Ontogeny of decapod crustacean hemocyanin: effects of temperature and nutrition.

Hemocyanin is present throughout the decapod crustacean's life, usually as one-hexamer and two-hexamer oligomers. Hemocyanins of some decapod crustaceans undergo changes in subunit composition and oxygen affinity during development. Maternal hemocyanin is taken up from the hemolymph via endocytosis by the oocyte. Embryo hemocyanin differs in subunit composition from hemocyanin of oocyte and adult crab and may represent the onset of hemocyanin synthesis. Complex changes in expression of hemocyanin subunits occur through megalopa and early juvenile stages of the crab Cancer magister, culminating in the pattern of adult hemocyanin. The influences of food availability and temperature on development, growth and hemocyanin ontogeny in early juvenile C. magister have been studied. Crabs were raised in warm or cold sea water and fed high or low levels of food for 6 months. While intermolt period was shorter in crabs fed high food levels, especially those raised in warm water, crabs reared in cold water with high food levels attained the largest sizes. Thus increased food availability affects growth more than increased temperature. Adult hemocyanin appeared at about the same number of weeks after the start of the experiment for crabs in the warm water/high food, warm water/low food and cold water/high food groups, even though warm water/low food crabs had molted fewer times. Crabs in the cold water/low food group expressed adult hemocyanin much later than the other groups. Molt stage and maturation from juvenile to adult are not absolutely coupled, and food availability has a greater influence than temperature on hemocyanin ontogeny.

Oxidant and acid aerosol exposure in healthy subjects and subjects with asthma. Part I: Effects of oxidants, combined with sulfuric or nitric acid, on the pulmonary function of adolescents with asthma.

Both peak flow decrements in children at summer camps and increased hospital admissions for asthma have been associated with summer "acid haze," which is composed of ozone and various acidic species. The objective of this study was to investigate the pulmonary effects of acid summer haze in a controlled laboratory setting. Twenty-eight adolescent subjects with allergic asthma, exercise-induced bronchospasm, and a positive response to a standardized methacholine challenge enrolled in the study; 22 completed the study. Each subject inhaled one of four test atmospheres by mouthpiece on two consecutive days. The order of exposure to the four test atmospheres was assigned via a random protocol: air, oxidants (0.12 parts per million [ppm]* ozone plus 0.30 ppm nitrogen dioxide), oxidants plus sulfuric acid at 70 micrograms/m3 of air, or oxidants plus 0.05 ppm nitric acid. Exposure to each of the different atmospheres was separated by at least one week. The exposures were carried out during alternating 15-minute periods of rest and moderate exercise for a total exposure period of 90 minutes per day. Pulmonary function was measured before and after exposure on both test days and again on the third day as a follow-up measurement. A postexposure methacholine challenge was performed on Day 3. Low methacholine concentrations were chosen for the postexposure challenge to avoid provoking a response. The protocol was designed to detect subtle changes in airway reactivity. The statistical significance of the pulmonary function values was tested using paired t tests. First, we compared the difference between baseline and postexposure measurements after air exposure on Day 1 with the differences between baseline and postexposure measurements after Day 1 exposure to each of the other three atmospheres. Second, we compared the difference between baseline and postexposure measurements after the Day 2 air exposure with the differences between baseline and postexposure measurements after the Day 2 exposure to each of the pollutant atmospheres. Third, we compared the difference between baseline measurements on Day 1 of each exposure atmosphere with measurements after exposure to the same atmosphere on Day 2 to detect delayed effects. No changes in any of the pulmonary function parameters were statistically significant when compared with changes after clean air exposure. Six subjects left the study because of uncomfortable symptoms associated with the exposures. These all occurred after exposure to pollutant atmospheres and not after exposure to clean air.(ABSTRACT TRUNCATED AT 400 WORDS)

The effects of ozone exposure on lactate dehydrogenase release from human and primate respiratory epithelial cells.

