Methoxyethyl Mercury Chloride Research Articles

When toxic chemicals refuse to die—An examination of the prolonged mercury pesticide use in Australia

Mercury, even in low concentrations, is known to cause severe adverse human health effects. In the early 1900s, mercury became a popular fungicide ingredient, leading to multiple poisoning incidents that forced much of the world to act upon phasing out mercury use in agriculture. These incidents spurred the advancement of mercury science and the implementation of international policies and regulations to control mercury pollution worldwide. Despite these developments internationally, Australia continued using methoxyethyl mercury chloride as a fungicide to treat sugarcane against the fungi Ceratocystis paradoxa (pineapple disease). At the request of the manufacturer and following pressure from Australian researchers and the Minamata Convention on Mercury, Australian authorities announced a ban on mercury-containing pesticide in May 2020. Australia’s unique reluctance to act on controlling this hazardous pollutant makes it an interesting case study for policy inaction that runs counter to global policy trends and evidence-based decision making. As such, it can provide insights into the challenges of achieving multilateral agreement on difficult environmental issues such as global warming. In this review, I discuss the scientific development and policy decisions related to mercury fates and exposure of wildlife and humans in Australia to mercury used in pesticide. The historical uses of mercury pesticide and poisoning incidents worldwide are described to contextualize Australia’s delayed action on banning and controlling this chemical product compared to other nations. Regulations on mercury use in Australia, which has not ratified the Minamata Convention on mercury, are compared to those of major sugarcane and pesticide producer nations (Brazil, China, Japan, India, Thailand, and United States) which have ratified the Convention and replaced mercury pesticides with alternative products. I discuss how mercury regulations have the potential to protect the environment, decrease human exposure to mercury, and safeguard the ban on mercury products. Ratifying the Minamata Convention would give Australia equal footing with its international counterparts in global efforts to control global mercury pollution.

The selective uptake of mercury by myocardial infarcts in the rat.

Abstract Rats with myocardial infarcts, sham operated and control animals were treated with methoxyethyl mercury chloride (MEMC) intra-peritoneally or with mercamphamide intravenously or intra-peritoneally and the mercury content in the hearts determined spectrophotometrically with dithizone after various time intervals. After MEMC treatment there was no difference between the amounts of mercury found in the hearts of rats with myocardial infarcts and controls. After injection of mercamphamide, mercury was taken up by hearts of rats with myocardial infarcts while those of sham operated and control animals remained free of mercury. Optimal results were yielded by 1 h experiments made within the first 24 postoperative hours. The selective uptake of mercury from organo-mercurials is much dependent on the organic part of the molecule present in the given individual compound.

Effect of Pesticides on the Nematode Pathogenic Bacteria, Bacillus macerans In vitro

Sensitivity of Bacillus macerans Schardinger, 1905, a potent biocontrolagent of root-knot nematode, to different pesticides was tested in vitro by filter paper disc method. The pesticides were metham sodium, phorate, aldicarb, carbofuran and formalin representing nematicides and HCH (BHC), endosulfan, malathion, quinalphos and carbaryl representing insecticides and agallol, . carbendazim, copper oxychloride, maneb, zineband ziram the fungicides. B. macerans was highly sensitive to metham sodium and formaldehyde with an inhibition zone diameter ranging from 20 to 44 m.m. While aldicarb was slightly inhibitory, phorate and carbofuran were non-inhibitory. All insecticides except quinalphos (1000 ppm only) and carbaryl were non-inhibitory. Among the fungicides tested, the systemic fungicide carbendazim was the safest. Methoxy ethyl mercury chloride, mancozeb, zineb and ziram were toxic to B. macerans . These fungicides showed statistically significant increase in inhibition among the different fungicides.

