Sublethal Poisoning Research Articles

Histopathological changes in Lithobates catesbeianus tadpoles used as biomarkers of pesticide poisoning

The use of biological indicators has increased in recent years with the aim of investigating environmental pollution in aquatic environments that are vulnerable to the constant use of pesticides. Some biomarkers can help assess the health status, indicating physical, metabolic, and behavioral changes under acute and sublethal poisoning. The mixture of the active ingredients cyproconazole and picoxystrobin is a widely used fungicide for the control of pests in cotton, rice, coffee, sugarcane, corn, soybean, and wheat. The objective of this study was to verify the occurrence of possible histopathological lesions in the liver and kidneys of bullfrog tadpoles (Lithobates catesbeianus) caused by a fungicide commercial formula composed of picoxystrobin and cyproconazole. The animals were subjected to different concentrations of the fungicide to determine the median lethal concentration (LC50-96h = 0.05 mg L-1), that is, the lethal dose for 50% of the animals in 96 h. After determining the value of LC50-96h, the animals were subjected to three sublethal concentrations (LC50-96h/2, LC50-96h/10, and LC50-96h/100). Through histological biomarkers, it was verified that this fungicide changed the morphology of the animals' kidney and liver tissues in a chronic way, impairing the functioning of organs that are essential for their survival and metamorphosis, which can result in an imbalance in the biodiversity of aquatic ecosystems.

Lead, cadmium, and other trace elements in the liver of golden eagles and white-tailed eagles: recent data from Poland and a systematic review of previous studies

The golden eagle (Aquila chrysaetos) and the white-tailed eagle (Haliaeetus albicilla), being apex predators and facultative scavengers, can bioaccumulate different environmental contaminants, including toxic elements that may adversely affect their health. We analyzed the levels of cadmium (Cd), lead (Pb), and other metals and metalloids, including arsenic (As), barium (Ba), beryllium (Be), cobalt (Co), chromium (Cr), copper (Cu), iron (Fe), magnesium (Mg), manganese (Mn), molybdenum (Mo), selenium (Se), thorium (Th), thallium (Tl), uranium (U), vanadium (V), and zinc (Zn) in liver samples taken from three golden eagles and 36 white-tailed eagles that were found dead across Poland to verify their exposure. We also used a systematic review to summarize the available literature data on Cd, Pb, and other studied elements in the liver of both eagle species. Analyses of trace elements in the liver samples of the Polish eagles revealed interspecific differences in Cd, Cu, and Mn and differences in Co, Mn, Tl, and Zn among study regions. All elements tested except Pb were below the suggested thresholds linked with adverse health effects in birds. The hepatic Pb found in almost half of all the tested individuals suggests environmental exposure to this toxic element. One of the tested white-tailed eagles had hepatic Pb above the threshold of sublethal poisoning. Although our results seem optimistic, as previous Polish studies showed a higher prevalence of birds with hepatic Pb exceeding the toxicity threshold, they indicate that exposure to this toxic metal could still pose an additional threat to the health of Polish eagles.Graphical abstract

A typical enzyme activity for glutathione conjugation indicates exposure of pacu to pollutants

Abstract Functional enzyme assays to detect sublethal poisoning of Neotropical fish are paramount. Accordingly, we assayed a glutathione S-transferase (GST) activity in liver and kidney cytosols from Piaractus mesopotamicus injected with methyl parathion or benzo[a]pyrene using the substrate 1-chloro-2,4-dinitrobenzene (CDNB), which is the usual substrate for assaying a known general activity of GST. Since the most reactive substrate is required to reveal specific changes in enzyme activity, we also used two alternative substrates, 1,2-dichloro-4-nitrobenzene (DCNB) and ethacrynic acid (ETHA). Activities with CDNB or ETHA did not change. However, assays with DCNB showed that methyl parathion caused a decrease in GST activity in the liver on the 24th, 48th and 96th hour after the injection. DCNB also revealed that GST activity in the liver increased seven days after benzo[a]pyrene injection, coming down to normal after fourteen days. Benzo[a]pyrene, but not methyl parathion, increased the activities with DCNB in cytosol from the kidney seven and fourteen days after the injection. Thus, a decreased liver GST activity assayed with DCNB corresponded to contamination of P. mesopotamicus with methyl parathion. The increase of this GST activity in the liver and the kidney correlates to pacu contamination with polycyclic aromatic hydrocarbons.

