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In the past several decades, a variety of efforts have been made in the United States to improve air quality, and ambient particulate matter (PM) concentrations have been used as a metric to evaluate the efficacy of environmental policies. However, ambient PM concentrations result from a combination of source emission rates and meteorological conditions, which also change over time. Dispersion normalization was recently developed to reduce the influence of atmospheric dispersion and proved an effective approach that enhanced diel/seasonal patterns and thus provides improved source apportionment results for speciated PM mass and particle number concentration (PNC) measurements. In this work, dispersion normalization was incorporated in long-term trend analysis of 11-500 nm PNCs derived from particle number size distributions (PNSDs) measured in Rochester, NY from 2005 to 2019. Before dispersion normalization, a consistent reduction was observed across the measured size range during 2005-2012, while after 2012, the decreasing trends slowed down for accumulation mode PNCs (100-500 nm) and reversed for ultrafine particles (UFPs, 11-100 nm). Through dispersion normalization, we showed that these changes were driven by both emission rates and dispersion. Thus, it is important for future studies to assess the effects of the changing meteorological conditions when evaluating policy effectiveness on controlling PM concentrations. Before and after dispersion normalization, an evident increase in nucleation mode particles was observed during 2015-2019. This increase was possibly enabled by a cleaner atmosphere and will pose new challenges for future source apportionment and accountability studies.

Evidence of the association between long-term exposure to particulate matter (PM) and chronic obstructive pulmonary disease (COPD) mortality from large population-based cohort study is limited and often suffers from residual confounding issues with traditional statistical methods. We hereby assessed the casual relationship between long-term PM (PMA total of 580,757 participants in southern China were enrolled in a prospective cohort study from 2009 to 2015 and followed up until December 2020. Exposures to PM at each residential address were obtained from the Long-term Gap-free High-resolution Air Pollutant Concentration dataset. Marginal structural Cox models were used to investigate the association between COPD mortality and annual average exposure levels of PM exposure.During an average follow-up of 8.0 years, 2250 COPD-related deaths occurred. Under a set of causal inference assumptions, the hazard ratio (HR) for COPD mortality was estimated to be 1.046 (95 % confidence interval: 1.034-1057), 1.037 (1.028-1.047), and 1.032 (1.006-1.058) for each 1-μg/mOur results support causal links between long-term PM exposure and COPD mortality, highlighting the urgency for more effective strategies to reduce PM exposure, with particular attention on protecting potentially vulnerable groups.

Background: Previous work reported increased rates of acute cardiovascular hospitalizations associated with increased PM2.5 concentrations in the previous few days across urban centers in New York State from 2005 to 2016. These relative rates were higher after air quality policies and economic changes resulted in decreased PM2.5 concentrations and changes in PM composition (e.g. increased secondary organic carbon), compared to before and during these changes. Changes in PM composition and sources may explain this difference. Objectives: To estimate the rate of acute cardiovascular hospitalizations associated with increases in source specific PM2.5 concentrations. Methods: Using source apportioned PM2.5 concentrations at the same NYS urban sites, a time-stratified case-crossover design, and conditional logistic regression models adjusting for ambient temperature and relative humidity, we estimated the rate of these acute cardiovascular hospitalizations associated with increases in mean source specific PM2.5 concentrations in the previous 1, 4, and 7 days. Results: Interquartile range (IQR) increases in spark-ignition emissions (GAS) concentrations were associated with increased excess rates of cardiac arrhythmia hospitalizations (2.3%; 95% CI = 0.4%, 4.2%; IQR = 2.56 μg/m3) and ischemic stroke hospitalizations (3.7%; 95% CI = 1.1%, 6.4%; 2. 73 μg/m3) over the next day. IQR increases in diesel (DIE) concentrations were associated with increased rates of congestive heart failure hospitalizations (0.7%; 95% CI = 0.2% 1.3%; 0.51 μg/m3) and ischemic heart disease hospitalizations (0.8%; 95% CI = 0.3%, 1.3%; 0.60 μg/m3) over the next day, as hypothesized. However, secondary sulfate PM2.5 (SS) was not. Increased acute cardiovascular hospitalization rates were also associated with IQR increases in concentrations of road dust (RD), residual oil (RO), and secondary nitrate (SN) over the previous 1, 4, and 7 days, but not other sources. Conclusions: These findings suggest a role of several sources of PM2.5 in New York State (i.e. traffic emissions, non-traffic emissions such as brake and tire wear, residual oil, and nitrate that may also reflect traffic emissions) in the triggering of acute cardiovascular events. Keywords: Cardiovascular hospitalizations, Air pollution, Source apportionment, Traffic emissions

Increased ambient air pollutant concentrations during pregnancy have been associated with reduced birth weight, but the etiologically relevant pregnancy time window(s) is/are unclear. In 76,500 singleton births in Monroe County, NY (2005–2016), who were 37–42 gestational weeks at delivery, we used generalized linear models to regress term birth weight against mean gestational month pollutant concentrations, adjusting for mean temperature, and maternal, infant, and medical service use characteristics. Overall, there were no clear patterns of term birth weight change associated with increased concentrations of any pollutant across gestational months. However, among Hispanic women only, increases in all pollutants, except O3, in multiple gestational months, were associated with decreased term birth weight. Each 3.25 µg/m3 increase in PM2.5 concentration in the 6th gestational month was associated with a −20.4 g (95% CI = −34.0, −6.8) reduction in term birth weight among Hispanic women, but a 4.1 g (95% CI = −2.5, 10.8) increase among non-Hispanic mothers (p for interaction

