Statistical analysis of air pollution panel studies: an illustration.

PURPOSE: The panel study design is commonly used to evaluate the short-term health effects of air pollution. Standard statistical methods are available for analyzing longitudinal data, but the literature reveals that these methods are poorly understood by practitioners. METHODS: We review standard statistical methods for modeling longitudinal data. Marginal, conditional, and transitional approaches are reviewed and contrasted with respect to their parameter interpretation and methods for accounting for correlation and dealing with missing data. We also discuss techniques for controlling for time-dependent and time-independent confounding and for exploring and summarizing panel study data. Notes on available software are provided. RESULTS: These methods are illustrated by using data from the 1999 to 2002 Seattle Panel Study. CONCLUSIONS: The quality of statistical analyses and presentation of results of panel studies could be improved if the methods we present were followed.

A community study of the effect of particulate matter on blood measures of inflammation and thrombosis in an elderly population.

BACKGROUND: The mechanism behind the triggering effect of fine particulate matter (PM) air pollution on cardiovascular events remains elusive. We postulated that elevated levels of PM would be associated with increased blood levels of inflammatory and thrombotic markers in elderly individuals. We also hypothesized that elevated PM would increase levels of cytokines in individuals with heart disease. METHODS: We measured these blood markers in 47 elderly individuals with (23) and without (16 COPD and 8 healthy) cardiovascular disease (CVD) on 2 or 3 mornings over a 5 or 10-day period between February 2000 and March 2002. Blood measures were paired with residence level outdoor PM measured by nephelometry. Analyses determined the within-individual effect of 24-hour averaged outdoor PM on blood measures. RESULTS: Analyses found no statistically significant effect of a same day 10 ug/m3 increase in fine PM on log transformed levels of CRP 1.21 fold-rise [95% CI: 0.86, 1.70], fibrinogen 1.02 fold-rise [95% CI: 0.98, 1.06], or D-dimer 1.02 fold-rise [95% CI: 0.88, 1.17] in individuals with CVD. One-day lagged analyses in the CVD subgroup found similar null results. These same models found no change in these blood markers at the same-day or 1-day lag in the group without CVD. In 21 individuals with CVD, a 10 mug/m3 increase in same-day PM was associated with a 1.3 fold-rise [95% CI: 1.1, 1.7] in the level of monocyte chemoattractant protein-1. CONCLUSION: We did not find consistent effects of low ambient levels of PM on blood measures of inflammation or thrombosis in elderly individuals.

Long-term exposure to air pollution and incidence of cardiovascular events in women.

BACKGROUND: Fine particulate air pollution has been linked to cardiovascular disease, but previous studies have assessed only mortality and differences in exposure between cities. We examined the association of long-term exposure to particulate matter of less than 2.5 microm in aerodynamic diameter (PM2.5) with cardiovascular events. METHODS: We studied 65,893 postmenopausal women without previous cardiovascular disease in 36 U.S. metropolitan areas from 1994 to 1998, with a median follow-up of 6 years. We assessed the women's exposure to air pollutants using the monitor located nearest to each woman's residence. Hazard ratios were estimated for the first cardiovascular event, adjusting for age, race or ethnic group, smoking status, educational level, household income, body-mass index, and presence or absence of diabetes, hypertension, or hypercholesterolemia. RESULTS: A total of 1816 women had one or more fatal or nonfatal cardiovascular events, as confirmed by a review of medical records, including death from coronary heart disease or cerebrovascular disease, coronary revascularization, myocardial infarction, and stroke. In 2000, levels of PM2.5 exposure varied from 3.4 to 28.3 microg per cubic meter (mean, 13.5). Each increase of 10 microg per cubic meter was associated with a 24% increase in the risk of a cardiovascular event (hazard ratio, 1.24; 95% confidence interval [CI], 1.09 to 1.41) and a 76% increase in the risk of death from cardiovascular disease (hazard ratio, 1.76; 95% CI, 1.25 to 2.47). For cardiovascular events, the between-city effect appeared to be smaller than the within-city effect. The risk of cerebrovascular events was also associated with increased levels of PM2.5 (hazard ratio, 1.35; 95% CI, 1.08 to 1.68). CONCLUSIONS: Long-term exposure to fine particulate air pollution is associated with the incidence of cardiovascular disease and death among postmenopausal women. Exposure differences within cities are associated with the risk of cardiovascular disease.