Aerial baiting for feral cats is unlikely to affect survivorship of northern quolls in the Pilbara region of Western Australia

Abstract ContextFeral cats (Felis catus) are known predators of northern quolls (Dasyurus hallucatus). Management to suppress feral cat densities often uses the poison sodium monofluoroacetate (compound 1080) in baits broadcast aerially. Eradicat® baits have demonstrated efficacy at reducing feral cat densities in some environments. However, these are not registered for use in northern Australia because their risk to non-target northern quolls remains unknown. AimsWe investigated the risks of aerially deployed feral cat Eradicat® baits containing 4.5mg of the poison 1080 on the survival of free-ranging northern quolls. MethodsThe study was conducted over a 20000-ha area in the Pilbara bioregion in Western Australia. Twenty-one wild northern quolls from a baited area and 20 quolls from a nearby reference area were fitted with radio-collars, and their survivorship was compared following the aerial deployment of over 9700 feral cat baits. Survivorship of quolls was assessed before and after the baiting campaign. Key resultsFive radio-collared quolls died at the baited area; four mortalities were due to feral cat predation, and the cause of one death was uncertain. At the reference area, seven radio-collared quolls were confirmed dead; three mortalities were due to feral cat predation, two from wild dog predation, and the cause of death of two could not be determined. Evidence for sublethal poison impacts on quolls, inferred by monitoring reproductive output, was lacking; average litter size was higher in quolls from the baited area than in those from the unbaited area, and within range of litters reported elsewhere, suggesting that acute effects of 1080 (if ingested) on reproductive success were unlikely. ConclusionsRadio-collared northern quolls survived the trial using Eradicat® baits, and females showed no acute effects of sublethal poisoning on the basis of reproductive output. A lack of quoll deaths attributed to 1080 poisoning suggests that the use of Eradicat® poses a low risk to northern quolls in the Pilbara. Importantly, the high level of mortalities associated with predation by feral cats, and to a lesser extent, canids, validates the threats of these introduced predators on quolls, suggesting that their control in areas where quolls are present is likely to be beneficial for the recovery of this species. ImplicationsLand managers aiming to conserve northern quolls in the Pilbara would see conservation benefits if they introduced an operational landscape-scale feral cat baiting program using Eradicat® baits, with appropriate monitoring.

The evaluation of oxidative damage of DNA after poisoning with nerve agents.

The potency of three nerve agents (sarin, soman, tabun) to induce oxidative damage of DNA in lymphocytes, liver and brain during lethal or sublethal poisoning was investigated. The single strand breaks or oxidative base DNA damage was evaluated with the help of Comet assay and a specific enzyme able to detect oxidative bases of DNA (endonuclease III). While sarin and soman administered at sublethal doses corresponding to 50% of their LD50 values were not able to induce oxidative damage of DNA, their lethal dose (LD50) induced the significant increase of the number of oxidative bases in DNA of hepatocytes. In addition, tabun administered at lethal dose (LD50) induced significant increase of the number of single strand breaks and oxidative bases of DNA in glial cells isolated from pontomedullar brain region. Thus, some nerve agents were able to induce oxidative damage in the peripheral as well as central compartment but only in the case of severe poisoning caused by lethal doses of nerve agents. This non-cholinergic effect of nerve agents has probably consequences with nerve agents-induced hypoxic status during acute cholinergic crisis and it can contribute to their long-term toxic effects.

