Research Watch: Nitrate can control arsenic cycling - ACS Publications

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Research▼Watch Pesticide–parasite link to frog deformities

David Senn and Harold Hemond faced a real mystery at heavily contaminated Upper Mystic Lake (UML) in Massachusetts. The Massachusetts Institute of Technology scientists knew that cycling of metals, including iron and arsenic, in natural waters depends on redox processes. Moreover, in a nonsulfidic lake, O2 levels are thought to be the main determinant for whether iron and arsenic appear in their oxidized forms. Yet, in most years they monitored UML, they found oxidized metals— As(V) and particulate Fe(III)—in the lake’s anoxic water column. The culprit they believe is nitrate, and it may help explain a host of other observations, including the dangerous levels of arsenic in Bangladesh groundwaters. Senn and Hemond believe that bacteria in the water oxidize either arsenic or iron through the reduction of nitrate, primarily to N2. As long as nitrate is present, the metals are oxidized. Significantly, in 1999, nitrate levels plummeted in UML’s deepest waters, and Fe(II) and As(III) levels rapidly increased in that region. UML’s sediments contain 200 to 2100 parts per million of arsenic, primarily from past industrial activity, and nitrate frequently exceeds 100 micromolar levels, primarily due to the in situ microbial oxidation of ammonium ions. Thus, nitrogen pollution may affect cycling of arsenic and possibly other contaminants, such as phosphates, mercury, and cadmium. Ironically, solid hydrous ferric oxide—the oxidized form of iron— often plays a dominant role in immobilizing dangerous As(V), which would lower toxicity. On the other hand, high levels of nitrate have been measured in Bangladesh groundwaters that also contain elevated levels of arsenic. (Science 2002, 296, 2373–2376)

Wood frogs exposed to common pesticides, such as atrazine and malathion, are more likely to have weakened immune systems, which appears to render the amphibians more susceptible to infections by limb-deforming trematode larvae, according to field and lab work by biologist Joseph Kiesecker of Pennsylvania State University. Although the research confirms that trematode infections are the main culprit for limb deformities, it raises the question of

taminant levels for drinking water. These frogs had lower numbers of white blood cells (eosinophils) in their blood and, in the presence of trematode larvae, a greater rate of infection. (Proc. Natl. Acad. Sci. U.S.A. 2002, 99, 9900–9904)

Toxicological link between common cold virus and pollutants

© 2002 NATIONAL ACAD. OF SCIENCES, U.S.A.

Nitrate can control arsenic cycling

Wood frog tadpoles exposed to pesticides are more susceptible to trematode infection.

whether pesticide pollution is contributing to the rapid increase in deformed frogs. Kiesecker monitored wood frogs (Rana sylvatica) in six ponds in Pennsylvania, three of which were exposed to agricultural runoff with detectable levels of organochlorine pesticides and organophosphorus compounds. Of the frogs exposed to the trematode larvae (which were introduced to the waters by infected snails), 28.6% in the runoff-contaminated ponds had limb deformities compared to only 4% in runoff-free ponds. Moreover, compared to frogs in trematode-free ponds, the infected frogs in the runoff-contaminated pond were 37% smaller, whereas infected frogs in runoff-free ponds were 22% smaller. Kiesecker also exposed tadpoles in his lab to malathion, esfenvalerate, and atrazine at EPA’s maximum con-

Cell studies indicate that ambient levels of certain pollutants found both indoors and outdoors can make common colds worse. Concurrent exposure to oxidants such as nitrogen oxide (NO2) or ozone (O3), and the common cold virus, rhinovirus-16 (RV-16), triggered significantly higher levels of proinflammatory agents than would be expected if the effects of either cellular stress were additive, indicating that these pollutants could exacerbate inflammation in people with upper and lower respiratory infections. Epidemiological studies indicate that pollutants increase the potential and magnitude for viral infections and can aggravate asthma, but until now, there has been little mechanistic and toxicological information linking environmental oxidants and viral infection. E. W. Spannhake and colleagues at the Johns Hopkins School of Public Health exposed human nasal epithelial cells and another line of cells found in the lower respiratory track to RV-16, and either NO2 (1–3 parts per million [ppm]) or O3 (0.1–0.3 ppm) for 3 hours. Each stimulant activated the inflammatory pathways in the cells, producing indicative cytokines and other proteins. However, the combined effect of RV-16 and midrange concentrations of NO2 was 42–250% greater than additive effects of the separate experiments, and 41–67% greater for midrange O3. Even though antioxidant treatments reduced cytokine production, the mechanisms behind

