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Responsive survey design is a technique aimed at improving the efficiency or quality of surveys by using incoming data from the field to make design changes. The technique was pioneered on large national surveys, but the tools can also be applied on the smaller-scale surveys most commonly used by sociologists. We demonstrate responsive survey design in a small-scale, list-based sample survey of students on the topic of sexual misconduct. We investigate the impact of individual incentive levels and a two-phase responsive design with changes to mode of contact as approaches for limiting the potential of nonresponse bias in data from such surveys. Our analyses demonstrate that a two-phase design introducing telephone and face-to-face reminders to complete the survey can produce stronger change in response rates and characteristics of those who respond than higher incentive levels. These findings offer tools for sociologists designing smaller-scale surveys of special populations or sensitive topics.

BACKGROUND: Exposure to fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] is linked to adverse cardiopulmonary health effects; however, the responsible constituents are not well defined. OBJECTIVE: We used a rat model to investigate linkages between cardiac effects of concentrated ambient particle (CAP) constituents and source factors using a unique, highly time-resolved data set. METHODS: Spontaneously hypertensive rats inhaled Detroit Michigan, CAPs during summer or winter (2005]2006) for 13 consecutive days. Electrocardiogram data were recorded continuously, and heart rate (HR) and heart rate variability (HRV) metrics were derived. Extensive CAP characterization, including use of a Semicontinuous Elements in Aerosol Sampler (SEAS), was performed, and positive matrix factorization was applied to investigate source factors. RESULTS: Mean CAP exposure concentrations were 518 μg/m3 and 357 μg/m3 in the summer and winter, respectively. Significant reductions in the standard deviation of the normal-to-normal intervals (SDNN) in the summer were strongly associated with cement/lime, iron/steel, and gasoline/diesel factors, whereas associations with the sludge factor and components were less consistent. In winter, increases in HR were associated with a refinery factor and its components. CAP-associated HR decreases in winter were linked to sludge incineration, cement/lime, and coal/secondary sulfate factors and most of their associated components. Specific relationships for increased root mean square of the standard deviation of successive normal-to-normal intervals (RMSSD) in winter were difficult to determine because of lack of consistency between factors and associated constituents. CONCLUSIONS: Our results indicate that specific modulation of cardiac function in Detroit was most strongly linked to local industrial sources. Findings also highlight the need to consider both factor analytical results and component-specific results when interpreting findings. [ABSTRACT FROM AUTHOR]

Toxicological effects have been observed in rats exposed to concentrated ambient particles (CAPs) from different regions of the United States. The objective of this study was to evaluate the cardiopulmonary and systemic effects of CAPs in Detroit. The authors stationed a mobile concentrator at a location near major traffic and industrial sources. Spontaneously hypertensive (SH) and Wistar-Kyoto (WKY) rats were exposed to fine CAPs (diameter < 0.1–2.5 μm) 8 h/day for 13 consecutive days. Animals were implanted with telemeters, and electrocardiogram data were recorded continuously. Bronchoalveolar lavage (BAL) fluid and plasma were analyzed. Comprehensive exposure monitoring was conducted, including CAPs components. CAPs exposure concentrations were 103–918 μg/m3 (mean = 502 μg/m3). The authors found no statistically significant differences in heart rate or SDNN (standard deviation of the normal-to-normal intervals), a measure of heart rate variability, between CAPs-exposed and control rats. The authors found significantly higher levels of C-reactive protein in the serum of CAPs-exposed SH rats compared with air-exposed animals. Protein in BAL fluid was elevated in WKY rats exposed to CAPs. Measurement of trace metals in lung tissue showed elevated concentrations of V, Sb, La, and Ce in CAPs-exposed SH animals versus controls. These elements are generally associated with oil combustion, oil refining, waste incineration, and traffic. Examination of wind rose data from the exposure period confirmed that the predominant wind direction was SSW, the direction of many of the aforementioned sources. These results indicate that ambient particles in Detroit can cause mild pulmonary and systemic changes in rats, and suggest the importance of local PM2.5 sources in these effects. [ABSTRACT FROM AUTHOR]