Reduced efficacy of baiting programs for invasive species: some mechanisms and management implications

‘Bait-resistance’ is defined as progressive decreases in bait efficacy in controlled pest species populations. Understanding the mechanisms by which bait-resistance can develop is important for the sustainable control of pests worldwide, for both wildlife conservation programs and agricultural production. Bait-resistance is influenced by both behavioural (innate and learned bait-avoidance behaviour) and physiological aspects of the target pest species (its natural diet, its body mass, the mode of action of the toxin, and the animal’s ability to biochemically break down the toxin). In this review, we summarise the scientific literature, discuss factors that can lead to innate and learned aversion to baits, as well as physiological tolerance. We address the question of whether bait avoidance or tolerance to 1080 could develop in the red fox (Vulpes vulpes), an introduced predator of significant economic and environmental importance in Australia. Sublethal poisoning has been identified as the primary cause of both bait avoidance and increased toxin-tolerance, and so, finally, we provide examples of how management actions can minimise the risk of sublethal baits in pest species populations.

Neuroprotective efficacy of newly developed oximes in comparison with currently available oximes in tabun-poisoned rats

The ability of two newly developed oximes (K361, K378) to reduce tabun-induced acute neurotoxic signs and symptoms was compared with the oxime K203 and trimedoxime using a functional observational battery. The neuroprotective effects of the oximes studied combined with atropine on rats poisoned with tabun at a sublethal dose (310μg/kg i.m.; 90% of LD50 value) were evaluated. Tabun-induced neurotoxicity was monitored by functional observational battery at 2h following tabun challenge. The results indicate that all tested oximes combined with atropine enable tabun-poisoned rats to survive till the end of experiment. Both newly developed oximes (K361, K378) combined with atropine were able to decrease tabun-induced neurotoxicity in the case of sublethal poisonings although they did not eliminate all tabun-induced acute neurotoxic signs and symptoms. Their ability to decrease tabun-induced acute neurotoxicity was slightly lower than that of trimedoxime and the oxime K203. Therefore, the newly developed oximes are not suitable for the replacement of commonly used oximes (especially trimedoxime and obidoxime) in the treatment of acute tabun poisonings.

Secondary poisoning risks from 1080-poisoned carcasses and risk of trophic transfer—a review

In New Zealand, sodium fluoroacetate (1080) is used for the control of unwanted terrestrial vertebrate pests, some of which are carriers of bovine TB, and for the conservation of native flora and fauna. One key advantage of 1080 used for animal pest control is that it is biodegradable. In this short review, we focus on the persistence of 1080 in carcasses and the risk of 1080-poisoned carcasses to dogs, and the possible risk of toxicity in other non-target species via trophic transfer. The slower breakdown of 1080 in poisoned carcasses under certain conditions (e.g. cold, dry conditions), and the risks of secondary poisoning, have to be understood and managed following use of this toxin in conservation or as part of TB eradication programs. Poisoned possum carcasses can pose a risk to dogs even up to 75 days after the control operation. Lower, less hazardous concentrations have been found in deer bone marrow after 213 days. When other species (e.g. insects or birds) come into contact with 1080 in carcasses, sub-lethal poisoning is more likely. In these cases, as with sub-lethal poisoning in any non-target animals, any 1080 ingested will be metabolised and excreted, and trophic transfer will be minimal when compared to more persistent poisons.

Evaluation of the Potency of Two Novel Bispyridinium Oximes (K456, K458) in Comparison with Oxime K203 and Trimedoxime to Counteract Tabun-Induced Neurotoxicity in Rats

The ability of two newly developed bispyridinium oximes (K456, K458) to reduce tabun-induced acute neurotoxic signs and symptoms was compared with oxime K203 and trimedoxime using the functional observational battery. The neuroprotective effects of the oximes studied combined with atropine on rats poisoned with tabun at a sublethal dose (200 μg/kg i.m.; 85% of LD50 value) were evaluated. Tabun-induced neurotoxicity was monitored by the functional observational battery and automatic measurement of motor activity at 2 hr after tabun challenge. The results indicate that all tested oximes combined with atropine enable tabun-poisoned rats to survive till the end of experiment. Both newly developed oximes (K456, K458) combined with atropine were able to decrease tabun-induced neurotoxicity in the case of sublethal poisonings although they did not eliminate all tabun-induced acute neurotoxic signs and symptoms. Their ability to decrease tabun-induced acute neurotoxicity was slightly higher than that of trimedoxime and oxime K203, but the difference in neuroprotective efficacy among all oximes studied is not large enough to make a decision about replacement of commonly used oximes (especially trimedoxime and obidoxime) in the treatment of acute tabun poisonings.