Phthalate exposure is widespread among pregnant women and may be a risk factor for preterm birth.To investigate the prospective association between urinary biomarkers of phthalates in pregnancy and preterm birth among individuals living in the US.Individual-level data were pooled from 16 preconception and pregnancy studies conducted in the US. Pregnant individuals who delivered between 1983 and 2018 and provided 1 or more urine samples during pregnancy were included.Urinary phthalate metabolites were quantified as biomarkers of phthalate exposure. Concentrations of 11 phthalate metabolites were standardized for urine dilution and mean repeated measurements across pregnancy were calculated.Logistic regression models were used to examine the association between each phthalate metabolite with the odds of preterm birth, defined as less than 37 weeks of gestation at delivery (n = 539). Models pooled data using fixed effects and adjusted for maternal age, race and ethnicity, education, and prepregnancy body mass index. The association between the overall mixture of phthalate metabolites and preterm birth was also examined with logistic regression. G-computation, which requires certain assumptions to be considered causal, was used to estimate the association with hypothetical interventions to reduce the mixture concentrations on preterm birth.The final analytic sample included 6045 participants (mean [SD] age, 29.1 [6.1] years). Overall, 802 individuals (13.3%) were Black, 2323 (38.4%) were Hispanic/Latina, 2576 (42.6%) were White, and 328 (5.4%) had other race and ethnicity (including American Indian/Alaskan Native, Native Hawaiian,1 racial identity, or reported as other). Most phthalate metabolites were detected in more than 96% of participants. Higher odds of preterm birth, ranging from 12% to 16%, were observed in association with an interquartile range increase in urinary concentrations of mono-n-butyl phthalate (odds ratio [OR], 1.12 [95% CI, 0.98-1.27]), mono-isobutyl phthalate (OR, 1.16 [95% CI, 1.00-1.34]), mono(2-ethyl-5-carboxypentyl) phthalate (OR, 1.16 [95% CI, 1.00-1.34]), and mono(3-carboxypropyl) phthalate (OR, 1.14 [95% CI, 1.01-1.29]). Among approximately 90 preterm births per 1000 live births in this study population, hypothetical interventions to reduce the mixture of phthalate metabolite levels by 10%, 30%, and 50% were estimated to prevent 1.8 (95% CI, 0.5-3.1), 5.9 (95% CI, 1.7-9.9), and 11.1 (95% CI, 3.6-18.3) preterm births, respectively.Results from this large US study population suggest that phthalate exposure during pregnancy may be a preventable risk factor for preterm delivery.

Previously, we found short-term increases in ambient particulate matter (PM) air pollutant concentrations were associated with increased serum fibrinogen levels in patients with cardiac disease. We now studied whether high blood levels of omega-3 (ω-3) fatty acids blunted this fibrinogen response to increased PM concentrations in these same patients. Plasma fibrinogen and ω-3 fatty acid levels (% of total identified fatty acids) were measured in blood samples collected from 135 patients treated at the University of Rochester Medical Center for myocardial infarction or stable ischemic heart disease requiring cardiac catheterization. Using ambient measurements of ultrafine, accumulation mode, and fine particles (PM2.5), Delta-C, and black carbon (BC), we regressed serum fibrinogen levels against pollutant concentrations over the previous 1–96 h, using interaction terms to estimate these associations separately for those with HIGH (> 5.12%) and LOWMED serum levels of ω-3 fatty acid (≤ 5.12%). Each 5.6 μg/m3 increase in PM2.5 concentration in the previous hour was associated with a 3.1% increase in fibrinogen (95% CI = 1.5%, 4.7%) in those subjects with LOWMED total ω-3 fatty acid levels, but only a 0.9% increase (95% CI = − 1.5%, 3.2%) in patients with HIGH total ω-3 fatty acid levels. This same pattern was observed with fish oil-derived docosahexaenoic and eicosapentaenoic acids but not alpha-linolenic (from plant oil or seeds). A similar finding was observed with BC in the prior 24 h, but not other PM. Thus, increased blood levels of fish-based ω-3 fatty acids attenuated increases in fibrinogen associated with short-term increases in ambient PM. Electronic supplementary material The online version of this article (10.1007/s11869-018-0586-0) contains supplementary material, which is available to authorized users.

To address limitations of observational epidemiology studies of air pollution and health effects, including residual confounding by temporal and spatial factors, several studies have taken advantage of ‘natural experiments’, where an environmental policy or air quality intervention has resulted in reductions in ambient air pollution concentrations. Researchers have examined whether the population impacted by these air quality improvements, also experienced improvements in various health indices (e.g. reduced morbidity/mortality). In this paper, I review key accountability studies done previously and new studies done over the past several years in Beijing, Atlanta, London, Ireland, and other locations, describing study design and analysis strengths and limitations of each. As new ‘natural experiment’ opportunities arise, several lessons learned from these studies should be applied when planning a new accountability study. Comparison of health outcomes during the intervention to both before and after the intervention in the population of interest, as well as use of a control population to assess whether any temporal changes in the population of interest were also seen in populations not impacted by air quality improvements, should aid in minimizing residual confounding by these long term time trends. Use of either detailed health records for a population, or prospectively collected data on relevant mechanistic biomarkers coupled with such morbidity/mortality data may provide a more thorough assessment of if the intervention beneficially impacted the health of the community, and if so by what mechanism(s). Further, prospective measurement of a large suite of air pollutants may allow a more thorough understanding of what pollutant source(s) is/are responsible for any health benefit observed. The importance of using multiple statistical analysis methods in each paper and the difference in how the timing of the air pollution/outcome association may impact which of these design features is most important is also discussed. Based on these and other lessons learned, researchers may provide a more epidemiologically rigorous evaluation of cause-specific health impacts of an air quality intervention or action. Keywords: Air pollution, Epidemiology, Accountability, Natural experiment, Confounding

Background: Previous studies suggest that pathways reducing oxidative stress may have a protective effect against adverse cardiac responses associated with ambient PM. However, few studies have directly assessed total antioxidant capacity (TAC) as a potential effect modifier of cardiac responses to increased ambient PM. Objectives: We examined if TAC modifies the association between ambient PM and markers of heart rate variability (HRV), repolarization, systemic inflammation, and systolic blood pressure (SBP) in post-infarction patients. Methods: We recruited 76 patients with a recent coronary event (myocardial infarction or unstable angina) who participated in a cardiac rehabilitation program from June 2006 to November 2009 in Rochester, New York. Ambient fine particle (PM2.5,≤2.5 μm in aerodynamic diameter), accumulation mode particle (AMP, 100-500 nm) and ultrafine particle (UFP, 10-100 nm) concentrations were measured continuously by fixed-site monitors. Markers of HRV and repolarization were measured by continuous Holter electrocardiogram (ECG) recordings before and during exercise sessions of the rehabilitation program. Blood pressure was measured and venous blood samples were collected before exercise to measure TAC and inflammation markers. We applied linear mixed models to assess changes in markers of HRV, repolarization, systemic inflammation, and SBP associated with increased PM concentrations in the low, medium and high TAC tertile groups, after adjusting for covariates including temperature, calendar time since the beginning of the study, visit number, month of year, and hour of day. Results: Based on subject-visits with available TAC, we observed increases in SBP, C-reactive protein, and fibrinogen, and decreases in rMSSD (square root of the mean of the sum of the squared differences between adjacent normal to normal intervals) and SDNN (standard deviation of normal to normal beat intervals) associated with increased PM2.5, AMP and UFP in the previous 6-120 h (e.g. change in SBP associated with each interquartile range (IQR) increase in PM2.5 lagged 0-5 h was 1.27 mmHg [95%CI: 0.09, 2.46 mmHg]). However, we did not observe a consistent pattern of effect measure modification by TAC for any combination of pollutant and outcome (e.g. changes in SBP associated with each IQR increase in PM2.5 lagged 0-5 h for the low, medium and high TAC tertile groups were 1.93 mmHg [95%CI: 0.23, 3.63 mmHg], -0.31 mmHg [95%CI: -2.62, 2.01 mmHg], and 1.29 mmHg [95%CI: -0.64, 3.21 mmHg], respectively. P for interaction=0.28). Conclusions: In a post-infarction population, total antioxidant capacity does not appear to modify the association between biomarkers of heart rate variability, repolarization, systemic inflammation, and systolic blood pressure and ambient PM concentrations in the previous 6-120 h.

