Student Research: Carrie J. Fields

, , 2003
Faculty Advisor: Jane Q. Koenig

Measurement of PM2.5 Concentrations and Cardiorespiratory Health Effects in Adult Subjects


Abstract

This research measured exposure assessment and health effects in sixteen older adults in Seattle during the winter of 2002-2003. In the attempt to elucidate the role of PM2.5 in cardiopulmonary system changes, this study looked at specific cardiovascular endpoints, such as pulse rate and blood pressure, traditional pulmonary endpoints such as lung function, and more innovative pulmonary endpoints, such as exhaled nitric oxide (eNO) and 8-isoprostane analyses of breath condensate. Subjects were observed for twelve consecutive days, during the months of October to March, the wood-burning season. winter in Seattle typically has high levels of outdoor particulate matter and variations in temperature, so it is considered to be an ideal study period. Observations involved a daily visit to the subject's home to collect the health data and to collect indoor, outdoor and personal air pollution information. The subjects were asked to fill out morning and evening symptom diaries and a general daily activity log, and answered technician questions regarding exposure to particles from cooking, stove burning and environmental tobacco smoke. Indoor, outdoor, and personal air pollution levels were measured using three personal data recorders placed in the living area of the subject's home, outside of the subject's home, and on the subject's person.

Data were analyzed using a linear mixed effects model with random intercept, controlling for age, gender, height, weight, pulse, and outdoor temperature. This model was used to determine the association between the subject's daily health measures and daily PM2.5 air pollution levels. In the analysis of 164 samples from the 16 subjects with respiratory disease (COPD or asthma), a range of eNO levels from 0.5 to 60.6 ppb was seen (mean ± SD=17.4±10.8). Statistical analysis shows that a 10 µg/m3 increase in personal PM2.5 relevant to each subject session average was associated with a 5.1 ppb (95%Cl: 2.2, 8.1) increase in eNO (p=0.001). Also, a 10 µg/m3 increase in outdoor PM2.5 relative to each subject session average was associated with a 6.5 ppb (95%CL: 0.56, 12.5) increase in eNO (p=0.032). A 10 µg/m3 increase in outdoor PM2.5 relative to each subject session average was also associated with a 0.3 liter/second (95%Cl: 0.00, 0.7) increase in peak expiratory flow. For corticosteroid users, a 10 µg/m3 increase in personal PM2.5 relative to each subject session average was also associated with a 0.05 L (95%Cl: 0.005, 0.1) increase in FEV1 (p=0.028). A 10 µg/m3 increase in personal PM2.5 relative to each subject session average was also associated with a 0.07 L (95%CL: 0.01, 0.1) increase in FVC (p=0.012). A weak association (p=0.089) was seen between a 10 µg/m3 increase in personal PM2.5 relative to each subject session average and an 8.9 pg/ml (95%Cl: -1.3, 19.1) increase in 8-isoprostane. No other significant associations were seen between any of the three measures of air pollution and any health effects.