[APWG] Science News, article on concerns to reexamine atrazine's safety

[scott_davis at blm.gov]

Scott Davis, Regional Science Coordinator
Bureau of Land Management
P. O. Box 25047
Building Fifty
Lakewood, Colorado  80225-0047

scott_davis at blm.gov
303-236-6646


http://www.sciencenews.org/view/feature/id/56253/title/Weed_Killer_in_the_Crosshairs

February 27th, 2010; Vol.177 #5 / Feature
Weed Killer in the Crosshairs
Concerns prompt reexamination of atrazine’s safety
By Janet Raloff
February 27th, 2010; Vol.177 #5 (p. 18)



Each year, American farmers and turf managers apply some 34 million
kilograms of atrazine to quash broad-leaved and grassy weeds. Most
treatments go to protect corn, sorghum, sugarcane and cotton, though golf
courses sometimes tap the weed killer to maintain immaculate fairways and
putting greens.


In recent years, however, questions have surfaced about atrazine’s safety,
especially after monitoring programs picked up the chemical in drinking
water and lab studies demonstrated the pollutant’s ability to emasculate —
if not deform — amphibians and fish. Last fall, the U.S. Environmental
Protection Agency announced it was reopening what industry had hoped was a
closed chapter on allegations in the United States of atrazine’s risks.


Atrazine, an organic compound belonging to the triazine family of
herbicides, stops pre- and post-emergent weeds by inhibiting electron
transport, ultimately blocking photosynthesis. The EPA reexamined data on
the herbicide’s putative toxicity four years ago as part of a systematic
review of the safety of older pesticides — those initially registered for
use before 1984. Atrazine was reregistered — meaning it could continue to
be sold — after the EPA concluded that its regulated use could continue
without posing undue risks to health and the environment. The chemical is
banned by the European Union and, ironically, in Switzerland, where
atrazine’s leading manufacturer, Syngenta, is headquartered.


In a surprising turnabout, the EPA instructed its Scientific Advisory Panel
on pesticides, a group of outside experts, to reevaluate the weed killer’s
safety through three meetings this year, the first of which took place
earlier this month. The panel will review human data and any studies,
including animal or test-tube assays, that might suggest risks to people.


EPA admits this new review was prompted by a flurry of recent news stories
and critical reports by advocacy groups, which continue to show that large
numbers of people are being exposed to atrazine through drinking water (SN:
11/3/01, p. 285) and which offer new data suggesting health concerns.


Among these new criticisms was a report in August by the Natural Resources
Defense Council: “Poisoning the Well: How the EPA is ignoring atrazine
contamination in surface and drinking water in the central United States.”
Its analysis of data that the EPA collected — but didn’t publicly release
—shows that traces of atrazine frequently pollute not only rivers but also
water exiting the tap, oftentimes at concentrations exceeding EPA’s
3-parts-per-billion limit for drinking water.


(Embedded image moved to file: pic15724.jpg)accessEnlarge(Embedded image
moved to file: pic11478.gif)magnifyAtrazine in the city
Source: M. Wu et al./NRDC August 2009


For its part, Syngenta Crop Protection, based in Greensboro, N.C., the
largest U.S. producer of atrazine, argues EPA’s new review is unnecessary.
“After seven Scientific Advisory Panels, 15 years of special review and the
reregistration [of atrazine] in 2006, the science stands for itself,” says
company toxicologist Tim Pastoor. Reviewing the data again “seems over the
top,” he contends, and poses unnecessary costs to taxpayers.


Yet there are plenty of new data that have not previously been part of any
systematic federal review.


Sentinels of risk


Atrazine’s ability to provoke hormonal perturbations in test animals is one
of the more dramatic signs of its toxicity to emerge throughout the past
decade, says biologist Tyrone Hayes of the University of California,
Berkeley. He points to studies from his lab (SN: 11/2/02, p. 275) and by
others that have demonstrated that this weed killer can inappropriately —
and sometimes quite deleteriously — boost estrogen concentrations in male
animals, from rats and fish to frogs and alligators.


The presence of too much estrogen or estrogen at the wrong time can not
only alter reproductive development but also can pose cancer risks, so
toxicologists have expressed concern over hormonal changes in test animals.
Whether atrazine poses such risks to people, however, remains unknown.


Robust data suggestive of hormonal effects, including partial gender
reassignment, come from amphibians and fish. And a review in the January
Environmental Health Perspectives by Jason Rohr and Krista McCoy of the
University of South Florida in Tampa includes more than a dozen papers out
since atrazine’s last regulatory review. The EHP review highlights a long
list of reproductive and developmental impacts in these animals.


(Embedded image moved to file: pic29358.jpg)accessEnlarge(Embedded image
moved to file: pic26962.gif)magnify
Source: P. Winchester et al./Acta Paediatrica


This analysis didn’t include all available studies, Rohr acknowledges,
because “we had very strict quality criteria,” requiring such things as
“proper experimental design, proper reporting or application of
statistics,” and data showing there had been no contamination of supposedly
unexposed animals.


