Mortality of sea lions along the central California coast linked to a toxic diatom bloom.

Over 400 California sea lions (Zalophus californianus) died and many others displayed signs of neurological dysfunction along the central California coast during May and June 1998. A bloom of Pseudo-nitzschia australis (diatom) was observed in the Monterey Bay region during the same period. This bloom was associated with production of domoic acid (DA), a neurotoxin that was also detected in planktivorous fish, including the northern anchovy (Engraulis mordax), and in sea lion body fluids. These and other concurrent observations demonstrate the trophic transfer of DA resulting in marine mammal mortality. In contrast to fish, blue mussels (Mytilus edulus) collected during the DA outbreak contained no DA or only trace amounts. Such findings reveal that monitoring of mussel toxicity alone does not necessarily provide adequate warning of DA entering the food web at levels sufficient to harm marine wildlife and perhaps humans.

Effects of sulfur dioxide or ammonium sulfate exposure, alone or combined, for 4 or 8 months on normal and elastase-impaired rats.

Normal and lung-impaired rats were compared after exposure to SO2 and/or (NH4)2SO4 for 4 or 8 months, or for 8 months plus 3 months recovery. Young adult male Sprague-Dawley rats were pretreated intratracheally with either physiologic saline (normal lungs) or porcine pancreatic elastase (impaired lungs). Rats from each pretreatment group were exposed to filtered air (control), to SO2 (1 ppm) or (NH4)2SO4 (0.5 mg/m3), or to combined SO2 + (NH4)2SO4 for 5 hr/day, 5 days/week. Morphologic, physiologic, and immunologic criteria were evaluated. At 4 months cellular immunologic responsiveness was not impaired, but physiologic changes were detected. Morphologic changes were apparent in all time periods. Elastase-induced changes included greater lung volumes, emphysema, and alveolar interstitial fibrosis. Pollutant effects included bronchiolar epithelial hyperplasia and changes in alveolar mean chord length (MCL). Relative to controls, bronchiolar epithelial hyperplasia and MCL increased in saline/pollutant groups, but decreased in elastase/pollutant rats at 4 months. The pretreatment/pollutant interaction was not observed at 8 months. Elastase effects persisted throughout the recovery period. Pollutant effects were more transitory, although alveolar septal fibrosis was greater in saline/(NH4)2SO4 rats at 8 months. Pulmonary function changes associated with elastase included increases in residual volume, functional residual capacity, and the residual volume/total lung capacity ratios. The alveolar plateau of single-breath washout (N2 slope) was significantly steeper in elastase-treated rats but less steep in animals exposed to SO2 or to (NH4)2SO4 than in those exposed to air only.

Pulmonary function in elastase-treated guinea pigs and rats exposed to ammonium sulfate or ammonium nitrate aerosols.

Three weeks following intratracheal instillations of elastase dissolved in saline, or saline alone, guinea pigs and rats were exposed for 5 or 20 days, 6 hr/day, 5 days/week to filtered room air, 1 mg/m3 ammonium sulfate [NH4)2SO4) or 1 mg/m3 ammonium nitrate (NH4NO3) aerosols. Pulmonary function evaluations conducted in guinea pigs showed no detrimental effects of (NH4)2SO4 or NH4NO3 exposure and very little effect of elastase treatment. Lung function changes in elastase-treated rats were consistent with a condition of experimentally induced pulmonary emphysema. Rats exposed to NH4NO3 aerosols showed no consistent exposure-related changes. Compared with air-exposed animals, rats exposed to (NH4)2SO4 aerosols had increased values of residual volume and functional residual capacity and decreased slope of single-breath N2 washout curves. We conclude that elastase treatment had no significant effect on lung function changes resulting from inhalation of (NH4)2SO4 aerosols. Lung function was more affected by (NH4)2SO4 exposure than by NH4NO3 exposure, and lung function changes were more pronounced in rats than in guinea pigs.

Experimental pulmonary emphysema induced in the rat by intratracheally administered elastase: morphogenesis.

Emphysema was produced experimentally in rats by administration of porcine pancreatic elastase at dose levels of 75, 100, 125, and 150 units elastase activity/100 g body wt. All doses studied were equally effective in producing emphysema. Dose levels of over 75 units activity/100 g offered no advantage in terms of degree or severity of emphysema produced; however, such doses exacerbated hemorrhage and edema, resulting in relatively high post-instillation mortality. Lesion morphogenesis at all doses tested paralleled those described in this and in other species by other investigators. The 75-unit activity produced a quantifiable degree of emphysema which was relatively constant among animals. Results suggest that because of group differences in susceptibility to elastase (or variations in batches of elastase), dose-range studies should be performed on each new group of animals.

Pulmonary toxicity of inhaled coal liquid aerosols (boiling range 230-450 degrees C).

The biological activity of materials produced in the direct liquefaction of coal is being assessed by a variety of test systems. In this study, the pulmonary toxicity of process solvent (PS) from the solvent refined coal-I (SRC-I) process was determined by histamine aerosol challenge tests and pulmonary function and morphologic evaluations. Guinea pigs inhaled aerosols of PS (boiling range, 230 to 450 degrees C) for 6 hr/day, 5 day/week, for up to 12 days in three different experiments. In the first experiment, 8-week-old animals inhaled 0 (controls), 0.15, or 0.60 mg/liter PS aerosols with a mass median aerodynamic diameter (MMAD) of 1.3 micrometer. Exposure to 0.15 mg/liter PS for 12 days resulted in depressed weight gain and marked hypersensitivity to inhaled histamine compared with sham-exposed control animals. Four of five animals exposed to 0.6 mg/liter PS died of respiratory failure during exposure. During the second experiment, 14-week-old animals inhaled 0 (controls) or 0.19 mg/liter PS (MMAD, 1.3 microns) for 1, 3, or 12 days. Hypersensitivity to aerosolized histamine occurred only after 12 days exposure to PS aerosols. At that time, morphologic lung evaluations showed mild to moderate pneumonitis and accumulation of exudate in bronchioles of PS-exposed animals. In the third experiment, pulmonary function evaluations were conducted on 4-week-old animals exposed to 0 (controls) or 0.19 mg/liter PS for 8 days. Functional changes measured in these animals (compared to controls) included increased gas trapping at low lung volumes, decreased quasi-static compliance, and decreased diffusion capacity of the lung for carbon monoxide. These studies showed that measurable changes in lung function were produced in guinea pigs after 8 to 12 days exposure to 0.15 or 0.19 mg/liter PS and that exposure to PS affected weight gain only in younger animals (4 and 8 weeks old) but not in 14-week-old animals.

Clinical and pathological effects of cigarette smoke exposure in beagle dogs.

To compare the clinical and pathological effects of high and low nicotine cigarette smoke 12 young adult male beagles were separated into four equal groups and exposed to smoke from high (4.6 mg) or low (1.4 mg) nicotine cigarettes, administered in six or 12 cigarettes per day. Two control groups, sham-exposed and nontracheostomized, consisted of three dogs each. The dogs were exposed seven days per week for five months. Tracheobronchitis developed in smoke-exposed dogs; gross lesions were generally confined to the lungs and tracheobronchial lymph nodes. Histopathological changes were found in all smoke-exposed dogs, with slightly more severe or extensive lesions in the dogs exposed to 12 cigarettes per day. The incidence and severity of rhinitis, turbinate basal epithelial cell hyperplasia, and squamous metaplasia were increased among dogs in the high nicotine cigarette groups.