An inhalation exposure study for particulate matter (PM) investigates links between exposure and observed changes in respiratory function by evaluating the interactions of chemical and physical properties of the PM with physiological mechanisms. Laboratory studies are useful in this regard, but provide limited information because of the difficulty in reproducing real atmospheric PM compositions and processes. To better understand the types of particles to which people are actually exposed in their daily lives, and the human health risks for source-specific PM, a real world assessment of the source-to-receptor pathways for ambient PM is vital. This was accomplished using a unique mobile air research laboratory (AirCARE1) which enables inhalation exposure studies in real-world settings. The overall goal of this study was to determine the effects of concentrated air particulates (CAPs) from 2 different urban atmospheres in Michigan on the lungs of ovalbumin-sensitized rats concurrently challenged with the allergen. Our work demonstrated that short-term (8 hours) exposure to ambient fine particulate matter (aerodynamic diameter ≤ 2.5 μ m; PM2.5) concentrated from 2 different urban atmospheres in Michigan induced distinct allergic responses in the lungs of rats. This paper presents detailed characterization of CAPs and their sources in an effort to define possible associations between the observed health effects and source-specific ambient PM2.5. [ABSTRACT FROM AUTHOR]

A collaborative research study was conducted in order to improve our understanding of the source-to-receptor pathway for ambient fine particulate matter (aerodynamic diameter ≤ 2.5 μ m; PM2.5) and subsequently to investigate the identity and sources of toxic components in PM2.5 responsible for adverse health effects in allergic humans. This research used a Harvard fine particle concentrator to expose Brown Norway rats, with and without ovalbumin-induced allergic airway disease, to concentrated air particles (CAPs) generated from ambient air in an urban Detroit community where the pediatric asthma rate was three times higher than the national average. Rats were exposed to CAPs during the exposure periods in July (mean = 676 μg/m3) and September (313 μg/m3) of 2000. Twenty-four hours after exposures lung lobes were either lavaged with saline to determine cellularity and protein in bronchoalveolar lavage fluid (BALF), or removed for analysis by inductively coupled plasma–mass spectrometry (ICP-MS) to detect ambient PM2.5-derived trace element retention. PM2.5 trace elements of anthropogenic origin, lanthanum (La), vanadium (V), manganese (Mn), and sulfur (S), were recovered from the lung tissues of CAPs-exposed rats. Recovery of those pulmonary anthropogenic particles was further increased in rats with allergic airways. In addition, eosinophils and protein in BALF were increased only in allergic animals exposed to CAPs. These results demonstrate preferential retention in allergic airways of air particulates derived from identified local combustion sources after a short-term exposure. Our findings suggest that the enhancement of allergic airway responses by exposure to PM2.5 is mediated in part by increased pulmonary deposition and localization of potentially toxic elements in urban air. [ABSTRACT FROM AUTHOR]

Abstract: Recent studies have indicated that the chemical composition of ambient PM2.5, or fine particulate matter (aerodynamic diameter <2.5μm), may be closely associated with the health effects induced by PM. Thus, identification of the sources of these components of PM2.5 is critical to understanding source-specific health risks posed by PM2.5. However, ambient PM measurements are typically 24-h average concentrations, masking the temporal variability of individual sources. These daily samples can limit our understanding of the associations between sources and observed heath effect parameters. In the present study, highly time-resolved sampling methods were utilized to characterize trace element concentrations and to obtain information on potential emission sources impacting a site in urban Detroit where a complex mixture of local point and mobile sources, as well as regional sources, is observed. Positive matrix factorization (PMF) was applied to 117 8-h PM2.5 filter samples from which six major factors were extracted including secondary aerosol, gasoline-powered vehicles, iron and steel manufacturing, diesel-powered vehicles, refining, and sludge incineration. In addition, PMF was applied to 268 30-min PM2.5 samples where six major source factors were identified including secondary aerosol, gasoline- and diesel-powered vehicles, iron and steel manufacturing, refining, sludge incineration, and cement/lime production. Contributions of various emission source factors and peak concentrations for each factor were characterized using detailed meteorology and, factor directionality analysis. Although some variations were observed between the 8-h integrated filter samples and the 30-min SEAS samples, the results from the two datasets are generally consistent, suggesting that 46% and 43% of ambient PM, respectively, is derived from local sources. These findings have advanced our understanding of temporal PM source-receptor relationships in a complex urban air shed. [Copyright &y& Elsevier]

