The toxicity of sodium monofluoroacetate (1080) to

Although many species of native invertebrates have been identified on toxic baits containing sodium monofluoroacetate (1080) following aerial operations for possum control, few quantitative data are available to determine the risk of primacy or secondary poisoning that may result from these exposures. This paper reports on a series of studies conducted to determine the risk of 1080 exposure to one such non-target insect, the native ant Huberia striata. Subsequent risk of secondary poisoning to insectivorous animals is extrapolated. Ants were exposed in the laboratory to cereal baits containing 0.15% sodium monofluoroacetate, with and without alternative sources of food, and mortality was compared with controls after 24 and 48 h. Acute mortality was significantly greater in both exposed groups and ants that died contained 1080 residues, indicating that some ants could consume lethal amounts of 1080 in cereal baits. However, the increase in mortality was relatively small (7% after 24 h and 12% after 48 h), indicating either that palatability of 1080 bait to this species is low, or that the toxin is not readily absorbed from this matrix. Additional trials were conducted to expose ants to 1080 in sugar-water, in order to determine the acute toxicity dose range. The oral LD50 at 48 h was 32 mg kg(-1), which was comparable to previous results obtained for the large-headed weta, Helmideina crassidens. The persistence of 1080 in ants consuming a sub-lethal dose was also determined, in order to assess risks of secondary poisoning to insectivores. Residues in ants receiving approximately 36 mg kg(-1) of 1080 declined rapidly, from a Peak of 5.51 mg kg(-1) 1 day after exposure, to 0.27 mg kg(-1) after 7 days. Potential risks to insectivorous birds were calculated using worst-case exposure assumptions, and were determined to be negligible.     

An updated review of the toxicology and ecotoxicology of sodium fluoroacetate (1080) in relation to its use as a pest control tool in New?Zealand

Sodium fluoroacetate (1080) is a vertebrate pesticide, originally developed in the 1940s and principally used for the control of unwanted introduced animals in New?Zealand and Australia. Fluoroacetate is also a toxic component of poisonous plants found in Australia, Africa, South America, and India. In relation to its use as a pesticide, recent research has focused on further elucidation of its potential sub-lethal effects, on animal welfare issues, on understanding and reducing its risk to non-target species, on its ecotoxicology, and fate in the environment following use in baits. 1080 acts by interfering with cellular energy production through inhibition of the tricarboxylic acid cycle and lethal doses can kill animal pests within 6?48 h of eating baits. Exposure to sub-lethal doses has been shown to have harmful effects on the heart and testes in animal studies, and strict safety precautions are enforced to protect contractors and workers in the pest control industry. Considerable care must be taken when using 1080 for the control of animal pests. Primary poisoning of non-target birds and secondary poisoning of dogs must be minimised to ensure that benefits in terms of conservation outcomes and pest and disease control significantly outweigh the risks associated with its use. Despite over 60 years of research and practical experience, the use of 1080 is still embroiled in controversy, while research efforts continue to improve its target specificity when it is used as a conservation tool or for Tb vector control.     

Memory retention of conditioned aversion training in New Zealand's alpine parrot,the kea

New Zealand pest control operations commonly deploy toxic sodium fluoroacetate (1080) baits to control introduced mammalian predators and protect vulnerable native fauna, yet the highly intelligent kea (Nestor notabilis) is at risk of mortality following ingestion of toxic baits intended for their protection. We tested the retention of conditioned aversion in 11 captive kea that had learned to avoid baits containing the bird repellent anthraquinone alongside color, olfactory, and taste cues. We revisited kea over increasing time intervals (3 days, 5 weeks, 3 months, 6 months, and 1 yr) offering them otherwise identical non-repellent baits. Kea retained their aversion until the final session, 1 year after previous exposure to reinforcement, and almost 2 years since previous exposure to repellent. Whether the kea forgot their aversion or the repeated exposures to non-repellent baits resulted in extinction of the aversion, our results indicate that kea are capable of remembering an aversion for long enough to be of practical use to conservation managers in reducing kea mortality through 1080 operations.     

