Particulate matter and manganese exposures in Indianapolis, Indiana.

The distribution of PM(2.5) and manganese (Mn) personal exposures was determined over a 4-month period in Indianapolis, IN, at a time when the gasoline additive, methylcyclopentadienyl manganese tricarbonyl (MMT), was not being used. The data collection period coincided with the data collection period in the Toronto, ON, study, where MMT had been used as a gasoline additive for over 20 years. The inferential or target population consisted of noninstitutionalized residents of the Indianapolis area during the monitoring period (from May 1996 through August 1996) who were at least 16 years old. The survey instruments used in this study (and also in Toronto) included a household screener form (HSF), a study questionnaire (SQ), and a time and activity questionnaire (TAQ). The SQ was administered to elicit information about the participant and his/her activities, occupation, and surroundings that might be relevant to his/her exposure to particles and Mn. In addition to the personal particulate matter (PM) and elemental 3-day monitoring, 240 participants completed a TAQ on a daily basis during the actual monitoring period. Also, a subset of participants had 3-day outdoor and indoor stationary monitoring at their home (approximately 58 observations), and sampling was conducted at a fixed site (approximately thirty-three 3-day observations). The quality of data was assessed and compared to the Toronto study in terms of linearity of measurement, instrument and method sensitivity, measurement biases, and measurement reproducibility. Twenty-six of the sample filters were subjected to two analyses to characterize the within-laboratory component of precision in terms of relative standard deviations (RSDs). The median RSD for Mn was 8.7%, as compared to 2.2% for Toronto. The quality assurance (QA) laboratory exhibited a clear positive bias relative to the primary laboratory for Al and Ca, but no systematic difference was evident for Mn. A high interlaboratory correlation (>0.99) was also attained for Mn. Mean field blank results for PM and Mn were 0.87 microg/m(3) and 0.71 ng/m(3), respectively, which were comparable to the Toronto study. The median RSDs for colocated fixed site and residential samples ranged from 2.2% to 9.0% for PM and from 8.8% to 15.3% for Mn, which were close to those observed in Toronto. For the PM(10), the 90th percentile indoors was 124 microg/m(3) compared with 54 microg/m(3) outdoors. This pattern was even more pronounced for the PM(2.5) data (90th percentiles of 92 microg/m(3) indoors vs 30 microg/m(3) outdoors). Personal PM(2.5) was somewhat higher than the indoor levels, but the percentiles seemed to follow the more highly skewed pattern of the indoor distribution. This difference was largely due to the presence of some smokers in the sample; e.g., exclusion of smokers led to a personal exposure distribution that was more similar to the outdoor distribution. The estimated 90th percentile for the nonsmokers' personal exposures to PM was 43 microg/m(3) compared with 84 microg/m(3) for the overall population. In general, the Indianapolis PM levels of a given type and cut size were somewhat higher than the levels observed in Toronto, e.g., the median and 90th percentile for the personal PM(2.5) exposures were 23 and 85 microg/m(3), respectively, in Indianapolis, while in Toronto, the corresponding percentiles were 19 and 63 microg/m(3). The cities' distributions of the proportion of the PM(10) mass in the 2.5-microm fraction appeared similar for the residential outdoor data (medians of 0.67 and 0.65 for Indianapolis and Toronto, respectively, and 90th percentiles of 0.83 for both cities). For the indoor data, Indianapolis tended to have a larger portion of the mass in the fine fraction (median of 0.80 compared to 0.70 for Toronto). Unlike the PM, the Indianapolis indoor Mn concentration levels were substantially lower than the outdoor levels for both PM sizes, and the median personal levels for Mn in PM(2.5) appeared to fall between the median indoor and outdoor levels. The personal Mn exposure distributions exhibited more skewness than the indoor or outdoor distributions (e.g., the means for the personal, indoor, and outdoor distributions were 7.5, 2.6, and 3.5 ng/m(3), respectively, while the medians were 2.8, 2.2, and 3.2 ng/m(3), respectively). At least a substantial portion of the high end of the personal exposure distribution appeared to be associated with occupational exposures to Mn. In general, the Mn levels in both cut sizes in Indianapolis were approximately 5 ng/m(3) smaller than those in Toronto (e.g., the estimated median and mean levels for personal Mn exposures in PM(2.5) were 2.8 and 7.5 ng/m(3), respectively, in Indianapolis, but were 8.0 and 13.1 ng/m(3) in Toronto). For the nonoccupational subgroups with no exposure to smoking and no subway riders in the two cities, the medians (2.6 ng/m(3) in Indianapolis and 7.8 ng/m(3) in Toronto) were similar to those for the overall populations, but the means were substantially smaller (3.1 ng/m(3) in Indianapolis and 9.2 ng/m(3) in Toronto). The median proportion of Mn in the fine fraction (relative to the PM(10) Mn) for Indianapolis was 0.39 for outdoors and 0.55 for indoors; these ratios were somewhat smaller than the corresponding Toronto medians (0.52 and 0.73). The study found high correlations for particulates and Mn between personal exposures and indoor concentrations, and between outdoor and fixed site concentrations, and low correlations of personal and indoor levels with outdoor and fixed site levels. The pattern was similar to that observed for Toronto, but slightly more pronounced. The PM(10) Mn concentrations (log scale) generally exhibited stronger associations among these various measures than the PM(2.5) Mn concentrations. Comparisons of the particulate distributions between PTEAM (Riverside, CA) and the Indianapolis and Toronto studies were also made.