Selective serotonin reuptake inhibitors (SSRIs), a class of antidepressants, were found to increase central nervous system (CNS) metastasis in mice. Our study investigated in humans whether antidepressants, and specifically SSRIs, increased the relative odds of CNS metastasis. We identified 189 cases of CNS metastasis amongst breast cancer, melanoma, and non-Hodgkin lymphoma subjects who were diagnosed with CNS metastasis or infiltration between January 1, 2005 and September 30, 2013 and 756 controls (patients without CNS metastasis or infiltration). Using logistic regression, we estimated the relative odds of CNS metastasis associated with antidepressant use adjusting for relevant covariates. The prevalence of antidepressants was 28.6 % in cases and 27.5 % in controls, whereas SSRIs were used in 16.9 % of cases and 17.3 % of controls. Among all patients, antidepressants were not associated with CNS metastasis or infiltration. No consistent patterns of association were observed in the analyses of other cancer subsets or exposure measures, with the possible exception of an increased risk of CNS metastasis associated with 'any SSRI use' among breast cancer patients (OR = 1.73, 95 % CI = 0.75, 4.04). We did not observe clear patterns of association, which may be due in part to the small sample size in many of our analyses.

Land use regression modeling (LUR) through local scale circular modeling domains has been used to predict traffic-related air pollution such as nitrogen oxides (NOX). LUR modeling for fine particulate matters (PM), which generally have smaller spatial gradients than NOX, has been typically applied for studies involving multiple study regions. To increase the spatial coverage for fine PM and key constituent concentrations, we designed a mobile monitoring network in Monroe County, New York to measure pollutant concentrations of black carbon (BC, wavelength at 880 nm), ultraviolet black carbon (UVBC, wavelength at 3700 nm) and Delta-C (the difference between the UVBC and BC concentrations) using the Clarkson University Mobile Air Pollution Monitoring Laboratory (MAPL). A Deletion/Substitution/Addition (D/S/A) algorithm was conducted, which used circular buffers as a basis for statistics. The algorithm maximizes the prediction accuracy for locations without measurements using the V-fold cross-validation technique, and it reduces overfitting compared to other approaches. We found that the D/S/A LUR modeling approach could achieve good results, with prediction powers of 60%, 63%, and 61%, respectively, for BC, UVBC, and Delta-C. The advantage of mobile monitoring is that it can monitor pollutant concentrations at hundreds of spatial points in a region, rather than the typical less than 100 points from a fixed site saturation monitoring network. This research indicates that a mobile saturation sampling network, when combined with proper modeling techniques, can uncover small area variations (e.g., 10 m) in particulate matter concentrations.

Background Perchlorate and similar anions compete with iodine for uptake into the thyroid by the sodium iodide symporter (NIS). This may restrict fetal growth via impaired thyroid hormone production. Methods We collected urine samples from 107 pregnant women and used linear regression to estimate differences in newborn size and gestational age associated with increases in perchlorate, thiocyanate, nitrate, and perchlorate equivalence concentrations (PEC; measure of total NIS inhibitor exposure). Results NIS inhibitor concentrations were not associated with newborn weight, length, or gestational age. Each 2.62 ng/μg creatinine increase in perchlorate was associated with smaller head circumference (0.32 cm; 95% CI: −0.66, 0.01), but each 3.38 ng/μg increase in PEC was associated with larger head circumference (0.48 cm; −0.01, 0.97). Conclusions These anions may have effects on fetal development (e.g. neurocognitive) that are not reflected in gross measures. Future research should focus on other abnormalities in neonates exposed to NIS inhibitors.

Using a quasi-experimental opportunity offered by greatly restricted air pollution emissions during the Beijing Olympics compared to before and after the Olympics, we conducted the current study to compare ultrafine particles (UFPs) and fine particles (PM2.5) in their associations with biomarkers reflecting multiple pathophysiological pathways linking exposure and cardiorespiratory events. Number concentrations of particles (13.0-764.7 nm) and mass concentrations of PM2.5 were measured at two locations within 9 km from the residence and workplace of 125 participating Beijing residents. Each participant was measured 6 times for biomarkers of autonomic function (heart rate, systolic and diastolic blood pressures), hemostasis (von Willebrand factor, soluble CD40 ligand, and P-selectin), pulmonary inflammation and oxidative stress (exhaled nitric oxide and exhaled breath condensate pH, malondialdehyde, and nitrite), and systemic inflammation and oxidative stress (urinary malondialdehyde and 8-hydroxy-2'-deoxyguanosine, plasma fibrinogen, and white blood cells). Linear mixed models were used to estimate associations of biomarkers with UFPs and PM2.5 measured 1-7 days prior to biomarker measurements (lags). We found that the correlation coefficient for UFPs at two locations (∼ 9 km apart) was 0.45, and at the same location, the correlation coefficient for PM2.5 vs UFPs was -0.18. Changes in biomarker levels associated with increases in UFPs and PM2.5 were comparable in magnitude. However, associations of certain biomarkers with UFPs had different lag patterns compared to those with PM2.5, suggesting that the ultrafine size fraction (≤ 100 nm) and the fine size fraction (∼ 100 nm to 2.5 μm) of PM2.5 are likely to affect PM-induced pathophysiological pathways independently.