Improving the efficacy of aerial poisoning of brushtail possums (Trichosurus vulpecula) through reduced fragmentation of bait

In New Zealand, aerial delivery of sodium fluoroacetate (1080) baits to poison introduced brushtail possums (Trichosurus vulpecula) is a key pest management tool. GPS-guided broadcast baiting systems should expose all possums to large amounts of toxic bait, but some possums still survive despite being poisoned. This sub-lethal poisoning might reflect bait fragmentation, so we measured bait size before and after broadcast sowing from helicopter-slung buckets with spinners used to fling bait laterally. Mean bait size was smaller after sowing than before. The amount of fragmentation differed between operations and between buckets. Small fragments were concentrated under the flight path suggesting that they were caused by the spinner. Fragmentation increased with spinner speed. Removing the spinner resulted in less fragmentation. Use of spinners may therefore adversely affect poisoning efficacy by producing sub-lethal bait fragments. Solutions to this bait fragmenation problem include reducing spinner speed, removing the spinner, or development of shatterproof baits. A reduction in the amount of fragmentation is likely to reduce the need to sow large numbers of baits, so our findings could enable major reductions in toxin use.

A Comparison of Neuroprotective Efficacy of the Oxime K203 and its Fluorinated Analogue (KR‐22836) with Obidoxime in Tabun‐Poisoned Rats

The ability of the newly developed bispyridinium compound K203 and its fluorinated analogue KR-22836 to reduce tabun-induced acute neurotoxic signs and symptoms was compared with the currently available reactivator of acetylcholinesterase-obidoxime. Tabun-induced neurotoxicity and the neuroprotective effects of all tested oximes in combination with atropine in rats poisoned with tabun at a sublethal dose (200 μg/kg intramuscularly (i.m.); 80% of LD(50) value) were monitored by a functional observational battery at 24 hr after tabun challenge. The results indicate that all tested oximes combined with atropine were able to survive tabun-poisoned rats 24 hr after tabun challenge while one non-treated tabun-poisoned rat died within 24 hr after tabun poisoning. All tested oximes combined with atropine were able to decrease tabun-induced neurotoxicity in the case of sublethal poisoning but they did not eliminate all tabun-induced acute neurotoxic signs and symptoms. While the ability to reduce tabun-induced acute neurotoxicity of obidoxime and K203 was similar, the neuroprotective efficacy of KR-22836 was slightly higher compared to other tested oximes. Thus, the newly developed fluorinated analogue of K203, called KR-22836, is able to slightly increase the neuroprotective effectiveness of antidotal treatment of acute tabun poisonings compared to K203 and currently available obidoxime.

A Comparison of the Potency of Newly Developed Oximes (K347, K628) and Currently Available Oximes (Obidoxime, HI-6) to Counteract Acute Neurotoxic Effects of Tabun in Rats

The ability of newly developed oximes (K347, K628) to reduce tabun-induced acute neurotoxic signs and symptoms was compared with currently available oximes (obidoxime, HI-6) using a functional observational battery. The neuroprotective effects of the oximes studied (K347, K628, obidoxime, HI-6) combined with atropine on rats poisoned with tabun at a sublethal dose (220 microg/kg i.m.; 80% of LD50 value) were evaluated. Tabun-induced neurotoxicity was monitored by a functional observational battery and automatic measurement of motor activity at 24 hours following tabun challenge. The results indicate that all tested oximes combined with atropine enable tabun-poisoned rats to survive 24 hours following tabun challenge. Both newly developed oximes (K347, K628) combined with atropine are able to decrease tabun-induced neurotoxicity in the case of sublethal poisonings but they do not eliminate all tabun-induced acute neurotoxic signs and symptoms. Their ability to decrease the tabun-induced acute neurotoxicity is higher than that of the oxime HI-6 and it is slightly slower than the neuroprotective efficacy of obidoxime. As the neuroprotective potency of both newly developed oximes (K347, K628) is not as high as the potency of obidoxime, they are not a suitable replacement for obidoxime for the treatment of acute tabun poisonings.

