeks or later, her fetus will still have been exposed to the harmful effects of cigarette smoking during cardiac development.”

About 36,000 babies are born with a heart defect each year, according to the American Heart Association.   A congenital heart defect (CHD) is a structural abnormality present at birth.   The defects result when a mishap occurs during heart development soon after conception.  Defects range from simple problems, such as “holes” between chambers of the heart, to severe malformations, such as the absence of one or more chambers or valves.

“From animal studies, we know that multiple components within cigarettes are harmful to the developing fetus and can cause mutations that might lead to birth defects,” Malik said.

In this population-based, case-controlled study, researchers investigated the association between congenital heart defects and maternal smoking.   Collaborating with the National Birth Defects Prevention Study (NBDPS), researchers studied 566 infants with a CHD and 491 infants without a CHD, along with all the children’s parents.  The disorders among the children included:

• left-sided or right-sided obstructive defects that can restrict blood flow through the aortic valve or the pulmonary valve;
• septal heart defects, which affect the heart chambers; and
• conotruncal heart defects, a group of defects, such as the condition in which the aorta and pulmonary arteries are transposed, disturbing the blood flow between the heart and lungs.

Mothers of both the infants with CHD and without CHD were asked whether they smoked from one month before pregnancy through the end of pregnancy.   Women’s exposure to tobacco smoke at home or work during the same period also was determined.

Thirty-four percent of women who had children with a CHD reported they smoked some time in the month prior to conception through the end of the first trimester.

Researchers found that women who had smoked in that period were 60 percent more likely to have infants with a CHD than women who said they had not smoked.  This was true even if women had taken prenatal vitamins and limited their alcohol intake, regardless of their age or race.

A subgroup analysis estimated that women who had an infant with a septal or right-sided obstructed heart defect were 80 percent more likely to have smoked during embryo development than women who had an infant without a heart defect.

Malik suggested that some biological mechanisms, such as apoptosis (programmed cell death — the cell dies if it becomes severely mutated as a means of protecting the entire organism), may play more of a role during septal and pulmonary valve development than during the development of other cardiac structures.

“We hope our study contributes to the existing knowledge of the harmful effects of maternal smoking and tobacco smoke exposure on the developing infant,” Malik said.   “We want to help develop a comprehensive approach to pre-conception clinical and public health interventions that will ultimately optimize the health of future generations.”

Malik said the study is limited because maternal tobacco exposure was self-reported after pregnancy and the study focused on a small number of patients.  Further study is needed to investigate the full impact of maternal smoking on the developing heart.

Malik and co-authors are analyzing more data to determine if these results among Arkansas women are reproducible in a larger sample from the NBDPS, which is more representative of the general U.S. population.

Co-authors are: Charlotte Hobbs, M.D., Ph.D.; Mario Cleves, Ph.D.; and Weizhi Zhao, M.S.

This study was funded by the Centers for Disease Control and Prevention, Division of Birth Defects and Developmental Disabilities; the National Institute of Child Health and Human Development; and the Arkansas Biosciences Institute, the major research component of the Tobacco Settlement Proceeds Act of 2000.

Statements and conclusions of study authors that are published in the American Heart Association scientific journals are solely those of the study authors and do not necessarily reflect association policy or position.  The American Heart Association makes no representation or warranty as to their accuracy or reliability.

NR06 – 1101 (SS06/Malik)

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