Measurements of extinct fission products in nuclear bomb debris: Determination of the yield of the Trinity nuclear test 70 y later.

This paper describes an approach to measuring extinct fission products that would allow for the characterization of a nuclear test at any time. The isotopic composition of molybdenum in five samples of glassy debris from the 1945 Trinity nuclear test has been measured. Nonnatural molybdenum isotopic compositions were observed, reflecting an input from the decay of the short-lived fission products (95)Zr and (97)Zr. By measuring both the perturbation of the (95)Mo/(96)Mo and (97)Mo/(96)Mo isotopic ratios and the total amount of molybdenum in the Trinity nuclear debris samples, it is possible to calculate the original concentrations of the (95)Zr and (97)Zr isotopes formed in the nuclear detonation. Together with a determination of the amount of plutonium in the debris, these measurements of extinct fission products allow for new estimates of the efficiency and yield of the historic Trinity test.

Inhaled diesel engine emissions reduce bacterial clearance and exacerbate lung disease to Pseudomonas aeruginosa infection in vivo.

Despite experimental evidence supporting an adverse role for air pollution in models of human disease, little has been done in the way of assessing the health effects of inhalation of whole mixtures from defined sources at exposure levels relevant to ambient environmental exposures. The current study assessed the impact of inhaled diesel engine emissions (DEE) in modulating clearance of Pseudomonas aeruginosa (P.a.) and the adverse effects of infection to the pulmonary epithelium. At DEE concentrations representing from high ambient to high occupational exposures, mice were exposed to DEE continuously for one week or six months (6 h/day), and subsequently infected with P.a. by intratracheal instillation. At 18 h following P.a. infection, prior exposure to DEE impaired bacterial clearance and exacerbated lung histopathology during infection. To assess the airway epithelial cell changes indicative of lung pathogenesis, markers of specific lung epithelial cell populations were analyzed by immunohistochemistry. Both ciliated and non-ciliated airway epithelial cell numbers were decreased during P.a. infection by DEE exposure in a concentration-dependent manner. Furthermore, the lung transcription regulator, thyroid transcription factor 1 (TTF-1), was also decreased during P.a. infection by prior exposure to DEE concordant with changes in airway populations. These findings are consistent with the notion that environmental levels of DEE can decrease the clearance of P.a. and increase lung pathogenesis during pulmonary bacterial infection.

Increased susceptibility to RSV infection by exposure to inhaled diesel engine emissions.

Although epidemiologic data strongly suggest a role for inhaled environmental pollutants in modulating the susceptibility to respiratory infection in humans, the underlying cellular and molecular mechanisms have not been well studied in experimental systems. The current study assessed the impact of inhaled diesel engine emissions (DEE) on the host response in vivo to a common pediatric respiratory pathogen, respiratory syncytial virus (RSV). Using a relatively resistant mouse model of RSV infection, prior exposure to either 30 microg/m3 particulate matter (PM) or 1,000 microg/m3 PM of inhaled DEE (6 h/d for seven consecutive days) increased lung inflammation to RSV infection as compared with air-exposed RSV-infected C57Bl/6 mice. Inflammatory cells in bronchoalveolar lavage fluid were increased in a dose-dependent manner with regard to the level of DEE exposure, concomitant with increased levels of inflammatory mediators. Lung histology analysis indicated pronounced peribronchial and peribronchiolar inflammation concordant with the level of DEE exposure during infection. Mucous cell metaplasia was markedly increased in the airway epithelium of DEE-exposed mice following RSV infection. Interestingly, both airway and alveolar host defense and immunomodulatory proteins were attenuated during RSV infection by prior DEE exposure. DEE-induced changes in inflammatory and lung epithelial responses to infection were associated with increased RSV gene expression in the lungs following DEE exposure. These findings are consistent with the concept that DEE exposure modulates the lung host defense to respiratory viral infections and may alter the susceptibility to respiratory infections leading to increased lung disease.