1947 –the Federal insecticide, Fungi-
cide and rodenticide act requires the
registration of all pesticides.
A troubled past
industry had hoped that atrazine’s
regulatory hurdles were over, but new
concerns have led to a fresh analysis.
1958 –atrazine is first registered.
1983 –registration standard for
atrazine is issued, and the document
notes concern about dietary carcinogenic risks from ground and water
contamination.
1988–ePa issues a preliminary notification of its intent to initiate a special
review under FiFra based on atrazine’s
carcinogenic potential.
1990 to 1992 –atrazine’s registrant
takes steps to reduce ground and
surface water contamination.
1991 –Under the safe drinking water
act, the ePa sets 3 ppb as the maximum level of atrazine in drinking water.
1994 – ePa institutes its special review
for triazine pesticides, including atrazine. at the time, atrazine has status
as a possible human carcinogen.
January and October 2003 – ePa concludes in interim reregistration decisions that atrazine is not likely to be a
human carcinogen and that there are
not sufficient data to confirm or refute
the hypothesis that atrazine exposure
may impact gonadal development in
amphibians. Before reregistration, the
Food Quality Protection act requires an
evaluation of food tolerances.
2004 – european Union bans atrazine.
April 2006 – in its reregistration decision, the ePa says that there is a
reasonable certainty that no harm will
result to the general U.s. population,
infants, children or other subgroups of
consumers from aggregate exposure to
cumulative residues of atrazine. Products containing atrazine are eligible for
reregistration.
2007 – ePa concludes that atrazine
does not adversely affect amphibian
gonadal development.
2009 – ePa releases atrazine ecological watershed monitoring data following a Huffington Post report about
atrazine in drinking water.
2010 –ePa launches a new evaluation
of atrazine’s safety.
According to Syngenta’s Pastoor, the
paper by Kloas’ team is “the most com-
prehensive, complete and extensive study
ever done on frogs looking at sexual devel-
opment.” Some 3,000 African clawed
frogs were exposed to five doses of atra-
zine spanning four orders of magnitude.
“And from that,” he says, “it was defini-
tively shown that atrazine has no effect.”
Rohr and McCoy omitted most data in
that paper from their review, however,
arguing its statistical deficiencies made
evaluation of the data “impossible.”
Previous EPA analyses of atrazine
safety had access to four earlier reviews
of animal data, Rohr notes — all funded
at least in part by industry. He maintains
that his is the first review that is free of
industry involvement. Funding for his
assessment came from the EPA, the
National Science Foundation and the U. S.
Department of Agriculture.
Two rat studies in the November
Toxicological Sciences point to an apparent stress response that may explain how
atrazine could alter reproductive development. EPA scientists showed that
the weed killer elevates stress-related
hormones such as adrenocorticotropic
hormone, or ACTH.
If levels of this hormone get out of
balance in females, it “can interfere
with normal regulation of the ovaries
and ovulation,” notes Ralph Cooper,
chief of endocrinology at EPA’s laboratory in Research Triangle Park, N.C.
This, in turn, “will interfere with fertility,” he points out. The hormone changes
“indicated to us that the pituitary was
responsive to atrazine directly,” he says,
“by secreting ACTH.” Similar changes
were seen in exposed male rats, suggesting a possible stress-system mechanism
by which atrazine might impair sex-hormone production in males.
The witnessed changes might help
explain the impaired reproduction previously linked to atrazine in animal studies,
including delayed puberty, impaired fertility and inflamed prostates (in the male
pups of exposed female rats), Cooper says.
However, he cautions, exposures in his
studies, though brief, far exceeded what
would ever occur in drinking water.
Several studies have linked problems in
human newborns to water supplies polluted with atrazine. The limitation of
these papers is substantial: The water
contained other farm chemicals that
might be toxic in high doses as well.
A paper in Acta Paediatrica in April
2009, for instance, identified a recurring
seasonal increase in U.S. birth defects for
babies conceived from April through July.
The data, compiled from 1996 to 2002
by the Centers for Disease Control and
Prevention, came from an assessment of
more than 30 million live births.
Surface-water contaminant measurements by the U.S. Geological Survey during the same years show these months
are when concentrations of agricultural
chemicals — chiefly nitrate fertilizers and
atrazine — peak, says Paul Winchester, a
neonatologist at the Indiana University
School of Medicine in Indianapolis.
Compared with the rest of the year,
Winchester’s team found, babies who
were conceived from late spring to early
U.S. birth defects and atrazine, 1996–2002
Atrazine
Birth defects
1,640
1. 4
Atrazine in surface water (μg/L)
1,620
1. 2
Cases/100,000 births
1,600
1.0
1,580
0.8
0.6
1,560
0.4
1,540
0.2
1,520
0.0
1,500
J FMAMJ J ASOND
Month of conception
soUrce: P. winchester et al./acta Paediatrica
Agrochemical Mean surface water level
April–July Other months
atrazine (μg/l) 1. 31 0.16
nitrate (mg/l) 1.94 1.65
Pesticides (μg/l) 0.14 0.05
Other chemical complicators
Unestablished cause research has
found a positive correlation between levels
of atrazine in surface water and birth defects
(graph). But the data are muddied because
levels of other chemicals (table) are also higher
during the start of farming season.
soUrce: P. winchester et al./acta Paediatrica
