Background: Animal models suggest that the cardiovascular effects of air pollution result in part from inflammation caused by proinflammatory mediators originating in the lung. In a human study of the cardiovascular effects of air pollution, we aimed to evaluate the potential association between air pollution levels and the fraction of exhaled nitric oxide (FE NO ), a non-invasive measure of airway inflammation. Methods: Breath samples were collected weekly between September and December 2000 in a community based group of elderly subjects (median age 70.7 years) in Steubenville, Ohio. The samples were analysed for NO. Air pollution levels were measured concurrently at a central site monitor. Results: An increase in the 24 hour average PM 2.5 concentration of 17.7 mg/m 3 was associated with an increase in FE NO of 1.45 ppb (95% CI 0.33 to 2.57) in models adjusted for subject, week of study, day of the week, hour of the day, ambient barometric pressure, temperature, and relative humidity. This represents a change of approximately 15% compared with the mean FE NO in the cohort (9.9 ppb). A significant association was also observed for a 24 hour moving average of ambient NO (0.83 ppb increase, 95% CI 0.26 to 1.40). In two-pollutant models, the magnitude and precision of the PM 2.5 effect was not reduced and the ambient NO effect was no longer significant. The associations between FE NO and PM 2.5 were significantly higher in subjects with a doctor's diagnosis of COPD (p value for interaction = 0.03). Conclusions: Ambient pollution may lead to airway inflammation as measured by FE NO . These subclinical inflammatory changes may be an important step in the pathogenesis of the cardiopulmonary effects induced by exposure to air pollution.

Bluefish Pomatomus saltatrix have experienced declines in recruitment and adult abundance along the US East Coast since the mid-1980s. At the onset of winter, young-of-the-year (YOY) bluefish exhibit a multimodal size distribution including larger, spring-spawned fish (spring cohort) and smaller, summer-spawned fish (summer cohort). Declines in the adult stock appear to coincide with declines in recruitment success of the summer cohort. We investigated the hypothesis that poor recruitment success of the summer cohort results from size-selective winter mortality. Winter mesocosm experiments were conducted to examine the effects of cohort of origin (spring vs. summer) and food availability (fed vs. unfed) on winter survival of YOY bluefish. Spring fish entered winter with significantly greater lipid reserves than summer fish. When fed, both cohorts stored lipids during late fall, depleted lipid reserves during winter, and experienced high overwinter survival. When starved, both cohorts mobilized lipids from multiple depots (liver, viscera, white muscle, red muscle, skin) and summer fish experienced starvation mortality ~6 wk prior to spring fish. Although summer fish were more susceptible to winter starvation than spring fish, their starvation endurance (> 90% survival probability after 120 d) appeared more than adequate to survive natural winter conditions. Interestingly, spring fish suffered a brief mortality event during January when water temperatures dropped briefly below 6°C, suggesting that larger individuals are less tolerant of acute cold stress. The remarkable starvation endurance of summer-spawned bluefish, coupled with their capacity for rapid lipid storage during fall and reduced rates of lipid depletion at low temperatures, implies that members of this cohort are physiologically well-equipped to survive their first winter of life. Our findings are inconsistent with the hypothesis that winter starvation accounts for decreased recruitment of the summer cohort to the western Atlantic stock.

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