Influence of maternal stress on uranium-induced developmental toxicity in rats

It has been demonstrated that uranium is an embryo/fetal toxicant when given orally or subcutaneously to pregnant mice. On the other hand, maternal stress has been shown to enhance the developmental toxicity of a number of metals. In this study, maternal toxicity and developmental effects of a concurrent exposure to uranyl acetate dihydrate (UAD) and restraint stress were evaluated in rats. Four groups of pregnant animals were given subcutaneous injections of UAD at 0.415 and 0.830 mg/kg/day on Days 6 to 15 of gestation. Animals in two of these groups were also subjected to restraint for 2 hr/day during the same gestational days. Control groups included restrained and unrestrained pregnant rats not exposed to UAD. Cesarean sections were performed on gestation Day 20, and the fetuses were weighed and examined for malformations and variations. Maternal toxicity and embryotoxicity were noted at 0.830 mg/kg/day of UAD, while fetotoxicity was evidenced at 0.415 and 0.830 mg/kg/day of UAD by significant reductions in fetal body weight and increases in the total number of skeletally affected fetuses. No teratogenic effects were noted in any group. Maternal restraint enhanced uranium-induced embryo/fetal toxicity only at 0.830 mg/kg/day, a dose that was also significantly toxic to the dams. As in previous studies with other metals, maternal stress enhances uranium-induced developmental toxicity at uranium doses that are highly toxic to the dams; however, at doses that are less acutely toxic the role of maternal stress would not be significant.     

Impacts on nontarget avian species from aerial meat baiting for feral pigs

Bait containing sodium fluoroacetate (1080) is widely used for the routine control of feral pigs in Australia. In Queensland, meat baits are popular in western and northern pastoral areas where they are readily accepted by feral pigs and can be distributed aerially. Field studies have indicated some levels of interference and consumption of baits by nontarget species and, based on toxicity data and the 1080 content of baits, many nontarget species (particularly birds and varanids) are potentially at risk through primary poisoning. While occasional deaths of species have been recorded, it remains unclear whether the level of mortality is sufficient to threaten the viability or ecological function of species. A series of field trials at Culgoa National Park in south‐western Queensland was conducted to determine the effect of broadscale aerial baiting (1.7 baits per km²) on the density of nontarget avian species that may consume baits. Counts of susceptible bird species were conducted prior to and following aerial baiting, and on three nearby unbaited properties, in May and November 2011, and May 2012. A sample of baits was monitored with remote cameras in the November 2011 and May 2012 trials. Over the three baiting campaigns, there was no evidence of a population‐level decline among the seven avian nontarget species that were monitored. Thirty per cent and 15% of baits monitored by remote cameras in the November 2011 and May 2012 trials were sampled by birds, varanids or other reptiles. These results support the continued use of 1080 meat baits for feral pig management in western Queensland and similar environs.     

Hoarding behavior by ship rats (Rattus rattus) in captivity and its relevance to the effectiveness of pest control operations

Hoarding of food items is well known among muroid rodents, but evidence for hoarding behavior among ship rats (Rattus rattus) is scant. Here, we characterize hoarding behavior in ship rats maintained in captivity after capture from the wild. After acclimatization to captivity, 40 ship rats (21 females, 19 males) were presented with baits in experiments designed to emulate a typical poison control operation for vertebrate pests in New Zealand: this involved first offering rats nontoxic cereal baits (of 2- or 6-g size) as a prefeed for three nights consecutively, followed by 6- or 12-g cereal baits laden with 0.15% 1080 on the fourth night. Seventy-eight percent of rats (31/40) hoarded food in distinct cache sites when presented with nontoxic baits although there was no significant effect of bait size or type on hoarding behavior and nor did hoarding behavior vary according to rat gender. When rats were presented with 1080-laden baits, the incidence of hoarding was reduced to 40%, due to the onset of toxicosis. This study indicates that R. rattus will show hoarding behavior analogous to other rat species when presented with an excess of cereal-based baits, at least under conditions of captivity and free from competition. This finding may have practical relevance: since 1080 is the principal toxin used against the major vertebrate pest species in New Zealand (the brushtail possum, Trichosurus vulpecula), ship rats have the potential to deplete supplies of prefeed and/or toxic baits intended for possum control. However, based on typical rat densities recorded in New Zealand native forest (c. 5 rats/ha), the degree of removal and manipulation of toxic baits observed by ship rats here is unlikely to impact adversely on the efficacy of possum control operations.     