Epidemiological studies have reported that elevated levels of particulate air pollution in urban communities are associated with increases in attacks of asthma based on evidence from hospital admissions and emergency department visits. Principal pathologic features of chronic airway diseases, like asthma, are airway inflammation and mucous hypersecretion with excessive amounts of luminal mucus and increased numbers of mucus-secreting cells in regions of the respiratory tract that normally have few or no mucous cells (ie, mucous cell metaplasia). The overall goal of the present project was to understand the adverse effects of urban air fine particulate matter (PM2.5; < or = 2.5 pm in aerodynamic diameter)* on normal airways and airways compromised with airway inflammation and excess mucus. Our project was specifically designed to (1) examine the chemical and physical characteristics of PM2.5 and other airborne pollutants in the outdoor air of a local Detroit community with a high incidence of childhood asthma; (2) determine the effects of this community-based PM2.5 on the airway epithelium in normal rats and rats compromised with preexisting hypersecretory airway diseases (ie, animal models of human allergic airway disease--asthma and chronic bronchitis); and (3) identify the chemical or physical components of PM2.5 that are responsible for PM2.5 -induced airway inflammation and epithelial alterations in these animal models. Two animal models of airway disease were used to examine the effects of PM2.5 exposure on preexisting hypersecretory airways: neutrophilic airway inflammation induced by endotoxin challenge in F344 rats and eosinophilic airway inflammation induced by ovalbumin (OVA) challenge in BN rats. A mobile air monitoring and exposure laboratory equipped with inhalation exposure chambers for animal toxicology studies, air pollution monitors, and particulate collection devices was used in this investigation. The mobile laboratory was parked in a community in southwestern Detroit during the summer months when particulate air pollution is usually high (July and September 2000). We monitored the outdoor air pollution in this community daily, and exposed normal and compromised rats to concentrated PM2.5 from this local urban atmosphere. Rats in the inhalation studies were exposed for 1 day or for 4 or 5 consecutive days (10 hours/day) to either filtered air (controls) or concentrated ambient particles (CAPs) delivered by a Harvard ambient fine particle concentrator. Rats were killed 24 hours after the end of the exposure. Biochemical, morphometric, and molecular techniques were used to identify airway epithelial and inflammatory responses to CAPs. Lung lobes were also either intratracheally lavaged with saline to determine cellular composition and protein in bronchoalveolar lavage fluid (BALF) or removed for analysis by inductively coupled plasma-mass spectrometry (ICPMS) to detect retention of ambient PM2.5--derived trace elements. The Harvard concentrator effectively concentrated the fine ambient particles from this urban atmosphere (10-30 times) without significantly changing the major physicochemical features of the atmospheric particles. Daily CAPs mass concentrations during the 10-hour exposure period (0800-1800) in July ranged from 16 to 895 microg/m3 and in September ranged from 81 to 755 microg/m3. In general, chemical characteristics of ambient particles were conserved through the concentrator into the exposure chamber. Single or repeated exposures to CAPs did not cause adverse effects in the nasal or pulmonary airways of healthy F344 or BN rats. In addition, CAPs-related toxicity was not observed in F344 rats pretreated with bacterial endotoxin. Variable airway responses to CAPs exposure were observed in BN rats with preexisting allergic airway disease induced by OVA sensitization and challenge. Only OVA-challenged BN rats exposed to CAPs for 5 consecutive days in September 2000 had significant increases in airway mucosubstances and pulmonary inflammation compared to saline-challenged/air-exposed control rats. OVA-challenged BN rats that were repeatedly exposed to CAPs in July 2000 had only minor CAPs-related effects. In only the September 5-day exposure protocol, PM2.5 trace elements of anthropogenic origin (La, V, and S) were recovered from the lung tissues of CAPs-exposed rats. Recovery of these specific trace elements was greatest in rats with OVA-induced allergic airway disease. Additional laboratory experiments using intratracheal instillations of ambient PM2.5 samples were performed to identify bioactive agents in the CAPs to which rats had been exposed in the inhalation exposure component. Because the most pronounced effects of CAPs inhalation were found in BN rats with OVA-induced allergic airways exposed in September, we used ambient PM2.5 samples that were collected on 2 days during the September CAPs inhalation exposures to use for instillation. Ambient PM2.5 samples were collected, fractionated into soluble and insoluble species, and then compared with each other and with total PM2.5 for their effects in healthy BN rats and those with OVA-induced allergic airway disease. Intratracheal instillation of the insoluble fraction of PM2.5 caused mild neutrophilic inflammation in the lungs of healthy rats. However, total PM2.5 or the soluble or insoluble fractions instilled in rats with OVA-induced airway inflammation did not enhance the inflammation or the airway epithelial remodeling that was evident in some of the BN rats exposed to CAPs by inhalation. Therefore, the results from this instillation component did not suggest what fractions of the CAPs may have been responsible for enhancing OVA-induced airway mucosubstances and pulmonary inflammation observed in the inhalation exposure component. In summary, inhaled CAPs-related pulmonary alterations in the affected OVA-challenged rats appeared to be related to the chemical composition, rather than the mass concentration, to which the animals were exposed. Results of the trace element analysis in the lungs of CAPs-exposed BN rats exposed in September suggested that air particles derived from identified local combustion sources were preferentially retained in allergic airways. These results demonstrate that short-term exposures to CAPs from this southwestern Detroit community caused variable responses in laboratory rats and suggest that adverse biological responses to ambient PM2.5 may be associated more closely with local sources of particles and weather patterns than with particle mass.