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Phosphine is a food fumigant, used until now as an insecticide and rodenticide. The present work researches the action of phosphine treatment on growth and sterigmatocystin production of several fungal strains. Production of sterigmatocystin decreased by a ratio of 100 to 500 or was abolished.
BACKGROUND: Acute pesticide poisoning (APP) is a well-recognized cause of morbidity and mortality but is not well described in developing countries. We describe the toxicoepidemiology of APP in Zimbabwe. METHODS: All cases of APP admitted to eight major referral hospitals in Zimbabwe from January 1998 to December 1999 (inclusive) were identified using ICD-9 codes and ward registers and relevant information recorded on a standard data collection sheet. RESULTS: There were a total of 914 single pesticide exposures. Almost half (49.1%) resulted from oral exposure to rodenticides, 42.2% from anticholinesterase-type pesticides (AChTP), mostly organophosphates (OP) that were responsible for over 90% of admissions from AChTP. Accidental and deliberate self-poisoning (27.1% and 58.6%, respectively) accounted for most cases with only eight homicides. The case fatality rate (CFR) in deaths/100 admissions was 6.8 [62 deaths; 95% Confidence Interval (CI) 5.2-8.6] and was significantly higher in males (9.4) than females (4.1) (CI for difference in proportions; 2.0-8.5). In addition, the CFR for deliberate self-poisoning (DSP), 6.5 deaths/100 admissions, was also significantly higher than that for accidental poisoning (0.8 deaths/100 admissions) (CI for difference in proportions 3.2-7.9). Organophosphates were implicated in 70.9% of all fatalities, with over 20% resulting from oral exposure to rat poison (RP). CONCLUSION: Organophosphates and rat poison (RP) are the leading causes of APP admissions to major referral hospitals in Zimbabwe, with most of the admissions being the result of deliberate self-poisoning. Greater control in the sale and use of these products could help prevent significant morbidity and mortality.
Under the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA), the US Environmental Protection Agency (EPA) has the authority to regulate the use of pesticides to prevent unreasonable adverse human health effects associated with pesticide exposure. Accordingly, the EPA requires pesticide registrants to perform studies evaluating the potential for pesticide handler exposure. Data from five such studies that included exposure measurements based on both external measurements and biological monitoring were used to examine methods of assessment, routes and determinants of exposure and dose to the pesticide chlorpyrifos. Eighty workers across four job classes were included: mixer/loaders (M/L, n = 24), mixer/loader/applicators (M/L/A, n = 37), applicators (A, n = 9) and re-entry scouts (RS, n = 10). Results showed that doses were highly variable and differed by job class (P < 0.05) with median total (inhalation and dermal combined) exposure-derived absorbed doses (EDADtot) of 129, 88, 85 and 45 microg/application for A, M/L/A, M/L and RS, respectively. Doses derived from the measurement of 3,5,6-trichloro- 2-pyridinol (3,5,6-TCP) in urine were similar in magnitude but differed in rank with median values of 275, 189, 122 and 97 microg/application for A, M/L, RS, and M/L/A, respectively. The relative contribution of dermal to inhalation exposure was examined by their ratio. The median ratios of exposure-derived absorbed dermal dose (EDADderm) (assuming 3% absorption) to exposure-derived absorbed inhalation dose (EDADinh) (assuming 100% absorption) across job classes were 1.7, 1.5, 0.44 and 0.18 for RS, M/L, A and M/L/A, respectively, with an overall median of 0.6. For 34 of 77 workers (44%), this ratio exceeded 1.0, indicating the significance of the dermal exposure pathway. Different dermal absorption factor (DAF) assumptions were examined by comparing EDADtot to the biomarker-derived absorbed dose (BDAD) as a ratio where EDADtot was calculated assuming a DAF of 1, 3 and 10%. Median ratios of 0.45, 0.71 and 1.28, respectively, were determined suggesting the DAF is within the range of 3-10%. A simple linear regression of urinary 3,5,6-TCP against EDADtot indicates a positive association explaining 29% of the variability in the 3,5,6-TCP derived estimate of dose. A multiple linear regression model including the variables EDADderm, EDADinh and application type explained 46% of the variability (R2 = 0.46) in the urinary dose estimate. EDADderm was marginally significant (P = 0.066) while EDADinh was not (P = 0.57). The EDADderm regression coefficient (0.0007) exceeded the coefficient for EDADinh (0.00002) by a factor of 35. This study demonstrates the value of the pesticide registrant database for the purpose of evaluating pesticide worker exposure. It highlights the significance of the dermal exposure pathway, and identifies the need for methods and research to close the gap between external and internal exposure measures.