The Concept of Hormesis in Developmental Toxicology

Animal bioassay experiments are frequently conducted to assess the toxicity of chemicals on the developing fetus. Experiments are normally conducted at dosage levels that are much higher than human exposure levels to elicit the toxic reproductive effect of the chemical in a limited number of litters. Recently there has been much discussion on the fact that some chemicals may have beneficial effects at low doses and become toxic at high doses. This concept, known as chemical hormesis, has been the focus of attention in many investigations. Here, we consider the prevalence of hormesis in developmental toxicology and show that current design of developmental toxicity testing does not accommodate the study of hormesis. If it can be proved that some developmental toxicants may have stimulatory low dose effects, then design and analysis of developmental toxicity experiments need to be revised by the scientific community and the regulatory agencies. Using a thorough analysis of an experimental data set, we further demonstrate that in order to establish the possible hormetic effects of a chemical in reproduction, often a multiple replication of the experiment may be necessary to examine such effects. Using a trend test, we illustrate that while it is possible that one replicate of a developmental toxicity experiment with a known teratogen shows strong evidence of hormesis, other replicates may show no sign of beneficial effects at low doses.     

Monomethylarsonic acid and dimethylarsinic acid: developmental toxicity studies with risk assessment

BACKGROUND: The toxicity of arsenic compounds is highly dependent on the valence and methylation state of the compound. Although there is extensive published literature on the potential developmental toxicity of inorganic arsenic compounds, little exists on organic arsenic compounds and, in particular, studies conducted in accordance with conventional regulatory guidelines appropriate for risk assessment are rare. The organic arsenic compounds, monomethylarsonic acid (MMAV) and dimethylarsinic acid (DMAV, also called cacodylic acid), are the active ingredients in pesticide products that are used mainly for weed control. MMAV and DMAV are also metabolites of inorganic arsenic formed intracellularly by most living organisms (animals, plants and bacteria). In mammals, this occurs predominantly in liver cells. METHODS: Conventional developmental toxicity studies of orally administered MMAV and DMAV in the Sprague-Dawley rat and New Zealand White rabbit were conducted in commercial contract laboratories in the late 1980 s for regulatory compliance. The results of these studies are summarized and presented to broaden the data available in the public domain. RESULTS: In both species, data shows an absence of dose-related effects at organic arsenic exposures that were not maternally toxic. MMAV doses of 0, 10, 100, and 500 mg/kg/day (rat) and 0, 1, 3, 7, and 12 mg/kg/day (rabbit) and DMAV doses of 0, 4, 12, and 36 mg/kg/day (rat) and 0, 3, 12, and 48 mg/kg/day (rabbit) were administered by oral gavage daily during organogenesis (Gestation Day [GD] 6-15, rat; GD 7-19, rabbit) and the litters examined at maternal sacrifice (GD 20, rat; GD 29, rabbit). After treatment with MMAV, maternal and fetal toxicity were observed at the highest doses of 500 mg/kg/day (rat) and 12 mg/kg/day (rabbit), but no treatment-related developmental toxicity at the lower doses, even in the presence of minimal maternal toxicity in the rat at 100 mg/kg/d. There was no evidence of teratogenicity associated with MMAV treatment. With DMAV, maternal and developmental toxicity were observed in the rat at 36 mg/kg/day, with a higher than spontaneous incidence of fetuses with diaphragmatic hernia. In the rabbit at 48 mg/kg/day, there was marked maternal toxicity, culminating for most females in abortion and with no surviving fetuses for evaluation. There was no treatment-related maternal or developmental toxicity in the rat or rabbit at 12 mg/kg/day. Based on pregnancy outcome, the developmental toxicity no observed adverse effect level (NOAEL) for orally administered MMAV were 100 and 7 mg/kg/day in the rat and rabbit, respectively, and for DMAV were 12 mg/kg/day in both species. CONCLUSIONS: Margins of exposure estimated based on conservative estimates of daily intakes of arsenic in all of its forms indicate that exposure to MMAV or DMAV at environmentally relevant exposure levels, by the oral route (the environmentally relevant route of exposure) is unlikely to pose a risk to pregnant women and their offspring.     