Anti-platelet medications may be less efficacious in certain clinical contexts. Recent studies suggest the need for a gender-specific, personalized approach to anti-platelet therapy. Our goal was to determine whether platelets from women and men activate differently in health and following

Objectives Increased air pollutant concentrations have been linked to several asthma-related outcomes in children, including respiratory symptoms, medication use, and hospital visits. However, few studies have examined effects of ultrafine particles in a pediatric population. Our primary objective was to examine the effects of ambient concentrations of ultrafine particles on asthma exacerbation among urban children and determine whether consistent treatment with inhaled corticosteroids could attenuate these effects. We also explored the relationship between asthma exacerbation and ambient concentrations of accumulation mode particles, fine particles (≤2.5 micrograms [μm]; PM 2.5 ), carbon monoxide, sulfur dioxide, and ozone. We hypothesized that increased 1–7 day concentrations of ultrafine particles and other pollutants would be associated with increases in the relative odds of an asthma exacerbation, but that this increase in risk would be attenuated among children receiving school-based corticosteroid therapy. Methods We conducted a pilot study using data from 3 to 10 year-old children participating in the School-Based Asthma Therapy trial. Using a time-stratified case-crossover design and conditional logistic regression, we estimated the relative odds of a pediatric asthma visit treated with prednisone ( n =96 visits among 74 children) associated with increased pollutant concentrations in the previous 7 days. We re-ran these analyses separately for children receiving medications through the school-based intervention and children in a usual care control group. Results Interquartile range increases in ultrafine particles and carbon monoxide concentrations in the previous 7 days were associated with increases in the relative odds of a pediatric asthma visit, with the largest increases observed for 4-day mean ultrafine particles (interquartile range=2088 p/cm 3 ; OR=1.27; 95% CI=0.90–1.79) and 7-day mean carbon monoxide (interquartile range=0.17 ppm; OR=1.63; 95% CI=1.03–2.59). Relative odds estimates were larger among children receiving school-based inhaled corticosteroid treatment. We observed no such associations with accumulation mode particles, black carbon, fine particles (≤2.5 μm), or sulfur dioxide. Ozone concentrations were inversely associated with the relative odds of a pediatric asthma visit. Conclusions These findings suggest a response to markers of traffic pollution among urban asthmatic children. Effects were strongest among children receiving preventive medications through school, suggesting that this group of children was particularly sensitive to environmental triggers. Medication adherence alone may be insufficient to protect the most vulnerable from environmental asthma triggers. However, further research is necessary to confirm this finding.

Central-site monitors do not account for factors such as outdoor-to-indoor transport and human activity patterns that influence personal exposures to ambient fine-particulate matter (PM(2.5)). We describe and compare different ambient PM(2.5) exposure estimation approaches that incorporate human activity patterns and time-resolved location-specific particle penetration and persistence indoors. Four approaches were used to estimate exposures to ambient PM(2.5) for application to the New Jersey Triggering of Myocardial Infarction Study. These include: Tier 1, central-site PM(2.5) mass; Tier 2A, the Stochastic Human Exposure and Dose Simulation (SHEDS) model using literature-based air exchange rates (AERs); Tier 2B, the Lawrence Berkeley National Laboratory (LBNL) Aerosol Penetration and Persistence (APP) and Infiltration models; and Tier 3, the SHEDS model where AERs were estimated using the LBNL Infiltration model. Mean exposure estimates from Tier 2A, 2B, and 3 exposure modeling approaches were lower than Tier 1 central-site PM(2.5) mass. Tier 2A estimates differed by season but not across the seven monitoring areas. Tier 2B and 3 geographical patterns appeared to be driven by AERs, while seasonal patterns appeared to be due to variations in PM composition and time activity patterns. These model results demonstrate heterogeneity in exposures that are not captured by the central-site monitor.

Rationale: Unprecedented pollution control actions during the Beijing Olympics provided a quasi-experimental opportunity to examine biologic responses to drastic changes in air pollution levels.Objectives: To determine whether changes in levels of biomarkers reflecting pulmonary inflammation and pulmonary and systemic oxidative stress were associated with changes in air pollution levels in healthy young adults.Methods: We measured fractional exhaled nitric oxide, a number of exhaled breath condensate markers (H+, nitrite, nitrate, and 8-isoprostane), and urinary 8-hydroxy-2-deoxyguanosine in 125 participants twice in each of the pre- (high pollution), during- (low pollution), and post-Olympic (high pollution) periods. We measured concentrations of air pollutants near where the participants lived and worked. We used mixed-effects models to estimate changes in biomarker levels across the three periods and to examine whether changes in biomarker levels were associated with changes in pollutant concentrations...

Background: Mechanisms underlying previously reported air pollution and cardiovascular (CV) morbidity associations remain poorly understood. Objectives: We examined associations between markers of pathways thought to underlie these air pollution and CV associations and ambient particle concentrations in postinfarction patients. Methods: We studied 76 patients, from June 2006 to November 2009, who participated in a 10-week cardiac rehabilitation program following a recent (within 3 months) myocardial infarction or unstable angina. Ambient ultrafine particle (UFP; 10–100 nm), accumulation mode particle (AMP; 100–500 nm), and fine particle concentrations (PM2.5; ≤ 2.5 μm in aerodynamic diameter) were monitored continuously. Continuous Holter electrocardiogram (ECG) recordings were made before and during supervised, graded, twice weekly, exercise sessions. A venous blood sample was collected and blood pressure was measured before sessions. Results: Using mixed effects models, we observed adverse changes in rMSSD [square root of the mean of the sum of the squared differences between adjacent normal-to-normal (NN) intervals], SDNN (standard deviation of all NN beat intervals), TpTe (time from peak to end of T-wave), heart rate turbulence, systolic and diastolic blood pressures, C-reactive protein, and fibrinogen associated with interquartile range increases in UFP, AMP, and PM2.5 at 1 or more lag times within the previous 5 days. Exposures were not associated with MeanNN, heart-rate–corrected QT interval duration (QTc), deceleration capacity, and white blood cell count was not associated with UFP, AMP, and PM2.5 at any lag time. Conclusions: In cardiac rehabilitation patients, particles were associated with subclinical decreases in parasympathetic modulation, prolongation of late repolarization duration, increased blood pressure, and systemic inflammation. It is possible that such changes could increase the risk of CV events in this susceptible population.

The purpose of this study was to examine the trends in the rates of stillbirth by race and ethnicity and to determine the risk factors of stillbirth.We used New Jersey data (1997-2005) for live births and fetal deaths. Cox proportional hazards model was used to estimate the risk of stillbirth associated with maternal risk factors and pregnancy complications.The rate of stillbirth was 4.4/1000 total births (3.4 for white and 7.9 for black non-Hispanics and 4.4 for Hispanics/1000 total births). The rates of stillbirth decreased from 3.8 in 1997 to 2.7/1000 total births in 2005 for white non-Hispanics but remained unchanged for other race/ethnicity groups. Adjusted relative risks for the risk factors associated with stillbirth were 1.3 (95% CI, 1.2-1.4) for maternal age ≥ 35 years, 1.9 (95% CI, 1.7-2.1) for black non-Hispanics, 2.8 (95% CI, 2.4-3.3) for no prenatal care, 40.2 (95% CI, 36.9-43.9) for placental abruption, 5.3 (95% CI, 3.4-8.2) for eclampsia, 3.5 (95% CI, 2.8-4.3) for diabetes mellitus and 1.7 (95% CI, 1.3-2.2) for preeclampsia.There was a decline in the rate of stillbirth but there were persistent racial disparities with the highest rates of stillbirth for black non-Hispanics.