Evaluation of the neuroprotective efficacy of individual oxime (HI-6) and oxime mixtures (HI-6 + trimedoxime, HI-6 + K203) in tabun-poisoned rats

The ability of the oxime HI-6 to reduce tabun-induced acute neurotoxic signs and symptoms was compared with the neuroprotective efficacy of two combinations of oximes (HI-6 + trimedoxime, HI-6 + K203) using a functional observational battery. Tabun-induced neurotoxicity and the neuroprotective effects of HI-6 alone, and HI-6 combined with trimedoxime or K203, in rats poisoned with tabun at a sublethal dose (200 μg/kg i.m.; 80% of LD50 value), were monitored by the functional observational battery at 24 hours following tabun challenge. The results indicate that both oxime mixtures tested, combined with atropine are able to allow tabun-poisoned rats to survive for 24 hours following tabun challenge, while one non-treated tabun poisoned rat and one tabun-poisoned rat treated with the oxime HI-6 alone combined with atropine, died within 24 hours following tabun challenge. The oxime HI-6 alone, as well as both oxime mixtures combined with atropine, were able to decrease tabun-induced neurotoxicity in the case of sublethal poisonings, but they did not eliminate all tabun-induced acute neurotoxic signs and symptoms. Their ability to reduce tabun-induced acute neurotoxcicity was almost the same, regardless of type of antidotal treatment. Thus, the tested combinations of oximes were not able to increase the neuroprotective effectiveness of the antidotal treatment of acute tabun poisonings compared to the individual oxime.

A Comparison of neuroprotective efficacy of newly developed oximes (K203, K206) and commonly used oximes (obidoxime, HI-6) in tabun-poisoned rats

The neuroprotective effects of newly developed oximes (K203, K206) and commonly used oximes (obidoxime, HI-6) in combination with atropine in rats poisoned with tabun at a sublethal dose (180 μg/kg i.m.; 80% LD50) were studied. The tabun-induced neurotoxicity was monitored by using a functional observational battery and an automatic measurement of motor activity. The neurotoxicity of tabun was monitored at 24 hours and 7 days following tabun challenge. The results indicate that K203 and obidoxime in combination with atropine allow all tabun-poisoned rats to survive within 7 days following tabun challenge, while 2 nontreated tabun-poisoned rats and 1 tabun-poisoned rat treated with K206 or HI-6 in combination with atropine died within 7 days. Only one of the newly developed oximes (K203) combined with atropine seems to be effective for a decrease in tabun-induced neurotoxicity within 24 hours after tabun sublethal poisoning, although it is not able to eliminate tabun-induced neurotoxicity completely. On the other hand, the neuroprotective efficacy of commonly used oximes (obidoxime and HI-6), as well as one of the new synthesized oximes (K206), is significantly lower in comparison with K203, according to the number of eliminated tabun-induced neurotoxic signs at 24 hours after tabun challenge. Due to its neuroprotective effects, K203 appears to be a suitable oxime for the antidotal treatment of acute tabun poisonings.