Assessment of hydroxypropyl methylcellulose, propylene glycol, polysorbate 80, and hydroxypropyl-β-cyclodextrin for use in developmental and reproductive toxicology studies

BACKGROUND: A series of studies were conducted to assess Polysorbate 80 (PS80), Propylene Glycol (PG), and Hydroxypropyl‐β‐Cyclodextrin (HPβCD), when compared with Hydroxypropyl Methylcellulose (MC) in developmental and reproductive toxicology (DART) studies. METHODS: In the rat fertility study, 20 mg/kg MC, 10 mg/kg PS80, 1,000 mg/kg PG, 500 mg/kg HPβCD or 1,000 mg/kg HPβCD were administered orally before/during mating, and on gestation Day (GD) 0–7, followed by an assessment of embryonic development on GD 14. In the rat and rabbit teratology studies, the doses of MC, PS80, PG, and HPβCD were the same as those in the fertility study. In these teratology studies, pregnant females were dosed during the period of organogenesis, followed by an assessment of fetal external, visceral, and skeletal development. RESULTS: In the rat fertility and rat teratology studies, PS80, PG, and HPβCD did not exhibit toxicity, when compared with MC. Similarly, in the rabbit teratology study, there was no PS80 or PG‐related toxicity, when compared with MC. However, individual rabbits in the 500 and 1,000 mg/kg HPβCD groups exhibited maternal toxicity, which included stool findings, decreased food consumption, and body weight gain. Furthermore, one rabbit each in the 500 and 1,000 mg/kg HPβCD groups exhibited evidence of abortion, which was considered secondary to maternal toxicity. CONCLUSIONS: Although HPβCD was not well tolerated in rabbits at doses of 500 and 1,000 mg/kg, PS80 and PG were comparable to MC and should be considered for use in developmental and reproductive toxicology studies. Birth Defects Res (Part B) 89:504–516,2010. © 2010 Wiley‐Liss, Inc.     

Current and future needs for developmental toxicity testing

A review is presented of the use of developmental toxicity testing in the United States and international regulatory assessment of human health risks associated with exposures to pharmaceuticals (human and veterinary), chemicals (agricultural, industrial, and environmental), food additives, cosmetics, and consumer products. Developmental toxicology data are used for prioritization and screening of pharmaceuticals and chemicals, for evaluating and labeling of pharmaceuticals, and for characterizing hazards and risk of exposures to industrial and environmental chemicals. The in vivo study designs utilized in hazard characterization and dose-response assessment for developmental outcomes have not changed substantially over the past 30 years and have served the process well. Now there are opportunities to incorporate new technologies and approaches to testing into the existing assessment paradigm, or to apply innovative approaches to various aspects of risk assessment. Developmental toxicology testing can be enhanced by the refinement or replacement of traditional in vivo protocols, including through the use of in vitro assays, studies conducted in alternative nonmammalian species, the application of new technologies, and the use of in silico models. Potential benefits to the current regulatory process include the ability to screen large numbers of chemicals quickly, with the commitment of fewer resources than traditional toxicology studies, and to refine the risk assessment process through an enhanced understanding of the mechanisms of developmental toxicity and their relevance to potential human risk. As the testing paradigm evolves, the ability to use developmental toxicology data to meet diverse critical regulatory needs must be retained.     