International audience; BACKGROUND: The findings of prior studies of air pollution effects on adverse birth outcomes are difficult to synthesize because of differences in study design. OBJECTIVES: The International Collaboration on Air Pollution and Pregnancy Outcomes was formed to understand how differences in research methods contribute to variations in findings. We initiated a feasibility study to a) assess the ability of geographically diverse research groups to analyze their data sets using a common protocol and b) perform location-specific analyses of air pollution effects on birth weight using a standardized statistical approach. METHODS: Fourteen research groups from nine countries participated. We developed a protocol to estimate odds ratios (ORs) for the association between particulate matter ≤ 10 μm in aerodynamic diameter (PM₁₀) and low birth weight (LBW) among term births, adjusted first for socioeconomic status (SES) and second for additional location-specific variables. RESULTS: Among locations with data for the PM₁₀ analysis, ORs estimating the relative risk of term LBW associated with a 10-μg/m³ increase in average PM₁₀ concentration during pregnancy, adjusted for SES, ranged from 0.63 [95% confidence interval (CI), 0.30-1.35] for the Netherlands to 1.15 (95% CI, 0.61-2.18) for Vancouver, with six research groups reporting statistically significant adverse associations. We found evidence of statistically significant heterogeneity in estimated effects among locations. CONCLUSIONS: Variability in PM₁₀-LBW relationships among study locations remained despite use of a common statistical approach. A more detailed meta-analysis and use of more complex protocols for future analysis may uncover reasons for heterogeneity across locations. However, our findings confirm the potential for a diverse group of researchers to analyze their data in a standardized way to improve understanding of air pollution effects on birth outcomes.

Background Epidemiologic studies consistently demonstrate an association between acute cardiopulmonary events and changes in air pollution; however, the mechanisms that underlie these associations are not completely understood. Oxidative stress and inflammation have been suggested to play a role in human responses to air pollution. The proteasome is an intracellular protein degradation system linked to both of these processes and may help mediate air pollution effects. Objectives In these studies, we determined whether acute experimental exposure to two different aerosols altered white blood cell (WBC) or red blood cell (RBC) proteasome activity in human subjects. One aerosol was fresh diesel exhaust (DE), and the other freshly generated secondary organic aerosol (SOA). Methods Thirty-eight healthy subjects underwent 2-hr resting inhalation exposures to DE and separate exposures to clean air (CA); 26 subjects were exposed to DE, CA, and SOA. CA responses were subtracted from DE or SOA responses, and mixed linear models with F-tests were used to test the effect of exposure to each aerosol on WBC and RBC proteasome activity. Results WBC proteasome activity was reduced 8% (p = 0.04) after exposure to either DE or SOA and decreased by 11.5% (p = 0.03) when SOA was analyzed alone. RBCs showed similar 8–10% declines in proteasome activity (p = 0.05 for DE alone). Conclusions Air pollution produces oxidative stress and inflammation in many experimental models, including humans. Two experimental aerosols caused rapid declines in proteasome activity in peripheral blood cells, supporting a key role for the proteasome in acute human responses to air pollution.

Background Skin cancer is the most common of all cancers and a public health concern of increasing magnitude in the U.S. Purpose A mid-year review of Healthy People 2010 found that the percentage of adults engaging in sun-safe practices increased from 59% in 2000 to 71% in 2005. This paper examines whether this increase in sun-safe practices in adults is an artifact caused by the change from 2000 to 2005 in the operational definition of "sun-safe practices" in the National Health Interview Survey (NHIS). Methods This study analyzed the 2000 and 2005 NHIS data sets in 2009 to examine changes in sun-safe practice prevalence estimates and to estimate the relative odds of practicing sun-safe behaviors associated with gender, age, race/ethnicity, education, and geographic region. Results Contrary to the Healthy People 2010 mid-year review, it was found that engaging in sun-safe practices by adults decreased from 59% (2000) to 55% (2005). A question order effect and use of images for use of sun-safe hats likely caused an artificial change in "cover-up" behavior estimates from 31% (2000) to 18% (2005) and wide-brim hat usage from 27% (2000) to 12% (2005). When eliminating data from these two questions added in 2005, the relative odds of practicing sun-safe behaviors was significantly lower for men in both 2000 and 2005 but were not different for other demographic characteristics. Conclusions The current analyses suggest that the increase in sun-safe behaviors in adults and a notable decrease in "hat use" may be due to methodologic artifacts. When operational definitions change, caution should be used in interpreting estimates over time.

Most previous studies (D’Ippoliti et al. 2003; Peters et al. 2001, 2005; Pope et al. 2006; Zanobetti and Schwartz 2005), but not all (Sullivan et al. 2005), that have investigated the triggering of myocardial infarction (MI) by particulate matter (PM) air pollution concentrations in the hours and days before MI onset have reported an association. Other studies have reported increased mortality due to MI or increased mortality or cardiovascular admissions among MI survivors associated with increases in PM over the previous few days (Braga et al. 2001; von Klot et al. 2005; Zanobetti and Schwartz 2007). Several studies have investigated whether certain subgroups are particularly susceptible and have reported increased cardiovascular effects among those with diabetes (Dubowsky et al. 2006; Goldberg et al. 2001; Liu et al. 2007; O’Neill et al. 2005; Zanobetti and Schwartz 2002) and among patients with chronic obstructive pulmonary disease (COPD) (Naess et al. 2007; Zanobetti and Schwartz 2005; Zanobetti et al. 2000). However, Zanobetti and Schwartz (2005) reported increased susceptibility among patients with COPD but not among persons with diabetes. Numerous researchers have reported that the percentage of infarctions that are nontransmural has been increasing (Goff et al. 2000; Hellermann et al. 2003; Kostis et al. 2007; Myerson et al. 2009; Roger et al. 2006, 2010; Rogers et al. 2008). More recently, Shao (2008) noted a similar secular trend in clinical presentation of MI to emergency departments (EDs) in New Jersey. In short, 72% of persons admitted to hospitals in New Jersey from 1990 through 1992 for MI had had transmural infarctions, and only 28% had had nontransmural infarctions. Since then, however, this pattern has reversed. From 2002 through 2004, most of the admissions for MI were for nontransmural infarctions (63%), with only 37% for transmural infarctions (Shao 2008). These changes may be due in part to improvements in preventive pharmacotherapies (statins, beta blockers, aspirin), interventional procedures [angioplasty, coronary artery bypass graft (CABG)], more sensitive diagnostic tests (troponins), and treatment of the MI upon ED arrival (reperfusion therapy, increased use of antiplatelet agents). It has not been reported whether PM with aerodynamic diameter ≤ 2.5 μm (PM2.5) triggers all infarctions, whether PM–MI associations differ in magnitude, or whether these associations are restricted to PM–transmural or PM–nontransmural infarctions alone. Such investigations may provide insight into the mechanisms by which PM may trigger cardiovascular events. Using the same data as Shao (2008), we attempted to replicate, in New Jersey, previous MI–PM2.5 studies that were conducted in other U.S. and European cities. We hypothesized that increases in mean PM2.5 concentration on the same day and a few days before ED arrival for MI may be associated with increased risk of MI and that these effect estimates would be greater for persons with diabetes and those with COPD than for individuals without these conditions. Further, we explored whether there were differences in risks associated with increases in ambient PM2.5 concentration between transmural and nontransmural infarctions.