Effect of particulate air pollution on lung function in adult and pediatric subjects in a Seattle panel study.

STUDY OBJECTIVE: To determine whether increased exposure to particulate matter air pollution (PM), measured with personal, residential, or central site monitoring, was associated with pulmonary function decrements in either adults with COPD or children with asthma. PARTICIPANTS: We studied 57 adults with or without COPD and 17 children aged 6 to 13 years with physician-diagnosed asthma in Seattle during a 3-year panel study. STUDY DESIGN AND MEASUREMENTS: Indoor and outdoor PM measurements were made at subjects' homes. The subjects wore personal exposure monitors for 10 consecutive 24-h periods, and PM was also measured at a central outdoor location. We assessed the within-subject effect of particulate exposure on FEV(1) and peak expiratory flow (PEF) in adults, and maximal midexpiratory flow (MMEF), PEF, FEV(1), and symptoms in children. RESULTS: FEV(1) decrements were associated with 1-day lagged central site PM

A case-crossover study of wintertime ambient air pollution and infant bronchiolitis.

UNLABELLED: We examined the association of infant bronchiolitis with acute exposure to ambient air pollutants. DESIGN: We employed a time-stratified case-crossover method and based the exposure windows on a priori, biologically based hypotheses. PARTICIPANTS: We evaluated effects in 19,901 infants in the South Coast Air Basin of California in 1995-2000 with a hospital discharge record for bronchiolitis in the first year of life (International Classification of Diseases, 9th Revision, CM466.1). EVALUATIONS/MEASUREMENTS: Study subjects' ZIP code was linked to ambient air pollution monitors to derive exposures. We estimated the risk of bronchiolitis hospitalization associated with increases in wintertime ambient air pollutants using conditional logistic regression. RESULTS: We observed no increased risk after acute exposure to particulate matter < or = 2.5 microm in aerodynamic diameter (PM2.5), carbon monoxide, or nitrogen dioxide. PM2.5 exposure models suggested a 26-41% increased risk in the most premature infants born at gestational ages between 25 and 29 weeks; however, these findings were based on very small numbers. CONCLUSIONS: We found little support for a link between acute increases in ambient air pollution and infant bronchiolitis except modestly increased risk for PM2.5 exposure among infants born very prematurely. In these infants, the periods of viral acquisition and incubation concurred with the time of increased risk. RELEVANCE TO PROFESSIONAL PRACTICE: We present novel data for the infant period and the key respiratory disease of infancy, bronchiolitis. Incompletely explained trends in rising bronchiolitis hospitalization rates and increasing number of infants born prematurely underscore the importance of evaluating the impact of ambient air pollution in this age group in other populations and studies.

Exhaled nitric oxide in children with asthma and short-term PM2.5 exposure in Seattle.

The objective of this study was to evaluate associations between short-term (hourly) exposures to particulate matter with aerodynamic diameters < 2.5 microm (PM2.5) and the fractional concentration of nitric oxide in exhaled breath (FE(NO) in children with asthma participating in an intensive panel study in Seattle, Washington. The exposure data were collected with tapered element oscillation microbalance (TEOM) PM2.5 monitors operated by the local air agency at three sites in the Seattle area. FE(NO) is a marker of airway inflammation and is elevated in individuals with asthma. Previously, we reported that offline measurements of FE(NO) are associated with 24-hr average PM2.5 in a panel of 19 children with asthma in Seattle. In the present study using the same children, we used a polynomial distributed lag model to assess the association between hourly lags in PM2.5 exposure and FE(NO) levels. Our model controlled for age, ambient NO levels, temperature, relative humidity, and modification by use of inhaled corticosteroids. We found that FE(NO) was associated with hourly averages of PM2.5 up to 10-12 hr after exposure. The sum of the coefficients for the lag times associated with PM2.5 in the distributed lag model was 7.0 ppm FE(NO). The single-lag-model FE(NO) effect was 6.9 [95% confidence interval (CI), 3.4 to 10.6 ppb] for a 1-hr lag, 6.3 (95% CI, 2.6 to 9.9 ppb ) for a 4-hr lag, and 0.5 (95% CI, -1.1 to 2.1 ppb) for an 8-hr lag. These data provide new information concerning the lag structure between PM2.5 exposure and a respiratory health outcome in children with asthma.