Do colours that deter birds affect cereal bait acceptance by possums (

Poisonous baits used for pest control in New Zealand commonly contain green dye and cinnamon oil to make them less attractive to birds. Research aimed at reducing the impact of poison based pest control on birds has shown that some birds are initially deterred from feeding on blue or, to a lesser extent, green coloured food and are attracted to yellow or red food. We determined whether colours that deter or attract birds affected the acceptance of non-toxic and toxic cereal baits by captive brushtail possums (Trichosurus vulpecula). Individual possums were offered, daily, a choice between a standard green dyed non-toxic cereal bait and either a blue dyed(17 possums) or yellow dyed non-toxic bait (16 possums) for 10 days. Following this, for the first group of 17 possums, 1080 toxin was added to either the green bait (9 possums) or blue bait (8 possums) and possums were offered the green versus blue choice again. Two additional groups that had not previously been fed cereal baits were also given a choice between blue and green baits, one of which was toxic. All possums offered non-toxic bait ate less on the first day of presentation than on subsequent days. There was no difference in acceptance of either blue or yellow coloured non-toxic bait compared to the standard green non- toxic bait on any days. Bait colour appeared to be unimportant in cereal bait choice and did not deter possums from eating any of the baits. The addition of toxin to baits did not significantly alter bait choice in any groups, although some individuals which had no previous experience with baits ate more toxic than non-toxic bait. These data suggest that adding a stronger bird deterring colour (i.e., blue) to poisonous baits is unlikely to adversely affect the acceptance of baits by possums.     

Ethyl t‐butyl ether: review of reproductive and developmental toxicity

Ethyl t‐butyl ether (ETBE) is a motor fuel oxygenate used in reformulated gasoline. Knowledge of developmental and reproductive toxicity potential of ETBE is critical for making informed decisions about acceptance and regulations. This review discusses toxicology studies providing information about effects on reproduction and the conceptus. Seven GLP‐compliant studies following widely accepted protocols have focused specifically on developmental and reproductive toxicity (DART) in rats and rabbits exposed to ETBE by gavage with doses up to 1,000 mg/kg body weight/day, the limit specified in standardized test guidelines. Other repeat‐dose general toxicology studies have administered ETBE to rodents for up to 180 days, and included reproductive organ weights, histology, or other indications of reproductive system structure or function. DART potential of the main ETBE metabolite t‐butyl alcohol and class‐related MTBE has also been studied. More GLP‐compliant studies exist for evaluating ETBE using well‐established, currently recommended protocols than are available for many other chemicals used today. The database for determining ETBE DART potential is adequate, although not all study details are currently easily accessible for peer‐review. ETBE does not appear to be selectively toxic to reproduction or embryofetal development in the absence of other manifestations of general toxicity. Studies using recommended methods for sample preservation and analysis have shown no targeted effect on the reproductive system. No embryofetal effects were observed in rabbits. Early postnatal rat pup deaths show no clear dose‐response and have largely been attributed to total litter losses with accompanying evidence of maternal neglect or frank maternal morbidity. Birth Defects Res (Part B) 89:239–263, 2010. © 2010 Wiley‐Liss, Inc.     

Effects of tert-butyl acetate on maternal toxicity and embryo-fetal development in Sprague-Dawley rats