Ambient air pollution has been linked to cardiovascular and respiratory morbidity and mortality in epidemiology studies. Frequently, oxidative and nitrosative stress are hypothesized to mediate these pollution effects, however precise mechanisms remain unclear. This paper describes the methodology for a major panel study to examine air pollution effects on these and other mechanistic pathways. The study took place during the drastic air pollution changes accompanying the 2008 Olympics in Beijing, China. After a general description of air pollution health effects, we provide a discussion of panel studies and describe the unique features of this study that make it likely to provide compelling results. This study should lead to a clearer and more precise definition of the role of oxidative and nitrosative stress, as well as other mechanisms, in determining acute morbidity and mortality from air pollution exposure.

Perchlorate is a commonly occurring environmental toxicant that may be transported across the placental barrier by the sodium-iodide symporter (NIS), possibly resulting in both increased perchlorate exposure and decreased iodide uptake by the fetus. Therefore, we measured levels of three physiologically relevant NIS-inhibitors (perchlorate, nitrate, and thiocyanate) and iodide in maternal and fetal fluids collected during cesarean-section surgeries on 150 U.S. women. Geometric means of perchlorate, thiocyanate, and nitrate levels in maternal urine (2.90, 947, and 47900 microg/L, respectively) were similar to previously published results, while urinary iodide levels (1420 microg/L) were significantly higher (p < 0.0001), likely because of prevalent prenatal vitamin use in the study population (74%). Thiocyanate levels were higher in the maternal serum, cord serum, and amniotic fluid of smokers compared to women with environmental tobacco smoke exposure and nonsmokers (p-values of 0.0006, 0.0011, and 0.0026, respectively). Perchlorate was detected in most samples: urine (100%), maternal serum (94%), cord serum (67%), and amniotic fluid (97%). Maternal urinary perchlorate levels were positively correlated with perchlorate levels in amniotic fluid (r = 0.57), indicating that maternal urine perchlorate is an effective biomarker of fetal perchlorate exposure. Maternal serum perchlorate was generally higher than cord serum perchlorate (median ratio 2.4:1 for paired samples), and maternal urine perchlorate was always higher than fetal amniotic fluid perchlorate levels (mean ratio 22:1); conversely, iodide levels were typically higher in fetal fluids compared to maternal fluids. We found no evidence of either disproportionate perchlorate accumulation or lack of iodide in the fetal compartment. In this panel of healthy infants, we found no association between cord blood levels of these anions and newborn weight length, and head circumference.

Objectives We explored the association between acute changes in daily mean pulmonary artery (PA) and right ventricular (RV) pressures and concentrations of ambient fine particulate matter [PM with aerodynamic diameter ≤2.5 μm (PM2.5)] as an explanation for previous associations between congestive heart failure (HF) hospital admissions and PM. Materials and methods In the Chronicle Offers Management to Patients with Advanced Signs and Symptoms of Heart Failure (COMPASS-HF) trial, to see whether management of ambulatory HF could be improved by providing continuous right heart pressure monitoring to physicians, the Chronicle Implantable Hemodynamic Monitor (Medtronic, Inc., Minneapolis, MN, USA) continuously measured multiple right heart hemodynamic parameters, heart rate, and activity trends in subjects with moderate/severe HF. Using these trial data, we calculated daily mean pressures, using only those time intervals where the subject was not physically active (n = 5,807 person-days; n = 11 subjects). We then studied the association between mean daily PA/RV pressures and mean ambient PM2.5 concentrations on the same day and previous 6 days. Results Each 11.62-μg/m3 increase in same-day mean PM2.5 concentration was associated with small but significant increases in estimated PA diastolic pressure [0.19 mmHg; 95% confidence interval (CI), 0.05–0.33] and RV diastolic pressure (0.23 mmHg; 95% CI, 0.11–0.34). Although we saw considerable differences in the magnitude of response by COMPASS-HF randomization group (total data access for physicians vs. blocked clinician access), season, left ventricular ejection fraction, and obesity, these effects were not significantly different. Conclusions These pilot study findings provide a potential mechanism for previous findings of increased risk of HF associated with ambient PM. However, because of the small number of subjects, a larger study is needed for confirmation.

Background and Purpose— Residence in the Southeastern United States (US) has been linked to increased stroke incidence and mortality. However, data on regional variability in overall cardiovascular disease (CVD) and specific coronary heart disease incidence are sparse. Methods— We assessed the risk of major CVD (nonfatal stroke, nonfatal myocardial infarction, or death from CVD) and specific CVD associated with region of residence (Northeast, Southeast, Midwest, and West) in 17 927 apparently healthy male participants of the Physicians’ Health Study. Subjects were aged 40 to 84, most were white (93%), and had no previous CVD at baseline. We used residence in the Northeast as the reference group and proportional hazards models to adjust for potential confounding. Results— We found no difference in risk of major CVD between regions of residence. Further, we found no consistent association between myocardial infarction and CVD death and region of residence. In contrast, we found a significantly increased risk of total stroke (HR, 1.22; 95% CI, 1.02 to 1.47) associated with residence in the Southeast compared with the Northeast. This relative risk was further increased for ischemic stroke (HR, 1.30; 95% CI, 1.06 to 1.58). We saw no difference in risk of any outcome when categorizing state of residence into tertiles based on mean winter temperature, mean summer temperature, or into 2 groups based on latitude. Conclusions— In this homogenous and well-characterized cohort of US male physicians, we found greater incidence of ischemic stroke, but not other vascular event s among those living in the Southeastern US, compared with other regions.

