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P. N. Klein

Publications and source records attributed to P. N. Klein.

9 recordsLinked to original sources
USGS2006

Chlorfenapyr and mallard ducks: Overview, study design, macroscopic effects, and analytical chemistry

The first commercial pesticide derived from a class of compounds known as halogenated pyrroles was registered for use in the United States in 2001. Chlorfenapyr degrades slowly in soil, sediment, and water and is highly toxic to birds. Information on biochemical or histological endpoints in birds is lacking; therefore, a two‐year study was conducted to provide information needed to develop diagnostic criteria for chlorfenapyr toxicosis. In the first year, male mallard ducks were fed concentrations of 0, 2, 5, or 10 ppm technical chlorfenapyr or 5 ppm of a formulated product in their diet during a 10‐week chronic exposure study. Survival, body weight, feed consumption (removal), behavior, and molt progression were monitored. Feed and liver were analyzed for chlorfenapyr and two metabolites. Five of 10 ducks in the 10‐ppm group died, and neurotoxic effects were observed in the 5‐and 10‐ppm groups. Feed removal increased for ducks receiving chlorfenapyr and body weights of 5‐ and 10‐ppm ducks were reduced. Loss of body fat, muscle atrophy, and bile retention were suggestive of metabolic disruption or a decreased ability to digest and absorb nutrients. Liver and kidney weights and liver and kidney weight/body weight ratios exhibited a positive response to concentrations of chlorfenapyr in the diet. Emaciation and elevated organ weight/body weight ratios are candidates for a suite of indicators of chronic chlorfenapyr exposure. Liver is the preferred tissue for chemical confirmation of exposure.

Environmental Toxicology and Chemistry↗
USGS1998

Comparative developmental toxicity of planar polychlorinated biphenyl congeners in chickens, American kestrels, and common terns

The effects of polychlorinated biphenyl (PCB) congeners, PCB 126 (3,3′,4,4′,5-pentaCB) and PCB 77 (3,3′4,4′-tetraCB), were examined in chicken ( Gallus gallus ), American kestrel ( Falco sparverius ), and common tern ( Sterna hirundo ) embryos through hatching, following air cell injections on day 4. PCB 126 caused malformations and edema in chickens starting at 0.3 ppb, in kestrels at 2.3 to 23 ppb, but in terns only at levels affecting hatching success (44 ppb). Extent of edema was most severe in chickens and least in terns. Defects of the beak were common in all species but with crossed beak most prevalent in terns. Effects on embryo growth were most apparent for PCB 126 in chickens and kestrels. The approximate 50% lethal dose (LD50) for PCB 126 in chickens was 0.4 ppb, in kestrels was 65 ppb, and in terns was 104 ppb. The approximate LD50 for PCB 77 in chickens was 2.6 ppb and in kestrels was 316 ppb. Induction of cytochrome P450 associated monooxygenase activity (ethoxyresorufin- O -dealkylase activity) by PCB 126 in chick embryo liver was about 800 times more responsive than in tern and at least 1,000 times more responsive than in kestrel. High concentrations of PCB 126 found in bald eagle eggs are nearly 20-fold higher than the lowest toxic concentration tested in kestrels. Concentrations of PCB 126 causing low-level toxic effects in common tern eggs are comparable to highest levels in common terns and Forster's terns in the field, suggesting additional involvement of other compounds in the Great Lakes.

Environmental Toxicology and Chemistry↗
USGS1996

Developmental toxicity of PCB 126 (3,3',4,4',5-pentachlorobiphenyl) in nestling American kestrels (Falco sparverius)

Planar PCB congeners are embryotoxic and teratogenic to birds including American kestrels. The developmental toxicity of 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126) was studied in the posthatching kestrel as a model for the eagle. Nestlings were dosed orally for 10 days with 5 μl/g body weight of corn oil (controls) or the planar PCB 126 at concentrations of 50, 250, or 1000 ng/g body weight. Dosing with 50 ng/g of PCB 126 resulted in a hepatic concentration of 156 ng/g wet weight, liver enlargement and mild coagulative necrosis, over 10-fold increases in hepatic microsomal ethoxyresorufin- O -dealkylase and benzyloxyresorufin- O -dealkylase, and approximately a 5-fold increase in methoxyresorufin- O -dealkylase. At this dose, mild to moderate lymphoid depletion of the spleen was apparent, as were decreased follicle size and content of the thyroid. At 250 ng/g, concentration of PCB 126 in the liver was 380 ng/g with increasing multifocal coagulative necrosis, decreased bone growth, decreased spleen weight with lymphocyte depletion of the spleen and bursa, and degenerative lesions of the thyroid. At 1000 ng/g, the liver concentration was 1098 ng/g, accompanied by decreased bursa weight, decreased hepatic thiol concentration, and increased plasma enzyme activities (ALT, AST, and LDH-L) in addition to the previous effects. Highly significant positive correlations were noted between liver concentrations of PCB 126 and the ratio of oxidized to reduced glutathone. These findings indicate that nestling kestrels are more susceptible to PCB 126 toxicity than adults, but less sensitive than embryos, and that planar PCBs are of potential hazard to nestling birds..

Fundamental and Applied Toxicology↗