This study investigated the potential adverse effects of tert-butyl acetate (TBAc) on maternal toxicity and embryo-fetal development after maternal exposure of pregnant rats from gestational days 6 through 19. TBAc was administered to pregnant rats by gavage at 0, 400, 800, and 1,600 mg/kg/day. All dams were subjected to a Caesarean section on day 20 of gestation, and their fetuses were examined for any morphological abnormalities. At 1,600 mg/kg, maternal toxicity manifested as increases in the incidence of clinical signs and death, lower body weight gain and food intake, increases in the weights of adrenal glands and liver, and a decrease in thymus weight. Developmental toxicity included a decrease in fetal weight, an increase in the incidence of skeletal variation, and a delay in fetal ossification. At 800 mg/kg, only a minimal developmental toxicity, including an increase in the incidence of skeletal variation and a delay in fetal ossification, were observed. In contrast, no adverse maternal or developmental effects were observed at 400 mg/kg. These results show that a 14-day repeated oral dose of TBAc is embryotoxic at a maternally toxic dose (i.e., 1,600 mg/kg/day) and is minimally embryotoxic at a nonmaternally toxic dose (i.e., 800 mg/kg/day) in rats. However, no evidence for the teratogenicity of TBAc was noted in rats. It is concluded that the developmental findings observed in the present study are secondary effects to maternal toxicity. Under these experimental conditions, the no-observed-adverse-effect level of TBAc is considered to be 800 mg/kg/day for dams and 400 mg/kg/day for embryo-fetal development.     

Large-Scale Poisoning of Ship Rats (

This paper describes the impact of nine poison operations on ship rats in four areas (35 ha to 3200 ha) of North Island forest. Poisoning with 1080, brodifacoum, or pindone killed 87- 100% of rats, based on trapping and tracking-tunnel indices. Rat populations took 4-5 months to recover. Operations to protect nesting birds should therefore coincide with the onset of nesting and be rePeated each year, although not necessarily with the same methods. Population reduction declined each year at Mapara, King Country, during three annual 1080 operations which used the same lures and baits, but remained high at Kaharoa, Bay of Plenty, where poison toxicity was higher, non- toxic bait was pre-fed, and poisoning methods varied each year. Mouse tracking rates increased in poisoned forests 3-6 months after poisoning if the initial kill of rats exceeded 90%, Peaked 7-9 months after poisoning, then declined to pre-poison levels. Future research should focus on how prey and non-prey species within a forest community respond to a temporary reduction in rat numbers, and on methods to maintain low rat densities after initial knock-down.     

Utilization of juvenile animal studies to determine the human effects and risks of environmental toxicants during postnatal developmental stages

BACKGROUND: Toxicology studies utilizing animals and in vitro cellular or tissue preparations have been used to study the toxic effects and mechanism of action of drugs and chemicals and to determine the effective and safe dose of drugs in humans and the risk of toxicity from chemical exposures. Testing in animals could be improved if animal dosing using the mg/kg basis was abandoned and drugs and chemicals were administered to compare the effects of pharmacokinetically and toxicokinetically equivalent serum levels in the animal model and human. Because alert physicians or epidemiology studies, not animal studies, have discovered most human teratogens and toxicities in children, animal studies play a minor role in discovering teratogens and agents that are deleterious to infants and children. In vitro studies play even a less important role, although they are helpful in describing the cellular or tissue effects of the drugs or chemicals and their mechanism of action. One cannot determine the magnitude of human risks from in vitro studies when they are the only source of toxicology data. METHODS: Toxicology studies on adult animals is carried out by pharmaceutical companies, chemical companies, the Food and Drug Administration (FDA), many laboratories at the National Institutes of Health, and scientific investigators in laboratories throughout the world. Although there is a vast amount of animal toxicology studies carried out on pregnant animals and adult animals, there is a paucity of animal studies utilizing newborn, infant, and juvenile animals. This deficiency is compounded by the fact that there are very few toxicology studies carried out in children. That is one reason why pregnant women and children are referred to as "therapeutic orphans." RESULTS: When animal studies are carried out with newborn and developing animals, the results demonstrate that generalizations are less applicable and less predictable than the toxicology studies in pregnant animals. Although many studies show that infants and developing animals may have difficulty in metabolizing drugs and are more vulnerable to the toxic effects of environmental chemicals, there are exceptions that indicate that infants and developing animals may be less vulnerable and more resilient to some drugs and chemicals. In other words, the generalization indicating that developing animals are always more sensitive to environmental toxicants is not valid. For animal toxicology studies to be useful, animal studies have to utilize modern concepts of pharmacokinetics and toxicokinetics, as well as "mechanism of action" (MOA) studies to determine whether animal data can be utilized for determining human risk. One example is the inability to determine carcinogenic risks in humans for some drugs and chemicals that produce tumors in rodents, When the oncogenesis is the result of peroxisome proliferation, a reaction that is of diminished importance in humans. CONCLUSIONS: Scientists can utilize animal studies to study the toxicokinetic and toxicodynamic aspects of drugs and environmental toxicants. But they have to be carried out with the most modern techniques and interpreted with the highest level of scholarship and objectivity. Threshold exposures, no-adverse-effect level (NOAEL) exposures, and toxic effects can be determined in animals, but have to be interpreted with caution when applying them to the human. Adult problems in growth, endocrine dysfunction, neurobehavioral abnormalities, and oncogenesis may be related to exposures to drugs, chemicals, and physical agents during development and may be fruitful areas for investigation. Maximum permissible exposures have to be based on data, not on generalizations that are applied to all drugs and chemicals. Epidemiology studies are still the best methodology for determining the human risk and the effects of environmental toxicants. Carrying out these focused studies in developing humans will be difficult. Animal studies may be our only alternative for answering many questions with regard to specific postnatal developmental vulnerabilities.     

