Maternal Exposure to Weed, Rodent Killers Raises Risk Of Congenital Heart Defect
Exposure to certain pesticides during the first trimester of pregnancy increases a woman's risk of bearing an infant with a severe congenital heart defect that disrupts oxygenation of the blood. An analysis involving more than 1,800 infants with congenital heart defects indicates that early maternal exposure to rodenticides nearly quintuples the risk, while exposure to herbicides almost triples the risk.1
The researchers used a subset of data from a case-control study conducted from 1981 through 1989 to identify genetic and environmental risk factors for congenital heart defects. That subset, which includes 1,832 infants with congenital heart defects and 771 infants without such defects, provides detailed information on the type and frequency of pesticide exposure and its timing in relation to conception.
The analysis included infants with congenital heart defects who were born in the Baltimore-Washington area in 1987-1989 and treated at one of the region's six pediatric cardiology centers, as well as a random sample of infants without heart defects born in the area during that period. Interviews conducted with the children's parents, generally before the children's first birthday, covered socioeconomic and demographic data, family history of congenital heart and other defects, and maternal and paternal exposure to environmental contaminants.
After a preliminary analysis indicating that heart defects as a group are not associated with pesticide exposure, the researchers focused on one type of malformation that was twice as common among infants whose mothers had been exposed as among those whose mothers had not been exposed. In this malformation, called transposition of the great arteries, the aorta arises from the right instead of the left ventricle, while the pulmonary artery originates in the left instead of the right ventricle; as a result, the body's supply of oxygenated blood is disrupted.* In addition to the 66 infants with transposed arteries, 114 infants had other abnormalities affecting the flow of blood from the heart; these infants made up a second comparison group.
The three groups were similar in race, age and exposure to most environmental contaminants. However, the families of infants with transposed arteries were more likely than those of controls to be of low socioeconomic status (74% vs. 60%). In addition, the mothers of such infants were more likely than those of control infants to have been exposed to solvents (6% vs. 2%), and the fathers were more likely to have been exposed to pesticides (62% vs. 45%).
Exposure to a pesticide of any kind was reported by 44% of the mothers of infants with transposed arteries, 26% of the mothers of those with other abnormalities affecting the flow of blood out of the heart and 27% of the mothers of infants without heart defects. Small proportions in each group (6-11%) reported exposure occurring at least once a week. The most common mode of exposure for all three groups was by hand-held spray (14-21%), but the greatest difference among groups was for exposure to pellets, to powder or to poison disguised as food (3-11%). Bivariate analysis indicated significant associations between transposed arteries and exposure to chemical rodent killers (unadjusted odds ratio of 3.5) or weed killers (3.7). The use of pellets, powders or food imitators was the only mode of exposure associated with the malformation (4.0). No overall trend was evident according to frequency of exposure, although too few women had been exposed once a week or more for meaningful analysis. None of these factors had significant effects on the risk of other abnormalities affecting the flow of blood from the heart.
After adjustment for socioeconomic and demographic characteristics, medical history and paternal pesticide exposure, a logistic regression analysis found that infants whose mother had been exposed to weed killers or rodent killers had significantly elevated odds of being born with transposed great arteries (2.8 and 4.8, respectively). Exposure to rodent killers did not affect a woman's risk of bearing a child with other malformations affecting the flow of blood from the heart. No women whose children had such defects reported exposure to herbicides during the first trimester or the three months preceding conception.
An examination of the effect of the timing of pesticide exposure in relation to conception revealed that maternal exposure to a pesticide of any kind during the first trimester of pregnancy or the preceding three months significantly increased the risk that an infant would be born with transposed arteries (odds ratio of 2.1); exposure before or after that period had no effect. When the analysis focused on specific types of pesticides, however, rodenticide exposure and herbicide exposure had significant effects when they occurred 4-6 months before conception (6.1 and 4.7, respectively) or during the six months centering on conception (5.1 and 3.6, respectively).
The researchers note that currently available weed, insect and rodent killers use more than 600 pesticide chemicals in as many as 50,000 formulations and that they were not able to determine the specific chemicals to which women were exposed. They were, however, able to identify chemical categories (such as anticoagulants, the predominant chemicals used in rodenticides) that call for further examination, and they stress the need to examine the effects of pesticide exposure in larger samples. Nevertheless, they conclude that transposition of the great arteries "is associated with environmental pesticide exposure during the periconceptional period of pregnancy."--F. Althaus
1. Loffredo CA et al., Association of transposition of the great arteries in infants with maternal exposures to herbicides and rodenticides, American Journal of Epidemiology, 2001, 153(6):529-536.
*Because of the transposition, the aorta carries deoxygenated rather than oxygenated blood out of the heart to be distributed throughout the body.