Objectives: We reported previously that 24-hr moving average ambient air pollution concentrations were positively associated with ventricular arrhythmias detected by implantable cardioverter defibrillators (ICDs). ICDs also detect paroxysmal atrial fibrillation episodes (PAF) that result in rapid ventricular rates. In this same cohort of ICD patients, we assessed the association between ambient air pollution and episodes of PAF. Design: We performed a case–crossover study. Participants: Patients who lived in the Boston, Massachusetts, metropolitan area and who had ICDs implanted between June 1995 and December 1999 (n = 203) were followed until July 2002. Evaluations/Measurements: We used conditional logistic regression to explore the association between community air pollution and 91 electrophysiologist-confirmed episodes of PAF among 29 subjects. Results: We found a statistically significant positive association between episodes of PAF and increased ozone concentration (22 ppb) in the hour before the arrhythmia (odds ratio = 2.08; 95% confidence interval = 1.22, 3.54; p = 0.001). The risk estimate for a longer (24-hr) moving average was smaller, thus suggesting an immediate effect. Positive but not statistically significant risks were associated with fine particles, nitrogen dioxide, and black carbon. Conclusions: Increased ambient O3 pollution was associated with increased risk of episodes of rapid ventricular response due to PAF, thereby suggesting that community air pollution may be a precipitant of these events.

The authors evaluated the association between ventricular arrhythmias detected by implantable cardioverter defibrillators and ambient air pollution concentrations in the hours immediately before the arrhythmia. Patients given implantable cardioverter defibrillators at the New England Medical Center in Boston, Massachusetts, between mid-1995 and 1999 who lived within 40 km of a central monitoring site (n = 203) were followed until July 2002. The authors used a case-crossover design to study the association between ambient air pollution and up to 798 confirmed ventricular arrhythmias among 84 subjects. The authors found that interquartile range increases in 24-hour moving average particulate matter less than 2.5 mum in aerodynamic diameter and ozone were associated with 19% and 21% increased risks of ventricular arrhythmia, respectively. For each, there was evidence of a linear exposure response, and the associations appeared independent. These associations were stronger than associations with mean concentrations on the same calendar day and previous calendar days. The authors did not find associations with pollutant concentrations less than 24 hours before the arrhythmia. Cases with a prior ventricular arrhythmia within 72 hours had greater risk associated with air pollutants than did cases without a recent arrhythmia. These results confirm previous findings and suggest that matching of pollution periods to arrhythmias is important in detecting such associations.

Epidemiologic studies have demonstrated a consistent link between sudden cardiac deaths and particulate air pollution. We used implanted cardioverter defibrillator (ICD) records of ventricular tachyarrhythmias to assess the role of air pollution as a trigger of these potentially life-threatening events. The study cohort consisted of 203 cardiac patients with ICD devices in the Boston metropolitan area who were followed for an average of 3.1 years between 1995 and 2002. Fine particle mass and gaseous air pollution plus temperature and relative humidity were measured on almost all days, and black carbon, sulfate, and particle number on a subset of days. Date, time, and intracardiac electrograms of ICD-detected arrhythmias were downloaded at the patients' regular follow-up visits (about every 3 months). Ventricular tachyarrhythmias were identified by electrophysiologist review. Risk of ventricular arrhythmias associated with air pollution was estimated with logistic regression, adjusting for season, temperature, relative humidity, day of the week, patient, and a recent prior arrhythmia. We found increased risks of ventricular arrhythmias associated with 2-day mean exposure for all air pollutants considered, although these associations were not statistically significant. We found statistically significant associations between air pollution and ventricular arrhythmias for episodes within 3 days of a previous arrhythmia. The associations of ventricular tachyarrhythmias with fine particle mass, carbon monoxide, nitrogen dioxide, and black carbon suggest a link with motor vehicle pollutants. The associations with sulfate suggest a link with stationary fossil fuel combustion sources.

Five methods of sampling lead-contaminated dust on carpets were evaluated and compared in 33 New Jersey homes of children with elevated blood lead levels. The five sampling methods were (1) wipe, (2) adhesive label, (3) C18 sheet, (4) vacuum, and (5) hand rinse. Samples were collected side by side on the same carpets within the homes. Among the five methods the wipe and vacuum methods showed high percentages of detectable samples, good reproducibility, and significant correlations with other methods. C18 sheets and adhesive labels collected the least quantity of lead dust, with high percentages of undetectable samples. Because of the limited ability of sampling lead on carpets and the relatively high cost for laboratory analysis, C18 sheets or adhesive labels are not considered feasible sampling techniques. The hand rinse method also was not feasible for carpet sampling, because it was difficult to conduct in the field and laboratory, and it was subject to inconsistency and cross contamination. Wipes, which collected lead dust from carpet surfaces, were believed to be the most appropriate method for measuring lead from carpets accessible to children. However, because of the low pickup from carpets, wipes may not be an appropriate measuring tool to assess the levels of total lead contamination in carpets. The authors recommend using surface wipe sampling to measure accessible lead from carpets for exposure assessment, and vacuum sampling to obtain the information on total lead accumulation.

High-efficiency particulate air (HEPA) filtered vacuum cleaners are recommended by the U.S. Department of Housing and Urban Development for cleaning lead-contaminated house dust. We performed a randomized field study to determine whether a conventional (non-HEPA) vacuum cleaner could achieve cleaning results comparable with those of a HEPA vacuum cleaner. We compared the lead loading reductions of these two vacuum cleaners in a total of 127 New Jersey homes of lead-exposed children. We used wet towelettes and a vacuum sampler to collect lead dust from carpets and upholstery before and after vacuum cleaning. The vacuum sampling data showed that the HEPA and non-HEPA vacuum cleaners resulted in 54.7% (p = 0.006) and 36.4% (p = 0.020) reductions in lead loading, respectively, when used on soiled carpets, although the overall difference in lead loading reduction between the two vacuum cleaners was not statistically significant (p = 0.293). The wipe sampling data did not show any significant lead loading reduction for either of the vacuum cleaners, suggesting that both vacuum cleaners fail to clean the surfaces of carpet effectively, considering that wipe sampling media simulate surface contact. On upholstery, the wipe sampling data showed a significant reduction in lead loading for the non-HEPA vacuum cleaner (22.2%, p = 0.047). Even with the significant reduction, the postcleaning lead loadings on upholstery were similar to those on carpets. The similar lead loading results for carpets and upholstery indicate that soiled upholstery may be as important a source of childhood lead exposure as carpets.