Behavioral effects of prenatal methoxy-ethyl-mercury chloride exposure in rat pups

A number of neurotoxic drugs, when administered prenatally, induce neurobehavioral impairments and cause delay of the developmnet of central nervous functions, without morphological malformations. Experiments were undertaken to clarify the behavioral teratogenicity of the fungicide methoxy-ethyl-mercury chloride (MEMC). CFY rat dams were treated with different doses of MEMC during 7th–15th days of gestation (2.0, 0.62 and 0.02 mg/kg daily), perorally. Development of gait, motor coordination, behavior patterns in an open field test, swimming, and conditioned avoidance learning were tested at different ages of rat pups. MEMC did not cause any mortality of dams, but there was a mild ataxia at the 2.0 mg/kg treatment. While birthweight, number of offspring, ear-eye opening and gait were normal, unexpectedly high mortality occurred perinatally. After weaning, open field behavior was nearly normal, there was a mild decrease of rearing, grooming and ambulation and an initial preference for the periphery of the open field decreased. Ambulation increased significantly in 90-day-old pups. Motor coordination on a rotorod decreased in 23- and 36-day-old pups, but increased in 90-day-old pups at the 2.0 mg/kg dose. There was no difference among groups in amphetamine sensitivity tested in a swim stress test. During avoidance conditioning, pups treated with the two higher doses performed poorly when compared to controls and the latency of the positive conditioned response was lengthened significantly. Our results show a dose-dependent behavioral teratogenicity of this organomercurial fungicide. The so called no effect level—as far as the neurobehavioral impairments due to prenatal exposure are concerned—is 0.02 mg/kg daily.

Toxic effects of three mercurial compounds on survival, and histology of the kidney of the catfish Clarias batrachus (L.)

In Clarias batrachus methylmercuric chloride (CH 3HgCl) was 1.18 and 10.05 times more toxic than mercuric chloride (HgCl 2) and emisan 6 (methoxyethyl mercury chloride), respectively, for 96 hr. A similar trend was observed at 24, 48, and 72 hr. Exposure of the catfish to sublethal concentrations of these mercurials for 14 and 28 days caused progressive changes in the kidney. The diameter of the proximal convoluted tubules was increased, the epithelial cells were hypertrophied, and the lumen was reduced and filled with secretory material and sloughed-off cells. In 14-day emisan 6-treated fish, some glomeruli were also degenerated. Exposure of the catfish to toxicologically safe concentrations of the mercurials for 90 days caused vacuolation, atrophy, and extensive damage of the tubules in HgCl 2- and CH 3HgCl-treated fish, and hypertrophy and vacuolation of epithelial cells of some tubules in the emisan 6-treated fish. Regeneration was noticed in the 90-day HgCl 2-exposed group. After 180 days of exposure, however, histology of the kidney appeared normal in all the groups.

Investigations on the mutagenicity of two organomercurial pesticides, ceresan and agallol 3, in Drosophila melanogaster

Two organomercurial fungicides, Ceresan containing phenyl mercury acetate and Agallol 3 containing methoxyethyl mercury chloride, were investigated for their mutagenicity in Drosophila melanogaster. The fungicides, administered by both larval and adult feeding techniques, were evaluated for their efficacy in inducing dominant lethals, sex-linked recessive lethals, and II-III translocations in the male germ cells. Both fungicides failed to induce significant dominant lethals, sex-linked recessive lethals, and II-III translocations when administered in the larval diet ( P > 0.05). But Ceresan in the adult diet brought about a significant increase in the frequency of sex-linked recessive lethals ( P < 0.05). Broodwise analysis revealed that spermatids and spermatocytes were more sensitive than others to all the concentrations of Ceresan and Agallol 3 used. The mutagenic implications of such fungicides in the human environment are discussed.

Fungicidal control of Rhizoctonia solani in soil amended with organic manures

SUMMARYAmendments of nutrient‐deficient soil with three organic manures and one non‐edible oil‐cake reduced the disease controlling potential of methoxyethyl mercury chloride (MEMC), quintozene and carbendazim used as seed treatments on cowpea and cotton against seedling rot caused by Rhizoctonia solani.Biogas sludge (BGS) and farm yard manure (FYM) nullified the activity of MEMC and quintozene and reduced markedly the efficacy of carbendazim. Humic acid extracted from BGS inactivated MEMC and carbendazim but had little effect on quintozene. Green manure (Sesbania aculeata) slightly reduced the efficacy of MEMC only. Soil amendment with mahua (Madhuca indica) cake and soil drench with its aqueous extract greatly reduced the efficacy of the three fungicides.