Ozone is the most persistent, wide-spread air pollutant in the United States. Over one half of the population of the US lives in cities or suburban areas which do not meet the National Ambient Air Quality Standard for ozone which is 0.12 ppm averaged over 1 h. Controlled laboratory exposures of human subjects have shown that ozone exposure produces decreased pulmonary function, hyperresponsiveness to inhaled methacholine, inspiratory pain, and airway inflammation as assessed by bronchoalveolar lavage. However, the cellular mechanisms responsible for such effects are incompletely known. The present study examined the effects of ozone exposure at 0.50 ppm for 3 h on three types of cultured respiratory epithelial cells; primary cultures of human nasal cells and primate bronchial cells, and the A549 type II pneumocyte-derived cell line. Cells were grown to confluent monolayers in plastic 6-well plates and then exposed to ozone or filtered air on a tilting platform over a heated water bath. Lactose dehydrogenase release was significantly increased following ozone exposure of all cell types; a 75% increase from human nasal cells (P = 0.0002), a 79% increase from primate bronchial cells (P = 0.003), and a 69% increase from A549 cells (P = 0.02). These data suggest that even brief ozone exposure causes membrane injury to cultured human respiratory epithelial cells.

Pulmonary function changes in children associated with fine particulate matter.

During winter months many neighborhoods in the Seattle metropolitan area are heavily affected by particulate matter from residential wood burning. A study was conducted to investigate the relationship between fine particulate matter and pulmonary function in young children. The subjects were 326 elementary school children, including 24 asthmatics, who lived in an area with high particulate concentrations predominantly from residential wood burning. FEV1 and FVC were measured before, during and after the 1988-1989 and 1989-1990 winter heating seasons. Fine particulate matter was assessed using a light-scattering instrument. Analysis of the relationship between light scattering and lung function indicated that an increase in particulate air pollution was associated with a decline in asthmatic children's pulmonary function. FEV1 and FVC in the asthmatic children dropped an average of 34 and 37 ml respectively for each 10(-4) m-1 increase in sigma sp. This sigma sp increase corresponds to an increase in PM2.5 of 20 micrograms/m3. It is concluded that fine particulate matter from wood burning is significantly associated with acute respiratory irritation in young asthmatic children.

Respiratory effects of inhaled sulfuric acid on senior asthmatics and nonasthmatics.

The objective of this study was two-fold: (1) to investigate the response of asthmatic subjects who were 60 to 75 y of age to inhaled sulfuric acid, and (2) to compare that response to findings from healthy subjects in the same age group. Nine subjects who had asthma and eight healthy subjects participated. Each subject was exposed to clean air, an inert ammonium sulfate aerosol, or 70 micrograms/m3 sulfuric acid during a 40-min exposure period composed of 30 min at rest and 10 min of light exercise on a treadmill. The sulfuric acid was delivered twice, one preceded by a lemonade drink to neutralize oral concentrations of ammonia. Exposures were separated by at least 1 wk. Oral ammonia levels and pulmonary function parameters (forced expiratory volume in one second, forced vital capacity, and total respiratory resistance) were measured before and after each exposure. None of the functional parameters in either group showed significant changes. However, total respiratory resistance changes from baseline after sulfuric acid exposure were significantly higher (+16%) in the asthmatic subjects, compared with the healthy subjects (-6%). These data suggest that older subjects are not at increased risk for adverse respiratory effects from inhalation of sulfuric acid by virtue of age alone, and older subjects with asthma are slightly more vulnerable than are their healthy peers.

Theophylline mitigates the bronchoconstrictor effects of sulfur dioxide in subjects with asthma.

The objective of the study was to investigate the ability of a sustained-release (SR) theophylline tablet (Uniphyl; Purdue Frederick Co., Norwalk, Conn.) to block or mitigate sulfur dioxide (SO2)-induced bronchoconstriction in adult subjects with asthma. Eight subjects participated in a double-blind, crossover study with a 400 mg theophylline tablet or placebo once a day for a week before a 10-minute SO2 challenge. FEV1 and total respiratory resistance (RT) were measured before and after the SO2 challenge and on a different day before and after an air exposure. After exposure to SO2, average values of FEV1 dropped 16% after placebo treatment and 7% after theophylline treatment. The corresponding percentages for RT were a 37% increase after placebo and a 7% increase after theophylline treatment. Analysis of variance demonstrated a significant difference between the SO2-induced decrease in FEV1 and increase in RT after SR theophylline treatment compared with that of placebo treatment. Thus, we conclude that SR theophylline tablets, taken at this concentration for 1 week, mitigate SO2-induced bronchoconstriction.