A case-control study of bladder cancer in two northern counties of New Jersey was conducted to investigate a tumour that has been considered to be strongly associated with industrial and environmental exposures. The study population included 75 bladder cancer cases and 142 controls. Cases and controls were matched for race, sex, age, place of birth and place of residence. Statistically significant associations with bladder cancer and risk ratios of greater than 2.0 were found for cigarette smoking and for working in dye, petroleum (fuel) or plastics industries. No statistically significant association was found for: cigar and pipe smoking; caffeine, saccharine and alcohol consumption; and life time occupational history of working in other than dye, petroleum and plastics industries. No statistically significant differences between cases and controls were found in family history of cancer. Risk ratios of at least 2.5 (but without statistical significance possibly because of sample size) were found for workers in rodenticide and printing industries, for cable workers and for cancer in the spouses of bladder cancer cases. Simultaneous multiple primary cancer sites were found in 9.3% of the bladder cancer patients; this is higher than the 0.2-8% reported in the medical literature. The life time occupational history of the bladder cancer cases points to industrial determinants: some are known (petroleum and dye industries) but the association with the plastics industry is new. If our findings are confirmed, investigations will be needed to determine whether any specific chemical or combination of chemicals used in the plastics industry is responsible for bladder cancer induction.
A method for the determination of tetramine in postmortem specimens is reported. Tetramine is an organosulfur rodenticide. Parathion, an organophosphorous insecticide, was adopted as the internal standard. Both were extracted from biological materials by benzene and purified by an aluminum oxide column. The extract was analyzed by a gas chromatograph equipped with a nitrogen-phosphorous detector. The extraction efficiency was greater than 90%, and the limit of detection was 0.05 microgram/g for the liver. The standard curve was linear in the range 0.5-50 micrograms/g for the liver, and the correlation coefficient was equal to 0.9993.
In October 1988, five of seven members of a Florida family were poisoned with thallium, constituting the largest outbreak of acute thallium poisoning in the United States since thallium was banned as a rodenticide in 1972. Three patients had an acute severe neuropathy with respiratory depression; one died. The other two had no symptoms. No cases were identified among nonhousehold relatives or friends, or in the community. Of the more than 100 environmental specimens collected at the family household and tested by atomic spectroscopy, three empty and four unopened glass soft drink bottles of the same lot number yielded thallium in a concentration fatal to humans. All family members who consumed the soft drink were poisoned (5/5) as compared with none of those who did not (0/2). Because poisoning was clustered to the family and police investigators provided evidence that the poisoning was deliberately targeted to the family, it was assumed that no other soft drink bottles contained thallium, and it was decided not to recall all soft drink bottles with the same lot number. A year later a neighbor of the family was arrested and convicted of the murder.
Lawn-care herbicides are a type of pesticide regulated under federal and state pesticide legislation. The Michigan Department of Agriculture implements herbicide regulation to protect the public's health and welfare. Yet, due to gaps that exist in all levels of government in the regulation of lawn-care herbicide application, the public is placed at risk. The federal pesticide legislation (Federal Insecticide, Fungicide, and Rodenticide Act) provides for a lower standard of safety in the classification of herbicides applied in the residential context as opposed to the agricultural context. Michigan legislation (The Pesticide Control Act) exempts from the law persons applying general herbicides on their own premises. The state does not require public notification of risks or safety precautions prior to commercial application of these herbicides. Furthermore, on-site inspections are not performed for residential application of herbicides and the state applicator certification program is not assessed for effectiveness.
A three-year-old Border collie was presented with a two-week history of lethargy, stiff gait, polydipsia and polyuria. Biochemical analysis revealed hypercalcaemia. Serum concentrations of 25-hydroxyvitamin D (25[OH]D) and 1,25-dihydroxyvitamin D (1,25[OH]2D) were markedly elevated and parathyroid hormone was undetectable. Subsequent analysis of the dog's diet revealed that the food contained excessive amounts of vitamin D. The hypercalcaemia resolved following treatment with bisphosphonates and dietary change. Hypervitaminosis D was diagnosed in a second unrelated dog, which had been fed the same brand of dog food as case 1. The dog was also hypercalcaemic and had markedly elevated serum concentrations of 25(OH)D and 1,25(OH)2D. Hypervitaminosis D in dogs has been reported to occur secondarily to ingestion of either rodenticides containing cholecalciferol or antipsoriatic ointments that contain vitamin D analogues. Hypervitaminosis D has also been reported following the treatment of hypoparathyroidism. To the authors' knowledge, this is the first report of hypervitaminosis D in dogs following the accidental over supplementation of a commercial diet with vitamin D. While the benefits of adequate dietary vitamin D are well established in dogs, the potential deleterious effects of over supplementation of vitamin D should also be acknowledged.