Detrimental effects of highly efficient interference competition: invasive Argentine ants outcompete native ants at toxic baits

The Argentine ant (Linepithema humile) is an invasive species that disrupts the balance of natural ecosystems by displacing indigenous ant species throughout its introduced range. Previous studies that examined the mechanisms by which Argentine ants attain ecological dominance showed that superior interference and exploitation competition are key to the successful displacement of native ant species. The objective of this research was to test the hypothesis that effective interference competition by Argentine ants may also be detrimental to the survival of Argentine ant colonies where Argentine ants and native ants compete at toxic baits used to slow the spread of Argentine ants. To study this hypothesis, we examined the competitive interactions between Argentine ants and native odorous house ants, Tapinoma sessile, in the presence and absence of toxic baits. Results showed that Argentine ants aggressively outcompete T. sessile from toxic baits through efficient interference competition and monopolize bait resources. This has severe negative consequences for the survival of Argentine ants as colonies succumb to the toxic effects of the bait. In turn, T. sessile avoid areas occupied by Argentine ants, give up baits, and consequently suffer minimal mortality. Our results provide experimental evidence that highly efficient interference competition may have negative consequences for Argentine ants in areas where toxic baits are used and may provide a basis for designing innovative management programs for Argentine ants. Such programs would have the double benefit of selectively eliminating the invasive species while simultaneously protecting native ants from the toxic effects of baits.     

Effect of pH, light intensity and population on the toxicity of the pesticide carbofuran to the blue-green alga Nostoc muscorum.

The effect of pH, light intensity and population on the toxicity of the pesticide furadan (containing 3% carbofuran as the active ingredient) was studied on the nitrogen fixing blue-green alga Nostoc muscorum. It was observed that all these factors had effects on the toxicity of the pesticide. The blue-green alga grew better in the pH range of 7.5-10, whereas the acidic pH of 5-6 retarded growth. The pesticide was more toxic to alga in the medium of pH 5-6, whereas reduction in toxicity was noticed in alkaline pH of 7.5-10. The alga grew slowly in a light intensity of 1,500 lux in comparison to a light intensity of 3,000 lux, and no growth occurred in the dark. The toxicity of the pesticide gradually decreased with increasing light intensity. The toxic effect of the pesticide was increased when the initial population level was low, and increasing the initial population reduced the toxicity.     