A comparison of the neuroprotective efficacy of newly developed oximes (K117, K127) and currently available oxime (obidoxime) in tabun-poisoned rats

The potency of newly developed bispyridinium compounds (K117, K127) to reduce tabun-induced acute neurotoxic signs and symptoms was compared with currently available oxime (obidoxime) using functional observational battery. The neuroprotective effects of atropine alone and atropine combined with one of three bispyridinium oximes (K117, K127, obidoxime) on rats poisoned with tabun at a sublethal dose (180 μg/kg i.m.; 80% of LD50 value) were studied. Tabun-induced neurotoxicity was monitored using a functional observational battery and automatic measurement of motor activity at 24 h following tabun challenge. The results indicated that all tested oximes combined with atropine enabled tabun-poisoned rats to survive 24 h following tabun challenge while one tabun-poisoned rats died within 24 h after tabun poisoning when the rats were treated with atropine alone. Newly developed oxime K127 combined with atropine was the most effective in decreasing tabun-induced neurotoxicity in the case of sublethal poisonings among all oximes tested. Nevertheless, the differences of neuroprotective efficacy between K127 and obidoxime are not sufficient to replace obidoxime by K127 for the treatment of acute tabun poisonings.

The Evaluation of the Neuroprotective Effects of Bispyridinium Oximes in Tabun-Poisoned Rats

Tabun (O-ethyl-N,N-dimethyl phosphoramidocyanidate) belongs to the group of highly toxic organophosphorus compounds that may be used as chemical warfare agents for military as well as terrorist purposes. Tabun differs from other highly toxic organophosphates by the fact that commonly used antidotes are not able adequately to prevent tabun-induced acute toxic effects. The neuroprotective effects of four bispyridinium oximes (K075, trimedoxime, HI-6, obidoxime) in combination with atropine on rats poisoned with tabun at a sublethal dose (150 μg/kg im; 80% of LD50 value) were studied. Tabun-induced neurotoxicity was monitored using a functional observational battery and automatic measurement of motor activity at 24 h and 7 d following tabun challenge. The results indicated that all tested oximes combined with atropine enabled tabun-poisoned rats to survive 7 d following challenge. Trimedoxime combined with atropine was the most effective antidote in decreasing tabun-induced neurotoxicity in the case of sublethal poisonings among all oximes tested. Due to its neuroprotective effects, trimedoxime may be considered to be more suitable oxime for the antidotal treatment of acute tabun exposure than currently used oximes (obidoxime, HI-6) and the newly synthesized oxime K075.

Effects of Exposure to Pheromone and Insecticide Constituents of an Attracticide Formulation on Reproductive Behavior of Oriental Fruit Moth (Lepidoptera: Tortricidae)

The effect of exposure to both the pheromone and insecticide constituents of an attracticide formulation on subsequent pheromonal response of male oriental fruit moth, Grapholita molesta (Busck) (Lepidoptera: Tortricidae), was tested in several wind tunnel bioassays. Male response to the attracticide formulation was significantly reduced in all behavioral categories, including source contact 1 h after sublethal exposure (both by voluntary contact in the wind tunnel and forced application in the laboratory) to the attracticide formulation containing inert ingredients, pheromone, and insecticide. Sublethal exposure to the attracticide formulation in the laboratory (forced application) 24 h before the bioassay resulted in a significantly lower proportion of males subsequently responding to attracticide droplets in the wind tunnel. However, voluntary contact of male moths with the toxic formulation in the wind tunnel had no effect on subsequent response 24 h later. Exposure of males to different constituents of the attracticide formulation demonstrated that both pheromone and insecticide exerted effects on subsequent male pheromonal response. Exposure to the formulation containing the inert ingredients plus the pheromone (no insecticide) significantly reduced male behavioral responses to an attracticide droplet in the wind tunnel 1 h but not 24 h after exposure, compared with males treated with inert ingredients alone. Response to attracticide droplets was further reduced by exposure to the entire attracticide formulation containing inert ingredients, pheromone and insecticide at both 1 and 24 h postexposure. Similarly, males exposed to inert ingredients plus pheromone were less likely to orient to female-produced plumes 1 h but not 24 h after exposure than males treated with inert ingredients alone. Response to female-produced plumes was further reduced at 1 h but not at 24 h after exposure to the entire attracticide formulation. Mating success of males was significantly reduced by exposure to the entire attracticide formulation but not to the formulation without insecticide when placed with females 1 and 24 h postexposure. These findings suggest that sublethal poisoning of males exposed to the attracticide formulation will enhance the effectiveness of this formulation under field conditions.