Respiratory obstruction resulting from a discrete haematoma within the dorsal tracheal membrane was seen in an 11-year-old neutered female greyhound that had been involved in a fight two days earlier. There was no history or evidence of rodenticide toxicity or other coagulopathy, and it is suggested that the tracheal haematoma resulted from trauma. A right third intercostal thoracotomy was performed and this allowed resection of the haematoma from within the dorsal membrane of the cranial thoracic trachea, relieving the obstruction with no subsequent signs of dyspnoea. Intramural haematoma should be considered as a rare differential diagnosis for dogs presenting with acute respiratory obstruction.
Phosphine is a food fumigant, used until now as an insecticide and rodenticide. The present work researches the action of phosphine treatment on growth and aflatoxin production of 23 Aspergillus strains. Production of aflatoxins B1, B2, G1, and G2 decreased in almost all cases by a ratio of 10 to 100. Phosphine treatment therefore seems favorable to prevent growth of various Aspergillus strains, in the context of keeping food safe.
Details of cases involving the inadvertent exposure of birds to eight toxic substances are recorded. The organophosphate insecticides dichlorvos, diazinon and malathion produced respiratory symptoms which in the former and latter cases were initially thought to be caused by infectious disease. Birds which consumed feed containing fenitrothion showed nervous signs before death. On three separate occasions feral starlings (Sternus vulgaris) were found dead and their gizzard contents contained mevinphos. The rodenticide warfarin was associated with petechial haemorrhages in the skeletal muscles and on the serosal surfaces of one hen. Cyanogenic glycosides from Eucalyptus cladocalyx were responsible for the sudden deaths of ducks and guinea fowl. 'Ornamental dough' containing sodium chloride was fed to birds which were deprived of water and they showed diarrhoea and nervous disorders before death.
Forty-four free-living stoats were collected from five game estates in England and examined for evidence of disease. All the macroscopic lesions were attributable to the trauma associated with being trapped or shot. There were no significant microscopic lesions in 27 (61 per cent) of the stoats. There was evidence of nematode parasitism in the intestines of six stoats (14 per cent), and in the lungs of five stoats (11 per cent), and of pulmonary granulomatous inflammation or microgranulomas in five stoats. In two of the stoats, blood-filled cavities in the liver were suggestive of peliosis hepatis, possibly associated with infection by Bartonella species or with sublethal exposure to anticoagulant rodenticides.
The potential chemical contamination incidents investigated by the Veterinary Laboratories Agency (VLA) between 1990 and 2002 are reviewed. Incidents were identified in the course of the VLA's surveillance of food animal disease and further investigations were carried out on behalf of the Food Standards Agency in order to identify and control the contamination of food animals and animal products with chemical hazards. In total 876 incidents were investigated, of which 588 involved the poisoning of cattle with heavy metals. There were 63 incidents involving the exposure of cattle, sheep, pigs and poultry to the accidental misuse of veterinary medicines, pesticides or rodenticides, and 50 incidents involving their exposure to microbiological toxins, particularly botulism.
The history of the antithrombotic agents--aspirin, heparin, warfarin, and the thrombolytics--is a rich and lively odyssey of serendipity, perseverance, vision, and conflict involving a number of striking personalities. The history of aspirin spans ages and continents from Hippocrates' analgesic for women in labor to the rediscovery of the white willow bark by English country scholar Reverend Edward Stone. Bayer chemist Felix Hoffmann reinvented aspirin for his ailing father; suburban physician L.L. Craven pioneered the prophylactic antithrombotic uses of aspirin; and Sir John Vane elucidated aspirin's mechanism of action as the inhibition of prostaglandin synthetase. Heparin was discovered by McLean, working as a medical student in 1915 in search of a pure procoagulant in dog liver. His original impure material differed somewhat from today's heparin, but purified heparin was rapidly accepted for a myriad of clinical uses; to this day, diverse new properties of this complex glycosaminoglycan continue to be elucidated. The oral anticoagulants emerged from veterinary research in the 1920s on a hemorrhagic disorder afflicting cattle that consumed spoiled sweet clover hay. Several chance encounters led Karl Link and his University of Wisconsin team to the identification of dicumarol as the offending agent in 1939 and its widespread therapeutic use by Wright and others in the 1940s. Link later developed warfarin as a rodenticide, but its use in humans soon followed in the 1950s. Vitamin K was discovered in the 1930s; its involvement in the mechanism of the anticoagulant agents was not delineated until the 1970s. The intrinsic ability of clotted blood to liquify and the fibrinolytic properties of normal urine were noted in the 1800s. Tillett and Sherry's group stumbled on the fibrinolytic properties of streptokinase in the 1930s and pioneered the therapeutic use of streptokinase in the 1940s and of urokinase in the 1960s. Several teams found tissue-type plasminogen activator in various body sites beginning in the 1940s, leading to its cloning and widespread use in the 1980s; anisoylated plasminogen-streptokinase activator complex is an example of rational drug design. The discoverers of these diverse agents have not only provided physicians with a potent armamentarium of antithrombotic drugs but also helped elucidate much basic science and vividly demonstrated the merits of perseverance, independent thought, and adherance to the scientific method.