SEPTEMBER 1, 2002 / ENVIRONMENTAL SCIENCE & TECHNOLOGY



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Widespread gene flow documented Scientists in Australia have found that genes from genetically modified (GM) canola can rapidly spread to nearby fields in which conventional canola is grown. This first comprehensive study on genetic pollution shows that “cross-pollination between commercial canola fields occurs at low frequencies but to considerable distance.” The team of researchers from the Cooperative Research Center for Australian Weed Management and the Universities of Adelaide and Western Australia, tested more than 48 million individual plants in 63 conventional canola fields located near GM canola fields. The fields were in three Australian states with a diverse range of environments. The researchers took advantage of the fact that Australian farmers planted GM canola resistant to acetolactate synthase-inhibiting herbicides for the first time in 2000. Because the GM variety is homozygous, any crosses will contain copies of the herbicideinhibiting gene and can therefore be detected unambiguously. When the crops were mature, the researchers took 10 samples containing at least 100,000 seeds from three locations in each tested field. Although resistant genes were found in 63% of the tested fields, only a few fields had more than 0.03% resistance overall. No evidence of cross-pollination was detected more than 3 km from any GM fields, but the researchers stress that the number of fields they sampled was not large. Although the researchers say that all previous pollination studies show cross-pollination occurs more frequently closer to the source field, the Australian study was notable for bucking that trend. “Samples from the leading edges of fields did not always have a higher level of resistance,” the researchers report. (Science 2002, 296, 2386–2388)

Hazards and ecological risks of transgenics Introducing genetically modified organisms into the environment may 346 A



put wild populations at a greater risk of extinction than previously thought, according to new computer models developed by two Purdue University scientists. Although the models specifically address the risks and hazards of transgenic fish, the researchers claim that they can also be applied to other organisms. To determine the fate of a transgene and the affected wild organisms, William Muir and Richard Howard used a unique risk assessment method, concentrating on six components of an organism’s life cycle—juvenile viability, adult viability, female fecundity, male fertility, age at sexual maturity, and mating advantage. Various processes that influence these fitness PHOTODISC

the synergism are not completely clear. (Environ. Health Perspect. 2002, 110, 665–670)

cause population extinction). The level of hazard associated with an invasion is compared to that of exotic invasive species, which can disrupt ecosystems and cause species displacement. When the researchers examined various combinations of the fitness parameters that can lead to invasion and extinction hazards, they found three new ways that a transgene could result in an extinction hazard. The scenario that resulted in the most extreme risk was when the transgene increases both male mating success and adult viability but decreases male fertility. Although not as extreme, two other scenarios, when the transgene increases male mating success but decreases adult viability, and when the transgene increases adult viability but decreases male fertility, also posed an extinction hazard for wild populations. (Transgenic Res. 2002, 11, 101–114)

Human-induced warming trend

The risk of wild populations going extinct because of genetically modified fish escaping into the environment may be greater than previously thought.

parameters, such as predator avoidance, disease resistance, or swimming speed, were not included because only the net effect is important. Estimates of the net fitness parameters were then combined into mathematical models to determine whether transgenic organisms are more likely to survive and reproduce than wild populations. The researchers differentiated between risk and hazard, defining risk as “the probability a transgene will spread into natural conspecific [of the same species] populations,” and hazard as “the probability of species extinction, displacement, or ecosystem disruption given that the transgene has spread”. Their approach addressed risk relative to two kinds of hazards: extinction (when a transgene spreads to a natural population and leads to a local extinction event) and invasion (when a transgene spreads to a natural population but the negative effects on the fitness parameters are not great enough to

ENVIRONMENTAL SCIENCE & TECHNOLOGY / SEPTEMBER 1, 2002

Increasing levels of greenhouse gases are to blame for the recent tropospheric warming trend, concludes an analysis of more than 130 years of climate data by scientists at the Hadley Centre for Climate Prediction and Research and the University of Oxford in the United Kingdom. Beginning with the 1960s, the modeling results point to anthropogenic causes of rising surface temperatures, with negligible contributions from natural effects, such as solar radiation and volcanic eruptions. The analysis paints a much different picture for the early 20th century. Before industries began emitting large quantities of CO2 and other greenhouse gases into the atmosphere, the model predicts that a combination of both greenhouse gases and natural effects contributed to warming. On the basis of the modeling results, the scientists estimate that humans are now responsible for a 0.5 °C increase in average surface temperatures per century. The situation could be worse, however. The model predicts that approximately one-third of the human-induced warming trend has been offset by the cooling effects due to anthropogenic sulfate and possibly volcanic aerosols. (J. Geophys. Res. 2002, 107, 10.1029/2000JD000028)