Geology topics

David J. Hoffman

Publications and source records attributed to David J. Hoffman.

42 records · Page 3Linked to original sources

USGS1984

Evaluation of potential embryotoxicity and teratogenicity of 42 herbicides, insecticides, and petroleum contaminants to mallard eggs

Results are reported for the embryotoxicity of 42 environmental contaminants applied externally to mallard ( Anas platyrhynchos ) eggs including crude and refined petroleum, and commercial formulations of herbicides and insecticides. Many of the petroleum pollutants were embryotoxic and moderately teratogenic and had LD 50 s of 0.3 to 5 μl per egg (∼6–90 μg/g egg). The most toxic was a commercial oil used for control of road dust followed by South Louisiana crude oil, Kuwait crude, no. 2 fuel oil, bunker C fuel oil, and industrial and automotive waste oil. Prudhoe Bay crude, unused crankcase oil, aviation kerosene, and aliphatic hydrocarbon mixtures were less toxic ( LD 50 s of 18 to over 75 μl) and less teratogenic. The LC 50 s of herbicides and insecticides in aqueous emulsion were measured by egg immersion; the most toxic were paraquat and trifluralin ( LC 50 s of about 1.5 Ibs/A; 1.7 kg/ha). Propanil, bromoxynil with MCPA, methyl diclofop, prometon, endrin, sulprofos, and parathion were toxic ( LC 50 s of 7 to 40 Ibs/A; 7.8–44.8 kg/ha), whereas 2,4-D, glyphosate, atrazine, carbaryl, dalapon, dicamba, methomyl, and phosmet were only slightly toxic or not toxic ( LC 50 s of 178 to over 500 Ibs/A; 199–560 kg/ha). Pesticides in nontoxic oil vehicle applied by microliter pipet were up to 18 times more toxic than when applied in water vehicle, which was probably due to better penetration of the pesticide past the eggshell and its membranes. Teratogenic effects and impaired embryonic growth are reported and results discussed in terms of potential hazard at field levels of application. A discussion is provided on the effects of pollutants on the eggs of other species of birds under laboratory and field conditions.

Archives of Environmental Contamination and Toxico↗

USGS1984

Comparative toxicity of acephate in laboratory mice, white-footed mice, and meadow voles

The LD50 (95% confidence limits) of the organophosphorus insecticide acephate was estimated to be 351, 380, and 321 mg/kg (295–416, 280–516, and 266–388 mg/kg) for CD-1 laboratory mice ( Mus musculus ), white-footed mice ( Peromyscus leucopus noveboracensis ), and meadow voles ( Microtus pennsylvanicus ), respectively. In a second study, these species were provided mash containing 0, 25, 100, and 400 ppm acephate for five days. Brain and plasma cholinesterase activities were reduced in a dose-dependent manner to a similar extent in the three species (inhibition of brain acetyl-cholinesterase averaged for each species ranged from 13 to 22% at 25 ppm, 33 to 42% at 100 ppm, and 56 to 57% at 400 ppm). Mash intake, body or liver weight, plasma enzyme activities (alkaline phosphatase, alanine and aspartate aminotransferase), hepatic enzyme activities (aniline hydroxylase, 7-ethoxycoumarin O-deethylase, and glutathione S-transferase), and cytochrome content (P-450 and b 5 ) were not affected by acephate ingestion, although values differed among species. In a third experiment, mice and voles received 400 ppm acephate for 5 days followed by untreated food for up to 2 weeks. Mean inhibition of brain acetylcholin-esterase for the three species ranged from 47 to 58% on day 5, but by days 12 and 19, activity had recovered to 66 to 76% and 81 to 88% of concurrent control values. These findings indicate that CD-1 laboratory mice, white-footed mice, and meadow voles are equally sensitive to acephate when maintained under uniform laboratory conditions. Several factors ( e.g. , behavior, food preference, habitat) could affect routes and degree of exposure in the field, thereby rendering some species of wild rodents ecologically more vulnerable to organophosphorus insecticides.

Archives of Environmental Contamination and Toxico↗

USGS1983

Lead accumulation and depression of δ-aminolevulinic acid dehydratase (ALAD) in young birds fed automotive waste oil

The effects of a 3-week dietary exposure to automotive waste crankcase oil (WCO) were examined in 1-week-old mallard ( Anas platyrhynchos ) ducklings and pheasant ( Phasianus colchicus ) chicks. Treatment groups consisted of birds exposed to 0.5, 1.5, or 4.5% WCO, to 4.5% clean crankcase oil (CCO), or untreated controls. In both species, red blood cell ALAD activity was significantly inhibited after one week by 50 to 60% in the 0.5% WCO group and by 85 to 90% in the 4.5% WCO group due to the presence of lead. Growth, hematocrit, and hemoglobin were not significantly affected at the end of three weeks. Plasma aspartate aminotransferase (AST) activity was higher in mallards after three weeks of ingesting either 4.5% WCO or 4.5% CCO, suggesting an oil-related effect due to components other than lead. Treatment had no effect on plasma concentration of uric acid, glucose, triglycerides, total protein, or cholesterol. Lead analysis showed the WCO to contain 4,200 ppm Pb and the CCO to contain 2 ppm. Tissues of mallards were examined for accumulation of lead and the order of accumulation at the end of three weeks was kidney > liver > blood ∼ brain.