1. Alpha-chloralose, formed by the condensation of glucose with chloral, is used as a rodenticide and in the control of bird pests. 2. In two cases of poisoning with alpha-chloralose the clinical features included coma and generalized convulsions resembling the effects of strychnine more than those of chloral hydrate. 3. The principles of management are the support of vital functions in the unconscious patient and removal of unabsorbed poison by gastric lavage. Diazepam may be used to control convulsions.
1. Data on deaths from pesticide poisoning occurring in England and Wales between 1945 and 1989 (no data are available for 1954) have been collated; pesticides were responsible for only 1012 (1.1%) of the 87,385 deaths from poisoning (excluding those due to carbon monoxide) occurring over this 44 year period. At least 73% of all pesticide fatalities were due to suicide and overall there was a predominance of males (male:female ratio 2.4:1). No deaths from pesticide poisoning in children under 10 years have been reported since 1974 although almost 50% of suspected pesticide poisoning incidents involve this age group. 2. Herbicides were responsible for 787 (78%) fatal poisonings, 110 (11%) were caused by insecticides, 69 (6.8%) by rodenticides, 30 (3.0%) by wood preservatives and 16 (1.6%) by other pesticides. 3. The herbicide, paraquat, was responsible for 570 of 1012 (56%) deaths and, although there has been a progressive decline in the annual number of deaths from paraquat poisoning since 1982, paraquat remains the most common cause of fatal pesticide poisoning in England and Wales. 4. Sodium chlorate caused 113 (11.2%) deaths, most of these fatalities occurring between 1965 and 1983; only one death has been recorded since 1984. The phenoxyacetate herbicides resulted in 50 deaths; 2,4-D was implicated most commonly. Sixty-eight deaths were due to organophosphorus insecticides; demeton-S-methyl, malathion and mevinphos were involved most frequently. Only eight deaths resulted from organochlorine insecticides and two of these also involved an organophosphorus insecticide.(ABSTRACT TRUNCATED AT 250 WORDS)
1. Between 1982 and 1988, 239,350 children under 10 years old attended 20 A & E Departments in England and Wales (22 departments throughout the UK in 1988) as a result of a home accident. 15,144 of 239,350 were suspected cases of poisoning and 514 attendances involved pesticides. 2. 501 of 514 children who attended hospital were under 6 years old and 41% were thought to have ingested a rodenticide, 37% an insecticide or other animal poison, 13% an herbicide or fungicide and 9% other pesticides. 3. Overall 189 of 514 children were admitted to hospital and of these 189 cases 35% were discharged home in less than one day; 94% left hospital within 2 days. 4. Using these data we estimate that over the period of study approximately 1,850 children annually attended an Accident and Emergency Department in the UK with suspected pesticide poisoning and that some 450 were admitted to hospital. However, the morbidity from this cause is low and no deaths from pesticide poisoning have been reported in children in England and Wales for more than two decades.
1. Between 1989 and 1991, 121,708 children less than 10 years old attended 22 Accident and Emergency (A & E) Departments in the UK as a result of an accident at home; 6,478 of these were cases of suspected poisoning. 2. Two hundred and fifty (124 boys and 126 girls) of 6,478 cases involved pesticides. Forty two per cent of these children were thought to have been poisoned by rodenticides, 33% by a different animal poison, 13% by an herbicide or fungicide, 7% by creosote and 5% by mothballs; a pattern similar to that observed in previous years. 3. Fifty-seven of 250 children (23%) were admitted to hospital. The proportion of children admitted to hospital between 1989 and 1991 is smaller than that observed between 1982-1988 (37%). Forty-six per cent of children were discharged home within one day and 95% within 2 days, whereas between 1982 and 1988 only 35% of children were discharged within one day. No child died during the study confirming the low morbidity. 4. Using these data we estimate that between 1989 and 1991 approximately 1,500 children annually attended an A & E Department in the UK with a diagnosis of suspected pesticide poisoning and that some 350 children were admitted each year.