During the 1980s the Republic of Ireland experienced repeated severe pollution episodes. Domestic coal burning was a major source of this pollution. In 1990 the Irish government introduced a ban on the marketing, sale, and distribution of coal in Dublin. The ban was extended to Cork in 1995 and to 10 other communities in 1998 and 2000. We previously reported decreases in particulate black smoke (BS*) and sulfur dioxide (SO2) concentrations, measured as total gaseous acidity, in Dublin after the 1990 coal ban (Clancy et al. 2002). In the current study we explored and compared the effectiveness of the sequential 1990, 1995, and 1998 bans in reducing community air pollution and in improving public health. We compiled records of daily BS, total gaseous acidity (SO2), and counts of cause-specific deaths from 1981 to 2004 for Dublin County Borough (1990 ban), county Cork (1995 ban), and counties Limerick, Louth, Wexford, and Wicklow (1998 ban). We also compiled daily counts of hospital admissions for cardiovascular, respiratory, and digestive diagnoses for Cork County Borough (1991 to 2004) and counties Limerick, Louth, Wexford, and Wicklow (1993 to 2004). We compared pre-ban and post-ban BS and SO2 concentrations for each city. Using interrupted time-series methods, we estimated the change in cause-specific, directly standardized mortality rates in each city or county after the corresponding local coal ban. We regressed weekly age- and sex-standardized mortality rates against an indicator of the post- versus pre-ban period, adjusting for influenza epidemics, weekly mean temperature, and a season smooth of the standardized mortality rates in Coastal counties presumably not affected by the bans. We compared these results with similar analyses in Midlands counties also presumably unaffected by the bans. We also estimated the change in cause-specific, directly standardized, weekly hospital admissions rates normalized for underreporting in each city or county after the 1995 and 1998 bans, adjusting for influenza epidemics, weekly mean temperature, and local admissions for digestive diagnoses. Mean BS concentrations fell in all affected population centers post-ban compared with the pre-ban period, with decreases ranging from 4 to 35 microg/m3 (corresponding to reductions of 45% to 70%, respectively), but we observed no clear pattern in SO2 measured as total gaseous acidity associated with the bans. In comparisons with the pre-ban periods, no significant reduction was found in total death rates associated with the 1990 (1% reduction), 1995 (4% reduction), or 1998 (0% reduction) bans, nor for cardiovascular mortality (0%, 4%, and 1% reductions for the 1990, 1995, and 1998 bans, respectively). Respiratory mortality was reduced in association with the bans (17%, 9%, and 3%, respectively). We found a 4% decrease in hospital admissions for cardiovascular disease associated with the 1995 ban and a 3% decrease with the 1998 ban. Admissions for respiratory disease were not consistently lower after the bans; admissions for pneumonia, chronic obstructive pulmonary disease (COPD), and asthma were reduced. However, underreporting of hospital admissions data and lack of control and comparison series tempered our confidence in these results. The successive coal bans resulted in immediate and sustained decreases in particulate concentrations in each city or town; with the largest decreases in winter and during the heating season. The bans were associated with reductions in respiratory mortality but no detectable improvement in cardiovascular mortality. The changes in hospital admissions for respiratory and cardiovascular disease were supportive of these findings but cannot be considered confirming. Detecting changes in public health indicators associated even with clear improvements in air quality, as in this case, remains difficult when there are simultaneous secular improvements in the same health indicators.

Many epidemiologic studies of the health effects of exposure to ambient air pollution use measurements from central-site monitors as their exposure estimate. However, measurements from central-site monitors may lack the spatial and temporal resolution required to capture exposure variability in a study population, thus resulting in exposure error and biased estimates. Articles in this dedicated issue examine various approaches to predict or assign exposures to ambient pollutants. These methods include combining existing central-site pollution measurements with local- and/or regional-scale air quality models to create new or "hybrid" models for pollutant exposure estimates and using exposure models to account for factors such as infiltration of pollutants indoors and human activity patterns. Key findings from these articles are summarized to provide lessons learned and recommendations for additional research on improving exposure estimation approaches for future epidemiological studies. In summary, when compared with use of central-site monitoring data, the enhanced spatial resolution of air quality or exposure models can have an impact on resultant health effect estimates, especially for pollutants derived from local sources such as traffic (e.g., EC, CO, and NO(x)). In addition, the optimal exposure estimation approach also depends upon the epidemiological study design. We recommend that future research develops pollutant-specific infiltration data (including for PM species) and improves existing data on human time-activity patterns and exposure to local source (e.g., traffic), in order to enhance human exposure modeling estimates. We also recommend comparing how various approaches to exposure estimation characterize relationships between multiple pollutants in time and space and investigating the impact of improved exposure estimates in chronic health studies.

Five methods of sampling lead-contaminated dust on carpets were evaluated and compared in 33 New Jersey homes of children with elevated blood lead levels. The five sampling methods were (1) wipe, (2) adhesive label, (3) C18 sheet, (4) vacuum, and (5) hand rinse. Samples were collected side by side on the same carpets within the homes. Among the five methods the wipe and vacuum methods showed high percentages of detectable samples, good reproducibility, and significant correlations with other methods. C18 sheets and adhesive labels collected the least quantity of lead dust, with high percentages of undetectable samples. Because of the limited ability of sampling lead on carpets and the relatively high cost for laboratory analysis, C18 sheets or adhesive labels are not considered feasible sampling techniques. The hand rinse method also was not feasible for carpet sampling, because it was difficult to conduct in the field and laboratory, and it was subject to inconsistency and cross contamination. Wipes, which collected lead dust from carpet surfaces, were believed to be the most appropriate method for measuring lead from carpets accessible to children. However, because of the low pickup from carpets, wipes may not be an appropriate measuring tool to assess the levels of total lead contamination in carpets. The authors recommend using surface wipe sampling to measure accessible lead from carpets for exposure assessment, and vacuum sampling to obtain the information on total lead accumulation.

Comparability of dust lead measurements has been a difficult problem due to different sampling and analysis techniques. This paper compares two dust sampling techniques, the U.S. Department of Housing and Urban Development (HUD) dust wipe method and the Lioy, Wainman, Weisel (LWW) sampler. The HUD method specifies using a moist towelette to pick up as much dust as possible in a specified area and estimates total lead loading. The LWW sampler collects the dust on preweighed wetted filter media, and provides greater standardization of the sampling path and pressure applied. LWW samples were analyzed using inductively coupled plasma mass spectronomy (no samples below minimum detection limit), while HUD samples were analyzed using flame atomic absorption (32% of samples below minimum detection limit). A bootstrapping technique was used in the analysis to contend with those HUD samples below the minimum detection limit. Mixed model equations were generated to predict HUD values from LWW results, and to examine the effects of sampling location, time, and method. The results indicate that the two samplers performed similarly under field conditions, although the LWW sampler produced consistently lower lead loading estimates. LWW values that predicted HUD lead clearance values of 100 micrograms/ft2 for floors and 500 micrograms/ft2 for window sills were 72 micrograms/ft2 and 275 micrograms/ft2, respectively. To examine internal reproducibility, duplicate samples were taken using both the HUD and LWW methods. Correlation results within paired samples indicated a statistically significantly higher (p < 0.001) internal reproducibility for lead loading, for the LWW sampler (r = 0.87), than for the HUD method (r = 0.71). Some of the differences appeared to be related to the analytical methods.