Common Pesticide Linked to Birth Defect, Study SuggestsLast Updated: September 28, 2012. Children of Texas mothers living where atrazine most used were more likely to have nasal passage blockage.
FRIDAY, Sept. 28 (HealthDay News) -- A common herbicide called atrazine may be associated with a rare birth defect of the nasal cavity, a new study suggests.
Atrazine -- the most widely used herbicide in the United States, particularly in corn crops -- is believed to be an endocrine disruptor, which means that it may interfere with the hormone system in humans.
The new study looked at the link between atrazine and choanal atresia, a birth defect in which tissue formed during fetal development blocks the back of the nasal passage. The condition affects a baby's ability to breathe. Surgery is the typical treatment.
Although few risk factors for choanal atresia have been identified, it's believed that chemicals that disrupt a mother's hormone system may be associated with the risk, according to study author Philip Lupo, an assistant professor of pediatrics -- hematology/oncology at Baylor College of Medicine and Texas Children's Cancer Center.
He and his colleagues found that mothers who lived in Texas counties with the highest levels of atrazine use were 80 percent more likely to have children with choanal atresia -- or a less severe form of the condition called choanal stenosis -- than those in counties with the lowest levels of atrazine use.
"Our results warrant more detailed exploration before any public health or policy-related recommendations are made, but this study is a good first step in trying to understand the origin of this birth defect, including a possible role of atrazine," Lupo said in a Baylor news release.
The study appears Sept. 28 in the Journal of Pediatrics.
While the study found an association between the herbicide atrazine and the birth defect choanal atresia, it did not prove cause-and-effect.
The Children's Choanal Atresia Foundation has more about choanal atresia.
SOURCE: Baylor College of Medicine, news release, Sept. 28, 2012