Neuroprotective effects of currently used antidotes in soman-poisoned rats

The neuroprotective effects of antidotes (atropine, obidoxime, obidoxime/atropine mixture) on rats poisoned with soman at a sublethal dose (54 μg/kg, im, 80% of LD 50 value) were studied. The soman-induced neurotoxicity was monitored using a functional observational battery (FOB) and an automatic measurement of motor activity. The neurotoxicity of soman was monitored at 24 h and 7 days following soman challenge. The results indicate that obidoxime alone is not able to protect the rats from the lethal effects of soman. Three soman-poisoned rats treated with obidoxime alone died within 24 h. On the other hand, atropine alone or combined with obidoxime allows all soman-poisoned rats to survive within 7 days following soman challenge. Atropine alone and combined with obidoxime seems to be relatively effective antidotal treatment for the elimination of soman-induced neurotoxicity in the case of sublethal poisonings, although the antidotal mixture is significantly less effective than atropine alone because obidoxime can counteract the beneficial effects of atropine. Obidoxime appears to be practically ineffective to diminish soman-induced neurotoxicity. The neuroprotective effects of antidotal mixture consisting of atropine and obidoxime depend on the antimuscarinic effects of atropine only. Thus, the replacement of obidoxime by more effective acetylcholinesterase (AChE) reactivators is necessary to increase the neuroprotective efficacy of antidotal treatment in the case of soman poisonings.

Neuroprotective Effects of Antidotes in Soman-Poisoned Rats

1. The neuroprotective effects of antidotes (atropine, obidoxime/atropine mixture, HI-6/atropine mixture) on rats poisoned with soman at a sublethal dose (48 micrograms/kg i.m.; 60% of LD50 value) were studied. The neurotoxicity was monitored using a functional observational battery (FOB) and an automatic measurement of motor activity. The neurotoxicity of soman was monitored at 24 h and 7 d following soman poisoning. 2. The results indicate that atropine alone and the oxime HI-6 in combination with atropine seem to be effective antidotal treatment for the elimination of soman-induced neurotoxicity in the case of sublethal poisonings. 3. On the other hand, the combination of obidoxime with atropine appears to be practically ineffective in diminishing neurotoxic soman-induced symptoms. 4. Dealing with neuroprotective effects of antidotes, the oxime HI-6 in combination with atropine seems to be more suitable antidotal mixture than obidoxime in combination with atropine even in the case of sublethal poisoning with nerve agents.

The environmental and ethical implications of lead shot contamination of rural lands in North America

Lead shot deposited in fields and woodlands near shooting rangesand intense, upland, hunting adds an enormous tonnage of lead toenvironments, worldwide. This contamination is not remedied bybanning lead shot use only for waterfowl hunting. Lead pelletsdisintegrate extremely slowly, during which time they may beingested from the soil by wild birds, livestock, or silage-makingmachinery, and cause sublethal or fatal lead poisoning. Leadpellet corrosion products contaminate soil, surface waters, andground waters, often exceeding permissible levels. Plants do notconcentrate much lead from the soil, except when grown in acidicsoils of heavily-contaminated shooting ranges. Inheavily-contaminated sites, earthworms ingest leadcompounds which are bioaccumulated in higher consumersof food webs. Non-toxic substitutes made from steelor bismuth are available internationally and areeffective for all types of hunting and targetshooting. Many nations are slow to require their use,despite the marked awareness of the problems of leadshot contamination and toxicosis. This is due tohunters and international sport shooting organizationsopposing the use of non-toxic substitutes and overtemphasis by government agencies on the burden ofscientific proof for every situation, rather thantaking preventative action according to thePrecautionary Principle. The ethical approach ofDenmark and The Netherlands, which banned all uses oflead shot, is advocated as a precedent for othernations to adopt.