BACKGROUND

The Centers for Medicare & Medicaid Services (CMS) and Veterans Health Administration (VA) will report 30-day stroke readmission rates as a measure of hospital quality. A national debate on whether social risk factors should be included in models developed for hospital profiling is ongoing.

OBJECTIVE

To compare a CMS-based model of 30-day readmission with a more comprehensive model that includes measures of social risk (such as homelessness) or clinical factors (such as stroke severity and functional status).

DESIGN

Data from a retrospective cohort study were used to develop a CMS-based 30-day readmission model that included age and comorbid conditions based on codes from the International Classification of Diseases, Ninth Revision, Clinical Modification (model 1). This model was then compared with one that included administrative social risk factors (model 2). Finally, the CMS model (model 1) was compared with a model that included social risk and clinical factors from chart review (model 3). These 3 models were used to rank hospitals by 30-day risk-standardized readmission rates and examine facility rankings among the models.

SETTING

Hospitals in the VA.

PARTICIPANTS

Patients hospitalized with stroke in 2007.

MEASUREMENTS

30-day readmission rates.

RESULTS

The 30-day readmission rate was 12.8%. The c-statistics for the 3 models were 0.636, 0.646, and 0.661, respectively. All hospitals were classified as performing "as expected" using all 3 models (that is, performance did not differ from the VA national average); therefore, the addition of detailed clinical information or social risk factors did not alter assessment of facility performance.

LIMITATION

A predominantly male veteran cohort limits the generalizability of these findings.

CONCLUSION

In the VA, more comprehensive models that included social risk and clinical factors did not affect hospital comparisons based on 30-day readmission rates.

PRIMARY FUNDING SOURCE

U.S. Department of Veterans Affairs.

Ozone is an important constituent of ambient air pollution and represents a major public health concern. Oxidative injury due to ozone inhalation causes the generation of reactive oxygen species and can be genotoxic. To determine whether ozone exposure causes genetic damage in peripheral blood lymphocytes, we used a well-validated cytokinesis-block micronucleus Cytome assay. Frequencies of micronuclei (MN) and nucleoplasmic bridges (NB) were used as indicators of cytogenetic damage. Samples were obtained from 22 non-smoking healthy subjects immediately before and 24-hr after controlled 4-hr exposures to filtered air, 100 ppb, and 200 ppb ozone while exercising in a repeated-measure study design. Inhalation of ozone at different exposure levels was associated with a significant dose-dependent increase in MN frequency (P < 0.0001) and in the number of cells with more than one MN per cell (P <  .0005). Inhalation of ozone also caused an increase in the number of apoptotic cells (P = 0.002). Airway neutrophilia was associated with an increase in MN frequency (P = 0.033) independent of the direct effects of ozone exposure (P < 0.0001). We also observed significant increases in both MN and NB frequencies after exercise in filtered air, suggesting that physical activity is also an important inducer of oxidative stress. These results corroborate our previous findings that cytogenetic damage is associated with ozone exposure, and show that damage is dose-dependent. Further study of ozone-induced cytogenetic damage in airway epithelial cells could provide evidence for the role of oxidative injury in lung carcinogenesis, and help to address the potential public health implications of exposures to oxidant environments.