Compound toxicity screening and structure-activity relationship modeling in Escherichia coli

Synthetic biology and metabolic engineering are used to develop new strategies for producing valuable compounds ranging from therapeutics to biofuels in engineered microorganisms. When developing methods for high-titer production cells, toxicity is an important element to consider. Indeed the production rate can be limited due to toxic intermediates or accumulation of byproducts of the heterologous biosynthetic pathway of interest. Conversely, highly toxic molecules are desired when designing antimicrobials. Compound toxicity in bacteria plays a major role in metabolic engineering as well as in the development of new antibacterial agents. Here, we screened a diversified chemical library of 166 compounds for toxicity in Escherichia coli. The dataset was built using a clustering algorithm maximizing the chemical diversity in the library. The resulting assay data was used to develop a toxicity predictor that we used to assess the toxicity of metabolites throughout the metabolome. This new tool for predicting toxicity can thus be used for fine-tuning heterologous expression and can be integrated in a computational-framework for metabolic pathway design. Many structure-activity relationship tools have been developed for toxicology studies in eukaryotes [Valerio (2009), Toxicol Appl Pharmacol, 241(3): 356-370], however, to the best of our knowledge we present here the first E. coli toxicity prediction web server based on QSAR models (EcoliTox server: http://www.issb.genopole.fr/～faulon/EcoliTox.php).     

An assessment of the probability of secondary poisoning of forest insectivores following an aerial 1080 possum control operation

Assays for the toxin sodium monofluoroacetate (compound 1080) were undertaken on arthropods collected from toxic baits after a brushtail possum (Trichosorus vulpecula) control operation in Nothofagus forest in central North Island, New Zealand. The 1080 concentrations measured (mean 57 mu g per g, max 130 mu g per g) are considerably higher than those reported by other researchers who collected arthropods randomly after control operations. These data, together with published information on sensitivities to 1080, as well as diet and consumption rates, were used to calculate the median lethal doses of arthropods that have fed on 1080 baits for a number of vertebrate insectivores found in Nothofagus forest. The results indicate small insectivores that feed on, or close to, the ground (e.g., tomtit Petroica macrocephala, robin P. australis, hedge sparrow Prunella modularis, and the short-tailed bat Mystacina tuberculata) may be vulnerable to secondary poisoning. For instance, a tomtit will receive the median lethal dose of 1080 from 1.32 g (i.e., 14.7% of its daily food intake) of arthropods containing 57 mu g per g of 1080. Because of their greater sensitivity to 1080 poisoning, bats are at much greater risk; a short-tailed bat will receive the median lethal dose of 1080 from as little as 0.04 g (0.7% of its daily food intake) of arthropods containing 57 mu g per g of 1080.     

Laboratory and field performance of an indoxacarb bait against German cockroaches (Dictyoptera: Blattellidae)

Experimental indoxacarb powder and gel baits were evaluated in the laboratory, and a gel bait was evaluated in subsequent field studies against the German cockroach, Blattella germanica (L.). In continuous exposure tests, LT50 values were 1.90 and 1.10 d for 0.25 and 1% indoxacarb powder baits, respectively. However, 0.25% indoxacarb gel bait had an LT50 value of 0.68 d, similar to a 0.05% abamectin gel bait formulated with the same bait base. There was no difference in toxicity between fresh and 7-d-old gel bait deposits. A pyrethroid-resistant strain of German cockroaches was significantly resistant to both abamectin and indoxacarb gel baits. Gel bait contained approximately 40% water, desiccated rapidly at 25-28 degrees C and 30-45% RH, but did not rehydrate when held at 56.7% RH for 3 d. Powder indoxacarb baits contained <1% water and did not desiccate or gain water. Indoxacarb gel bait (0.25%) was relatively nonrepellent (approximately 30%) and had positive maximum performance index values (approximately 100) in Ebeling choice box experiments. In field experiments in cockroach-infested kitchens, the 0.25% indoxacarb gel bait significantly reduced visual counts of German cockroaches approximately 74% at 3 d and >95% at 14 d. Indoxacarb baits are toxic, relatively nonrepellent, and can significantly reduce German cockroach populations.