Trends observed across the studies that did make the cut indicate that
atrazine alters rates of amphibian metamorphosis, reduces immune function
in 33 of 43 measures and increases risk of infection in 13 of 16 measures.
Exposure to the weed killer altered at least one aspect of gonad structure
and function in seven of 10 studies, with some animals exhibiting “sexually
ambiguous” gonad tissue. Atrazine also altered sperm production in the two
studies that investigated it and changed sex-hormone concentrations in six
of seven studies.


This review’s findings contradict those reported in a February 2009 paper
in Toxicological Sciences by Werner Kloas of the Leibniz-Institute of
Freshwater Ecology and Inland Fisheries, in Berlin, and his coauthors (one
of whom, Alan Hosmer, is a Syngenta employee).


According to Syngenta’s Pastoor, the paper by Kloas’ team is “the most
comprehensive, complete and extensive study ever done on frogs looking at
sexual development.” Some 3,000 African clawed frogs were exposed to five
doses of atrazine spanning four orders of magnitude. “And from that,” he
says, “it was definitively 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.


(Embedded image moved to file: pic24464.jpg)accessEnlarge(Embedded image
moved to file: pic05705.gif)magnifyAtrazine at the surface
Map source: USGS watershed regressions for pesticides atrazine model at
infotrek.er.usgs.gov/warp; chart source: "Pesticides in the Nation's Stream
and Ground Water." 1992-2001/USGS


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.


Tied together, with caveats


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 inApril 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 summer showed a 3 percent higher
rate of birth defects, such as spina bifida, cleft lip, urogenital defects
and Down syndrome. And while a mix of farm pesticides usually showed up in
that seasonal runoff into waterways, Winchester observes that “far and
away, the most prevalent pesticide — and the one which exceeds safety
limits most often — is atrazine.” The weed killer’s statistically
significant association with birth defects is intriguing, he says, and
deserves further exploration.


A related investigation linked atrazine concentrations in Indiana
drinking-water supplies to the chance that a baby would be very small at
birth. “Atrazine concentrations above 0.1 part per billion were associated
with, on average, a 17 percent increase in the risk of having a small
baby,” says Hugo Ochoa-Acuña of Purdue University in West Lafayette, Ind.
Such contamination, well below the EPA’s 3-ppb limit, can be common.
Biweekly drinking-water data suggested that in Fort Wayne, Ind., for
example, atrazine concentrations exceed 0.2 ppb on 265 days a year, and
exceed 0.5 ppb more than one out of every three days.


Each 1 ppb increase of atrazine in drinking water, for consumption averaged
throughout a pregnancy, increased by 15 percent a woman’s chance of giving
birth to a baby in the lowest 10 percent of weight for its gestational age.
Such babies have a poorer chance of survival.


The weed killer’s correlation with low birth weight proved most robust for
contamination during a woman’s third trimester, the Purdue team reports in
the October Environmental Health Perspectives. “And that makes sense,”
Ochoa-Acuña explains, “because most of a baby’s growth occurs during the
last trimester. So a small effect there would produce a big difference.”


As Winchester’s group found, many other pesticides tended to coexist with
atrazine in water, but their levels weren’t nearly as high.


At his agency’s February Scientific Advisory Panel meeting, the EPA’s Aaron
Niman reviewed these and additional new studies correlating the levels of
atrazine in drinking water to birth defects and low birth weights. The
strength of Winchester’s study, he said, “is that it provides for an
overall snapshot of trends in both birth defects and atrazine levels in the
environment. For this reason, it’s useful in hypothesis generation … [but]
can only be used to demonstrate correlation” — not causation.


The study by Ochoa-Acuña’s team is “probably the strongest” linking the
weed killer to birth outcomes, Niman said, because it offers individual
exposure estimates and is able to adjust for several potentially
confounding factors, such as seasonality. Still, Niman acknowledged, there
are limitations to even this study. But he also noted that this is to be
expected when looking at complex, real-world exposures — not the controlled
environments of lab rats.


Overall, researchers concede that no smoking guns exist regarding atrazine
risks. Data are suggestive, based on high-dose rodent tests, real-world
wildlife exposures and epidemiological surveys of people exposed to a mix
of pollutants.


Although there have been charges that Syngenta has hidden troubling data
from regulators and the public, Pastoor counters that the company’s
research “is publicly available,” and that “EPA has all of our raw data”
for every study. Indeed, he says, “When we submit a study, it undergoes the
kind of scrutiny that would rival an Internal Revenue Service review.”


So regardless of the concerns that have been circulating in news accounts
and reports by public interest groups, Pastoor says he’s confident that as
long EPA bases its new safety assessment on science, “any further opening
up of atrazine’s scientific history is welcome.”
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