Sample design, sampling weights, imputation, and variance estimation in the 1995 National Survey of Family Growth.

OBJECTIVES: Cycle 5 of the National Survey of Family Growth (NSFG) was conducted by the National Center for Health Statistics (NCHS) in 1995. The NSFG collects data on pregnancy, childbearing, and women's health from a national sample of women 15-44 years of age. This report describes how the sample was designed, shows response rates for various subgroups of women, describes how the sampling weights were computed to make national estimates possible, shows how missing data were imputed for a limited set of key variables, and describes the proper ways to estimate sampling errors from the NSFG. The report includes both nontechnical summaries for readers who need only general information and more technical detail for readers who need an in-depth understanding of these topics. METHODS: The 1995 NSFG was based on a national probability sample of women 15-44 years of age in the United States and was drawn from 14,000 households interviewed in the 1993 National Health Interview Survey (NHIS). Of the 13,795 women eligible for the NSFG, 10,847 (79 percent) gave complete interviews. RESULTS: This report recommends using weighted data for analysis and a software package that will estimate sampling errors from complex samples (for example, SUDAAN or comparable software). The rate of missing data in the 1995 NSFG was very low. However, missing data were imputed for 315 key variables, called "recodes." Of the 315 recodes defined for Cycle 5, 271 variables had missing data on less than 1 percent of the cases; only 44 had 1 percent or more with missing data. These missing values were imputed for all of these 315 variables. The imputation procedures are described in this report.

Regulation of the raffinose permease of Escherichia coli by the glucose-specific enzyme IIA of the phosphoenolpyruvate:sugar phosphotransferase system.

In enteric bacteria, chromosomally encoded permeases specific for lactose, maltose, and melibiose are allosterically regulated by the glucose-specific enzyme IIA of the phosphotransferase system. We here demonstrate that the plasmid-encoded raffinose permease of enteric bacteria is similarly subject to this type of inhibition.

Victims of crime: the internist's role in treatment.

This article reports a case study on a crime victim identified and treated in an internal medicine residency program. Recent findings on crime and violence in the United States are reviewed with a particular focus on the psychologic and medical aftermath faced by victims. A unique role for the internist is suggested in the management of such sequelae. Research studies suggest that victims of crime, especially violent crime, evidence one or more of several clusters of acute and delayed emotional responses that typically progress through three stages of a recovery process. Physician awareness of these symptom clusters should result in increased understanding and improved assessment/treatment of crime victims.

Tissue plasminogen activator as an alternative to vena cava interruption in recurrent pulmonary thromboembolism.

We have described a woman with pulmonary thromboembolism (PTE) who had acute dyspnea, chest pain, and hypotension during adequate heparin therapy. Pulmonary angiography was consistent with recurrent PTE. The patient was given intravenous TPA and showed significant improvement. Repeat angiography showed resolution of the thrombus in the right main pulmonary artery. The patient did not require vena cava interruption.

Lysis of growing yeast-form cells of Candida albicans by echinocandin: a cytological study.

Yeast form cells of Candida albicans 6406 were treated with echinocandin, a new antifungal agent, which, in the absence of osmotic protection, provoked the lysis of exponentially growing cells. Lysis did not occur in stationary-phase cells and when protein synthesis was blocked. In intact cells, the synthesis of glucan, but not other important wall components, was partially inhibited. A cytological study of the effects of echinocandin at lytic doses (3.0 microgram ml-1) on osmotically protected yeast cells revealed a substantial thinning of the bud cell wall and derangement of its constitutive layers within 5-10 min, showing that the balance of wall growth was quickly and critically affected by the drug. Associated with this effect, a number of membranous bodies of myelin-like appearance were often seen in close proximity to the plasmamembrane of the emerging bud. Later during treatment (15 min onwards) membranous, convoluted bodies were detected in the nuclear and other intracytoplasmic membranes. Subsequent lytic events, unevenly distributed in cell population, eventually brought about complete lysis of the cell cytoplasmic structure. These results suggest that echinocandin may block a biosynthetic step during wall construction, or that it could alter wall metabolism as a result of a primary interaction with membranes.

Characteristics of Staphylococcus aureus associated with lysogenic conversion to loss of beta-hemolysin production.

Staphylococcus aureus strains 7-8 and 57 that produce beta-hemolysin but not staphylokinase (beta + K-) were lysogenically converted by certain serological group F bacteriophages to the loss of beta-hemolysin production and the gain in staphylokinase production (beta-K+). Serological group A phage 42E was found to convert S. aureus strains 7-8(beta-K-) and 57 (beta + K-) to beta - K-. Conversion of beta-hemolysin by lysogenization of a serological group A phage has not previously been reported. Phage 42E conversions differed from the group F conversions since staphylokinase was not affected. This indicates that conversion to beta-K+ involves separate loci on the phage chromosome. Several characteristics associated with virulence of staphylococci of human or animal origin other than staju;plomase production (coagulase, DNase, lipase, gelatinase, mannitol fermentation, and phage-sensitivity patterns) were not correlated with lysogenic conversions to loss of beta-hemolysin.