Methoxyethylmercury nephrotoxicity: effects on enzymuria and kidney function.

The fungicide, methoxyethylmercury chloride, was given in a saline solution to four groups of Sprague-Dawley C D rats (5 male, 5 female) as a single injection (IP) of 0, 0.5, 1.0, and 2.0 mg Hg/kg. In a three-day period, no changes were observed in urine collected every 24 h from rats given 0 or 0.5 mg Hg/kg; 1 mg Hg/kg induced only a transient increase of urine gamma glutamyl transferase (x 4) and alkaline phsophatase (x 2.5) on the day 2; 2.0 mg Hg/kg caused an early increase of enzymuria (day 1 and day 2) and a decrease of Na+, Cl-, K+, urea, and creatinin excretion. Urine enzymes and total mercury excretion were higher in males. These time-related variations of enzymuria, compared to previous results with Hg Cl2, could reflect the existence of metabolites more toxic than the native compound.

The role of antagonists in the chemical control of Fusarium oxysporum f. sp. narcissi

Treatment of narcissus bulbs with methoxy ethyl mercury chloride, pimaricin or thiram provided control of basal rot and primary root rot, caused by Fusarium oxysporum f. sp. narcissi and secondary root rot and ‘skin disease’ caused by F. oxysporum ff. spp. A similar treatment with formal in was only effective against basal rot and root rot. Newly formed roots of bulbs treated with the mercurial, pimaricin or thiram became more heavily colonized by Penicillium and Trichoderma spp. than those of untreated or formal in-treated bulbs. Especially P. janthinellum and T. viride appeared to protect the roots against the pathogens. These fungi were found to be antagonistic to F. oxysporum f. sp. narcissi and F. oxysporum ff. spp., both in experiments in vitro and in vivo. A synergism between P. janthinellum and thiram was observed with respect to inhibition of mycelial growth of F. oxysporum f. sp. narcissi in vitro and to control of root rot and basal rot in vivo. In vitro, similar effects were found for pimaricin and organic mercury. Pimaricin was found to stimulate the production of antibacterial metabolites by Cylindrocarpon destructans in vitro. In the field, a synergistic effect was observed between pimaricin and C. destructans with respect to control of basal rot.

Toxicity of organic mercury compounds. IV. Metabolism and excretion of alkoxyethylmercury compounds in mice.

Metabolism and excretion of alkoxyethylmercury compounds in mice were studied, and their gastrointestinal absorption was discussed. The total mercury and the organic mercury in blood, liver, kidney, and excreta at time intervals after a single subcutaneous injection of methoxyethylmercury chloride (MEMC) and n-propoxyethylmercury chloride (n-PEMC) were determined. Initially, the greater part of mercury in the blood, liver, and kidney was found as organic forms, but thereafter the organic mercury rapidly decreased with decrease of the total mercury. During 120 hr, the ratio of excretion of mercury in urine/feces was 2/1 after injection of MEMC and 1/2 after injection of n-PEMC, and more than half of the mercury in urine were in organic forms. Mercury in the feces was not determined as the organic form and was a chemically stable compound. It is most likely that the fecal mercury is mercuric sulfide, since it was formed from inorganic mercury ion in the cecum. Inorganic mercury was found in the gastric contents initially after oral administration of MEMC. The release of inorganic mercury in the stomach indicates a reason for the poorer gastrointestinal absorption of alkoxyethylmercury compounds.

Toxicity of organic mercury compounds. III. Uptake and retention of mercury in several organs of mice by long term exposure of alkoxyethylmercury compounds.