Archives of Environmental Contamination and Toxico↗

USGS1982

Effects of lindane, paraquat, toxaphene, and 2,4,5-trichlorophenoxyacetic acid on mallard embryo development

The effects were determined of externally treating mallard ( Anas platyrhynchos ) eggs with two insecticides (lindane and toxaphene) and two herbicides (paraquat and 2,4,5-T) with formulations and concentrations similar to field applications. Paraquat was the most embryotoxic of the four compounds regardless of the type of vehicle. The LC50 for paraquat was 1.5 lb of active ingredient/ acre in aqueous emulsion and 0.1 lb/acre in the oil vehicle. The other compounds had LC50's that were several orders of magnitude higher. Both paraquat and toxaphene caused some mortality at 1/2 of the field level of application. Paraquat impaired growth and was slightly teratogenic at 1/2 of the field level of application, but required higher concentrations (1.5 to 3 times the field level) to produce brain and visceral defects. Lindane was teratogenic, resulting in multiple defects but only at doses that were greater than five times the field level of application. Toxaphene resulted in defects of the joints at doses close to or exceeding the LC50. The herbicide 2,4,5-T resulted in few toxic effects and relatively few abnormal survivors with gross defects. The overall embryotoxicity with either vehicle was paraquat > lindane > toxaphene > 2,4,5-T on a lb per acre basis. However the potential hazard at exposures of up to five times the field level of application was paraquat > toxaphene; neither lindane nor 2,4,5-T constituted much of a hazard. Both paraquat and lindane were more toxic on a lb-peracre basis when administered in oil vehicle but only paraquat represented a potential hazard at five times the field level of application.

Archives of Environmental Contamination and Toxico↗

USGS1981

Effects of malathion, diazinon, and parathion on mallard embryo development and cholinesterase activity

The effects of external exposure of mallard ( Anas platyrhynchos ) eggs to malathion, diazinon, and parathion were examined using formulations and concentrations similar to field applications. Treatment with aqueous emulsion simulated exposure at the rate of 100 gal per acre (153 liters/hectare) with three to six different doses per compound with treatment at 3 and 8 days of embryonic development. Treatment with a nontoxic oil vehicle simulated exposure at the rate of 11 gal per acre (16.8 liters/hectare) with three to six different doses per compound. The order of embryotoxicity on a pounds-per-acre basis was parathion > diazinon > malathion with either vehicle. However, the potential hazard under conditions of up to five times the maximum field level of application was greater for malathion because of the high permissible level of application for malathion on certain crops. Parathion, the most embryotoxic of the three, had the most pronounced effects when an oil vehicle was used, as reflected by an LC 50 of about 2 lb of active ingredient per acre, stunted growth, and a high frequency of malformations involving distortion of the axial skeleton, particularly in the cervical region. All three compounds resulted in significant depression of plasma and brain cholinesterase activity, but parathion caused the most depression throughout development, which was still apparent in hatchlings. Treatment with either distilled water or oil vehicle alone did not result in any of these effects seen with organophosphorous insecticides.

Environmental Research↗

USGS1978

Embryotoxic effects of crude oil in mallard ducks and chicks

Recent studies in this laboratory have revealed that surface applications of microliter amounts of some crude and fuel oils that coat less than 10% of the egg surface reduce hatching considerably in different avian species. Applications of paraffin compounds that coat equal areas of the egg surface do not reduce hatching suggesting that toxicity is due to causes other than asphyxia. In the present study, 1–10 μl of South Louisiana crude oil, an API reference oil, were applied to the surface of fertile mallard ( Anas platyrhynchos ) and chicken ( Gallus gallus ) eggs. Early embryolethality was greater in mallard embryos than in chick embryos, but later embryolethality that coincided with the time of rapid outgrowth of the chorioallantoic membrane was more prevalent in chick embryos. The overall incidence of embryolethality was similar in both species. Retardation of growth as reflected by embryonic body weight, crown-rump length, beak length, and general appearance was more pronounced in chick than mallard embryos. Teratogenic defects were more frequent in chick embryos, and incomplete or abnormal ossification of the skull was the most common. External application of equivalent amounts of a mixture of paraffin compounds present in crude oil had virtually no embryotoxic effects in either species, suggesting that other components including aromatic hydrocarbons and organometallics may cause the embryotoxicity.

Toxicology and Applied Pharmacology↗