From air to clothing: characterizing the accumulation of semi-volatile organic compounds to fabrics in indoor environments.

Uptake kinetics of semi-volatile organic compounds (SVOCs) present indoors, namely phthalates and halogenated flame retardants (HFRs), were characterized for cellulose-based cotton and rayon fabrics. Cotton and rayon showed similar accumulation of gas- and particle-phase SVOCs, when normalized to planar surface area. Accumulation was 3-10 times greater by rayon than cotton, when normalized to Brunauer-Emmett-Teller (BET) specific surface area which suggests that cotton could have a longer linear uptake phase than rayon. Linear uptake rates of eight consistently detected HFRs over 56 days of 0.35-0.92 m3 /day.dm2 planar surface area and mass transfer coefficients of 1.5-3.8 m/h were statistically similar for cotton and rayon and similar to those for uptake to passive air sampling media. These results suggest air-side controlled uptake and that, on average, 2 m2 of clothing typically worn by a person would sequester the equivalent of the chemical content in 100 m3 of air per day. Distribution coefficients between fabric and air (K') ranged from 6.5 to 7.7 (log K') and were within the range of partition coefficients measured for selected phthalates as reported in the literature. The distribution coefficients were similar for low molecular weight HFRs, and up to two orders of magnitude lower than the equilibrium partition coefficients estimated using the COSMO-RS model. Based on the COSMO-RS model, time to reach 95% of equilibrium for PBDEs between fabric and gas-phase compounds ranged from 0.1 to >10 years for low to high molecular weight HFRs.

Can myocardial infarction be rapidly identified in emergency department patients who have left bundle-branch block?

STUDY OBJECTIVES: Fibrinolytic therapy is recommended for patients who have chest pain and left bundle-branch block (LBBB). However, the presence of baseline ECG abnormalities makes early accurate identification of acute myocardial infarction (AMI) difficult. The predictive ability of clinical and ECG variables for identifying patients with LBBB and AMI has not been well studied. We sought to determine the prevalence and predictors of myocardial infarction among patients presenting to the emergency department with LBBB on the initial ECG who were evaluated for myocardial infarction. METHODS: All patients presenting to the ED were prospectively risk stratified on the basis of clinical and historical variables. ECGs from patients with LBBB were compared retrospectively with previously published criteria for identification of AMI. The ability of a new LBBB to predict AMI was also determined. RESULTS: Twenty-four (13%) of the 182 patients with LBBB had AMI. Clinical and historical variables were similar in patients with and without AMI. A new LBBB had a sensitivity of 42% and a specificity of 65%. The presence of concordant ST-segment elevation or depression had specificities and positive predictive values of 100%; however, sensitivities were only 8% and 17%, respectively. The best diagnostic criterion was the presence of concordant ST-segment elevation or depression on the ECG or an initially elevated creatine kinase MB (sensitivity, 63%; specificity, 99%). CONCLUSION: ECG criteria for identifying patients with AMI and LBBB identify only a small minority of patients with AMI. Treating all patients with LBBB and chest pain with fibrinolytics would result in treatment of a significant number of patients without AMI.

Effectiveness of excimer laser coronary angioplasty in acute myocardial infarction or in unstable angina pectoris.

This study was conducted to evaluate the feasibility, safety, and acute results of percutaneous excimer laser coronary angioplasty (ELCA) in acute coronary syndromes. Fifty-nine patients were treated with ELCA (308 nm), including 33 patients with unstable angina pectoris (UAP) (35 vessels with 39 lesions) and 26 patients with acute myocardial infarction (AMI) (26 vessels with 29 lesions). In each patient the target lesion had a complex morphology. Overall, 71% of the patients had contraindications for pharmacologic thrombolytic agents or glycoprotein IIb/IIIa receptor antagonists. All patients received adjunct balloon dilation followed by stent implantation in 88% of patients with AMI versus 76% of patients with UAP (p = NS). Quantitative angiography was performed at an independent core laboratory; 86% laser success and 100% procedural success was achieved in the AMI group versus 87% laser success and 97% procedural success in the UAP group (p = NS). In the AMI group, the minimal luminal diameter increased from 0.77 +/- 0.56 to 1.44 +/- 0.47 mm after lasing to a final 2.65 +/- 0.47 mm versus 0.77 +/- 0.38 to 1.35 +/- 0.4 mm after lasing to 2.66 +/- 0.5 mm final in the UAP group. A prelaser percent stenosis of 76 +/- 17% for the AMI group versus 70 +/- 16% for the UAP group (p = NS) was decreased after lasing to 52 +/- 16% for the AMI group versus 51 +/- 14% for the UAP group (p = NS) and to a final stenosis of 15 +/- 17% for the AMI group versus 12 +/- 15% for the UAP group (p = NS). A 96% laser-induced reduction of thrombus burden area was achieved in the AMI group versus 97% in the UAP group (p = NS). Preprocedure Thrombolysis In Myocardial Infarction flow of 1.3 +/- 0.9 in the AMI group versus 2.3 +/- 1.2 for the UAP group (p = 0.01) increased to a final flow of 3.0 +/- 0 for the AMI group versus 3.0 +/- 0 for the UAP group (p = NS). There were no deaths, cerebrovascular accident, emergency bypass surgery, acute closure, major perforation or major dissection, distal embolization, or bleeding complications in either group. One patient with AMI had localized perforation (caused by guidewire) without sequelae and 1 patient with UAP had an abnormal increase in creatine kinase levels. All 59 patients survived the laser procedure, improved clinically, and were discharged. Thus, early experience in patients with acute coronary syndromes suggest that percutaneous ELCA is feasible and safe.

Effects of erythromycin or rifampin on losartan pharmacokinetics in healthy volunteers.

BACKGROUND: Losartan is metabolized by CYP2C9 and CYP3A4 to an active metabolite, E3174, which has greater antihypertensive activity than the parent compound. Coadministered drugs that inhibit or induce metabolic processes may therefore alter the pharmacokinetics and pharmacologic response of losartan and E3174. OBJECTIVE AND METHODS: Ten healthy volunteers were studied to assess the effects of CYP3A4 inhibition and nonspecific P450 enzyme induction on the pharmacokinetics of losartan and E3174. Subjects completed three 1-week phases separated by 6 days: 50 mg losartan every morning, losartan plus 500 mg erythromycin four times a day, and losartan plus 300 mg rifampin (INN, rifampicin) twice a day. On the eighth day of each phase, serial plasma concentrations of losartan and E3174 were obtained over 32 hours and steady-state pharmacokinetics were determined. RESULTS: Rifampin decreased the area under the concentration-time curve from time zero to 24 hours after the dose (AUC[0-24]) of losartan by 35% (349 +/- 246 versus 225 +/- 130; p = 0.0001) and decreased the AUC(0-24) of E3174 by 40% (1336 +/- 445 versus 792 +/- 302; p < 0.005). Losartan oral clearance was increased by 44% (p = 0.0001). The half-life values of both compounds were decreased by 50% (p < 0.005). In contrast, erythromycin did not significantly affect the AUC(0-24) or half-life of either losartan or E3174. CONCLUSIONS: Rifampin is a potent inducer of losartan and E3174 elimination. Given the magnitude of the effect, this interaction is likely to be clinically significant. On the basis of the minimal inhibitory effects observed with erythromycin, CYP3A4 appears to play a minor role in the in vivo metabolism of losartan to E3174. Further studies are needed to define the contribution of other isozymes, particularly CYP2C9, to the pharmacokinetics of losartan and E3174.