Uptake and accumulation of alkoxyethylmercury compounds in several organs of mice, in comparison with alkylmercury compounds, were studied. Diets containing various organic mercury compounds were continuously fed to mice, and organic mercury in the organs was extracted with dithizone-carbon tetrachloride and determined by gas chromatography. Histological studies in mice poisoned by methoxyethylmercury chloride showed a prominent damage of the kidney, and proliferation of glial cells and atrophy of nervous cells in the cerebrum. In all of the compounds administered, the organic mercury was found in the liver and kidney. The ratio of the mercury contents in blood to plasma was higher in ethylmercury chloride than in alkoxyethylmercury compounds. Ethylmercury chloride was highly incorpolated into the brain, while alkoxyethylmercury compounds were at much slower rates. The mercury contents in the brain at onset of the neural symptoms were much lower in methoxyethylmercury than in ethylmercury. In the brain after administration of alkoxyethylmercury compounds, it appeared to be present as an inorganic mercury for the most part, in contrast with significant amounts of the organic mercury in the case of the alkylmercury. It may be presumed that manifestation of the symptoms after exposure of organic mercury compounds is not merely related to mercury levels and not always in need of organic forms in the brain.

Alteration of electroencephalogram and evoked potential in rats induced by organic mercury.

An organic mercurial compound, methoxy‐ethyl‐mercury chloride (MEMC) has been studied for its subacute neurotoxic effects by means of EEG and evoked potentials, in male rats. Poisoning by MEMC during four weeks causes characteristic alterations of the electroencephalogram: i.e. increases the α1; β1; β2 frequency, analysed by integration of spectral frequency. The amplitude and duration of the cortical evoked potentials were also changed.

Rhizoctonia solanicontrol and effect on potato yields

Abstract Pre-planting tuber dips of benomyl and thiabendazole were compared as alternatives to organic mercury for Rhizoctonia solani control in two field trials. At suitable rates, all chemicals reduced the stem canker phase of Rhizoctonia solani Kuhn compared with untreated controls. A high concentration of benomyl 0.5% a.i. was necessary to give stem canker control equal to that of 0.015% organic mercury as methoxyethyl mercury chloride. Reducing the benomyl rate to 0.25% a.i. significantly reduced the degree of control. Major differences in level of stem canker between different treatments did not affect yields in the first trial, but produced significant reductions in the second year on an earlier crop.

The examination of organomercury compounds and their formulations by thin-layer chromatography.

Thin-layer chromatographic methods for the separation and identification of organomercury compounds have been developed and applied to the examination of commercial-quality organomercurials and seed-dressing formulations. The organomercury compounds, in the form of their chlorides, are separated on silica gel by continuous development with cyclohexane-acetone (4 + 1), and detected as orange-brown spots by spraying the plate successively with copper sulphate and sodium sulphite-potassium iodide reagents. If organomercury salts other than chlorides are present, they must be converted into the chlorides by adding aqueous sodium chloride solution to the spotting solvent.A method for the semi-quantitative assay of inorganic mercury [as mercury(II)] in the compounds, at levels between 1 and 14 per cent., is also described. The inorganic mercury [as mercury(II) chloride] is separated by using carbon tetrachloride-acetone (7 + 3) as the developing solvent and is determined by visual comparison with standards.Little or no mercury-containing impurity was found in samples of phenylmercury nitrate, phenylmercury acetate and phenylmercury chloride examined, but methoxyethylmercury chloride and ethoxyethylmercury chloride samples contained as many as five mercury-containing impurities and up to 12 per cent. of inorganic mercury compounds.

Resistance to mercury ofPyrenophora avenae(conidial stateHelminthosporium avenae) in New Zealand seed oats

Abstract Each of 53 samples of New Zealand seed oats harvested in the 1966–7 season was examined for the presence of Pyrenophora avenae Ito and Kuribay, before and after treatment with an organomercurial seed dressing. Colonies grew from 27 untreated samples and from eight treated samples. A number of isolates of the fungus were further tested for resistance to mercury by growing them on agar containing different concentrations of mercuric chloride, methoxyethyl mercury chloride, and phenyl mercury chloride. All colonies grew well at low concentrations, and in the case of mercuric chloride. grew better in the presence of small amounts of mercury than in its absence. Results of pot tests for infection after treatment agree well with those from agar plate tests.