Analysis of Toxic and Essential Elements in the Blood and Feathers of Humboldt Penguins ( Spheniscus humboldti) at Punta San Juan, Peru.

Whole blood, serum, and feather samples from 29 Humboldt Penguins ( Spheniscus humboldti) at the Punta San Juan Marine Protected Area, Peru, were analyzed for 55 toxic and essential elements by using inductively coupled plasma mass spectrometry. Mercury (Hg) was analyzed by cold vapor atomic fluorescence. Maximum Hg concentrations in serum (0.0056 mg/g), whole blood (0.297 mg/kg), and feathers (1.8 mg/kg dry weight) were at levels generally not considered to cause health impairment. Of the elements analyzed, only eight (aluminum, calcium, iron, Hg, potassium, magnesium, sodium, and zinc) were detected in serum. These elements, plus selenium and titanium, were also quantifiable in whole blood. Feather analysis detected quantifiable values for the elements found in serum, plus arsenic, boron, barium, copper, manganese, and titanium. Results indicate this important breeding population of endangered penguins did not appear to be exposed to environmental elemental contaminants at levels detrimental to health and reproductive success. However, identification of measurable concentrations of toxic elements at low levels underscores the need for continued environmental monitoring, particularly in the face of expanding regional human populations and industrial growth. These results provide important reference data for temporospatial monitoring of this and other penguin populations.

ASSESSMENT OF POLYCHLORINATED BIPHENYLS, ORGANOCHLORINE PESTICIDES, AND POLYBROMINATED DIPHENYL ETHERS IN THE BLOOD OF HUMBOLDT PENGUINS ( SPHENISCUS HUMBOLDTI) FROM THE PUNTA SAN JUAN MARINE PROTECTED AREA, PERU.

Persistent organic pollutants were assessed in Humboldt Penguins ( Spheniscus humboldti) from the Punta San Juan Marine Protected Area, Peru, in the austral winter of 2009. Plasma samples from 29 penguins were evaluated for 31 polychlorinated biphenyl (PCB) congeners and 11 organochlorine pesticides (OCPs) by using gas chromatography coupled to an ion trap mass spectrometer and for 15 polybrominated diphenyl ether (PBDE) congeners by using gas chromatography coupled with high-resolution mass spectrometry. The detection rate for PCBs in the samples was 69%, with congeners 105, 118, 180, and 153 most commonly detected. The maximum ΣPCB concentration was 25 ng/g. The detection rate for DDT, DDD, and/or DDE was higher than for other OCP residues (90%; maximum concentration=10 ng/g). The detection rate for PBDEs was 86%, but most concentrations were low (maximum ΣPBDE concentration=3.81 ng/g). This crucial breeding population of S. humboldti was not exposed to contaminants at levels detrimental to health and reproductive success; however, the identified concentrations of legacy and recently emerged toxicants underscore the need for temporal monitoring and diligence to protect this endangered species in the face of regional human population and industrial growth. These results also provide key reference values for spatial comparisons throughout the range of this species.

Carcinogenicity and DNA adduct formation of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and enantiomers of its metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol in F-344 rats.

4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is metabolized to enantiomers of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), found in the urine of virtually all people exposed to tobacco products. We assessed the carcinogenicity in male F-344 rats of (R)-NNAL (5 ppm in drinking water), (S)-NNAL (5 ppm), NNK (5 ppm) and racemic NNAL (10 ppm) and analyzed DNA adduct formation in lung and pancreas of these rats after 10, 30, 50 and 70 weeks of treatment. All test compounds induced a high incidence of lung tumors, both adenomas and carcinomas. NNK and racemic NNAL were most potent; (R)-NNAL and (S)-NNAL had equivalent activity. Metastasis was observed from primary pulmonary carcinomas to the pancreas, particularly in the racemic NNAL group. DNA adducts analyzed were O (2)-[4-(3-pyridyl)-4-oxobut-1-yl]thymidine (O (2)-POB-dThd), 7-[4-(3-pyridyl)-4-oxobut-1-yl]guanine(7-POB-Gua),O (6)-[4-(3-pyridyl)-4-oxobut-1-yl]deoxyguanosine(O (6)-POB-dGuo),the 4-(3-pyridyl)-4-hydroxybut-1-yl(PHB)adductsO (2)-PHB-dThd and 7-PHB-Gua, O (6)-methylguanine (O (6)-Me-Gua) and 4-hydroxy-1-(3-pyridyl)-1-butanone (HPB)-releasing adducts. Adduct levels significantly decreased with time in the lungs of rats treated with NNK. Pulmonary POB-DNA adducts and O (6)-Me-Gua were similar in rats treated with NNK and (S)-NNAL; both were significantly greater than in the (R)-NNAL rats. In contrast, pulmonary PHB-DNA adduct levels were greatest in the rats treated with (R)-NNAL. Total pulmonary DNA adduct levels were similar in (S)-NNAL and (R)-NNAL rats. Similar trends were observed for DNA adducts in the pancreas, but adduct levels were significantly lower than in the lung. The results of this study clearly demonstrate the potent pulmonary carcinogenicity of both enantiomers of NNAL in rats and provide important new information regarding DNA damage by these compounds in lung and pancreas.

(S)-N'-Nitrosonornicotine, a constituent of smokeless tobacco, is a powerful oral cavity carcinogen in rats.

Currently, smokeless tobacco products are being proposed as an alternative mode of tobacco use associated with less harm. All of these products contain the tobacco-specific carcinogen N'-nitrosonornicotine (NNN). The major form of NNN in tobacco products is (S)-NNN, shown in this study to induce a total of 89 benign and malignant oral cavity tumors in a group of 20 male F-344 rats treated chronically with 14 p.p.m. in the drinking water. The opposite enantiomer (R)-NNN was weakly active, but synergistically enhanced the carcinogenicity of (S)-NNN. Thus, (S)-NNN is identified for the first time as a strong oral cavity carcinogen in smokeless tobacco products and should be significantly reduced or removed from these products without delay in order to prevent debilitating and deadly oral cavity cancer in people who use them.

Toxicological effects of the aquatic herbicide, fluridone, on male water mites (Hydrachnidiae: Arrenurus: Megaluracarus).

The acute toxicities for technical grade fluridone (Sonar™) and the commercial formulation of fluridone (Sonar®AS) were assessed for male water mites (Hydrachnidiae: Arrenurus: Megaluracarus). Signs of toxicity were evaluated by detection of locomotor dysfunction or death after exposure to concentrations of 100,000, 10,000, 1,000, and 100 µg/L of Sonar™ and 10,000, 5,000, 1,000, 100, and 10 µg/L of Sonar®AS in US EPA, moderately hard reconstituted water (MHRW). The median effective concentration (EC50) was 891 and 631 µg/L for Sonar™ at 48 and 96 h and less than 10 µg/L for Sonar®AS at 96 h. Increased duration of exposure to Sonar®AS from 48 to 96 h had a significant effect on increasing the rate of combined morbidity and mortality. At the lowest concentration of Sonar®AS tested, which is half the concentration allowed within 400 m of any functioning potable water intake for human usage, 40% of the mites were adversely affected at 48 h and 70% were affected after 96 h of exposure. This study demonstrates that Sonar®AS is 60-fold more toxic to water mites than the active ingredient alone. At currently acceptable application rates of 90-150 µg/L fluridone, the addition of ingredients classified as inert, as in Sonar®AS, result in an increased risk of adverse effects on populations of male water mites (Arrenurus: Megaluracarus) in aquatic ecosystems.